Course Code: NCM 106

 

CARE OF CLIENTS ACROSS THE LIFESSPAN WITH PROBLEMS IN INFLAMMATORY AND IMMUNOLOGIC

REACTIONS, CELLULAR ABERRATIONS, ACUTE BIOLOGIC CRISIS, INCLUDING EMERGENCY AND

DISASTER  NURSING

General Objective

 

Demonstrate comprehensive safe and effective nursing care utilizing the concepts of acute biologic

crisis

Risk  Assessment and Screening Procedures

 

Focus:

 

Standard assessment of the critically ill patients

focused history-taking

discriminating PE - airway, breathing circulation

 hemodynamics status 

 

Focus:

-results and implications of diagnostic/laboratory examinations

Acute biologic crisis/multiorgan problem

Non-invasive: ECG, cardiac rhythms,

Invasive: ABG, hemodynamic monitoring, CVP, pulmonary capillary wedge pressure (PCWP)

 

Focus:

 Concurrent Diseases in Pregnancy

 

 A. Cardiac Diseases

Right Sided Heart Failure

Left Sided Heart Failure

Myocardial infarction

Cardiac Arrhythmias

 

 B.  Hemolytic  Disorders

RH Incompatibility

ABO Incompatibility

 

 C. Metabolic Disorder

DKA

Thyroid Crisis

Hepatic Coma

 

 D. Renal  Disorder

Chronic Renal Failure

 

 E. Toxemias of Pregnancy

Pre-eclampsia

Eclampsia

 

 E. Infectious Diseases

TORCH

 

F. Emergency Delivery

Standard Assessment of Critically ill Patients

 

Definition and Scope of the Problem

High-risk pregnancy

High-risk pregnancy: life or health of mother or fetus is jeopardized

For mother, high risk status arbitrarily extends through puerperium (30 days after childbirth)

Maternal complications usually resolved within 1 month of  birth

Perinatal morbidity may continue for months or years 

High risk diagnosis imposes crisis on family

Loss of pregnancy before anticipated date

Development of gestational diabetes mellitus with its

      potential complications

 

Neonate who does not meet cultural, societal, or familial

norms and expectations

 

Definition and Scope of the Problem

Maternal health problems

Leading causes of maternal mortality

ü  Pregnancy-induced hypertension

ü  Pulmonary embolism

ü  Hemorrhage

Factors related to maternal death include:

ü  Lack of prenatal care

ü  Low educational attainment

ü  Unmarried status

ü  Nonwhite race

 

Definition and Scope of the Problem

Assessment begins w/ the first prenatal

visit & continuous through puerperium

FACTORS:

Maternal age : < 18 y/o or nullipara >30y/o

Maternal height: 60 inches/ 153 cm or less

Weight: Obesity (>20% of standard weight)

 

Assessment of risk factors

Biophysical risks

Genetic disorders, nutritional and general health status, and medical or obstetric-related illnesses

 

Sociodemographic risks arise from mother and family

Lack of prenatal care, low income, marital status, and ethnicity

 

Environmental factors include:

Hazards in workplace and environment, including noxious chemicals, radiation, infections, and

pollutants

 

Psychosocial risks

Maternal behaviors and adverse lifestyles that have negative effect on health of mother or fetus

 

Nursing Role in

Antepartal Assessment for Risk

 

Psychologic considerations

Women undergoing antepartal assessments  are anxious

Tests due to suspected fetal compromise, deterioration of maternal condition, or both

 

Psychologic considerations

Third trimester women concerned about protecting themselves and fetuses and consider themselves

vulnerable

 

Label of high risk increases sense of vulnerability

 

Psychologic Implications of

High Risk Pregnancy

When woman is diagnosed with high-risk pregnancy, she and her family will likely experience stress

related to the diagnosis

The woman may exhibit various psychologic responses, including:

ü  Anxiety

ü  Low self-esteem and guilt

ü  Frustration

ü  Inability to function

 

Antepartum Testing

Biophysical Assessment

 

Magnetic resonance imaging

Examiner evaluates:

ü  Fetal structure

ü  Placenta (position, density, and presence of gestational trophoblastic disease)

ü  Quantity of amniotic fluid

ü  Maternal structures (uterus, cervix, adnexa, and pelvis)

ü  Biochemical status of tissues and organs

ü  Soft tissue, metabolic, or functional anomalies

ü   

Biochemical Assessment

Amniocentesis

Maternal

ü  Hemorrhage

ü  Fetomaternal hemorrhage

ü  Infection

ü  Labor

ü  Abruptio placenta

ü  Damage to intestines or bladder

ü  Amniotic fluid embolism

 

AMNIOCENTESIS – refers to aspiration of a sample of amniotic fluid for examination of fetal cells

 

Percutaneous umbilical blood sampling (PUBS) or cordocentesis 

Direct access to fetal circulation

Insertion of needle directly into a fetal umbilical vessel under ultrasound guidance

Maternal assays

ü  Alpha-fetoprotein (AFP)

Maternal serum levels screened for neural tube defects (NTDs)

80% to 85% of open NTDs and abdominal wall defects can be detected early

Recommended for all pregnant women

ü  Coombs’ test

Rh incompatibility

Detects other antibodies for incompatibility with maternal antigens

INDIRECT COOMBS’ TEST – used for search  for

          agglutination of Rh positive RBCs to determine 

          whether antibodies are present in maternal blood

 

 

Laboratory Studies & Diagnostic tests

COMPLETE BLOOD COUNT – provides info on #, type & health of RBC.

PREGNANCY TEST (Hcg)

SERUM  ALPHA-FETOPROTEIN

ULTRASOUND (UTZ)– refers to the use of high frequency- sound waves passed through the maternal

abdomen. 

BLOOD GLUCOSE & GLYCOSYLATED  HEMOGLOBIN

SEROLOGIC TESTS – to determine presence & type of STD. 

CULTURES – to determine type of infectious agent. 

 

 

Cardiovascular System

1. The cardiovascular system consists of the heart, and vessels, arteries, capillaries and veins.

 

1. A functional cardiovascular system is vital  for supplying oxygen and nutrients to             tissues and

removing wastes from them.

 

Structure of the Heart

ü  The heart is a hollow, cone-shaped, muscular pump within the thoracic cavity.

 

Structure of the Heart

ü  Size and Location of the Heart

1.  The average adult heart is 14 cm long and 9 cm wide.

                      2.  The heart lies in the mediastinum under the sternum;

                            its apex extends to the fifth intercostal space.

 

ü  Coverings of the Heart

1. The pericardium encloses the heart.

2. It is made of two layers: the outer, tough connective tissue fibrous pericardium surrounding a more

delicate visceral pericardium (epicardium) that surrounds the heart.

 

ü  Wall of the Heart

 

1. The wall of the heart is composed of three distinct layers.

2. The outermost layer, the epicardium, is made up of connective tissue and epithelium, and houses

blood and lymph capillaries along with coronary arteries.  It is the same as the visceral pericardium.

3. The middle layer called myocardium consists of cardiac muscle and is the thickest layer of the heart

wall.

4. The inner endocardium is smooth and is made up of connective tissue and epithelium, and is

continuous with the endothelium of major vessels joining the heart.

a. The endocardium contains the  Purkinje fibers.

 

ü  Heart Chambers and Valves

 

1.    The heart has four internal chambers: two atria on top and                 two ventricles below.

                                a.   Atria receive blood returning  to the heart and

                                      have  thin walls and ear-like auricles  projecting

                                      from their exterior.

                                 b.  The thick-muscled ventricles pump blood to

                                        the body.

 

2.    A septum divides the atrium and ventricle on each side. 

       Each also has an atrioventricular (A-V) valve to ensure one   

               way flow of blood.

                                a.The right A-V valve (tricuspid) and left A-V valve

                                    (bicuspid or mitral valve) have cusps to which

                                    chordae tendinae attach.

                                b.Chordae tendinae are, in turn, attached to

                                    papillary muscles in the inner heart wall that   

                                   contract during ventricular contraction to

                                   prevent the backflow of blood through the A-V

                                   valves.

 

1. The superior and inferior vena cavae bring de-oxygenated blood from the body  to the right atrium.

 

1. The right ventricle has a thinner wall than does the left ventricle because it must pump blood only as

far as the lungs, compared to the left ventricle pumping to the entire body.

 

1. At the base of the pulmonary trunk leading to the lungs is the pulmonary valve, which prevents a

return flow of blood to the ventricle.

 

1. The left atrium receives blood from four pulmonary veins.

 

1. The left ventricle pumps blood into the entire body through the aorta, guarded by the aortic valve that

prevents backflow of blood into the ventricle.

 

 

ü  Skeleton of the Heart

 

1. Rings of dense connective tissue surround the pulmonary trunk and aorta to provide attachments for

the heart valves and fibers.

2. These tough rings prevent dilating of tissue in this area.

 

 

 

ü  Path of Blood through the Heart

 

1. Blood low in oxygen returns to the right atrium via the venae cavae and coronary sinus.

2.   The right atrium contracts, forcing blood through the tricuspid valve into the right ventricle.

3. The right ventricle contracts, closingthe tricuspid valve,

         and forcing blood through the pulmonary valve into the   

         pulmonary trunk and arteries

1. The pulmonary arteries carry blood to the lungs where it  can rid itself of excess carbon dioxide and

pick up a new supply of oxygen.

2. Freshly oxygenated blood is returned to the left atrium of the heart through the pulmonary veins.

3. The left atrium contracts, forcing blood  through the left bicuspid valve into the  left ventricle.

4. The left ventricle contracts, closing the         bicuspid valve and forcing open the       aortic valve as

blood enters the aorta for distribution to the body.

 

 

Simplified Path of Blood Flow

Blood Supply to the Heart

 

1. The first branches off of the aorta, which carry freshly oxygenated blood, are the right and left

coronary arteries that feed the heart  muscle itself.

2. Branches of the coronary arteries  feed many capillaries of the myocardium.

3. The heart muscle requires a continuous supply of freshly oxygenated blood, so smaller branches of

arteries often have anastomoses as alternate pathways for blood, should one pathway become

blocked.

 

1. Cardiac veins drain blood from the heart muscle and carry it to the    coronary sinus, which empties

into       the right atrium.

 

ü   Heart Actions

The cardiac cycle consists of the atria beating in unison (atrial systole) followed by the contraction of

both ventricles, (ventricular systole) then the entire heart      relaxes for a brief moment (diastole).

 

ü  Cardiac Cycle

 

1. During the cardiac cycle, pressure         within the heart chambers rises and falls with the contraction

and relaxation of atria and ventricles

2. When the atria fill, pressure in the        atria is greater than that of the ventricles, which forces the A-V

valves open.

3. Pressure inside atria rises further as they contract, forcing the remaining blood into the ventricles.

 

ü  Heart Sounds

 

1. Heart sounds are due to vibrations  in heart tissues as blood rapidly changes velocity within the heart.

2. Heart sounds can be described as a "lubb-dupp" sound.

3. The first sound (lubb) occurs as ventricles contract and A-V valves are closing.

4. The second sound (dupp) occurs as ventricles relax and aortic and pulmonary valves are closing.

 

ü  Cardiac Muscle Fibers   

A mass of merging fibers that act as a unit is called a functional syncytium; one exists in the atria

(atrial syncytium) and one in the ventricles (ventricular syncytium).

 

ü  Cardiac Conduction System           

1. Specialized cardiac muscle tissue conducts impulses throughout the myocardium and comprises the

cardiac conduction system.               

2. A self-exciting mass of specialized cardiac muscle called the sinoatrial node (S-A node or pacemaker),

located on the posterior right atrium,   generates the impulses for the heartbeat.                           

3. Impulses spread next to the atrial syncytium, it contracts, and impulses travel to the junctional fibers

leading to the atrioventricular  node (A-V node) located in the septum.

 

1. Junctional fibers are small, allowing the atria to contract before the impulse spreads rapidly over the

ventricles.

 

1. Branches of the A-V bundle give rise to Purkinje fibers leading to papillary muscles; these fibers

stimulate contraction of the papillary muscles at the same time the ventricles contract.

 

Cardiac Diseases

 

Cardiac Disease

Affects a small percentage of pregnant women

 

Rheumatic Heart Disease : most common  in the past.

 

Congenital disease : most common cardiac problem encountered in pregnancy now

 

Incidence

ü  Successful  txt of congenital anomalies or mitral stenosis from RHD allows girls to reach childbearing

age & bear children.

ü  What affects childbearing women is that they already have the disease like hypertension w/c could

lead to disorders of the heart & its structures

 

Cardiovascular Disorders

ü  Incidence of congenital heart lesions increased in children of mothers with congenital heart disease

Preconception counseling crucial

ü  Major cardiovascular changes during pregnancy that affect women with cardiac disease are:

Increased intravascular volume

Decreased systemic vascular resistance

Cardiac output changes during labor and birth

Intravascular volume changes that occur just after childbirth

ü  Normal heart compensates for increased workload

Diseased heart is hemodynamically challenged

ü  Degree of disability often more important in treatment and prognosis

ü  Miscarriages increase

ü  Preterm labor and birth more prevalent

ü  Maternal mortality rate of more than 50% during pregnancy associated with pulmonary

hypertension

ü  Woman with cardiac disease must be assessed and diagnosed as soon as possible

 

Cardiovascular Disorders

ü  Peripartum cardiomyopathy (PPCM)

ü  Rheumatic heart disease (RHD)

ü  Mitral valve stenosis

ü  Mitral valve prolapse (MVP)

ü  Infective endocarditis

ü  Eisenmenger’s syndrome

ü  Atrial septal defect (ASD)

ü  Tetralogy of Fallot

ü  Marfan syndrome

ü  CV Physiology of Pregnancy

 

v  Blood volume increases 30 to 50%

ü  Plasma volume increase  more than RBC mass leading to physiologic anemia

ü  An estrogen mediated stimulation of the renin-angiotensin system results in retention of NA and

water

v  HR  increases 10 to 20 bpm

v  CV Physiology of Pregnancy

v   CO increase up to 45% by 24 wks

ü  These increases begin during the 1st trimester

ü  Peak by 20-24 wks and are sustained until term

ü  In early pregnancy an increase in SV (20-30%) is responsible to the increase in CO

ü  Later in pregnancy, the increase in HR is responsible since SV decreased due to IVC compression

v  Concurrently there is a substantial reduction in SVR by 21% with decreases in BP and decreases in

PVR by 34%

 

 

CV Physiology of Pregnancy

 

Symptoms and PE of normal pregnancy mimic cardiac disease

ü  Exertional dyspnea and orthopnea

ü  Fatigue and Presyncope

ü  Lower extremity edema

ü  a and v waves may be pronounced in CVP tracing

ü  Maximal apical impulse is displaced

ü  1st Heart sound the pulmonary component of 2nd might are accentuated

ü  3rd HS is heard in 80% of pregnant women

 

Murmurs frequently develop during pregnancy

ü  Soft, mid-systolic, and heard along the left sternal border is heard in 90% women

ü  Anemia might accentuate it

ü   Intensity may increase as CO increases

 

Cervical venous hums and a continuous murmur due to increased mammary blood flow may

also be heard Echocardiography is warranted if:

ü  Diastolic, continuous, or loud systolic murmurs (>2/6)

ü  A fixed split 2nd sound

ü  Associated with symptoms or an abnormal EKG

 

In normal pregnant women, echocardiography demonstrates:

ü  Minor increases in the left  and right ventricular diastolic dimensions (within the normal range)

 

During labor:

ü  CO  increases 45% above pre-labor values

ü  Uterine contraction “boluses” the patient

It might increase CO up to 65% of pre-labor values

ü  The BP increases with uterine contractions/pain

 

Immediately after delivery

ü  The cardiac filling pressure increase dramatically due to the decompression of the vena cava and

the return of uterine blood into the systemic circulation

CO might increase to 80% of pre-labor values

ü  The cardiovascular adaptations associated with pregnancy regress by approximately 6 weeks after

delivery

 

 

Physiology of Pregnancy

 

Pregnancy is also a hypercoagulable state

ü  Decreased in Protein activity

ü  Stasis

ü  Venous hypertension

 

Effect of Pregnancy on the cardiovascular system

 

Pregnancy

 

↑Blood volume,↑ cardiac output, HR,& stroke volume

 

↑ cardiac workload

 

Normal heart with heart disease

 

 

Prenatal Period

Assessment Findings

Evidence of cardiac decompensation especially when blood volume peaks  (weeks 28-32)

 

Signs of Cardiac Decompensation 

ü Dyspnea

ü Palpitations

ü Pulse irregularity

ü Chest pain

ü Cough

ü crackles @ base of the lungs

ü Sweating,Orthopnea

ü Weakness

ü Progressive generalized edema

ü Pallor

 

Intrapartal Period

 

Labor  increase  risk of CHF  milking effect of contractions &  delivery ↑es bld  volume to heart.

 

The New York Heart Association (NYHA) Grading of

   Functional capacity of the heart

 

Classification

 

Class 1:    No limitation of activity

Class 2:    Slight limitation of activity

Class 3:    Considerable limitation of  activity

Class 4:    Symptoms present even at rest

 

Classification

Class I ( Uncompromised )

Physical activity is not limited by angina or symptoms of cardiac insufficiency

Class II : Slightly Compromised

                 Comfortable at rest but normal activity causes fatigue, palpitations, dyspnea, or angina.

 

 

Class III ( Markedly Compromised)

                  Comfortable at rest but normal activity causes excessive fatigue, palpitation, Dyspnea or

angina.

 

Class IV ( Severely Compromised)

                 Unable to perform any activity w/out discomfort

                 May experience angina or signs of cardiac insufficiency

                 while at rest

 

Classification of risk

The WHO classification

 

What is the mortality associated  with the various cardiac lesions ?

 

Mortality associated with specific cardiac lesions

What is the prognosis for a woman with a cardiac disease depending on the NYHA classification?

What are the clinical features in a normal pregnancy which can mimic a cardiac disease ?

What are the criteria to diagnose cardiac disease during

 pregnancy ?

 

Heart Failure

 

Heart failure is a medical term that describes an inability of the heart to keep up its work load of

pumping blood to the lungs and to the rest of the body.

 

Signs of low cardiac output

ü  Lethargy, dizziness, confusion, agitate

ü  Oliguria

ü  Weak pulse, tachycardia

ü  Narrow pulse pressure

ü  Cool, moist skin

ü  Sign of etiology or precipitating factor

 

Signs of high cardiac output

ü  Pulse full, bounding

ü  Wide pulse pressure

ü  Warm skin

ü  Prominent PMI

ü  Soft Systolic ejection murmur at LSB

 

Sign of etiology or precipitating factor

ü  Rheumatic Fever

Strep throat from the streptococcal infection begins a disease process where the heart valves are

damaged

 affects the connective tissues of the body.

ü  Cardiomyopathy

 stretching and enlarging of the heart cavity that occurs making the heart weak so it does not pump

correctly

ü  Hypertrophic Cardiomyopathy

Defects in their contractile proteins, make cells too weak

They hypertrophy to do the same amount of work as normal cells

 

Need more oxygen and perform less efficiently, so the person is prone to heart failure and may suffer

sudden death during exertion

 

Hypertrophic Cardiomyopathy

 

Ventricular Failure

occurs when there are weak spots in the ventricular walls causing a bulge, or an aneurysm.

 

Atherosclerosis

                gradual clogging of the arteries by fatty, fibrous deposits

tiny lump of fibrous tissue grows as the artery tries to repair the damage. 

Cholesterol accumulates and more tissue builds up. 

 

PCI may be the best option

( > 2nd trimester )

 

Left Sided Heart Failure

 

Left-Sided Valvular Disorders

Mitral valve disorders

Mitral valve stenosis

Mitral valve regurgitation

Mitral valve prolapse

Aortic valve disorders

Aortic valve stenosis

Aortic valve regurgitation

Cardiac Disease

Left-sided heart failure

ü  Orthopnea

ü  Paroxysmal nocturnal

ü  dyspnea

 

Left-Sided Heart Failure

ü  Blood accumulates in left ventricle

ü  Left ventricle thickens and enlarges: hypertrophy

ü  Blood backs up into lungs

ü  Cough and shortness of breath result

 

LEFT-SIDED HEART FAILURE

ü  DYSPNEA

ü  DRY COUGH

ü  CRACKLES

ü  WHEEZES

ü  ORTHOPNEA

ü  HEMOPTYSIS

ü  “Paroxysmal” NOCTURNAL DYSPNEA

ü  CHEYNE-STOKES RESPIRATIONS

ü  FATIGUE

ü  WEAKNESS

ü  CYANOSIS

ü  NOCTURIA

ü  TACHYCARDIA

ü  Serious: life threatening

                Pulmonary Edema

 

Mitral Stenosis           

Rheumatic MS is the most common valvular abnormality in pregnant women (60%)

 Associated with pulmonary congestion, edema, and atrial arrhythmias during pregnancy or soon after

delivery

 increased BV load and CO associated with pregnancy lead to an increase in left atrial volume and

pressure, elevated pulmonary venous filling pressures, dyspnea, and decreased exercise tolerance

Increases in the maternal HR decrease the diastolic filling period, further increasing left atrial pressure

and decreasing CO

increased atrial pressure may cause arrhythmias

Predictors of adverse maternal outcomes

Mitral valve area less than 1.5 cm2

Abnormal functional class before pregnancy

Fetal mortality increases with deteriorating maternal functional capacity

30 % when the mother has  NYHA class IV

For women with mild or moderate symptoms

Medical therapy is directed to the treatment of volume overload

ü  Diuretic therapy but avoiding hypotension and tachycardia

ü  Na+ restriction

ü  Reduction of physical activity

Beta-blockers decrease HR and prolong the diastolic filling period which provides symptomatic benefit

Development of AF requires prompt treatment, including cardioversion.

Beta-blockers and digoxin for rate control

Procainamide and quinidine are frequently used if suppressive antiarrhythmic therapy is needed

 

Due to the increased risk of systemic embolism in patients with MS and AF anticoagulant therapy is

indicated

 

NYHA class III / IV or a valve area of less than 1.0 cm2

Percutaneous balloon mitral valvuloplasty (PBMV) or valve surgery BEFORE conceiving appear to allow

pregnancy with fewer complications than women treated medically

Percutaneous aortic balloon valvuloplasty

 

PBMV, during the 2nd trimester, has been associated with normal deliveries and excellent fetal

outcomes

Fetal risks associated with exposure to radiation may be reduced by avoiding exposure during the first

half of pregnancy

 

The uterus must be shielded and the patient should be informed about the possible risks

 

Mitral valvuloplasty has also been performed under TEE guidance

 

Percutaneous mitral balloon valvotomy prior to conception or during pregnancy

Open cardiac surgery has been performed during pregnancy for severe MS

Maternal outcomes are similar to the non-pregnant

Fetal loss in 10 to 30 % of cases

 

MS: Anesthesia management

ü  Careful clinical evaluation early on in conjunction with the OB team to have a clear plan

ü  ICU consultation

ü  Vaginal delivery is the usual approach

ü  Hemodynamic goals:

Avoidance of tachycardia and fluid overload

Preservation sinus rhythm

Increase of BV, CO and HR  during pregnancy and labor may result in pulmonary congestion,

tachycardia and atrial fibrillation

ü  Monitoring:

A-LINE and probably PAC

Labor and delivery is associated with an increase of 8 to 10 mm Hg in the left atrial and pulmonary

wedge pressures

PAC used before and during delivery facilitates  the management of hemodynamics in women with

advanced disease

 

 

ü  Epidural anesthesia to achieve effective pain control

A mixture of LA and opioids is ideal

Pain control and minimization of  BV/CO  increase after delivery

 

Assisted-delivery devices during the second stage of delivery eliminate hemodynamic effects of

valsalva maneuver during “pushing”

 

Cesarean section should be performed when there are obstetrical indications for it

 

Mitral Regurgitation

 

Women with symptomatic MR may benefit from mitral-valve surgery (preferably repair )before

becoming pregnant.

However, LV dysfunction associated with MR  is unlikely to improve after surgery and will increase

maternal risk during pregnancy

Diuretics and vasodilators may be indicated

 

When Will You Hear Murmurs?

If a valve is stenotic, you will hear a murmur of blood shooting through the narrow opening when the

valve is open

 

If a valve is regurgitant, you will hear a murmur of blood leaking back through when the valve should

be closed

 

Aortic Stenosis

 

ü  Congenital valvular abnormalities are usually the cause of AS in young women in the US

ü  Severe AS is poorly tolerated during pregnancy

Maternal and perinatal mortality  of 17%  and 32% have been reported

ü  The pressure gradient is responsible for the HD changes seen in AS

The increased LVSP needed to maintain systemic arterial blood pressure increases stress in the

ventricular wall

 

Lt ventricular hypertrophy develops leading to diastolic dysfunction, fibrosis, diminish coronary blood

flow reserve and late systolic failure

 

ü  Patients who are symptomatic or who have a peak outflow gradient of more than 50 mm Hg are

advised to delay conception until after surgical correction

ü  Termination of pregnancy should be strongly considered if the patient is symptomatic before the

end of the 1st  trimester

ü  Aortic-valve replacement and palliative aortic balloon valvuloplasty have been performed during

pregnancy with associated maternal and fetal risk

 

Biological valves

 

Aortic Stenosis

Hemodynamic goals:

Maintain normovolemia

NSR

Tachycardia decrease diastolic filling time

Atrial “kick” is responsible for up to 40% of ventricular filling in this patients

 

Baseline SVR

 

Aortic Stenosis

normal physiological changes of pregnancy can precipitate heart failure in patient with severe AS

 

The further increase of CO and BV during labor in face of the fixed CO of AS patients may precipitate:

ü  Tachycardia which  decreased diastolic time (and coronary perfusion time) and increases O2

consumption

ü  Increases LVEDP

ü  Ischemia might result

 

Vaginal delivery is preferred

ü  Instrumental delivery to avoid hemodynamic changes of the valsalva manuver

ü  Oxytocin may decrease SVR an increase PAP

 

Monitoring:

ü  A-line

ü  CVP , PAC

 

Epidural analgesia

ü  Pain control and also minimizes BV/CO  increase after delivery

ü  Avoid epinephrine “test dose”

ü  Careful titration to avoid sudden decrease of SVR

ü  Dilute LA with opioids to minimize sympathectomy

 

Cesarean section

GA has traditionally being advocated to avoid sudden decreases of SVR

Opiod based induction

Fetal depression. Pediatric team must be aware

Case reports of epidural anesthesia with positive outcomes

Careful titration of LA and fluid replacement/vasopressors to counteract sympathectomy

Phenylephrine possible a better choice over ephedrine

Aortic Regurgitation

 

AI may be due to a dilated Ao annulus (as in Marfan's syndrome), a bicuspid Ao valve, or previous

endocarditis

 

The reduced SVR of pregnancy reduces the volume of regurgitated blood

 

Women with an abnormal functional capacity or left ventricular dysfunction are predicted to have a

high risk of abnormal maternal outcomes, but few data concerning this population are available

 

Aortic Insufficiency

Isolated AI can usually be managed with vasodilators and diuretics

ACE inhibitors should be discontinued during pregnancy, and other agents, such as hydralazine or

nifedipine, should be substituted

 

Clinical and echo assessment should be performed before conception in women with AI due to Marfan's

syndrome

Even in the absence of overt cardiac abnormalities, this syndrome predisposes women to

unpredictable, but increased, risk during pregnancy.

 

Pulmonary Edema

 

 Pathophysiology

 

Pulmonary Edema

Capillary fluid moves into alveoli

ü  Lung becomes stiffer

ü  Harder to inhale

ü  Less gas exchange in alveoli

ü  Crackles

ü  Frothy sputum

Hemoglobin not completely oxygenated

Pulmonary hypertension

Hemodynamic objectives

Maintain the PAP as low as possible and the systemic pressure within the 15% above and below the

basal level (the systemic pressure should always be higher than pulmonary pressure)

 

Avoid dysrhythmias and tachycardia, and maintain sinus rhythm

 

 

 

Chest x-ray of rt. lung

A. Normal pulmonary vessels

B. General increase pulmonary vessels

C. Pulmonary congestion

D. Pulmonary hypertension

 

Pulmonary hypertension

   Pregnancy and labor CV changes against goals:

Uterine contraction after delivery returns a large bolus of blood to the circulation. This can be poorly

tolerated in patients with severe PHTN

 

The sudden hypervolemia can be treated with vasodilators, such as nitroglycerine, and diuretics.

 

A BP cuff inflated between the arterial and venous pressures around the thighs, can suddenly and

reversibly decrease RV filling by reducing venous return

 

Air or amniotic fluid embolism could acutely increase pulmonary pressure

 

Monitoring:

 a-line and CVP or PAC should be used for monitoring or for drug administration

 

Nursing managements

Administration of oxygen and intubation and mechanical ventilation if respiratory failure occurs.

Positioning the patient to promote circulation

Monitor I and O

Monitoring pulse rate and blood pressure

Examining skin turgor and mucous membranes for signs of DHN.

 

Assessment symptoms of fluid overload.

 

PULMONARY EMBOLISM

 

Pulmonary Embolism

obstruction of the base or one or more branches of the pulmonary arteries by the thrombus (or

thrombi) that originates somewhere in the venous system or in the right side of the heart.

 

 Gas exchange is impaired in the lung mass supplied by the obstructed vessel.

 

Massive pulmonary embolism is life threatening and can cause death within the first 1 to 2 hours after

the embolic event.

 

Common in pregnancy, oral contraceptive use, congestive heart failure, hypercoagulable

states, and prolonged immobility.

 

Most thrombi originates in the deep veins of the legs.

 

Clinical Manifestations

Symptoms depend on the size of the thrombus and the area of the pulmonary artery occlusion.

 

ü  Dyspnea is the most common symptom. Tachypnea is the most frequent sign

ü  Chest pain is common, usually sudden in onset and pleuritic in nature it can be substernal and

may mimic angina pectoris

ü  Fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis,  syncope, shock, and sudden

death may occur

ü  Multiple small emboli in the terminal pulmonary arterioles stimulate symptoms of

bronchopneumonia or heart failure

 

Assessment and Diagnostic Methods

ü  Ventilation-perfusion scan, pulmonary angiography, chest radiograph

 

ü  Electrocardiogram (ECG), tachycardia, PR interval and T-wave changes, peripheral vascular studies

and arterial blood gas (ABG) analysis (for hypoxemia)

 

Prevention

ü  Ambulation or leg exercises in patients on bed rest

ü  Anticoagulant therapy before abdominothoracic surgery and every 8 to 12 hours until discharge

from hospital

ü  Application of intermittent pneumatic leg compression devices

 

Right Sided Heart Failure

 

Shunts

A shunt is an opening or connection that lets blood move from one side of the circulation to the other

Most shunts occur in the heart and move blood either from the left to the right or from the right to the

left

Because the left side is stronger, blood is usually pushed from the left to the right side

 

Left-to-Right Shunt

Right-to-Left Shunt

Cardiac Disease

Right-side heart failure

ü  Distended liver and spleen

ü  Ascites

ü  Peripheral edema

 

Right-Sided Heart Failure

Blood backs up into veins

Causes peripheral edema and organ engorgement

Less common than left-sided HF

 

Jugular venous pressure estimation

ü  RIGHT-SIDED HEART FAILURE

ü  JUGULAR VEIN DISTENSION

ü  DEPENDENT PERIPHERAL EDEMA

ü  ASCITES

ü  WEIGHT GAIN

ü  FATIGUE

ü  WEAKNESS

 

ü  SPLENOMEGALY

ü  HEPATOMEGALY

ü  GI DISCOMFORT

ü  NOCTURIA

ü  TACHYCARDIA

 

RHD

Streptococcal pharyngitis infection

â

Scarring of the heart valves

â

Stenosis of the openings between chambers of the heart

 

Causes

ü  Atrial Septal Defects

ü  Ventricular Septal Defects

ü  Patent Ductus Arteriosus

 

R-L Shunt

Occur through Septal Defect or PDA when pulmonary vascular resistance exceeds peripheral

resistance & pulmonary hypertension occurs.                                                                                    

EISENMENGER SYNDROME

ATRIAL SEPTAL DEFECT

 

Produces L-R shunt because pressure of the

 L side of the heart is higher than the R side.

ü  Pregnancy is well tolerated with no complications

ü  However pulmonary HPN can occur because the additional blood moves to the R side of the heart is

transported into the lungs.

 

VSD

ü  Common @ birth

ü  Asymptomatic when pregnant

ü  Fatigue or pulmonary congestion may occur

 

If heart failure occurs they are managed as nonpregnant patients

 

 

                Bacterial endocarditis is common with unrepaired defects, antibacterial prophylaxis is usual.

PDA

ü  The communicating shunt b/w PA & Aorta

ü  If untreated physiologic effects are related to size

ü  If small, tolerated during pregnancy unless complicated by P HPN

ü  Antibiotics is recommended as they are commonly be infected.

 

R-L SHUNT

TOF

Combination of four defects:

ü  Ventricular septal defect

ü  Pulmonary valve stenosis

ü  Right Ventricular Hypertrophy

ü  Displacement of Aorta ( overrides the RV)

 

Symptoms of TOF

ü  Cyanosis

ü  Clubbing of fingers

ü  Inability to tolerate activity

 

ü  If treated ( repaired), & -cyanosis may do well in pregnancy

If uncorrected – death.

EISENMENGER SYNDROME

ü  Cyanotic heart condition

ü  Pulmonary resistance equals or exceeds systemic resistance to blood flow

ü  Several underlying congenital defects:    

                                                 - Large VSD

 -Large patent ductus arteriosus

MITRAL VALVE PROLAPSE

ü  One of the most common cardiac conditions

ü  Associated with ASD and Marfan Syndrome

ü  Leaflets of the valve prolapsed into the left atrium during ventricular contraction

 

Nursing Diagnoses

ü  Decrease Cardiac Output

ü  Activity Intolerance r/t imbalance between oxygen supply & demands

ü  Fluid Volume Excess r/t impaired cardiac pump and water & sodium retention

ü  Deficient Knowledge regarding diet and fluid restriction

 

 Nursing Interventions

ü  Monitor maternal ECG & FHT continuously.

ü  Explain to client that vaginal delivery is preferred over C-section.

ü  Monitor client’s response to stress of labor & watch for signs of decompensation.

ü  Administer O2 & pain medication as ordered, epidural preferable.

ü  Position client in side-lying/low semi-fowler’s position.

ü  Provide calm atmosphere.

ü  Encourage” open glottal” pushing during second stage of labor

ü  Monitor VS, any bleeding, strict I&O, lab test values, daily weight, & diet.

ü  Promote bed rest in appropriate position.

ü  Assist with activities as needed.

ü  Prevent infection.

ü  Facilitate non stressful mother/baby interaction.

ü  Promote frequent rest periods & adequate

                sleep, decrease stress.

ü  Teach client to recognize & report signs of infection, importance of prophylactic antibiotics.

ü  Monitor  uterine contractions

ü  Compare V/S to baseline & normal values expected during pregnancy.

 

Management

 

Antepartum Care

 

The chief aim of management of the patient in pregnancy is to keep patient within her cardiac reserve.

It is preferable to have detailed baseline information prior of pregnancy.

Limiting activity is helpful in severely

                affected women with ventricular dysfunction,

left heart obstruction, or class III or IV symptoms.

Hospital admission by mid-second

                trimester may be advisable for some.

 

Problems should be identified early and treated aggressively, especially pregnancy induced

hypertension, hyperthyroidism, infection, and anemia.

 

Arrhythmias should be treated if warranted

Premature atrial or ventricular beats are

common in normal pregnancy, and in

patients with preexisting arrhythmias,

 

Pregnancy may exacerbate their frequency

and hemodynamic severity.

These usually are not treated.

 

Sustained tachyarrhythmias, such as

atrial flutter or atrial fibrillation, should be

treated promptly.

 

If possible, all antiarrhythmic drugs should

be avoided during the first trimester, and

those known to be teratogenic should be

avoided throughout pregnancy.

 

 Anticoagulation therapy

Oral therapy with warfarin is effective and

logistically easy.

 

However, it can affect embryonic organ development, although some evidence shows that a dosage of

5 mg per day may not be teratogenic.

 

 Fetal intracranial bleeding is a risk throughout pregnancy, particularly during vaginal delivery, unless

warfarin is stopped before labor.

  

* Heparin in adjusted subcutaneous doses

does not cross the placenta and so has no teratogenic effects.

 

However, it may cause maternal

thrombocytopenia and osteoporosis and is

less effective in preventing thrombosis in

patients with prosthetic valves.

 

Mechanical prosthetic heart valves

 Anticoagulation therapy

More recent guidelines recommend either

(1) adjusted-dose heparin during the entire pregnancy or

 

(2) adjusted-dose heparin until the 13th week of gestation, warfarin from the 14th week to the middle

of the third trimester, and then restart adjusted-dose heparin.

 

 Anticoagulation therapy

 

* Low-molecular-weight heparin in adjusted

                doses is easier to administer and has been

                suggested as an alternative to adjusted-dose unfractionated heparin.

 

 

Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic  agents

during pregnancy.

 

Peripartum management

Cesarean section is indicated only for the

following conditions:

 Aortic dissection

Marfan syndrome with dilated aortic root

Taking warfarin within 2 weeks of labor.

 

 

Peripartum care

 Peripartum care

Peripartum care

 

Forceps or vacuum extraction should be

                considered at the end of the second stage of labor to shorten and ease delivery.

 

 Peripartum care

Postpartum monitoring

 

Because hemodynamics do not return to baseline for many days after delivery, patients at

intermediate or high risk may require monitoring for at least 72 hours postpartum.

 

 

 Peripartum care

Lactation should be encouraged unless patient is in failure.

 Cardiac output is not compromised during lactation.

Lactation is a pathway for fluid excretion and diuretic requirement may actually fall.

Cardiopulmonary Resuscitation

of the Pregnant Woman

For cardiac arrest, standard resuscitative efforts with few modifications implemented

 

If defibrillation needed, paddles must be placed one rib interspace higher than usual

 

MEDICATION

DIURETICS: Loop diuretics ex. Lasix (K+loss)

VASODILATORS:isosorbide(Isordil),Apresolin

 

INOTROPICS: cardiac glycoside: digoxin please check s/s dig toxicity (grn-yellow halos around

objects/lights, n/v/anorexia), Check serum level & hold dose if  AP=<60 bpm

 

 Digitalis-strengthen the heart’s contractions increasing blood flow

 

Beta BLOCKERS: carvedilol or Coreg is often the beta blocker of choice for CHF

 

ACE INHIBITORS: enalapril, lisinopril,catopril

 

Vasodilators-relax blood vessels which lowers the resistance to blood flow.  More blood reaches

the tissues and the heart works no harder than before.

 

Aldosterone antagonist: (Diuretic) K+ sparing such as spironolactone or Aldactone

 

Diuretics-increase the output of salt and water in urine

 

What is warfarin fetal embryopathy ?

 

Which is the ideal contraceptive for women with heart disease ?

 

Question

   A client develops left-sided heart failure. An appropriate nursing diagnosis is?

1.Activity intolerance

2.Ineffective airway clearance

3. Deficient fluid volume

4.Pain

 

Answer?  # 1

Activity intolerance:

Left sided heart failure impairs cardiac output and affects gas exchange in the lungs.

 

 Exchange of O2 and CO2 is compromised.  Clients tire easily and may be unable to complete simple

activities.

 

 Clients with Left-sided heart failure usually experience FVE

Question

   A client develops right sided heart failure. Which of the following s/s would the nurse

expect to find?

                1.             Pulmonary edema

                2.             Edematous legs and ankles

                3.             Decreased heart rate

                4.             Increased urinary output

 

Answer?  #2

Clients with right sided heart failure develop edema in the lower extremities and dependent body

areas as a result of increase capillary pressure.

 

The workload of the heart is increased leading to tachycardia

 

Pulmonary edema is a complication of left sided heart failure

Conclusion

Appropriate contraceptive and family planning advice as well as pre-conceptional counselling are also

important.

The concerted efforts of a team consisting of the

                obstetrician, cardiologist, anaesthetist, cardiothoracic surgeon, neonatologist, and paediatric

cardiologist are mandatory to ensure optimal results.

 

Evaluation

 

The evaluation of a woman with clinically significant valvular heart disease should occur before

conception and entail a full cardiac assessment

The history should focus on the patient's exercise capacity, current or past evidence of heart failure,

and associated arrhythmias

Cardiac hemodynamics, including PAP and the severity of valve dysfunction, should be assessed by

echo

Exercise testing may be useful if the history is inadequate to allow an assessment of functional

capacity

During pregnancy evaluation each trimester and whenever there is a change in symptoms, in order to

assess any deterioration in maternal cardiac status is the rule

 

SURGICAL PROCEDURES

ü  HEART VALVE REPAIR OR REPLACEMENT

ü  PACEMAKER INSERTION

ü  CORONARY ARTERY BYPASS

ü  MECHANICAL ASSIST DEVICES

ü  HEART TRANSPLANTATION

 

Prosthetic Heart Valves

 

Women with mechanical valves have a higher rate of thromboembolism and higher 10-year mortality,

despite a lower rate of valve loss

Pregnancy does not appear to increase the rate of failure of mechanical prostheses

 

associated with an estimated maternal mortality of 1 to 4% with death usually resulting from

complications of prosthetic-valve thrombosis.

 

Heart valve repair

Examples of remodeling

Angioplasty

catheterization using a balloon to flatten fatty deposits, used to treat atherosclerosis or other

conditions with blocked arteries.

 

artery of an arm or leg is used to guide the catheter through to  the blocked artery.

 

An uninflated balloon on the top of a smaller tube is threaded through the larger tube and centered in

the plaque narrowed area.

 

The balloon inflates compressing the plaque against the walls and increasing the open area.

SURGICAL PROCEDURES

Check for Medical Emergency: Acute Pulmonary Edema: frothy sputum, “impending doom”, panic,

orthopnea, cough  w/“pink-tinged sputum”

 

TX: add morphine to relieve  anxiety, slow rr, and decrease peripheral vascular resistance plus cardiac

glycoside (Digoxin), and loop diuretic(Lasix), bronchodilators, and oxygen for hypoxia

 

Myocardial Infarction

 

Cholesterol plaques deposited in the walls of coronary artery

                                                 ↓

Hardening of arterial walls and narrowing of the inner channel of the artery

                                                    ↓ 

      Arteries cannot deliver enough blood to maintain normal function of the parts of the  body

                                                 ↓ 

Eventually, the inner chamber of the artery is completely blocked

Artery Structure

 

Atherosclerosis in a Nutshell

Lipids get into the vascular endothelium

White blood cells try to clear them away à foam cells

 

 

Fatty Streaks and Atherosclerotic Plaques

Atherosclerosis in a Nutshell

WBCs and vascular endothelium release growth factors that

promote plaque formation

Plaques block the arteries

 

Arteriosclerotic Cardiovascular Ischemia

Acute:      Myocardial Infarction                                                                                                            

Chronic: Ischemic Cardiomyopathy                  (Dilated Cardiomyopathy)

People Live with Atherosclerosis – But Die of Thrombosis!

 

ü  Clinical Manifestations

ü  Chest pain

Sudden, not relieved by rest or NTG

ü  Shortness of breath

ü  Anxiety and restlessness

ü  Diaphoresis

ü  Cold, clammy perspiration

ü  Pallor

ü  Dizziness or lightheadedness

ü  Nausea and vomiting

ü   

ü  Assessment

                P              - provoking

                Q             - quality

                R              - radiation

                S              - severity

                T               -  timing

 

ü  Laboratory tests

ü  CK-MB

ü  LDH

ü  Myoglobulin

ü  TROPONIN

 

An Acute MI (AMI) Leaves Behind an

Area of Yellow Necrosis

 

ü  Complications of AMI

ü   Heart failure

ü   Cardiogenic shock

ü   Pericarditis

ü   Thromboemboli

ü   Rupture of the heart

ü   Ventricular aneurysms

 

 

Morbidity and Mortality

Acute MI in 0.0075% (7.5 in 100,000)

Overall mortality in pregnancy 28%

First trimester           0%

Second trimester    21%

Third trimester         40%

Puerperium   up to  75%

 

 

 

 

Highest mortality rates

Delivery within 2 weeks of MI

(+) pregnancy complications

 

Fetal mortality 35%

 

ü  Risk factors for MI

ü  Older maternal age, multiparity

ü  Smoking, obesity, DM

ü  Hypertension

ü  History of cardiovascular disease

ü  Cocaine abuse

 

ü  Management

ü  Position during labor

ü  Oxygen therapy

ü  Epidural anesthesia

ü  CVP monitoring

 

Post myocardial infarction

 

Cardiac Arrhythmias

Is an abnormal electrical conduction or automaticity causing changes in the heart rate and rhythm.

 

ü  Predisposing factors:

ü  Congenital

ü  Myocardial Ischemia, MI

ü  Organic heart disease

ü  Drug effect and toxicity

ü  Conductive tissue degeneration

ü  Electrolyte imbalance

ü  Acid-base imbalance

ü  Cellular hypoxia

 

ü  Pathophysiology

Result in the disturbance in the excitability, automaticity, or conductivity

Heart rate and rhythm are altered, reducing cardiac output

 

Assessment

ü  Asymptomatic

ü  Palpitation

ü  Chest pain

ü  Dizziness

ü  Weakness, fatigue

ü  Feeling of impending doom

ü  Irregular heart rhythm

ü  Bradycardia or tachycardia

ü  hypotension

ü  Syncope

ü  LOC

ü  Diaphoresis

ü  Pallor

ü  Cold, clammy skin

ü   

ü  Life-threatening: pulselessness, (-) respiration, no palpable blood pressure 

 

Diagnosis 

ü  ECG- change in heart rate, rhythm 

ü  Blood chemistry : electrolyte imbalance

 

Normal Sinus Rhythm

Normal Sinus Rhythm

                                Occurs when the electrical impulse starts at the regular rate and rhythm in the

sinus node and travels at through the normal conduction pathway

 

Characteristics:

ü  Ventricular and atrial rate: 60 to 100 in adult

ü  Ventricular and atrial rhythm: Regular

ü  QRS duration: Usually normal, but may be regularly abnormal 

ü  P wave: Normal and consistent shape; always in front of QRS

ü  PR interval: Consistent interval between 0.12 and 0.20 seconds

ü  P: QRS ratio 1:1

 

Types of Sinus node Dysrhythmias

A. Sinus Bradycardia 

                                occurs when the sinus node creates an impulse at a slower rate than normal.

Characteristics:

ü Ventricular and atrial rate: Less than 60 in adult

ü Ventricular and atrial rhythm: Regular

QRS duration: Usually normal but may be regularly abnormal 

P wave: Normal and consistent

     interval between 0.12 and

     0.20 seconds

P: QRS ratio 1:1

Management

ü The urgency of treatment depends on the effect of the slow rate on maintenance of  CO

ü Atropine, 0.5 to 1.0 mg given IV push block vagal stimulation to the SA Node & therefore accelerate

heart rate.

ü If  bradycardia persists a pacemaker  ( electrical device used to re-establish muscular

contraction of an arrested heart or to steady heartbeat)  may be required. 

 

B. Sinus Tachycardia

Occur when the sinus node create an impulse at a faster than normal rate.

may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia CHF, pain,

hypermetabolic states, fever, anxiety or sympathomimetic medication.

Ventricular and atrial rate: Greater than 100 in the adult

Venticular and atrial rhythm: Regular

QRS duration: Usually normal, but may be regularly abnormal 

P wave: Normal and consistent shape, always in front of the QRS, but may be buried in the preceding

T wave. 

P: QRS ratio 1:1 

 

As the heart rate increases, the diastolic falling time decreases, result in reduced cardiac

output and subsequent symptoms of syncope and low blood pressure. If the heart cannot

compensate for the decreased ventricular falling the pt may develop acute pulmonary

edema

Management

ü It is usually directed at abolishing its causes.

ü Calcium channel blockers and Beta-blockers may be used to reduce the heart rate quickly.

 

C. Sinus Arrhythmias

Occur when the sinus node create an impulse at an irregularly rhythm 

 rate usually increase with inspiration and decrease with expiration.

   Non respiratory cause includes heart disease and valvular disease, but these are rarely seen.

Ventricular and atrial rate: 60 to 100 in the adult

Ventricular and atrial rhythm: Irregular

QRS duration: Usually normal, but may be regularly abnormal

P wave: Normal and consistent shape, always in front of the QRS.

PR interval: Consistent interval between 0.12 and 0.20 second

P: QRS ratio: 1:1

Atrial Dysrhythmias

A. Premature Atrial Complex  

single ECG complex that  occur when an electrical impulse  start in  the atrium  before the next normal

impulse  of the sinus node.

 

may be caused by caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety, hypo kalemia (low

potassium level), hyper metabolic states or atrial ischemia, injury or infarction. 

Characteristics:

ü  Ventricular and atrial rate: Depend on the underlying rhythm

ü  Ventricular and atrial rhythm: Irregular

QRS duration: The QRS that follows the early P wave is usually normal, but it may be abnormal. 

P wave: An early and different P wave may be seen or may be hidden in the T wave;

Other P wave in the strip is consistent. 

PR interval: The early P wave has a shorter than normal PR interval, but still between 0.12 And 0.20

seconds  

P: QRS ratio: Usually 1:1

Management

ü  If PACs are in frequent, no treatment is necessary.

ü  If they are frequent (more tan 6 per minute) this may herald  a worsening diseases  state or the

onset of more serious  dysrhythmias, such as atrial fibrillation.

 

Treatment is directed toward the cause.

PAC’s should be monitored for increasing frequency

 

B. Atrial Flutter

 Occur in the atrium and creates impulse at an atrial rate between 250 and 400 time per minute.

Because the atrial rate is faster than the AV node can conduct, not all atrial impulse are conducted into

the ventricle causing a therapeutic block at the AV node.

Characteristics:

ü  Ventricular and atrial rate: Atrial range between 250 and 400 ventricular rates usually Range

between 75 and 150

ü  Ventricular and atrial rhythm: Usually Regular 

P wave:  Saw –toothed shape. These waves referred to as F wave

PR interval; Multiple F waves may make it difficult to determine the PR interval. 

P: QRS ratio: 2:1, 3:1, or 4:1 

Sign and Symptoms 

ü  Chest pain

ü  Shortness of breath

ü  Low blood pressure.

Management

ü  The urgency of treatment depend on the ventricular response rate& resultant symptoms

ü  A Calcium channel blocker such as Diltiazem (cardizem) may be used to slow AV Nodal

conduction  used with caution in the patient with CHF, hypotension

ü  Digitalis & Quinidine preparation may be used.

ü  A beta –adrenergic block drug such as Esmolol may be used.

ü  If drug therapy is un successful, trial flutter will often respond to cardiversion.

ü  Small doses of electrical current are often successful

 

C. Atrial Fibrillation

                May occur for a very short time (paroxysmal) or it may be chronic

 most common dysrhythmias that cause patients seek medical attention

shorter time in diastole reduce the time available for coronary artery perfusion, thereby increasing the

risk for myocardial ischemia.

 

 erratic atrial contraction promotes the formation of a thrombus within the  atria  increasing the risk of

stroke (brain attack).

Characteristics:

ü  Ventricular and atrial rate: Atrial rate is 300 and 600 in untreated atrial fibrillation

ü  Ventricular and atrial rhythm: Highly irregular

QRS shape and duration: usually normal but may be abnormal

P wave:  No discernible P waves; irregular undulating waves are seen and are referred to as

fibrillatory or waves.

PR interval: Cannot be measured

P: QRS ratio: many:1

Management

ü  Cardioversion (restoration of normal heart rhythm may be indicated for atrial fibrillation that has

been present for less than 48 hours, a condition termed acute onset of atrial fibrillation

ü  Acute onset, the medication  quinidine, Ibutilide,flecanide, dofetilide, profafenon,

procanamide, dysopyramide or amiodirone may be given  to achieve  conversion  to sinus

rhythm

ü  Intravenouse adenosine (adenocard,adenescan) has also been use for conversion, as well as  to

assist  in the diagnosis.

ü  Calcium channel blocker and beta blocker are effective in controlling the ventricular rate in 

atrial fibrillation

ü  Use Digoxin is recommended to control the ventricular rate those patient  with  poor  cardiac

function

ü  Aspirin may be substituted for warfarin.

 

Junctional Dysrhythmias

ü  Premature Junction Complex

an impulse that starts in the AV nodal before the next normal sinus impulse reaches the AV node

Premature junction complex are less common than PAC’s

ü  The criteria for premature junction complex are the same as for PACs except for the Pwave and the

PR interval.

ü  The Pwave may be absent QRS, or may occur before the QRS but with a PR interval of less than

0.12 second

ü  Treatment for frequency premature junction complexes is the same as for frequent PACs.

 

Junctional Dysrhythmias

 

B. Junctional Rhythm

Junctional or idionodal rhythm occur when the AV node, instead of the sinus node, become the

pacemaker of the heart.

Characteristics:

ü  Ventricular and atrial rate: 40 to 60

ü  Ventricular rhythm: Regular

QRS duration: Usually normal but may be abnormal  

P wave: May be absent, after the QRS complex, or before the QRS; may be inverted, especially in lead

II 

PR interval: If P wave is in front of the QRS, PR interval is less than 0.12 second 

P: QRS ratio1:1 or 1:1 

 

C. Atrioventicular Nodal Reentry Tachycardia

Occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted

back into the same area over and over again at a very fast rate.

It has an abrupt onset and an abrupt cessation with a QRS of normal duration had been called

paroxysmal atrial tachycardia (PAT) 

Characteristics: 

ü  Ventricular and atrial rate: atrial rate 150-250; vent rate: 75-250

ü  Ventricular and atrial rhythm: Regular; sudden onset and termination of the tachycardia

QRS duration: Usually normal but may be abnormal  

P wave: usually very difficult to discern 

PR interval: If P wave is in front of the QRS, PR interval is less than 0.12 second 

P: QRS ratio1:1 or 2:1 

 

Ventricular Dysrhythmias

 

A. Premature Ventricular Complex

Caused by acute MI other form of heart disease, pulmonary disease, electrolyte disturbance, metabolic

instability and drug abuse

The wave of impulse originates from an ectopic Focus (Foci) within the ventricles at rate faster than

the next normally occurring beat.

Because the normal conduction pathway is by passed configuration of the PVC is wider than normal

and is distorted in appearance.

 PVC’s may occur in regular sequence with normal rhythm.

Characteristics:

ü  Ventricular and atrial rate: Depend on the underlying rhythm.

ü  Ventricular and atrial rhythm: Irregular

QRS duration: 0.12 second or longer shape is bizarre and abnormal

P wave: none

PP interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 second

P: QRS ratio 0:1, 1:1

Management

ü  standard treatment is Lidocaine hydrochloride (Xylocaine) by IV push

ü  Be alert to the development of confusion, slurring of speech and diminished mentation because

lidocaine toxicity affects the CNS.

ü  If ventricular premature beats occur in conjunction with bradysrhythmias, atropine may be chosen

to accelerate the heart rate and eliminate the need for ectopic beat.

ü  Atropine should be used with caution in acute MI. the injured myocardium may not be able to

tolerate the

accelerated rate.

 

B. Ventricular Tachycardia

Ventricular tachycardia (VT) is designed as three or more PVCs in a row, occurring at a rate

exceeding 100 beats per minute.

 causes are similar to those for PVC

 VT is an emergency because the patient is usually unresponsive and pulse less

Characteristics:

ü  Ventricular and atrial rate: 100to200 beats per minute 

ü  Ventricular and atrial rhythm: Usually Regular 

P wave: atrial rate and rhythm may be indeterminable. 

PR interval: Very Irregular  

P: QRS ratio: difficult to determine 

Ventricular Tachycardia

Management  

ü  Cardioversion may be the treatment of choice, especially if the patient is unstable.

ü  VT in a patient who is unconscious and without a pulse treated in the same manner as ventricular

fibrillation immediate defibrillation is the action of choice.

 

C. Ventricular Fibrillation

                 rapid but disorganized  ventricular rhythm that cause of ventricular  fibrillation  are the

same  as for VT

may  also  result from untreated or unsuccessfully treated  VT, electrical shock

Characteristics:

ü  Ventricular rate: Greater than 300 per minute  

ü  Ventricular and atrial rhytm: Extremely irregular 

QRS duration Irregular

Management

ü  Immediately fibrillation and activation of emergency service

ü   importance of defibrillation is evident in one of the recent change in basic life support.

ü  Placing a call for emergency assistant and calling for a defibrillator takes precedence over initiating

Cardio pulmonary resuscitation in adult victim.

ü  Application of an automatic external  defibrillator AED is included in basic life support

ü  Administering Vaso active and anti arrhythmia medication alternating with defibrillation are

treatment used to try convert the rhythm to normal sinus rhythm.

 

D. Idioventricular Rhythm

also called ventricular escape rhythm, occur when the impulse starts in the conduction system below

the AV node.

  Commonly cause the patient to lose consciousness and experience other  signs and symptoms  of

reduced cardiac out put .

Intervention may include identify the underlying cause, administering

Intravenous atropine andvasopressor medication. Initiating emergency transcutaneous pacing.

Bed rest is prescribed so as not to increase the cardiac work load

Characteristics:

ü  Ventricular and atrial rate: Between 20and 40 if the rate exceeds 40 

ü  Ventricular and atrial rhythm: Regular 

QRS duration: Bizarre, abnormal, duration is 0.12 second or more.

Commonly called flat line, ventricular a systole characterized by QRS complexes,  P wave may be

apparent for a short duration in two different leads.

no heart beat, no palpable pulse and no respiration.

 

E. Ventricular Asystole

  Assessment to identify  the possible cause which may be hypoxia, acidosis, severe electrolyte

imbalance, drug overdose or hypothermia.

Management

ü  CPR and emergency service as necessary to keep the patient alive. 

ü  Transcutaneous pacing may be attempted.  

ü  A bolus of intravenous epinephrine should be administered and repeated  3 to 5 minutes interval 

 

HEART BLOCK

 

Conduction Abnormalities

The nurse first to identify is the underlying rhythm.(eg, sinus rhythmia) then the PR interval is

assessed for the possibility of an AV block.

AV block occurs when the conduction of impulse through the AV nodal are/ is decreased or stopped.

These block can caused by medication (eg,digitalis, calcium channel blockers, beta blocker).

Clinical sign and symptoms of a heart block vary with the resulting ventricular rate and the severity of

any underlying disease processes.

 treatment is based on the hemodynamic effect of the rhythm

 

Types of Conduction Abnormalities

 

A.      First Degree Block

                     Occurs when all the atrial impulse are conducted through the AV node into the ventricle

at a rate slower than normal

 

Characteristics:

Ventricular and atrial   rate: Depend on the underlying rhythm. 

Ventricular and atrial rhythm: Depend on the underlying rhythm. 

QRS duration; usually normal 

P wave: In front of QRS complex; shows sinus rhythm, regular shape. 

P: QRS ratio1:1

 

 

 

B.1     Second Degree Atrioventricular Block Type I

 

                                Second degree type I heart block occurs when all but one of the atrial impulse are

conducted. Through the  AV node into the ventricles. Each atrial impulse a take longer time for

conduction than the one before, until one impulse is fully blocked.

 

Characteristics:

ü  Ventricular and atrial rate: Depend on the underlying rhythm

ü  Ventricular and atrial rhythm: The PP interval is regular if the patient has  an underlying  normal

sinus rhythm; the RR interval characteristically reflect a pattern of change .

 

QRS duration: Normal may be abnormal

 

B.2      Second Degree Atrioventricular Block Type II

Occurs when only some of the atrial impulses are conducted through the AV node into the ventricles

 

C. Third Degree Atrioventricular Block

Occur when no atrial impulse is conducted through the AV node into the ventricle In the third degree

heart block

  two impulses stimulate  the heart :one stimulate the ventricle ,represent by the QRS complex, and

one stimulate the atria .

Characteristics:

ü  Ventricular and atrial rate: Depend on the escape and underlying atrial rhythm. 

ü  Ventricular and atrial rhythm:The PP interval is regular and the RR interval is regular; however 

the PP interval is not Equal to the RR interval. 

QRS duration: Depend on the escape of rhythm 

P wave: Depend on the underlying rhythm 

P: QRS ratio: More P wave than QRS complexes  

Management  

ü  IF the patient is short of breath, complaints of chest pain or lightheadedness, or has low BP:

Intravenous bolus of Atropine is the initial treatment of choice.

ü  If the patient does not respond to atropine or has acute MI, trascutaneous pacing should be started.

A permanent pacemaker may be necessary if the block persist.

ü  Major assessment include all possible  cause of the dysrhythmia and the dysrhythmia’s effect  on

the heart’s ability  to pump adequate blood volume.

ü  When cardiac  output is reduced, the amount of O2 reaching  the tissue and vital organ is

diminished producingthe s/sx associated  with dysrhythmia.

 

Nursing Assessment 

ü  A health history is obtained to identify  any previous occurrence of decreased cardiac output  such

as syncope (fainting), lightheadedness , dizziness , fatigue, chest discomfort  and palpitation 

ü   Coexisting condition that could be a possible cause of  heart block or dysrhythmia (heart disease,

chronic obstructive pulmonary disease ) may be also identified.

ü  All medications  prescribed and over the counter (supplements herbs and nutritional) may be

reviewed.

ü  nurse conducts physical assessment  to the patient  with diminished cardiac output  especially the

level of LOC

ü  nurse directs attention to the skin which may be pale and cool.

ü  Signs of fluid retention, such as neck vein distention and crackles and wheezes auscultated in the

lungs.

ü  nurse auscultates for extra heart sounds ( especially S3 and S4 ) and for  heart murmur, measure

blood pressure indicates reduced cardiac output.

 

 

Nursing Diagnosis

ü  Decreased cardiac output

ü  Anxiety related to fear of the unknown

ü  Deficient knowledge  about the dysrhythmias and its related treatment.

 

Collaborative Problems and Potential Complication

ü  May developed over time : a heart failure

Thromboembolic

 

Cardiopulmonary Resuscitation

of the Pregnant Woman

Fetus should be monitored during the cardiac arrest

 

THERAPEUTIC MANAGEMENT

CLASS I AND   II

ü  Limit physical activity

ü  Avoid excessive weight gain

ü  Prevent infection

ü  Undergo physical assessment for the development of CHF

ü  pulmonary edema, or cardiac dysrythmias

 

CLASS III AND IV

ü  To prevent cardiac decompensation and development of CHF

ü  Protect the fetus from hypoxia and IUGR.

 

ü  Bed rest

- increased risk of thrombus formation

 

DRUG THERAPY

ü  ANTICOAGULANTS

Clotting factors increase

Thrombolytic activities decrease

Subcutaneous heparin

Enoxaparin (Lovenox)

ü  ANTIDHYRHYTHMICS

Must balance benefits to the mother against possible harm to the fetus

Digoxin, Adenosine , Ca Channel Blockers appears to be safe

Beta Blockers causes  neonatal respiratory depression, sustained bradycardia and hypoglycemia 

ü  ANTI-INFECTIVES

For endocarditis

Gram –positive Staph are common to IV drug users

Maternal Gonorrhea infection may cause rapidly developing endocarditis

Amoxycillin, Penicillin, Ampicillin, Gentamicicn, Ceftraxone, or Vancomycin

 

Cardiovascular Disorders

 

Heart transplantation

Increasing numbers of heart recipients are successfully completing pregnancies

Before conception, woman must be assessed for quality of ventricular function and potential rejection

of transplant

Vaginal birth is desired, but transplant recipients have an increased rate of cesarean births

Neonate may exhibit immunosuppressive effects during first week of life

Breastfeeding not advised for infants of mothers taking cyclosporine  

Nursing Process:

The Pregnant Woman with Cardiac Disease

 

ASSESSMENT

Health history

                (prepregnancy cardiac status)

Medical history

Family historyReview

ü  Level of exercise performance

v Breathing pattern

v Peripheral tissue perfusion

ü  Cardiopulmonary status

 

NORMAL

ü Fatigue

ü Chest pain

ü Dyspnea

ü Orthopnea

ü Palpitations

 

ABNORMAL

ü  Symptoms at rest

ü  Exertional chest pain

ü  Severe dyspnea

ü  PND

ü  Dysrhythmia (>120bpm)

Medication intake

Emotional status

Cultural background

ü  Family size

ü  Role expectations

Physical Examination

ü  Subjective symptoms

ü  Objective signs

§ Increasing fatigue, DOB (with usual activities)

§ Frequent cough

§ Palpitations (“heart is racing”)

§ Swelling:  face, fingers, feet

§ Weak and irregular PR

§ Progressive, generalized edema

§ Crackles at base of lungs

§ Orthopnea

§ Cyanosis of lips and nailbeds

Laboratory and Diagnostic Tests

ü  Urinalysis

ü  Blood work (CBC, blood chemistry)

ü  Baseline ECG or 2D echocardiogram

ü  CXR

ü  Fetal UTZ, NST (non-stress test)

Nursing Diagnoses

ü  Fear

ü  Knowledge deficit

ü  Risk for Self-care deficit (bathing, grooming, dressing, etc.)

ü  ↑ peripartum risk

ü  Cardiac condition

ü  Fatigue or activity intolerance

 

Focus of Treatment

To minimize stress to the heart

Management

ü  Restriction of activity

ü  Nutrition counseling

ü  Medication

 

v  Prenatal period

Promote rest

 

If CO inadequate

↓

Peripheral vasoconstriction

↓ 

Uterine/placental constriction

 

REST Program

Rest periods

(naps and sleeptime)

CBR at week 30 of pregnancy

Left lateral recumbent position

 

 

v  Intrapartum period

Mode of delivery

Vaginal birth under epidural anesthesia

 

NURSE ALERT!

Cesarean section not recommended

Dramatic fluid shifts

↑ blood loss

Sustained hemodynamic changes

INTRAPARTUM PERIOD

ü  Vital signs monitoring

ü  Color and temperature check

 

NURSE ALERT! 

PR = > 100 bpm

RR = > 25 cpm

Pale, cool, and clammy skin may indicate cardiac shock

 

ü  ABG to assess oxygenation status

ü  ECG and BP monitoring

 

For cardiac decompensation,

ü  digitalis

ü  diuresis

ü  supplemental oxygen

 

v  Postpartum period

First 24 to 48 hours

most hemodynamically difficult

 

 

Extravascular fluid remobilized into vascular compartment

↓

Cardiac output increases

↓

Intra abdominal pressure reduced

↓ 

Pressure on veins removed

↓ 

Splanchnic vessels engorge

↓ 

Blood flow to the heart increased

(reflex bradycardia)

POST PARTUM PERIOD

Care tailored to functional capacity

position HOB, patient

CBR with or without BRP

progressive ambulation

 

NURSE ALERT!  Monitor vital signs 

ECG Rhythm Interpretation

ECG Basics

 Objectives

To recognize the normal rhythm of the heart - “Normal Sinus Rhythm.”

 

To recognize the 13 most common rhythm disturbances.

 

To recognize an acute myocardial infarction on a 12-lead ECG.

 

Electrocardiogram

 

1.An electrocardiogram is a recording of the electrical changes that occur during a cardiac cycle.

2.The first wave, the P wave, corresponds  to the depolarization of the atria.

3.The QRS complex corresponds to the depolarization of ventricles and hides the repolarization of

atria.

4.The T waves end the ECG pattern  and corresponds to ventricular

   repolarization.

 

 

Regulation of the Cardiac Cycle

 

1.The amount of blood pumped at any one time must adjust to the current needs of the body (more is

needed during strenuous exercise).                               

2.The S-A node is innervated by branches of the sympathetic and parasympathetic divisions, so the

CNS controls heart rate.

3. Sympathetic impulses speed up and parasympathetic impulses slow down heart

rate.                               

4.Impulses from cerebrum or hypothalamus may also influence heart rate, as do body temperature

and the concentrations of certain       ions.

 

ELECTROCARDIOGRAM

12-lead electrocardiogram is a representation of the heart's electrical activity recorded from electrodes

on the body surface

12 –Lead ECG Placement

Impulse Conduction & the ECG

Sinoatrial node

 

AV node

 

Bundle of His

 

Bundle Branches

 

Purkinje fibers

Normal Impulse Conduction

Sinoatrial node

 

AV node

 

Bundle of His

 

Bundle Branches

 

Purkinje fibers

The “PQRST”

                     P wave - Atrial                                             depolarization

 

 

 

The PR Interval

Atrial depolarization

+

delay in AV junction

 (AV node/Bundle of His)

 

 (delay allows time for the atria to contract before the ventricles contract)

 

Pacemakers of the Heart

 

ü  SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.

ü  AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.

ü  Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

ü  The ECG Paper

Horizontally

One small box - 0.04 s

One large box - 0.20 s

Vertically

One large box - 0.5 mV

 

Every 3 seconds (15 large boxes) is marked by a vertical line.

This helps when calculating the heart rate.

 

NOTE: the following strips are not marked but all are 6 seconds long.

 

 

How to Analyze a Rhythm

Rhythm Analysis

                Step 1:     Calculate rate.

                Step 2:     Determine regularity.

                Step 3:     Assess the P waves.

                Step 4:     Determine PR interval.

                Step 5:     Determine QRS duration.

Step 1: Calculate Rate

 

ü  Option 1

Count the # of R waves in a 6 second rhythm strip, then multiply by 10.

Reminder: all rhythm strips in the Modules are 6 seconds in length.

ü  Option 2

Find a R wave that lands on a bold line.

Count the # of large boxes to the next R wave. If the second R wave is 1 large box away the rate is

300, 2 boxes - 150, 3 boxes - 100, 4 boxes - 75, etc. 

 

Memorize the sequence:

300 - 150 - 100 - 75 - 60 - 50

 

Step 2: Determine regularity

 

Look at the R-R distances (using a caliper or markings on a pen or paper).

Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular? Irregularly irregular?

 

Step 3: Assess the P waves

 

Are there P waves?

Do the P waves all look alike?

Do the P waves occur at a regular rate?

Is there one P wave before each QRS?

 

Step 4: Determine PR interval

 

Normal: 0.12 - 0.20 seconds.

                                                    (3 - 5 boxes)

 

Step 5: QRS duration

 

Normal: 0.04 - 0.12 seconds.

                 (1 - 3 boxes)

 

Rhythm Summary

 

Rate                                                        90-95 bpm             

Regularity                                               regular

P waves                                                   normal

PR interval                                              0.12 s

QRS duration                                          0.08 s 

 

Normal Sinus Rhythm

Normal Sinus Rhythm (NSR)

 

Etiology: the electrical impulse is formed in the SA node and conducted normally.

 

This is the normal rhythm of the heart; other rhythms that do not conduct via the typical pathway are

called arrhythmias.

 

NSR Parameters

Rate                                        60 - 100 bpm         

Regularity                               regular

P waves                             normal

PR interval                              0.12 - 0.20 s

QRS duration                     0.04 - 0.12 s 

Any deviation from above is sinus tachycardia,

sinus bradycardia or an arrhythmia

 

Arrhythmia Formation

Arrhythmias can arise from problems  in the:

ü  Sinus node

ü  Atrial cells

ü  AV junction

ü  Ventricular cells

 

SA Node Problems

The SA Node can:

ü fire too slow

ü fire too fast

Sinus Bradycardia

 

Sinus Tachycardia

 

Atrial Cell Problems

Atrial cells can:

ü  fire occasionally from a focus

ü  fire continuously due to a looping re-entrant circuit

 

Premature Atrial  Contractions (PACs)

 

Atrial Flutter

A re-entrant pathway occurs when an impulse loops and results in self-perpetuating impulse formation.

 

Atrial Cell Problems

AV Junctional Problems

The AV junction can:

ü  fire continuously due to a looping re-entrant circuit

ü  Block  impulses coming from the SA Node

 

  Paroxysmal   Supraventricular Tachycardia

 

AV Junctional Blocks

 

Ventricular Cell Problems

Ventricular cells can:

ü  fire occasionally from 1 or more foci

ü  fire continuously from multiple foci

ü  fire continuously due to a looping re-entrant circuit

 

Premature Ventricular Contractions (PVCs)

 

Ventricular Fibrillation

 

Ventricular Tachycardia

DYSRHYTHMIAS

 

Dysrhythmias are disorders of the formation or conduction (or both) of the electrical impulse

within the heart.

These disorders can cause disturbances of the heart rate, the heart rhythm, or both

Initially evidenced by  hemodynamic effect they cause (eg, a change in conduction may change

the pumping action of the heart and cause decreased blood pressure)

 

Diagnosed by analyzing the ECG waveform.

 

Electrical impulse stimulates and paces the cardiac muscle & normally originates in the SA node, near

superior vena cava in the right atrium.

 

Electrical impulse occurs at a rate ranging between 60 - 100 times a minute in the adult.

 

Sinus rhythm promotes cardiovascular circulation.

 

Electrical impulse causes mechanical contraction of the heart muscle.

 

 

Electrical stimulation is called depolarization; mechanical contraction is called systole

 

Electrical relaxation is called repolarization; mechanical relaxation is called diastole

 

 

Normal Sinus Rhythm

 

Rate is between 60 and 100 beats/minute

The rhythm is regular

All intervals are within normal limits

There is a P for every QRS and a QRS for every P

The P waves all look the same

 

Sinus Bradycardia

Impulse in the sinus node is created at a slower rate.

Rate is lower than 60 beats/minute

The rhythm is regular

All intervals are within normal limits

There is a P for every QRS and a QRS for

every P

 

Sinus Bradycardia

The P waves all look the same

Caused by beta-blocker, digitalis, or calcium channel blockers.  Normal for athletes

Don’t treat unless there are symptoms.  Can use pacing or atropine

 

Atropine, 0.5 to 1.0 mg given rapidly as an intravenous (IV) bolus, is the medication of choice in

treating sinus bradycardia.

 

It blocks vagal stimulation, thus allowing a normal rate to occur.

 

Rarely, catecholamines and emergency transcutaneous pacing also may be implemented.

Sinus Tachycardia

Impulse in the sinus node is created at a faster rate. Rate above 100 beats/minute

 

The rhythm is regular. All intervals are within normal limits.

 

There is a P for every QRS and a QRS for every P. The P waves all look the same.

 

Sinus Tachycardia

Caused by fever, stress, caffeine, nicotine, exercise, or by increased sympathetic tone

 

may be caused by acute blood loss, anemia, shock, hypervolemia, hypovolemia, congestive heart

failure, pain, hypermetabolic states

 

Treatment is to take care of the underlying cause

 

Treatment if ischemia occurs

                administration of beta-adrenergic blocker, calcium channel blocker

 

Sinus Arrhythmia

Rate is between 60 and 100 beats/minute

The rhythm is irregular.

The SA node rate can increase or decrease with respirations

All intervals are within normal limits

There is a P for every QRS and a QRS for every P.

The P waves all look the same

Ask the patient to stop breathing and the rate will become regular

P-P and R-R are shorter during inspiration and longer during expiration.

More common in children and athletes

 

 

 

 

Atrial Flutter/ saw-toothed waves

 

Atrial rate is between 250 and 350 beats/minute.  Ventricular rate can vary

The rhythm is regular or regularly irregular

There is no PR interval.  QRS may be normal 2:1 to 4:1 f waves to every QRS

There are no P waves; they are now called flutter waves or F waves

Problem: Loss of atrial kick and ventricular conduction is too fast or too slow to allow good filling of

the ventricles

Treatment 

ü  Calcium channel blocker ,Beta adrenergic blocker

ü  Amiodarone, ibulitide, procainamide, flecainide. propafenone if arrythmia is present for less than 48

hrs.

ü  Anticogulation before cardioversion

ü  Synchronized cardioversion

 

 

Atrial Fibrillation/ more F waves

 

Atrial rate is between 350 and 600 beats/minute;  ventricular rate can vary

The rhythm is irregular

There is no PR interval;  QRS may be normal

Atrial Fibrillation/ more F waves

There are many more F waves than QRSs

 

Unlike flutter where the f wave will appear the same, in fib the f waves are from different foci so

they are different

 

  Treatment is the same as atrial flutter

Rate is between 100 and 200 bpm

Rhythm is regular, but can change to different rhythms

No PR interval; QRS is wide and aberrant

There may be a P wave, but it is not related to the QRS

 

Hematologic Disorders

 

Iron-deficiency Anemia

 

Anemia

  reduced ability of the blood to carry oxygen to the cells.

 

In pregnancy

 Hgb <10mg/dl & Hct ↓30%

 

Reduces O2-carrying capacity of blood

 

Heart compensates by ↑CO

 

↑ Cardiac workload

 

Ventricular function is stressed

 

CHF

 

Normal Values

ü  Packed RBC volume (HEMATOCRIT)

ü  An indirect index of the O2-carrying capacity

 

Effects

ü  Blood loss at birth not well tolerated

ü  Increased risk for blood transfusions

 

Pregnancy

 

↑maternal plasma volume & ↓ total RBC

 

↑ nutrient carrying capacity of the plasma but ↓ the viscosity of whole blood

(disproportionate rise in bld constituents)

 

Hemodilution

 

↓in Hgb concentration

 

Anemia

 

Fetus requirement for Iron

+

Poor general nutrition

(economic status/nausea & vomiting)

 

Maternal depletion of iron stores

 

Iron-deficiency anemia

ü  Accounts for about 90% of anemia cases in pregnancy

ü  Associated with LBW and preterm births

 

Iron Deficiency Anemia

   Iron absorbed from duodenum into bloodstream

 

Binds to transferrin

 

Transported to liver, spleen and bone marrow

 

Incorporated into hemoglobin

(stored as ferritin)

 

 

Microcytic (small-sized RBC)

 

Hypochromic (↓ Hgb than the average RBC)

 

Deficient iron stores results from:

ü  Poor nutritional status

ü  Heavy menstrual flow

 

Management

Oral iron supplements

ü Prophylactic therapy 30-60 mg/day

ü Therapeutic regimen 120-180 mg/day

Dietary instruction:  food sources

ü Liver

ü Meats

ü Whole or enriched bread/cereals

ü Deep green leafy vegetables

ü Legumes

ü Dried fruits

§Nursing Care

ü Diet history during prenatal visits

ü Dietary teaching PRN

ü Assess other needs (emotional support, financial aid, etc.)

ü Provide for appropriate resources or referral

Nursing considerations

ü Take with orange juice or vitamin C

ü Iron is best absorbed in an acid medium 

ü IF NOT TOLERATED, IM or IV Dextran

Folic acid deficiency anemia

 

Folic acid deficiency anemia

ü  Accounts for about 1 – 5 % of anemia cases in pregnancy

ü  Common in multiple gestations

 

Megaloblastic (enlarged RBC)

 

Effects

ü  Early abortion

ü  Abruptio placenta (premature placental separation)

 

Folic acid

 Folacin (Vitamin B)

ü  normal RBC formation

ü  prevents neural tube defects

v cleft lip

v   cleft palate

 

Nutritional instruction

ü  RDI (recommended dietary intake) 400micrograms/day

 

Therapeutic regimen:  1 mg/day

 

Food sources

ü  Fortified ready-to-eat cereals

ü  Green leafy vegetables

ü  Oranges

ü  Broccoli

ü  Asparagus

ü  Liver

Blood Incompatibilities

OVERVIEW : ANATOMY AND PHYSIOLOGY

 

ü  STRUCTURES OF THE HEMATOLOGIC SYSTEM

ü  BLOOD

ü  BLOOD VESSELS

ü  BLOOD FORMING ORGANS

BONE MARROW

SPLEEN

LIVER

LYMPH NODES

THYMUS GLAND

 

COMPOSITION OF THE BLOOD

ü  PLASMA ( 55%)

ü  CELLULAR COMPONENTS (45%)

99% - erythrocytes

1% - leucocytes and thrombocytes

 

BLOOD FORMING ORGANS

ü  BONE MARROW

Site of hematopoeisis or blood cell formation

One of the largest organs of the body, making up 4% to 5% of total body weight

Consists of cellular components  (red marrow) separated by fat (yellow marrow)

 

BLOOD COMPONENTS

ü  ERYTHROCYTES

Biconcave disc; no nucleus, chiefly sacs of hemoglobin

PRIMARY FUNCTION:

To transport oxygen from the lungs to the various tissues of the body and to assist in the transport of

carbon dioxide from tissues to the lungs

 

Two portions of erythrocytes:

ü  IRON – carried on the heme portion

ü  PROTEIN – on the second portion

 

 Iron- small intestine as ferritin  when required  released into the plasma binds

to transferrintransported into the membranes of the RBC in the marrow      incorporated into

hemoglobin

 

v  LEUKOCYTES

Are spherical cells that are whitish in color because they lack hemoglobin

PRIMARY FUNCTION:

Involved in the  protection from bacteria and other foreign substances

 

TWO CELL TYPES:

v  Granulocytes

Eosinophils – involved in phagocytosis and allergic reactions 

Basophils – prevention of clotting and allergic reaction 

Neutrophils – involved in phagocytosis 

 

v  Agranulocytes

Monocytes – phagocytosis

Lymphocytes – produce substances against foreign cells

 

THROMBOCYTES (PLATELETS)

Minute cell fragments surrounded by a plasma membrane

and containing granules

 

PRIMARY FUNCTION:

Forms platelet plugs, releases chemicals necessary for blood clotting

 

PLASMA

Liquid part of the body, yellow in color because of pigments

 

3 MAJOR TYPES OF PLASMA PROTEINS:

ü  Albumin – prevents the plasma from leaking into tissues

ü   Globulins – transports other substances and protects the body against infection

ü   fibrinogen – a protein molecule that can be activated to form fibrin important in clotting

process

 

ü  SPLEEN

Located under the diaphragm to the left of the stomach Destroys old imperfect RBCs, breaks down

hemoglobin released from these destroyed cells, stores platelets and filters antigens

3         types of tissues:

White pulp – filled with WBC, esp. lymphocytes and macrophages

Red pulp – contains vascular enlargements that stores RBCs and platelets

Marginal pulp – contains end of arteries and other blood vessels

 

ü  LIVER

Largest glandular organ of the body

Main production site for prothrombin and most blood clotting factors

Converts bilirubin to bile and stores extra iron within the protein ferritin

 

ü  LYMPH NODES

Fleshy pea sized structures found in groups or chains throughout the body

Traps infection and foreign materials by acting like a sieve

   Blood Incompatibility Between the Pregnant  and Fetus

 

 

Rh Incompatibility

The Rh-negative Blood type

Is

An autosomal recessive trait

 

A person must receive a gene for this characteristics from both parents

Alternative Names   

ü  Rh-induced hemolytic disease of the newborn

ü  Hydrops fetalis

Rh incompatibility

 -  excessive destruction of RBC which develops when  a pregnant woman has an Rh(-) blood type

                             +

the fetus she carries has Rh(+) blood type

 

 

 

 

 

 

antigen is

named “Rh” because

 it was

1st identified in

the blood of

rhesus monkeys

 

Causes 

During pregnancy, red blood cells from the fetus can get into the mother's bloodstream as she

nourishes her child through the placenta

 

If mother is Rh-negative, her system cannot tolerate the presence of

Rh (+) RBC

 

mother's immune system treats

the Rh (+) fetal cells as if they

were:

                                                1. a foreign substance

                                                2. makes antibodies against

                                                    the fetal blood cells

 

If some of fetus' blood passes into the mother's blood stream, her body will produce antibodies in

response

 

mother is said to be sensitized

(the process by which a person produces antibodies against the antigens of a different

species, eg. Measles virus is called

 

These anti-Rh antibodies

 may cross the placenta

into the fetus,

where they destroy

 the fetus's circulating red blood cells

 

Due to the excessive   destruction of fetal blood

 

becomes deficient in RBC

 

cannot deliver

Sufficient oxygen to fetal cells

 

 

Erythroblastosis Fetalis

                disease in fetus or newborn caused by transplacental transmission of maternal antibody, 

resulting from maternal and fetal blood group incompatibility

 

Incidence

First-born infants : not affected -- unless the mother has had previous miscarriages or abortions,

which could have sensitized her system

R: takes time for the mother to develop antibodies against the fetal blood.

 

Second child who is also Rh-positive

may be harmed.

Symptoms   

ü  Polyhydramnios (before birth)

ü  Hypotonia

ü  Motormental Retardation

ü  Slowly or rapidly increasing jaundice

ü  Prolonged jaundice

ü  Hyperbilirubinemia: bilirubin level in the blood is increased yellowish discoloration of the skin,

mucous membrane, sclera and other organs

 

Manifestation

ü  Yellowish discoloration = JAUNDICE or ICTERUS

 

                Icterus Index :representing the bilirubin concentration in the blood plasma 4-6 units

 

The observations of HDN will include:

ü  Hepatosplenomegaly

ü  Icterus Gravis – anemia & deep                                                                              jaundice

 

Hydrops Fetalis – generalized edema

 

The observations of HDN will include:

ü  Kernicterus -  excessive staining of brain cells with bilirubin              

results:                                    

                                - Brain damage

                                - Mental retardation

                                - Nerve deafness

                                - Muscle spasticity

                                - Athethoid movement

                                - Death

 

Assessment / Diagnosis

1.  All pregnant woman should be tested for:

blood group

Rh factor

Routine antibody screening

Blood transfusions

2. If the mother is Rh (-), the father of

                the infant is tested to determine his Rh status.

                *an Rh (-) father and mother will only produce Rh (-) offspring who will not be

affected by Rh incompatibility*

3.  Rh (-) pregnant  woman who has Rh (+) husband will have to undergo:  an anti-D antibody

titer                            (INDIRECT COOMBS TEST)

 

Done on the 16th–20th wk of  pregnancy

                IF the titer is normal (less than 1.8), no intervention is immediately necessary

BUT, a repeat indirect Coombs test will  be made on the 7th -8th month of pregnancy

= IF  results are normal, mother will be allowed to progress on with pregnancy and deliver full term.

= once baby is delivered, his blood will be examined for the Rh factor

= IF  baby is Rh (-), there’s no problem.

= IF  baby is Rh (+),he will undergo cord blood examination to determine presence of maternal

antibodies in  baby’s blood stream, (DIRECT COOMBS TEST)

 

DIRECT COOMBS TEST

IF baby is Rh (+)

and (-)for Coombs test

 

mother will be given

RhoGam

 

BUT If baby is Rh (+) and (+) for Coombs test

 

 useless to give

RhoGam to the mother

 

IF the INDIRECT COOMBS TEST of a Rh (-) pregnant woman with a Rh (+) husband is positive at the

start

 

pregnancy will be allowed to progress

But Amniocentesis will have to be repeated at regular intervals

 

 If studies revealed that  fetus is severely affected, signs & symptoms of     

    Erythroblastosis Fetalis will be observed.

 

 

 

 

*due to excessive  RBC destruction and efforts of the fetus to make more RBC ensue*

 

Laboratory & Diagnostic Findings

 

SPECTROPHOTOMETER

used to read amniotic fluid collected

Readings are obtained to determine fluid density

Plotted on graph & correlated w/ gestational age

                     amt of bilirubin resulting from the hemolysis of RBCs can be estimated.

 

c. Antibody Titer

 drawn at  first prenatal visit on all Rh negative women

drawn at 28 & 36 weeks & again at delivery or abortion.

Normal value is 0.

Ratio: Normal is1:8

If titer is absent or minimal (1:8) no therapy is needed.

A rising titer indicates the need for RhoGAM & vigilant monitoring of fetal wellbeing.

 

What is Rhogam ?

 

 

Management of Erythroblastosis Fetalis:

ü  Fetal intrauterine transfusion

ü  Exchange transfusion

ü  Phototherapy

 

Fetal Intrauterine Transfusion

Purpose:

                     - to replace destroyed RBC’s

 

 Procedure:

Amniotic cavity is penetrated and fetal  peritoneal cavity is entered by means of a special needle with

radiopaque dye and a  catheter is threaded into it

75-100 ml of type O, Rh (-) PRBC will be given to the fetus

                                *the blood to be transfused to the fetus should be exactly the same as that of the

mother so as not to be destroyed by the antibodies*

FHR and mother’s v/s monitoring

reaction to the dye should also be observed

If  satisfactory,  mother is discharged and readmitted after 7-10 days for another fetal intrauterine

transfusion until fetus is mature.

 

Exchange Transfusion

Purpose  : relieves  baby’s anemia  

                                        : lowers blood’s concentration   of the bilirubin

 

Procedure:

ü  umbilical stump is left longer than usual

ü  Wrapped in saline saturated gauze to prevent drying of the stump

ü  NPO for 3 hrs prior to  transfusion 

ü  Plastic catheter is inserted into umbilical vein and small amounts  (10-20ml)of infants blood are

withdrawn.

ü  Equal  amounts of type O, Rh (-) blood is transfused

                venous catheter for fluids, meds;              arterial catheter for extraction of blood           

ü  Procedure is continued  until most of the infants blood (around 500 ml) has been replaced with Rh 

(-) blood

 

ü  1ml of Calcium Gluconate is injected after each 100-200 ml of donor blood

                -in order to replace ions depleted   by citration (acid –citrate- dextrose mixture) of

donor blood*

 

 

 

 

 

Exchange Transfusion

NURSING RESPONSIBILITIES:

 

ü  Make sure that thedonor blood is around 37 degrees Celsius to prevent cardiac arrest

ü  monitor CVP

ü  Give antibiotics as ordered

ü  Monitor for v/s

ü  Monitor for serum glucose

ü  Observe for muscle twitching and other signs of hypocalcemia

 

Phototherapy

Photo oxidation by the use of  artificial blue light (bililight) in order to convert bilirubin to an excretable

one

 

NURSING RESPONSIBILITIES:

ü  Cover infants eyes*

ü  Cover infants genetalia*

ü  Increase fluid intake*

ü  Expose all areas of the body*

ü  Assess for loose green stools*

ü  Assess temperature every 2hrs*

ü  Monitor bilirubin level*

 

 

Prevention   

               Completely preventable.

 

Rh-negative mothers  to be closely monitored

    by obstetricians during pregnancy.

 

If father is Rh-positive,  mother is given a mid-term injection of RhoGAM ;second injection within

afew days of delivery.

 

injections prevent the development of antibodies against Rh-positive blood.

 

An Rh positive person can receive Rh negative blood with no untoward effects

   ( if all other factors are compatible)

 

Rh negative blood cannot receive Rh positive blood because they are not born with

antibodiesagainst the Rh factor.

 

Pregnancy

Nursing Management

 

Administer RhoGAM to the unsensitized Rh-negative client as appropriate

 

RhoGAM must be administered to the mother w/in 72h of delivery

 

Type & cross match of the mother’s blood & newborn’s cord blood must be done before administration

to determine the need for the drug.

 

Administer RhoGAM to the unsensitized Rh-negative client as appropriate

 

Do not give RhoGAM to the newborn.

 

The dose may be given w/in 3-72h after a miscarriage or abortion.

 

Do not administer IV. Administer into the deltoid muscle

 

Monitor for side effects (anemia, pain at injection site, fever.

 

May decrease antibody response to some live virus vaccines, such as measles, mumps and rubella.

 

2.Focus mgt. of sensitized Rh-negative mother on close monitoring of fetal well being

 

3. Provide management for ABO incompatibility

Phototherapy

Initiation of early feeding & exchange blood transfusion

 

4. Provide client family teaching & counseling.

 

Rh Factor

The dose must be repeated after each subsequent delivery.

 

 RhoGAM 300 mcg is the standard dose.

RhoGAM Rho (d) immune globulin, human

ABO Incompatibilty

type O

( universal donor but cannot receive from other blood type)

 

ABO Incompatibility

Reaction in an infant with type B blood is more serious

 

Hemolysis happens with first pregnancy (antibodies  to A and B cell types are present from birth)

 

Large IgM ( do not cross the placenta)

 

Infant is not born anemic

 

Hemolysis begins with birth

 

Destruction may extend for up to 2 weeks

 

Pre term infants do not seem to be affected ( receptor sites for ant A and B antibodies do not appear

on RBC till late in fetal life)

 

Even in mature NBs, direct Coomb’s test: weakly positive ( few ant A & B sites)

Reticulocyte count ( immature or newly formed RBC ) usually elevated as infant attempts to replace

destroyed cells

 

Jaundice occurs due to RBC destruction

 

 

THROMBOPHLEBITIS and THROMBOSIS

 

Etiology

ASSESSMENT

MEDICAL MANAGEMENT

ANTICOAGULANTS

Metabolic Disorders

 

Normal glucose metabolism

Glucose enters bloodstream from food source

Insulin aids in storage of glucose as fuel for cells

 

Insulin resistance is defined as insensitivity of cells to insulin, therefore resulting in increased levels

of insulin and glucose in the bloodstream

 

Metabolic changes in pregnancy

Caloric requirement for a pregnant woman is 300 kcal higher than the non-pregnant woman’s basal

needs

 

Placental hormones affect glucose and lipid metabolism to ensure that fetus has ample supply of

nutrients

 

Lipid metabolism:

Increased lipolysis (preferential use of fat for fuel, in order to preserve glucose and protein)

 

Glucose metabolism:

Decreased insulin sensitivity

Increased insulin resistance

 

Increased insulin resistance

Due to hormones secreted by the placenta that are “diabetogenic”:

Growth hormone

Human placental lactogen

Progesterone

Corticotropin releasing hormone

Transient maternal hyperglycemia occurs after meals because of increased insulin resistance

 

Relative baseline hypoglycemia

Proliferation of pancreatic beta cells (insulin-secreting cells) leads to increased insulin secretion

Insulin levels are higher than in pregnant than nonpregnant women in fasting and postprandial states

Hypoglycemia between meals and at night because of continuous fetal draw

Blood glucose levels are 10-20% lower

 

Lipid metabolism

Increased serum triglyceride (300%) and cholesterol (50%) levels

Spares glucose for fetus, since lipids do not cross the placenta

Provides building blocks for increased steroid hormone synthesis

 

Insulin Synthesis

Produced within the pancreas by cells, islets of langerhans – identified by Paul Langerhans in 1869

Islets of Langerhans – 1 million islets

cells – secrete glucagons

cells – produce insulin, most abundant

 

Somatostatin suppress secretion of  insulin and glucagon

 

History of Insulin

1920 – Insulin is first discovered by Fredrick Banting and Charles Best

November 1922 - Eli Lilly and Company is first to produce large amounts of insulin

1923 - MacLeod and Banting receive Nobel Prize in Physiology and Medicine for insulin discovery

1964 - Dorothy Crowfoot Hodgkin receives Nobel Prize in Chemistry for determination of spatial

conformation of molecule

1980 - Frederick Sanger, British molecular biologist,  receives Nobel Prize in Chemistry for amino

acid structure determination

 

DIABETES MELLITUS and PREGNANCY

 

WHAT IS DIABETES?

Refers to  group of metabolic diseases that lead to high blood glucose levels due to defects in either:

ü  insulin secretion

ü  insulin action or both

 

WHAT IS DIABETES?

DIABETES MELLITUS

 

Is an endocrine disorder of carbohydrate metabolism

 

PATHOPHYSIOLOGY

Deficiency or ineffective Insulin

 

Glucose accumulates in the bloodstream

(Hyperglycemia)

 

Preexisting Conditions

For some women, pregnancy represents significant risk because it is superimposed on preexisting

illness

 

Unique maternal and fetal needs due to these conditions must be met in addition to usual pregnancy-

related feelings, needs, and concerns

 

Metabolic Disorders

Endocrine and metabolic disorders require careful management to promote maternal and fetal well-

being and positive pregnancy outcome

 

Diabetes mellitus is the most common endocrine disorder associated with pregnancy

 

What are the Signs and Symptoms?

ü  Polyuria (frequent urination)

Glucose concentration in blood is high

Reabsorbtion of glucose in the proximal renal tubuli is incomplete, glucose remains in urine

Osmotic pressure of urine increases

Inhibits reabsorbtion of water by kidney, resulting in increase urine production

ü  Dehydration

Lost water volume in kidney replaced from water held in body, increased thirst and increased fluid

intake –polydipsia

 

ü  Polyphagia

Increased appetite, no glucose delivered to muscles, tissues, body sends signal to brain to eat

something to renourish

 

ü  Weight loss and weakness

glucose cannot participate in crib cycle to be used as energy, use of fat as alternative energy source

 

ü  Vision changes

changes shapes of lens in eye

 

Importance of Control – Complications of Diabetes

 

ü  Diabetic Ketoacidosis

Fat break down accelerates and increase the production of fatty acids

Fatty acids converted into ketone bodies

Ketones are toxic at high levels

 

Symptoms - rapid, deep breathing, polyuria, nausea, vomiting, abdominal pain, altered states of mind

such as hostility, mania, confusion, lethargy, and hypotension, coma, death

 

ü  Hypoglycemia

Low blood sugar, too much insulin or not enough glucose to cover insulin treatment

 

Symptoms - sympathetic activation of the autonomic nervous system: immobilized panic, dread,

agitated, sweaty, seizures

 

ü  Amputations

Heal slowly

Fail to heal

Infection

ü  Vascular diseases

Damage to blood vessels

Diabetic retinopathy – growth of poor quality

new blood vessels in retina, retinal damage, blindness

Diabetic nephropathy – damage to kidney,

                                chronic renal failure – dialysis

Damage to arteries

Coronary artery disease, stroke, peripheral vascular,

                diabetic myonecrosis (‘muscle wasting’)

Diabetic foot – neuropathy and arterial disease

 

Gestational Diabetes

 

Hyperglycemia in mother means more than normal glucose crossing the placenta and going to the

fetus resulting to hyperinsulinism

 

Diabetes Mellitus

Before discovery of insulin in 1922, it was uncommon for a woman with diabetes to give birth to a

healthy baby

 

Pregnancy complicated by diabetes considered high risk

 

Care requires nurse fully to understand normal physiologic responses to pregnancy and altered

metabolism of diabetes

Effects of Pregnancy on Diabetes

 

Classification System: DM

 

WHAT’S THE DIFFERENCE?!

Type 1

Juvenile diabetes mellitus

Don’t be fooled by its name!!!

β-cells that produce insulin are destroyed. 

Results in insulin dependence:

Injection (most common), jet injection, indwelling catheters, & inhaled insulin.

Type 2

Adult onset diabetes mellitus

90% of cases are Type 2

Ineffective insulin activity

Insulin resistance

Eventually leads to insulin dependence:

Similar administrative techniques as Type 1.

 

Pregestational Diabetes:

Types 1 and 2

 

MAJOR TARGETED SITES OF  DRUG CLASSES

 

GESTATIONAL DIABETES

 

Risk factors for the development of Gestational Diabetes

ü  Previous large infants 9lbs or more

ü  Family History of DM

ü  Glucosuria on two successive occasions

ü  Obesity – weight >200lbs

ü  Unexplained pregnancy wastage

                (spontaneous abortions, stillbirths)

ü  Multiparity

ü  Presence of hydramnios

ü  Previous infant w/ a congenital anomaly

 

Gestational Diabetes (GDM)

 

Diabetes Mellitus

Metabolic changes associated with pregnancy

Pregestational diabetes mellitus

Preconception counseling

Maternal risks and complications

ü  Hydramnios

ü  Ketoacidosis

ü  Hypoglycemia

 

Fetal and neonatal risks

ü  Sudden and unexplained stillbirth

ü  Congenital anomalies

Cardiac defects

Central nervous system

Skeletal defects

Other problems that cause significant neonatal morbidity

 

 

Effect of Diabetes on Pregnancy

ü  The fetus is often large ( macrosomia)

ü  4x greater incidence of preeclampsia or

                 Eclampsia

ü  Increase incidence of hydramnios & if coupled

                w/ macrosomia, it can cause cardiopulmonary symptoms

ü  ↑ rate of CS deliveries (45%)

ü   Incidence of congenital anomalies ↑

ü   

Gestational Diabetes

 

Maternal diabetic acidosis is the most common cause of fetal death in pregnancy of a diabetic

mother

In ketoacidosis there is no oxygen and placental exchange at placental site results to:

ü  fetal asphyxia

ü  fetal death

If maternal ketoacidosis is not treated, risk of fetal death increases to between 50 -90 %

 

Macrosomia can be reduced by tight maternal blood glucose control before 32 weeks gestation

 

Polyhydramnios ( increased amniotic fluid greater than 2000 ml) occur in 10% of pregnant

diabetics.

 

Even if the newborn is large, he is basically immature or premature thus more likely to suffer from

respiratory distress syndrome (RDS)

 

PREGNANCY RELATED COMPLICATIONS OF DIABETES

 

Nursing Assessment

ü  Obtain & review client’s family & prenatal Hx

ü  Observe for the previously identified S/Sx & risk factors

ü  Assess client’s knowledge on diabetes & her normal physiological – psychological adaptations in

pregnancy

 

Explain importance of screening tests

 

Diabetic screening

Important especially for the following:

 

ü  History of delivery of large babies >9 lbs.

ü  Unexplained fetal loss

ü   Congenital anomalies in previous pregnancies

ü  Obesity

ü  Family history of diabetes

 

Nursing Assessment

ü  Obtain baseline V/S & FHR & record.

ü   Obtain results of OGTT & other screening & diagnostic test results

ü   Knowledge on the basic testing  procedures

ü   Assess psycho socioeconomic factors  w/ special consideration to the potential stress evoked by the

high risk pregnancy & high cost antepartum testing

 

TESTING TESTING …

Diagnosed according to the following standards:

Casual (not fasting) PG concentration: ≥200mg/dL

2 hour (fasting) PG concentration: ≥200mg/dL

8-hour (fasting) PG concentration:  ≥126mg/dL

Normal resting PG concentration ranges between: 80mg/dL – 100mg/dL

Fasting PG Test:

Detects PG concentrations between 100mg/dL – 125mg/dL

Inexpensive and fast

Oral Glucose Tolerance Test:

Detects PG levels between 140mg/dL - ≥200mg/dL

Takes longer since PG level is monitored for approximately two hours.

 

 

Medical Diagnosis

      The diagnosis should be established or ruled out by the evaluation of blood glucose levels.

 

LABORATORY & DIAGNOSTIC FINDINGS

ü  ↑Fasting Blood Sugar test (FBS)

ü  GLUCOSE SCREENING TEST

FBS (fasting blood sugar of at least 8 hours)

ORAL GLUCOSE TOLERANCE TEST (OGTT) Oral glucose of 50 mg is given and blood sugar is taken

one hour after oral glucose administration

 

Repeated for a 3-hour glucose tolerance test after a positive result of 1-hour screening

ü  GDM: Screening

Screening test

50 gm 1-hour glucose challenge test (GCT)

Screening thresholds

135mg/dL: 90% sensitivity

                (23% screen positive)

140mg/dL: 80% sensitivity

                (14% screen positive)

If patient screens positive, she goes on to take a 3-hour glucose tolerance test (GTT)

 

 

ü  Glycosylated hemoglobin test(HbAIc)

                In the normal 120-day life span of the red blood cell, glucose molecules join hemoglobin,

forming glycated hemoglobin.

 

A buildup of glycated hemoglobin within the red cell reflects the average level of glucose to which the

cell has been exposed during its life cycle.

 

Measures glycemic control 4-8 weeks before test was done.

 

Performed on women with pre-existing Diabetes.

 

Hgb A1C concentration near 10% is associated with fetal anomaly rate of 20-25%

 

Levels between 5 and 6% are associated with fetal malformation rates comparable to those observed

in normal pregnancies (2-3%)

 

Goal of normal or near-normal glycosylated hemoglobin (Hgb A1C) level for at least 3 months prior to

conception

 

 

ü  UTZ often done @ 18 weeks gestation to confirm gestational age & to survey for congenital

anomalies fetal structural anomalies, macrosomia, hydramios

ü  Urinalysis

ü  Opthalmic exam

ü  Weekly Non-Stress Test (NST) are administered beginning @ approximately 32 weeks gestation

ü  Maternal serum alpha-fetoprotein level

assess risk for neural tube defects

 

Medical Diagnosis 

ü  risk of intrauterine fetal demise in the antepartum period.

 

ü  Lung Maturity Studies (Amniocentesis)

determine L/S ratio and Phosphatidylglycerol (PG)

predictor of newborn’s ability to avoid RDS

 

Nursing Diagnoses

ü  Alteration in Carbohydrate Metabolism r/t diabetes

ü  Knowledge Deficit r/t diabetic self care during pregnancy

ü  Disturbance in self Concept r/t complications of pregnancy

ü  Alteration in Tissue Perfusion; Uteroplacental

ü  High risk for Infection

ü   High Risk for Impaired Skin Integrity

Major objectives of Nursing Care

ü  Identification of women at risk for diabetes & provisions of appropriate perinatal care.

ü  Maintenance of blood sugar levels.

ü  Provisions of adequate client education & counseling for safe self-management of mother &

fetus/newborn.

ü  Prevention or detection of potential complications

ü   Promotion of a positive psychosocial adjustments to childbearing through understanding &

acceptance of pregnancy  & diabetes.

 

Nursing Interventions

ü  Teach client the effects & interactions of diabetes & pregnancy & signs of hyper & hypoglycemia.

ü  Prepare & assist client for screening & other diagnostic tests.

ü  Teach client how to control diabetes in pregnancy. Advise on changes that need to be made in

nutrition & activity patterns to prevent complications.

ü   Advise client on how to prevent infection

ü  Discuss & demonstrate insulin self-injection

ü  Demonstrate how to self-monitor blood glucose level.

ü  Provide emotional & psychosocial needs.

 

Nursing Evaluation

ü  Understands the effects of her condition

ü  Recognizes symptoms of disease progression & reports them promptly.

ü  Implements the treatment plan of self care activities & prevents potential complications.

ü   Maintains adequate tissue perfusion & oxygenation to maternal-fetal unit.

ü   Delivers a healthy infant at or near term

 

SIGNS AND SYMPTOMS of HYPOGLYCEMIA

 (Insulin reaction)

ü  Shakiness, dizziness

ü  Pallor, cold, clammy skin

ü  Sweating

ü  Headache

ü  Blurred vision

ü   Disorientation, irritability

ü  Hunger

ü  Nervousness

 

TREATMENT:  Hypoglycemia

Give 12 fluid oz of orange juice (20 g CHO), 8 oz regular soft drink(not diet), 6-8 Lifesavers, 1 ½ tbs

honey, 1-2 tbs jam.

 

Administer glucagon if unable to swallow.

 

  NOTE: Wait 20 minutes before repeating the procedure.

 

INTERVENTIONS

DIET and NUTRITION

ü  1,800 – 2,200 calories/day divided into 3 meals and 3 snacks (20% CHON, 50% CHO, 30% fat)

ü  IVF supplementation if with nausea or vomiting (early pregnancy) or heartburn (late pregnancy)

ü  Low fat, high fiber diet

EXERCISE

Aerobic or anaerobic exercises; exercise program consulted with physician

THERAPEUTICS

ü  INSULIN

Combination of short-acting (regular) and Intermediate (NPH)

Ratio of 2:1 (NPH to regular) 30 minutes pre-breakfast and a 1:1 ratio 30 minutes pre-supper

Methods for Control

ü  Daily Injections

ü  Bolus insulin

ü  Basal insulin

ü  Two to five shots a day

 

Insulin Pump Therapy

Constant insulin delivery

One insulin type become the bolus

                insulin and the basal insulin

Catheter changed every three days

Regular Insulin

No alteration in structure of human insulin

Does not peak until 1 to 2 hours later because hexameric form must be converted to monomeric

form

Lasts about 4 to 6 hours in body

 

NPH

Neutral Protamine Hagedorn

Protamine and Zinc added

                to the insulin structure

These additions resulted in more of the hexameric form present in the mixture than the monomeric

form

Thus, more hexamers had to be transformed to monomers for insulin absorption

The duration, onset, and peak of the insulin prolonged

 

Glucagon

Brain can only use glucose, not alternative energy sources like fatty acids

Insulin stimulates liver to store glucose in the form of glycogen

In liver:   

1.Stimulates break down of glycogen stored in liver

2.Activates hepatic gluconeogenisis: (amino acids) are converted to glucose

 

Injection of this hormone is given to patients when seizures

from low blood sugars occur

 

Seizures most likely to occur during the middle of the night, most specifically when using Regular

insulin and NPH insulin

 

THERAPEUTICS

BLOOD GLUCOSE MONITORING

CBG (capillary blood glucose) monitoring TID AC or every 6 hours

 

Recent Developments

Constant glucose monitoring – sensor records blood glucose every 10 seconds and sends an

average of the glucose measurements every 5 minutes to the pump for 3 days

Calibration by glucometer still required

 

Symlin – analog of human amylin, a hormone that contributes to glucose control during postprandial

periods

Slows gastric emptying

Supresses glucagon secretion

 

Implanted Insulin Pump (not yet fully developed)

 

Transplants

Pancreas and kidney dual transplants have been successful, must take immunosuppressant for rest of

life

Islet cell injections – several injections must take place, not viable for the whole population because

costly and not enough supply, most take immunosuppressant for rest of life

 

Diabetic Ketoacidosis (DKA)

 

Diabetic ketoacidosis  <DKA> is near complete deficiency of insulin and elevated levels of

stress hormones

Glucagon

Cathecolamine

Cortisol

Growth hormone

 

DKA : acute metabolic complication of diabetes characterized by Hyperglycemia,

Hyperketonemia,Metabolic acidosis

 

DKA is a life-threatening complication in Pt. with untreated DM  (chronic high blood sugar or

hyperglycemia).

 

DKA occurs mostly in type 1 DM, less common in type 2 DM, may occur in situations of physiologic

stress.

 

 new undiagnosed Type 1 DM  frequently present  with DKA

 

Etiology

Precipitates DKA -- > 5I’ s

ü  Insulin deficiency  c relative or absolute increase in glucagon<Inadequate insulin administration>

ü  Infection   or Inflammation < pneumonia, UTI, gastroenteritis, sepsis>

ü  Ischemia or Infarction < cerebral, coronary, mesenteric, peripheral>

ü  Intra-abdominal process <pancreatitis, cholecystitis>

ü  Iatrogenesis  Drug < glucocorticoids,cocaine>

 

Pathophysiology

 

1. Hyperglycemia  : gluconeogenesis, glycogenolysis ,↓glucose uptake into cell <underutilization>

 

2. Ketosis  : lipolysis, ketogenesis , ↓ Peripheral tissue uptake ketone -- >ketonemia

 

3. Hypertriglyceridemia  : ↑free fatty acid

 

4. Osmotic diuresis  : hyperglycemia -- > renal loss glucose, Na & K -- >electrolyte imbalance

 

5. Volume depletion  : hyperglycemia, glucosuria & osmotic diuresis -- >dehydration

 

Signs and Symptoms

 

Initial symptoms of DKA

ü  Anorexia, nausea, vomiting, abdominal pain

ü  Polyuria, polydipsia

ü  Dehydration  -- > dry mucous membranes, tachycardia, hypotension

ü  Alterated mental function-- > somnolence, stupor,coma

ü  Fever is not a sign of DKA -- >signifies underlying infectio

 

Classic signs of DKA

ü  Kussmaul  ‘ s respirations <deep>  to compensate for metabolic acidosis with  acetone odor on

breath

Laboratory and Diagnostic Test

 

1. Glucose & ketone in serum & urine

2. Serum electrolyte, BUN, Cr, Ca, PO4

3. Blood gas : capillary or arterial blood gas

4. EKG : hypo/ hyperkalemia

5. CBC UA

1. Hemoculture

2. Urine culture

3. Throat swab culture

4. CSF culture

5. Chest x-ray

6. Omission of insulin

7. Physical or emotional stress ÏÅÏ

 

 

 

 

LABORATORY EVALUATION

 

Elevated blood glucose level, decreased bicarbonate, decreased arterial pH

 

Urine is strongly positive for sugar and ketone and moderate protein

 

Sodium potassium level decreased, increased creatinine, BUN level

 

Diagnosis

ü  Serum glucose > 300 mg/dl                                                                                                   <

euglycemic DKA-- > pregnancy, alcolhol drinking, stravation  >

 

ü  Acidosis : serum HCO3 < 15 mEq/ml  or pH < 7.25                                  < wide anion gap:

>15 mEq/L>                                                                                 severity of

DKA                                                                           Mild           : HCO3    > 15-18 mq/L  & pH  > 7.3

Moderate   :  HCO3      10-15 mq/L & pH  7.1-7.3

Severe      :   HCO3  <  10 mq/L      &  pH < 7.1                                                           

 

ü  Ketone : positive ketone in urine and / or serum

 

MANAGEMENT:

ü  Obtain blood and urine specimen

ü  perform PE stat

ü  start IVF of isotonic saline solution at a rate of 500 ml/hr- give insulin as directed

ü  monitor blood chemistry

ü  1 or more ECG tracings

ü  clear liquids

 

Treatment                 Confirm Dx  : ↑ BS, positive serum ketone, metabolic

                                                                    acidosis

Assess

Serum electrolyte : K, Na, Mg, Cl, HCO3, PO4

Acid-base status :  pH, H CO3, Pco2

Renal function : creatinine, urine output

Replace fluid

                Administer regular insulin/ RI

                                Assess patient 

                                What precipitated the episode

                                Initial appropriate work up

 

Measure capillary glucose every 1-2 hr/  E’lyte, anion gap every 4 hr for first 24 hr

Monitor  BP, PR, respiration, mental status, fluid intake/output every 1-4 hr

Replace K

Continue above until Pt. stable

Administer intermediate or long – acting insulin as soon as Pt. eating / overlap in insulin infusion &

subcutaneous injection.

Replace fluid

                DKA : volume & Na depletion

                0.9%NaCl or NSS  -- >     1 L/hr in 1-3 hr  <5-10                                                   

mL/kg/hr>    then

                0.45% NaCl or Nss/2-- >  150-300 mL/hr Pt. Na                                                   >150

mEq/L-- > NSS/2

                Pt. euglycemic DKA -- > 5% D/NSS/2

Severe DKA  volume depletion~ 5-6 L ,Na ~ 500 & Cl ~ 350 mEq

 

When BS  <  300 -250 mg/dl change to 5%DN/2  80-100 ml/hr  <Severe dehydration add NSS/2 >

Replace fluid

                                Adequate Fluid replace :

                ↑plasma volume

                ↑urine output

                ↑absorb/action insulin

↓release counter-regulatory hormone

 

Fluid replace : 50 % of volum in 6 hr & 50% in 24 hr

Measure BP, PR, urine out put,   E’ lyte,   crepitation -- > pulmonary edema

 

Administer regular insulin

RI -- > ↓blood sugar ,  inhibit ketone production

 

low dose intramuscular insulin injection

low dose continuous intravenous insulin infusion  

 

Potassium Supplement

Moderate to severe DKA  loss  K~ 300-1,000 mEq   or      3-5 mEq/kg

 

Rx  :RI ,iv fluid -- > K shift in cell, loss K in urine-- > hypokalemia  < cardiac arrhythmia ,muscle

weakness >

 

K supplement -- >urine > 40 ml/hr , k< 5.5 mEq/L, EKG normal

 

 

Monitor

In first 6 hr

BP, PR, RR, Mental status-- > q 15 min – 1 hr

skin turgor, plasma ketone

Urine output, urine glucose, urine ketone -- > q 1 hr

E’lyte,  BUN,Cr-- > q 4 hr

 

Long term F/U

K supplement 7-10 day

DM type 1 continue insulin usage

Advice control BS < 300 mg/dl

 

 

Thyroid Crisis

 

Where to look for Thyroid ?

Clinical Anatomy of Thyroid

Clinical Exam of Thyroid

Thyromegaly

 

 

Thyroid Diseases

                Management of thyroid diseases during pregnancy requires special considerations

 

                 Pregnancy induces major changes in thyroid function, and maternal thyroid disease can

have adverse effects on the pregnancy and the fetus

 

THYROID FUNCTION AND PREGNANCY

Altered thyroid function is associated with hormone changes in pregnancy as a result of increased

levels of HCG and estrogen.

Elevated levels of HCG may cause transient hyperthyroidism.

Pregnant and lactating women require additional iodine intake

Recommended average iodine intake is approximately  250 g/d

Thyroid Hormone is Essential for Normal Brain Development

Severe iodine deficiency, if inadequately

    treated, is a major cause of neurological damage

 

 

Physiologic

Changes in Pregnancy

 

free T4 and T3 increase slightly during the first trimester in response to elevated hCG. decline to nadir

in third trimester

 

TSH decreases slightly in first trimester.

 

 

The thyroid gland increases slightly

in size during pregnancy.

Effect to pregnant women:

 

If hyperthyroidism is inadequately treated, it may result in early

labor and pre-eclampsia.

Women with Grave’s disease/ hyperthyroidism (worsens during post partum period) are at high risk of

developing thyroid storm.

 

Considerations

Care requires coordination among several healthcare professionals.

 Avoiding maternal (and fetal) hypothyroidism is of major importance because of potential damage to

fetal neural development, an increased incidence of miscarriage, and  preterm   delivery.

Maternal hyperthyroidism and its treatment may be accompanied by coincident problems  in fetal

thyroid function.

Autoimmune thyroid disease is associated with both increased rates of miscarriage, for which the

appropriate medical response is uncertain at this time, and postpartum thyroiditis.

Universal screening of pregnant women for thyroid disease is not yet supported by adequate studies,

but case finding targeted to specific groups of patients who are at increased risk is strongly supported.

 

THYROID STORM

( Thyrotoxic crisis, Thyroid crisis)

 

DEFINITION

A severe, life threatening condition caused by an excess of thyroid hormones  

 

  Form of severe hyperthyroidism

    (Grave’s disease), usually of abrupt onset      

 

THYROID STORM

( Thyrotoxic crisis, Thyroid crisis)

 

DEFINITION

If untreated, May be fatal that may lead to stroke or heart attack.

 

Mortality rate is 10-20% if with proper        treatment and monitored closely.

 

Effect to fetus:

ü  Uncontrolled maternal hyperthyroidism may

lead to:

Fetal tachycardia

Small Gestational Age

Still births

Congenital malformations

Fetal hyperthyroidism (occurs if mother’s TSI (Thyroid Stimulating Immunoglobulins, antibody that

stimulates thyroid gland function) levels are very high.

 

TSI is measured at 3rd trimester

 

 

Hypothyroidism

                Untreated patients with hypothyroidism rarely conceive and carry a pregnancy.

                Treated hypothyroidism usually has no associated pregnancy complications.

                Some patients will require increased levothyroxine doses during their pregnancies.

                Monitor thyroid function tests each trimester and at other clinically indicated times.

 

                Prenatal vitamins can decrease the absorption of levothyroxine.

 

 

Hyperthyroidism

                90- 95% of hyperthyroidism in pregnancy is secondary to Graves’ Disease.

                A good pregnancy outcome can be expected in patients with good control.

                Untreated hyperthyroidism is associated with decreased fertility,  an increased rate of

miscarriage, intrauterine growth retardation (IUGR), premature labor, and perinatal mortality.

                Poorly controlled thyrotoxicosis is associated with thyroid storm especially at labor and

delivery.

                Beta Blockers and PTU can be safely used in pregnancy and in nursing mothers.

                PTU crosses the placenta but does not usually cause fetal hypothyroidism and goiter unless

used in high doses.

                Treatment goals favor mild hyperthyroidism over hypothyroidism.

 

Hyperthyroidism -Grave’s Disease

                Like other immune mediated diseases in pregnancy, Grave’s disease tends to improve in the

third trimester.

                Exacerbations may occur in the first trimester and postpartum.

                Neonatal and fetal thyrotoxicosis may occur because of transplacental passage of thyroid

stimulating antibodies.

 

Thyroid Failure - Organ Systems

                Cardiovascular

                                Decreased ventricular contractility

                                Increased diastolic blood pressure

                                Decreased heart rate

                Central Nervous

                                Decreased concentration

                                General lack of interest

                                Depression

                Gastro-instestinal

                                Decreased GI motility

                                Constipation

                Reproductive

                                Arrest of pubertal development

                                Reduced growth velocity

                                Menorrhagia, Amenorrhea

                                Anovulation, Infertility

                Hepatic

                                Increased LDL / TC

                                Elevated LDL + triglycerides

 

CAUSES

ü  Infections esp. of the lungs and throat

ü  Thyroid surgery

ü  Stopping/discontinuing hyperthyroidism medications

ü  Too high thyroid dose

ü  Treatment using radioactive iodine

ü  Pregnancy (Toxemia)

ü  Heart emergencies (heart attack/heart failure)

ü  Blood sugar changes

ü  DKA, insulin-induced hypoglycemia

ü  excessive palpation of thyroid

ü  Severe emotional stress

 

CLINICAL MANIFESTATION

               

ü  Hyperpyrexia (38.5 C/105-106F and above) –major sign/hallmark that differs thyroid storm from

hyperthyroidism)

ü  Extreme tachycardia (130 bpm and above)

ü  Exaggerated symptoms of hyperthyroidism with disturbances of a major system ( GI- wt

loss,diarrhea, abd’l pain, N & V; Cardio-  bp, edema, palpitations, arrythmias; Respi- SOB,

DOB, chest pain.)

ü  Altered neurologic/mental state  (CNS- disoriented, anxiety & irritability, confusion

restlessness, delirium, psychosis, exaggerated reflexes, coma)

ü   increased sweating

ü   weakness

 

MANAGEMENT  :

 

ü  Decrease circulating thyroid hormone levels and their formation

ü  Treat precipitating cause (infection)

ü  Temperature be lowered with hypothermia blanket or cooling mattress, ice packs, cool environment.

ü  Acetaminophen is preferred with aspirin.

ü  Sedatives (e.g. Phenobarbital) are given to reduce anxiety, irritability and hyperactivity.

ü  Phenothiazines in large doses may be prescribed to reduce emesis and anxiety

ü  Humidified oxygen is administered to improve tissue oxygenation and meet high metabolic

demands

ü  ABG level monitoring and pulse oximetry monitoring to monitor respiratory status

ü  Administer IVF, electrolytes and vasopressor agents ( treat dehydration and hypertension)

ü  Hydrocortisone is prescribed to improve adrenal insufficiency

ü  PTU (propylthiouracil)/methimazole (tapazole) administration –antithyroid drugs, decreases thyroid

hormone synthesis by blocking T4 to T3 conversion

ü  Give iodine, Na iodide, K iodide or Lugol’s solution to inhibit thyroid hormone release from the

thyroid gland

ü  Antithyroid drug therapy to the mother can induce fetal hypothyroidism, and transplacental passage

of TSH

receptor antibodies can cause fetal hyperthyroidism

ü  Administer digitalis if heart failure or atrial fibrillation occurs

ü  Give propanolol for sinus tachycardia.

                     (controls heart rate, reduces adrenergic hyperactivity symptoms

ü  Sustain nutritional requirements

ü  Close monitoring of thyroid hormones and TSH.

ü  Anti-thyroid drugs are administered usually at low levels. (Methimazole or PTU)

 

Why low dose? – drugs cross placenta and may potentially impair baby’s thyroid function and cause

fetal goiter

                     R: To minimize development of hypothyroidism              in baby.

PTU  is the drug of choice for maternal hyperthyroidism due to less transplacental passage

 

Beta Blockers can be used sparingly to treat palpitation and tremors.

 

                     R: used sparingly to avoid impaired fetal   

           growth

 

If allergic to Anti-thyroid drugs, Surgery is done but very rarely due to risks to mother and baby.

 

Surgery is contraindicated during a thyroid storm episode because of patient’s adrenergic

hyperactivity.

 

Radioiodine is also contraindicated to treat hyperthyroidism

 

R:  it crosses placenta and may result in permanent fetal hypothyroidism. Baby’s thyroid gland is

destroyed.

 

Mother can still breast milk even if treated with anti-thyroid drugs only lower amounts of PTU is

present.

 

Hypothyroidism should be corrected before initiation of pregnancy, replacement dosage should be

augmented early in pregnancy

 

euthyroidism should be maintained throughout.

 

Overt maternal hypothyroidism has been associated with damage to fetal intellectual

developmentpresumably because of inadequate transplacental supply of hormone during

early pregnancy

 

Mother can still breast milk even if treated with anti-thyroid drugs only lower amounts of PTU is

present.

 

Postpartum Thyroiditis

 

Postpartum thyroiditis is a destructive

autoimmune thyroiditis that begins with

a period of hyperthyroidism followed by

a period of hypothyroidism.

 

The gland is often enlarged.

 

Postpartum Thyroiditis

There is usually complete recovery but a chance of recurrence in subsequent pregnancies exists.

 

80-85% of patients will have positive antithyroid antibodies.

 

A radioactive iodine uptake scan can differentiate postpartum thyroiditis from an exacerbation of

Graves’ Disease.

 

Postpartum thyroiditis in an important consideration in women with postpartum depression.

 

Perchlorate blocks “Radioactive

Iodide Uptake” (RUI)

Thyroid Investigations

 

Nursing mothers who have radioactive iodine uptake scans should pump and discard their milk for 48-

72 hours after the test.

 

Hyperemesis Gravidarum

associated with abnormal thyroid function tests in a significant number of cases.

 

Hyperthyroidism may be the cause of hyperemesis or hyperemesis may be the cause of the

hyperthyroidism.

 

Thyroid Nodules

New thyroid nodules should be aggressively investigated during pregnancy because of a high

incidence of malignancy.

 

 Fine-needle aspiration cytology should be performed for dominant thyroid nodules discovered in

pregnancy.

 

Thyroid nodules recognized during pregnancy, or growing,are typically biopsied under ultrasound

guidance

 

If appropriate, surgery is performed in the midtrimester

 

Delay in treatment of low-grade tumors until

    after delivery is not considered a danger

 

Hepatic Coma

 

HEPATIC COMA

 

PORTAL-SYSTEMIC ENCEPHALOPATHY (PSE), HEPATIC ENCEPHALOPATHY

 

A clinical disorder seen in hepatic failure and cirrhosis.

 

Brain and nervous system damage that

                occurs as a complication of liver disorders.

 

PATHOGENESIS

 

WITH SEVERE LIVER IMPAIRMENT AND IF THERE IS ALSO PORTAL HYPERTENSION, AND SUBSEQUENT

BYPASSING OF THE LIVER FILTRATION SYSTEM OF BLOOD FLOWING IN FROM THE INTESTINES,

 

  TOXIC SUBSTANCES NORMALLY REMOVED BY THE LIVER ACCUMULATE IN THE BLOOD

 

   LEAD TO METABOLIC ABNORMALITIES, MOST SIGNIFICANTLY ELEVATED SERUM AMMONIA,WHICH

IS PRODUCED BY THE BODY WHEN PROTEINS ARE DIGESTED

 

   TRAVEL DIRECTLY TO THE BRAIN IMPAIRING THE FUNCTION OF BRAIN CELLS.

 

   IMPAIRED COGNITION, (THINKING PROCESS) NEUROMUSCULAR DISTURBANCES (A FLAPPING TREMOR

KNOWN AS ASTERIXIS), DECREASED LOC INCLUDING COMA AND DEATH.

 

HEPATIC ENCEPHALOPATHY TRIGGERS :

ü  EPISODES OF GASTROINTESTINAL BLEEDING –

                presence of blood in the upper GIT results in increased       ammonia and nitrogen

absorption from the gut.

 

ü  EXCESSIVE INTAKE OF DIETARY PROTEIN

 

ü  ELECTROLYTE ABNORMALITIES

    (ESP. DECREASE IN K, RESULTING FROM VOMITING OR TREATMENTS SUCH AS DIURETICS OR

PARACENTESIS)

    Decreased serum potassium levels and alkalosis may facilitate the conversion of NH4+

to NH3. 

 

ü  INFECTIONS - Infection may predispose to impaired renal function and to increased tissue

catabolism, both of which increase blood ammonia levels.

 

ü  RENAL DISEASE - Renal failure leads to decreased clearance of urea, ammonia, and other

nitrogenous compounds.

 

ü  ANY CONDITION THAT RESULTS IN ALKALOSIS   (ALKALINE BLOOD PH)

 

 

USE OF MEDICATIONS THAT SUPPRESS THE CENTRAL NERVOUS SYSTEM

(E.G. BARBITURATES OR BENZODIAZEPINE TRANQUILIZERS)

HEPATIC ENCEPHALOPATHY TRIGGERS :

SURGICAL PROCEDURES TO TREAT PORTAL HPN –e.g. operations to relieve pressure in the portal

vein by connecting it to the splenic vein or other systemic venous vessels, have the effect of diverting

incoming intestinal venous blood away from the liver. Ammonia-carrying blood will not be "purified" by

the liver.

"TIPS" procedure (transjugular intrahepatic portosystemic shunt)

 

CLINICAL SYMPTOMS

 

ü  AN ELEVATED BLOOD AMMONIA LEVEL IS THE CLASSIC LABORATORY ABNORMALITY REPORTED

IN PATIENTS WITH HEPATIC ENCEPHALOPATHY.

 

EARLY MANIFESTATIONS OF HEPATIC COMA

1. "DAY-NIGHT REVERSAL" - tend to sleep during the day and stay awake at night

2. IMPAIRMENT IN SPATIAL PERCEPTION - poor ability to copy or draw various simple images, e.g

cube, star, clock.

 

                This deficit can also be demonstrated by administering a "trail test" or "numbers connecting

test“.

3. ASTERIXIS – Hallmark of hepatic coma on physical examination.

   Detected by having patient hold out his outstretched arms and hands and cock his wrists back. In the

presence of asterixis, there is a non-synchronized, intermittent flapping motion at the wrists

 

STAGES OF PORTAL-SYSTEMIC ENCEPHALOPATHY

 

STAGE I PRODROMAL 

SUBTLE MANIFESTATIONS THAT MAY NOT BE RECOGNIZED

IMMEDIATELY;

                PERSONALITY  CHANGES,

                BEHAVIOR CHANGES (AGITATION,BELLIGERENCE)

                EMOTIONAL LABILITY (EUPHORIA, DEPRESSION)

                IMPAIRED THINKING,INABILITY TO CONCENTRATE,

                FATIGUE, DROWSINESS,SLURRED SPEECH

                 SLEEP PATTERN DISTURBANCES

 

STAGE II IMPENDING

                CONTINUING MEDICAL CHANGES,

                MENTAL CONFUSION

                 DISORIENTATION TO TIME, PLACE, PERSON,

                ASTERIXIS

 

STAGE III STUPOROUS

                 PROGRESSIVE DETERIORATION,

                MARKED MENTAL CONFUSION

                 STUPOROUS,DROWSY BUT AROUSABLE

                ABNORMAL EEG TRACING

                MUSCLE TWITCHING

                HYPERREFLEXIA

                ASTERIXIS

 

STAGE IV COMATOSE 

                UNRESPONSIVENESS,LEADING TO DEATH,            UNAROUSABLE,OBTUNDED, RESPONSE TO

PAINFUL           STIMULUS, NO ASTERIXIS, POSITIVE BABINSKI SIGN,       MUSCLE RIGIDITY, FETOR

HEPATICUS-LIVER BREATH-        MUSTY,SWEET ODOR, SEIZURES

 

                PROGNOSIS DEPENDS ON SEVERITY OF THE UNDERLYING CAUSE, PRECIPITATING FACTORS

AND DEGREE OF LIVER    DYSFUNCTION

 

MANAGEMENT

ü  THE GOALS OF TREATMENT INCLUDE LIFE SUPPORT, ELIMINATION OR TREATMENT OF THE CAUSES,

AND REMOVAL OR NEUTRALIZATION OF AMMONIA AND OTHER TOXINS.

 

                Checking an arterial ammonia level in the initial assessment

 

ü  Precipitants of hepatic encephalopathy, such as metabolic disturbances, GI bleeding, infection, and

constipation, should be corrected.

 

ü  Avoid medications that depress CNS function, especially benzodiazepines. Patients with severe

agitation and hepatic encephalopathy may receive haloperidol as a sedative.

 

ü  Patients with severe encephalopathy (ie, stage 3 or 4) who are at risk for aspiration should undergo

prophylactic endotracheal intubation.

 

ü  Low-protein diets are recommended for patients with cirrhosis, to decrease intestinal ammonia

production and prevent hepatic encephalopathy

 

ü  Cathartics  - Lactulose causes osmotic diarrhea, lessens the time available for intestinal bacteria to

metabolise protein into ammonia within the bowel.

 

ü  Antibiotics - Neomycin and other antibiotics, such as metronidazole, oral vancomycin,

paromomycin, and oral quinolones,rifaximin are administered to decrease the colonic concentration of

ammoniagenic bacteria

 

Medications containing ammonium (including certain antacids) should also be avoided

 

Treatments to increase ammonia clearance

 

ü  L-ornithine L-aspartate (LOLA) -LOLA is a stable salt of the 2 constituent amino acids. L-ornithine

stimulates the urea cycle, with resulting loss of ammonia

Treatments to increase ammonia clearance

 

ü  Zinc -Zinc deficiency is common in cirrhosis. zinc increases the activity of ornithine

transcarbamylase, an enzyme in the urea cycle.

 

 The subsequent increase in ureagenesis results in the loss of  ammonia ions.

 

 

ü  Sodium benzoate, sodium phenylbutyrate, sodium phenylacetate -Sodium

benzoateinteracts with glycine to form hippurate. The subsequent renal excretion of

hippurate results in the loss of ammonia ions.

 

5g of sodium benzoate p.o. BID can effectively control hepatic encephalopathy.

Treatments to increase ammonia clearance

 

ü  Sodium phenylbutyrate is converted to phenylacetate. Phenylacetate reacts with

glutamine to form phenylacetylglutamine.

 

This is subsequently excreted in the urine, with loss of ammonia ions.

 

ü  L-carnitine - improves hepatic encephalopathy symptoms in several small studies of patients with

cirrhosis.

 

EXAMS AND TESTS

ü  Coarse, "flapping" muscle tremor (ASTERIXIS) may be observed during voluntary movement.

ü   Mental status examination will be abnormal, particularly cognitive (thinking) tasks such as

connecting numbers with lines.

ü   Liver disease may be known or may be suspected, and signs of liver disease such as jaundice and

ascites  may be noted.

ü   Musty odor to the breath and the urine (occasional)

ü  Blood tests may be nonspecific, or may show liver failure.

ü  Blood chemistry may show low albumin, high bilirubin, or other abnormalities.

ü  Serum ammonia levels are usually high.

ü  PT may be prolonged and not correctable with Vitamin K.

ü  Cranial CT scan  may be normal, or may show general atrophy (loss of tissue).

ü  EEG shows abnormalities.

 

POSSIBLE COMPLICATIONS

ü  Brain swelling

ü  Brain Herniation

ü  Progressive, irreversible coma

ü  Permanent nervous system damage

ü  Increased risk of:

Sepsis

Respiratory failure

Cardiovascular collapse

Kidney failure

 

Side effects of medications

PREVENTION

                TREAT LIVER DISORDERS TO PREVENT SOME CASES OF HEPATIC ENCEPHALOPATHY.

                AVOID HEAVY DRINKING AND INTRAVENOUS DRUG USE TO PREVENT MANY LIVER

DISORDERS.

Maternal Phenylketonuria

Recognized cause of mental retardation caused by deficiency in enzyme phenylalanine hydrolase

Absence impairs body’s ability to metabolize phenylalanine, found in all protein foods

Toxic accumulation of phenylalanine in blood interferes with brain development

 

Key to prevention is identification of women with disorder

Renal Disorders

 

Renal Changes in Pregnancy

 

Renal Changes

Bladder capacity                     Increased

Glomerular filtration

    rate (GFR)                             ↑  by 50%

Renal plasma flow ↑ by up to 80%

Blood urea nitrogen (BUN)      Decreased

Creatinine                               Decreased

Glucose (in urine)                       Present

 

ACUTE RENAL FAILURE

 

ACUTE RENAL FAILURE

Sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days

 

Oliguria most common clinical situation

 

TYPES

Prerenal

                                occurs as a result of impaired blood flow

                hypoperfusion of the kidney

 

Intrarenal

                                actual parenchymal damage to the glomeruli or kidney tubules

 

Postrenal

                                obstruction in the kidney

 

CHRONIC RENAL FAILURE

 

CHRONIC RENAL FAILURE

                End stage renal disease (ESRD)

                Irreversible renal failure

                Fewer nephrons are functioning

                Remaining nephrons must filter more

                Hyperperfusion

                Hypertrophy

                Progressive, irreversible deterioration in renal function

 

                body’s ability to maintain metabolic and fluids and electrolyte balance fails

 

                Results in uremia and azotemia

CAUSES

CRF can develop insidiously over many years or it may result from episodes of ARF from which the

client has not recovered

DM (leading cause)

 

Pathophysiology

↓ renal blood flow

 

↓ GFR

 

Hypertrophy of remaining nephrons

 

Inability to concentrate urine

 

Decreased blood viscosity

    +

Increased blood pressure

    +

Decreased oxygen supply

 

Cardiovascular Consequences of CRF

 

Clinical manifestations

Severe anemia

Elevated serum creatinine level

Proteinuria in urine

Elevated BP

Flank pain with pyelonephritis

Edema

 

Goal of care

To preserve renal function

To provide an optimal quality of life for self and significant others

 

Medical management

Drug therapy

ü  Corticosteroids – Prednisone

ALERT:  suppresses insulin activity→infant hyperglycemic

 

ü  Progesterone

ü  Azathioprine (with kidney transplantation)

 

Nursing responsibilities

ü  Monitor vital signs, esp BP

ü  Emotional support, esp fetal status

ü  Stress reduction

ü  Restriction of activity

ü  Dialysis education

 

Surgical management

                Dialysis

                Peritoneal dialysis

                Hemodialysis

Further loss of nephron function

 

Loss of non-excretory renal function

 

Loss of excretory renal function

 

End- Stage Renal Disease

                CAUSES

ü  Diabetes mellitus

ü  Hypertension

ü  Chronic glomerulonephritis

ü  Pyelonephritis

ü  Obstruction of the urinary tract

ü  Hereditary lesions (eg. Polycystic kidney disease)

ü  Vascular disorder

ü  Infections

ü  Medications / toxic agents

ü  Environmental and occupational agents (eg. Lead, cadmium, mercury, chromium)

 

Pathophysiology

Stages of Kidney Failure

 

Stage I - (Reduced renal reserve)

                 Loss of nephron function (40% - 70%)

                Px usually does not have sx because the remaining              nephrons are able to carry out

the normal function of the   kidney

 

Stage II - (Renal insufficiency)

                Nephron function is lost (75% - 90%)

                Serum creatinine and blood urea nitrogen rise

                Kidney loses it’s ability to concentrate urine and anemia     developsPx may report polyuria

and nocturia

Stage III - (ESRD)

                Final stage of chronic renal failure

                Loss of nephron function (10%)

                All of the normal regulatory, excretory and hormonal          function of the kidney are

severely impaired

                Elevated creatinine and BUN levels as well as electrolyte   imbalances

                Dialysis is indicated

 

Clinical Manifestation

ü  Cardivascular: hypertension, pitting and periorbital edema, pericardial friction rub, pericardial

tamponade, hyperkalimia

 

ü  Integumentary: ecchymosis, purpura, thin brittle nails, coarse thinning hair, gray-bronze skin

color, dry flaky skin

 

ü  Pulmonary: crackles, thick tenacious sputum, depressed cough reflex, shortness of breath,

tachypnea, kussmaul type of respiration, uremic pneumonitis

 

ü  Gastrointestinal: ammonia odor of breath, metallic taste, mouth ulceration and bleeding,N/V,

constipation or diarrhea, bleeding in GIT

 

ü  Nuerologic: weakness, fatigue, confusion, disorientation, tremors, seizure, burning of sole of feet,

behavioral change

 

ü  Musculoskeletal: muscle craps, loss of muscle strength, renal osteodystrophy, bone pain, fracture,

foot drop

 

ü  Reproductive: amenorrhea, testicular atrophy, infertility, decrease libido

 

ü  Hematologic: anemia,thrombocytopenia

 

Assessment and Diagnostic Findings

1. Glomerular filtration rate

 24ᵒ urinalysis for creatinine clearance = decrease GFR

Increase BUN  level

Serum creatinine (most sensitive indicator of renal function

 

2. Na and H2O retention

 Kidney cannot concentrate or dilute urine normally

Retain Na and H2O = increase risk for edem, heart failure and HPN

Other px tends to lose salt and develop hypotension and hypovolemia

Vomiting and diarrhea may produce Na and H2O depletion which worsen the uremic state

 

3. Anemia

Inadequate erythropoietin production

Producing fatigue, angina and shortness of breath

 

4. Ca and Phosporous imbalance

Body does not normally respond to the increased secretion of parathormone

Active metabolite of vitaminD  normally manufactured by the kidney decreases

Uremic bone disease develops from the complex changes in Ca, PO4 and parathormone balance

Medical Management

1. Medications

 Antihypertensive - to manage HPN

 

Antiseisure agents - (Diazepam, Phenytoin)

 

Erythropoietin (Epogen) - to manage anemia

                     Administer via IV or SubQ tid

                     A/E: HPN, increased clotting of vascular access sites, seizure and depletion of iron stores

 Iron supplement

 

 PO4 binding agents - suitable for or select not to participate in dialysis or transplantation

 

 Antacids

Hyperphosphatemia and hypocalemia are treated with aluminium based antacid

Magnesium based antacid should be avoided to prevent magnesium toxicit

Medical Management

    Diet therapy

ü  Vitamin supplementation

ü  CHON restriction

ü  Potassium restriction

ü  Adequate caloric intake

ü  Fluid intake to balance fluid loses

ü  Na intake to balance Na loses

 

  Dialysis

                     Used to remove fluid and uremic waste products from the body when the kidney cannot

do so.

 

                     Used to treat px with edema that does not respond to tx, hepatic coma, hyperkalemiam

hypercalcemiam HPN and uremia

 

Types of Dialysis

Medical Management

Methods of Therapy

 

1.  Hemodialysis

 Commonly used method of dialysis

 Used for acutely ill and require short term dialysis (days to weeks)

 Used for ESRD who require long term or permanent therapy to prevent death

 Uses dialyzer (synthetic semipermeable membrane replacing the renal glomeruli and tubules as the

filter for the impaired kidneys)

Dialysis disequilibrium

Complication includes:

ü  Hypertriglyceridemia             

ü   Heart failure

ü  Coronary heart disease

ü   Angina pain

ü  Stoke

ü   Peripheral vascular insufficiency

ü   Hypotension

ü  Painful muscle cramping

ü  Exsanguinations

ü  Dysrhythmias

ü  Air embolism

ü  Dialysis disequilibrium

 

Nursing Diagnosis

Excess fluid volume r/t decreased urine output, dietary excesses and retention of Na and H2O

Imbalance nutrition: less than body requirements r/t anorexia, N/V, dietary restriction and altered oral

mucous membranes

Deficient knowledge regarding condition and tx regime

Activity intolerance r/t fatigue, anemia, retention of waste product and dialysis procedure

Low self-esteem r/t dependency, role changes, change in body image and sexual dysfunction

 

Nursing Management

Assessing fluid status and identifying potential source of imbalance

Implementing dietary program to ensure proper nutritional intake

Promoting positive feelings by encouraging increase self-care and greater independence

Report the health care provider the s/sx of decreased renal fxn

Worsening s/sx of renal failure (N/v, change in usual output, ammonia odor or breaths/sx of

hyperkalemia

s/sx of access problem (clotted fistula or graft andinfection)

Multiple dietary restrictions is required, including fluid intake, NA, K and CHON restriction

 

Pregnancy Induced Hypertension

 

“a condition in which vasospasm occurs during pregnancy in both small and large arteries”.

 

“TOXEMIAS OF PREGNANCY”

VASOSPASM

( constriction of Blood vessels)

 

↑ BP level

 

 

Physiology

Vasospasm

↓

Vascular effects

↓

Vasoconstriction

↓

Poor organ perfusion

↓

Increased blood pressure

 

Vasospasm

↓

Kidney effects

↓

Decreased GFR and

increased permeability of glomeruli membranes

↓

Increased levels of BUN, UA and creatinine

↓

Decreased urine output and proteinuria

Vasospasm

↓

Interstitial effects

↓

Diffusion of fluid from blood stream into interstitial tissue

↓

Edema

Predisposing Factors

Multiple pregnancy

Primiparas

Low socio – economic status

Multiparas

Hydramnios

 

Existing disease

cardiac, DM with vessel or renal involvement or essential HPN.

Symptoms of developing PIH

Rapid weight gain over 2 lb / wk. in the 2nd trimester 

1         lb / wk. in the 3rd trimester

Swelling of the face or hands & fingers.Face Hands

Flashes of light or dots before the eyes.

Dimness or blurring of vision

 Severe, continuous headache

Decreased urine output.

 

CLASSIC SIGNS

ü  Hypertension

ü  Edema

ü  proteinuria

PATHOPHYSIOLOGY

Significance and Incidence

Hypertensive disorders of pregnancy are most common medical complication reported during

pregnancy

 

Significant contributor to maternal and perinatal morbidity and mortality

 

Preeclampsia complicates approximately 12% to 20% of pregnancies

 

Morbidity and Mortality

Overall rate of maternal death from preeclampsia/eclampsia is 1.8 per 100,000

Leading cause—specific cause of death

 

Large disparity between rates of maternal death by race, in that:

African-American women more likely to die of preeclampsia than women of all other races

 

Classification

Hypertension, gestational or chronic, defined

Systolic BP greater than 140 mm Hg

 

Diastolic BP greater than 90 mm Hg

 

Mean arterial pressure (MAP) greater than 105 mm Hg

 

Hypertension, gestational or chronic, defined

Diagnosis of onset during pregnancy based on two measurements that meet criteria for gestational

BP elevation

HYPERTENSIVE

     DISORDERS IN PREGNANCY

ü  Gestational Hypertension(GH)

ü  Pre-Eclampsia

ü  Eclampsia

ü  Chronic Hypertension

ü  Chronic hypertension with superimposed preeclampsia

 

Classification

Gestational hypertension

Onset of hypertension without proteinuria after week 20 of pregnancy

GESTATIONAL HYPERTENSION

 

BP>140/90 or + 30mmhgSBP/+15mmhgDBP

Starts after 20th week of pregnancy

No proteinuria

BP returns to normal by 6 wks postpartum

Classification

ü  Preeclampsia

                Pregnancy-specific syndrome

                Hypertension develops after 20 weeks of             gestation in previously normotensive

woman

                Disease of reduced organ perfusion with presence             

of hypertension andproteinuria

ü  MILD PREECLAMPSIA

                                BP rising to 140/90 mmHg, taken on two occasions                            at least 6

hours apart

 

                                proteinuria of 1+ or 2+, on reagent test strip on                   random sample

                                Diastolic Pressure Value

                degree of peripheral arterial spasm.

                    Appearance of symptoms b/w 20th & 24th week of                              pregnancy

Orthostatic Proteinuria

long periods standing, excrete protein.

 1+ proteinuria ( about 1 gram per day)

 

 

 

Edema

weight gain à1st symptom a woman notices.

 Sudden weight gain (+3lb/mos in second trimester; +1lb/week in 3rd trimester; or       + 4.5lb/week at

any time)

 

Interventions

ü  Bed rest

ü  Diet

ü  Provision of emotional support

 

Patient education

Severe Preeclampsia

Assessment Findings

ü Headaches, epigastric pain, nausea & vomiting, visual disturbances, irritability

ü BP of 150-160/100-110mmhg

 

                     Severe hypertension, 30-40 mmHg on Bedrest.

 

ü  ↑edema & weight gain

                     Massive anasarca

ü  Proteinuria (5g/24hours) (4+) oliguria

ü   Hyperreflexia of 4+, possibly w/ clonus

ü   Less than 400 mL output in 24 hours.

                       Dizziness, headache, blurring vision, nausea and vomiting, epigastric pain, and

irritability.

 

ü  Changes from preeclampsia with tonic-clonic seizure attacks to comatose  state.

 

Severe Preeclampsia

Assessment

ü  Extensive edema

ü  Cerebral and visual disturbances

ü  Epigastric pain, nausea and vomiting

 

Interventions

ü  Bed rest

ü  Maternal and fetal vital signs monitoring

ü  Nutrition

ü  Patient education

                                - I and O

                                - Daily weight

ü  Seizure precautions

ü  Medications

                                -Anti-hypertensives

                                -Anti-convulsant

 

                Administration of Magnesium Sulfate

                                -acts on myoneural junction

                                 -diminishes neuromuscula   transmission

 

Nursing responsibilities

ü  Monitor vital signs, reflexes and urine output

 

                Antidote:  Calcium gluconate

 

ü  Promote bed rest as long as signs of edema or proteinuria are minimal, preferably side lying

ü  Provide well-balanced diet with adequate protein & roughage, low to moderate Na.

ü  Explain need for close follow-up, weekly or twice-weekly visits to physician

ü   Monitor I & O

ü   Review results of laboratory tests.

ü   Take daily weight.

ü   Do daily fundoscopic examination

ü   Institute seizure precautions.

Restrict visitors

Minimize all stimuli

Monitor for hyperreflexia

Adm. sedatives as ordered.

ü  Continue to monitor 24-48 hours post delivery.

ü  Administer medications as ordered; vasodilator of choice usually hydralazine   ( Apresoline)

 

Eclampsia

Assessment Findings

ü  Increased hypertension precedes convulsions followed by hypotension & collapse.

ü  Coma may ensue.

ü  Labor may begin, putting fetus in great jeopardy.

ü  Convulsions may recur.

 

 

ECLAMPSIA

20% of maternal mortality rate due to: (Moldenhauer & Sibai, 2003)

ü  Cerebral hemorrhage

ü  Circulatory collapse

ü  Renal failure

 

Fetal prognosis – poor

hypoxia and fetal acidosis

 

Abruptio placenta 

occurs due to vasospasm

 

Fetal mortality rate

10% à in preeclampsia

 

Fetal mortality rate

25% à in eclampsia

 

PREECLAMPSIA

HPN + Proteinuria + Edema

Eclampsia

Description

Most severe classification of PIH

High maternal mortality

 

 

Assessment

                Convulsions leading to coma

 

Interventions

ü  Tonic-clonic seizures

ü  Oxygen administration; pulse oximetry

ü  Cardiac monitoring

ü  Positioning

ü  Medications

ü  Termination of pregnancy

 

COMPLICATION

HELLP

                H – emolysis

                EL – elevated liver enzymes

                LP – low platelet

 

Description

                *Variation of PIH

                *Occurs in 1 in every 150 births

                *Maternal mortality 24%

                *Fetal mortality 35%

 

Assessment

ü  Nausea

ü  Epigastric pain

ü  Body malaise

ü  RUQ tenderness

 

Diagnostics & Laboratory studies

ü  PBS – hemolysis of RBC

ü  Platelet – thrombocytopenia

ü  ALT (alanine aminotransferase) and AST (aspartate aminotransferase) – elevated liver enzymes

 

Management

ü  TransfusionFFP or platelet

ü  IVF hydration and nutrition

ü  Termination of pregnancy

 

Eclampsia

Nursing Interventions

ü  Minimize all stimuli

ü  Darken room

ü  Limit visitors

ü  Use padded bedsides & bed rails

ü   Check vital signs & lab values frequently.

ü  Seizure precautions: airway, 02, & suction equipment should be available at bedside.

ü   Adm. Meds as ordered.

ü   Prepare for CS when seizure stabilized

ü   Continue monitoring 24-48h postpartum.

ü  Lateral recumbent position

                - avoids uterine pressure on the vena cava

                - prevents supine hypotension syndrome

 

                Bed rest

                evacuation of sodium

                encouraging diuresis.

 

ABSENCE OF MEDICATION

                90% of childbearing age women are working

difficult to leave work

                – little swelling

                -  little headache.

 

BEGINNING SIGNS OF HPN

seen weekly or more frequently.

 

NO CURE

bed rest

reduce symptoms

 

Chronic hypertension

Present before the pregnancy or diagnosed before week 20 of gestation

 

High BP that occurs before pregnancy or before the 20th week of pregnancy

 

Chronic Hypertension

Chronic hypertension associated with increased incidence

Abruptio placentae

Superimposed preeclampsia

Adverse pregnancy outcomes

Postpartum complications include:

Pulmonary edema

Renal failure

Hypertensive encephalopathy

Chronic Hypertension

Increased risk of perinatal deaths, rates of preterm birth, and small-for-gestational-age (SGA) infants

 

Lifestyle changes may be necessary

 

In postpartum, high risk women monitored for complications: renal failure, pulmonary edema, heart

failure, and encephalopathy

Chronic Hypertension

Antihypertensive drugs found in breast milk

Methyldopa is choice for woman needing medication for hypertension and wishing to breastfeed

 

CHRONIC HYPERTENSION WITH SUPERIMPOSED PREECLAMPSIA

Chronic HPN that has new occurrence of proteinuria or thrombocytopenia & ↑ liver enzymes

 

HELLP Syndrome

H – Hemolysis,       resulting in anemia &

          jaundice

EL – Elevated liver enzymes, resulting in

           epigastric pain & vomiting

LP – Low platelets,     resulting in thrombocytopenia, abnormal bleeding & clotting time, bleeding

gums,  petechia, & possibly DIC

 

HELLP SYNDROME

Characterized by:

RBC hemolysis

elevated liver enzymes

low platelet count related to severe vasospasm  leading to disseminated intravascular coagulation

( DIC ).

 

Platelet and RBC transfusion often are administered; coagulation factors are monitored

 

Labor is induced if AOG is more than 32 weeks; cesarean if less than 32 weeks.

 

Chronic hypertension with superimposed preeclampsia

Women with chronic hypertension may acquire preeclampsia or eclampsia

 

Extreme Edema

“puffiness on woman’s face and hands”

 

 palpated over bony surfaces

Tibia on the anterior leg

Ulnar surface of the forearm

Cheekbones

 

Assessing  type of Edema

Nonpitting edema

 

1+

 

2+

 

swelling cannot be indented with finger pressure.

 

tissue can be indented slightly.

Minimal edema of lower extremities.

 

moderate indentation.

Marked edema of the lower extremities

 

Assessing  type of Edema

3+

 

4+ pitting edema

 

 

deep indentation.

Edema of lower extremities, face, hands, and sacral area.

 

indentation so deep and remains after removal of the finger.

Generalized massive edema that includes ascites.

 

Reports about edema

UE edema

“my rings are so tight, I cant’ get them off”.

 

Facial edema

 “when I wake in the morning, my eyes are swollen shut”

or

 “I cant’ talk until I walk around awhile”.

Edema

reduce their urine output to approximately 400 – 600 mL / 24 hours

Criteria for admission to healthcare facility

BP – 160/110 mm Hg

With extensive edema

With marked proteinuria – 3+ to 4+

With cerebral or visual disturbances

With marked hyperreflexia

Oliguria – 500 ml or less

Criteria for admission to healthcare facility

 36 weeks of pregnancy with confirmed fetal lung maturity

 

 Less than 36 weeks and with immature lung function

 

Management

Women are hospitalized

Visitor restriction

Darken the room

Do not stress patients

 receives clear explanation

 Allow to express feelings

Take BP

every 4 hours

Obtain blood studies

assess renal & liver function & development of

           DIC

Blood typing and cross matching

Daily Hematocrit

Plasma estriol level

Electrolytes

Optic fundus

Obtain daily weight

Indwelling catheter: UO

 600 mL/ 24 hours

 more than 30 mL/ hour

24 hour urine sample for protein and creatinine clearance

 evaluate kidney function

Doppler auscultation at 4 – hour’s intervals

External fetal heart monitor

Record of fetal movements

“KICK COUNT”

Non – stress test or biophysical profile

O2 administration

Moderate to high in protein

Moderate in sodium

IV line emergency route

 

DRUGS USED IN PREGNANCY INDUCED HYPERTENSION

 

HYDRALAZINE (Apresoline)

INDICATION

Antihypertensive (peripheral vasodilator), used to decrease HPN

DOSAGE  :5 – 10 mg / IV

Administer slowly to avoid sudden fall in BP.

Maintain diastolic pressure over 90 mmHg inadequate placental perfusion can occur

HYDRALAZINE (Apresoline)

MAJOR ADVANTAGE:

increases CO and blood flow to the placenta

thus do not interfere with placental circulation.

 

LABETALOL  OR NIFEDIPINE

ANTIHYPERTENSIVE

 HYDRALAZINE (Apresoline)

Acts to lower BP by peripheral dilatation

Diastolic pressure  not be lowered below 80 to 90 mmHg

ANTIHYPERTENSIVES: HYDRALAZINE HCl (APRESOLINE) AND DIAZOXIDE (HYPERSTAT)

ANTIHYPERTENSIVES: HYDRALAZINE HCl (APRESOLINE) AND DIAZOXIDE (HYPERSTAT)

 

Nursing Care

                P –promote bed rest

                P – prevent convulsion

                P – Prepare the following

                E – Ensure high CHON diet, Na in moderation

                A – Antihypertensive drug (Apresoline)

                C – Convulsion, prevent

                E – Evaluate for MgS04 Toxicity

 

Magnesium Sulfate

MECHANISM OF ACTION

Prevents seizures and blocks neuromuscular transmission

 

SIDE EFFFECTS:

Flushing, thirst, absence of deep tendon reflexes, respiratory depression, cardiac arrhythmias, cardiac

arrest, decreased urinary output

Medical Management

Magnesium Sulfate

(Mgso4)

 

Acts upon the myoneural junction, diminishing neuromascular transmission

Promotes maternal vasodilation, better tissue perfusion

 

Prevents

CONVULSIONS

MAGNESIUM SULFATE

INDICATION:

Muscle relaxant, prevents seizures & uterine contractions in preterm labor.

Loading dose 4 – 6 g.

Maintenance dose 1 – g/ hour IV.

Infuse loading dose slowly over 15 – 30 mins.

Always administer a piggyback infusion.

MAGNESIUM SULFATE

Assess RR, UO, DTR’s, & clonus every hour.

UO should be over 30 mL/hr and RR over 12/min.

Serum Mg level should remain below 7.5 mEq/L (4 – 8 mg / dL – Mckinney)

Observe for CNS depression & Hypotonia in infant at birth.

 

Signs of overdose of Mg SO4

Decreased UO

Depressed respirations (less than 12 cpm) Assess deep respirations.

Reduced consciousness / altered sensorium

Maternal pulse oximeter reading lower than 95%

Sweating , flushing, Hypotension

A serum Mg above the therapeutic range

 

Signs of paralysis

 

Decreased or absence of DTR’sAssess for depressed patellar reflex.(absent or <1+)

 

Nursing Responsibilities when giving magnesium sulfate

Monitor client’s respirations, BP, & reflexes as well as urinary output frequently

Administer medication either IV or deep IM.

 

 ANTIDOTE: calcium gluconate or calcium chloride

GLUCONATE CALCIUM

Antidote for Mg SO4 intoxication

1 g/IV (10 mL of a 10% solution

Prepared at bedside when administering Mg SO4.

Administer at 5 mL/ min.

DIAZEPAM (Valium)

 Halt seizures

 5 – 10 mg / IV

 Administer slowly. Dose maybe repeated q 5 – 10 (up to 30 mg/hr)

 

DIAZEPAM (Valium )

SALT – POOR ALBUMIN

high – colloid solution used to treat severe Oliguria

Mg SO4 given IV 2 hrs before baby’s birth

 baby will be born with respiratory depression

 

drug crosses the placenta.

Fetal effects

Loss of variability of heartbeat

Reduced fetal breathing movements

Late deceleration

 

Drug Management

Pulmonary edema

Furosemide (Lasix) is given.

 

Digitalis 

- to strengthen contraction of the heart

TONIC – CLONIC SEIZURES

 

Preliminary signal or “aura”

 

TONIC PHASE

 

Muscles of the body contract

 

Back arches

Extremities becomes stiff / rigid

 

Jaw closes abruptly

 

Respirations stop

 

Woman may grow slightly cyanotic

CLONIC PHASE

 

Muscles contract and relax repeatedly

 

                                 Extremities                                         bladder &

                                waves widely                                         bowel muscles

contract & relax

                                 Inhales and

                                exhales irregularly                                   Urine & fecal                       

incontinence

 

                                May aspirate saliva                Breathing is not   

                                                                                 entirely effective

 

                                May aspirate saliva               Remains cyanotic  

Priority care: MAINTAIN PATENT AIRWAY

 Don’t put a tongue blade between the

   woman’s teeth

 Suction patient’s mouth and nose

 Administer O2 via face mask (8 – 10

    L/min)

 Asses O2 saturation via pulse oximeter.

 Apply external fetal monitor

 Turn the patient on her side

 

POSTICTAL STATE

 

 

Patient is in semicomatose stage

 

Cannot be roused except by painful stimuli

Priority care: MAINTAIN PATENT AIRWAY

 Extreme close observation

Painful stimulus of contractions

NOTE: Hearing is the last sense lost and the 1st one regained Continuously assess fetal heart sounds

and uterine contractions

Check for vaginal bleeding every 15 minutes

 

 

POSTPARTUM HYPERTENSION

10 14 days after birth

 usually occurs 48 hours after birth

 Monitoring BP

 Postpartum check – up

 

GRADING PATELLAR REFLEX

 0 – no response, hypoactive, abnormal.

1+ - somewhat diminished response but not        abnormal.

2+ - average response

3+ - brisker than average but not abnormal.

4+ - hyperactive, very brisk, abnormal.

 

GRADING ANKLE CLONUS

 

                Mild              – 2 movements

                Moderate – 3 to 5 movements

                Severe       – over 6 movements

 

Closely monitoring of maternal vital signs

( esp. BP ) and weight and FHT

Bedrest most of the day; side lying position; for 8-12 hours.

High protein ( 60-70g/day), Low sodium diet. Calcium ( 1200mg), magnesium, 2-6g of zinc; vitamin

C&E.

Health teachings for symptoms of mild and severe preeclampsia.

Administration of Magnesium Sulfate, Cortecosteroids and anti hypertensives as ordered.

 HPN drugs are excreted in breast milk.

Blood replacements.

Monitor for seizure activity and protection from injury.

Administer O2 as needed.

Prepare mother and her family for early induction of labor. Vaginal delivery is preferred over

cesarean.

Health teachings on contraception.

 

Infectious Diseases

 

A group of infections caused by viruses and protozoa that cause serious fetal problems when

contracted  by the mother during pregnancy.

 

TORCH INFECTIONS

 

 

infections transmitted to the fetus in utero OR during passage through the birth canal

 

TORCH INFECTIONS

    stands for

Toxoplasmosis

Others:  Include gonorrhea, syphilis, varicella, hepatitis A and B virus (HAV, HGBV), HIV, and group B

beta-hemolytic streptocci (GBS)

Rubella

Cytomegalovirus (CMV), causing Cytomegalic inclusion disease (CID)

Herpes simplex virus (HSV)

TOXOPLASMOSIS

a protozoan infection

 

Cause:  eating undercooked meat, although organism is spread most commonly by contact with cat

stool, or soil with cat litter

 

Manifestations:  almost none, except for a few days of malaise and posterior cervical

lymphadenopathy (influenza-like symptoms)

 

Toxoplasmosis

Cause: Toxoplasmosis protozoan - Toxoplasma Gondii, capable of causing intrauterine infection

 

Incidence: 1:1000 live births

TOXOPLASMOSIS

Effect on fetus:  Infant may be born with any of the following:

Central nervous system damage

Hydrocephalus

Microcephaly

Intracerebral calcifications

Retinal deformities

 

TOXOPLASMOSIS

Diagnostics

                                 - serum analysis for antibody titers

 

Management

-          Sulfadiazine (potentially harmful to 

     the fetus)

-          Pyrimethamine (anti-protozoal)

 

Pathophysiology:

parasite

primary natural host is the cat family

The organisms exist in 3 forms: oocyst, tachyzoite, tissue cyst.

The oocyst are excreted in cat feces

Ingestion of oocyst is followed by penetration of gastrointestinal  mucosa

 

Most maternal organs, including the placenta are “seeded”  by the protozoan

 

In the chronic form of the disease, organisms invade certain body tissues – brain, eyes and striated

muscle forming  tissue cysts

 

Signs & symptoms:

ü  Rarely produces symptoms

                 - IF present, they are generally nonspecific

ü  Mononucleosis-like illness with fever

ü  Lymphadenopathy

ü  Fatigue, Malaise,  Myalgia

ü  Fever , Skin rash, splenomegaly

 

BUT when the infection is transmitted from the woman through the placenta, condition is called

Congenital Toxoplasmosis

 

(Premature infants have a higher incidence) – triad of symptoms includes:

ü  Chorioretinitis

ü  Intracranial calcification

ü  Obstructive Hydrocephalus

 

Transmission:

contact with soil or litter boxes  contaminated with cat feces

 

Development of the infection in the mother is associated with:

ü  consumption of ingested raw or                                      undercooked meat

ü  unpasteurized milk

Transmission:

ü  Development of the infection in the mother is associated with:

via blood product transfusion (WBC)

poor hand washing after handling cat litter

Diagnosis and Laboratory studies

ü  Direct Isolation of the organism from body fluids or tissues

ü  Cerebrospinal fluid examination

ü  Serologic tests

Indirect Fluorescent antibody test

it measures antibodies to surface antigen (in mother)

IgG titers greater than 1:256 – acquired a recent infection   

IgM titers greater than 1:256 – acquired an acute infection

 

ü  Radiologic studies

                                a. a skull film or CT scan of the head

                                b. long bone film

ü  Other studies

                     a. ophthalmologic examination

 

Effects

ü  Maternal effects: Flu-like symptoms in acute phase

 

ü  Fetal effects:  Miscarriages in early pregnancy (harmful to the fetus if it is contracted between 10

and 24 weeks of pregnancy)

 

ü  Neonatal effects: CNS lesions can result in: hydrocephaly,  microcephaly, chronic retinitis, seizures

 

Management:

ü  The efficacy of treatment of pregnant women  and infants with congenital infection is unclear

 

ü  Treatment of acute maternal toxoplasmosis appears to reduce the risk of fetal wastage, and

decrease the congenital infection

 

Drug of choice:

Pyrimethamine (1mg/kg/day orally) + sulfadiazine (25-100mg/kg/day)

should be use after the 1st trimester

Pyrimethamine is a folic acid antagonist

 

Folic Acid  (2mg/6mg, 3x a wk)

 

Prevention:

ü  Advise the pregnant women to have someone else clean the cat litter box

ü  If there’s no one else to perform the cleaning -  should wear the gloves

ü  avoid eating raw meat

ü  all fruits and vegetables –washed carefully

ü  do hand washing

 

Other infections (like Hepatitis B, Syphilis, Varicella and Herpes Zoster)

Hepatitis B

Cause: infection with 

ü  Hepatitis A (HAV) orHepatitis B (HBV) - common

Manifestations:  Fever, malaise, nausea, vomiting, liver

                                Tenderness, Jaundice (late symptom)

Incidence:

acutely affected- approx 1% die  of liver disease

85%-90% - completely recover and develop immunity to hepatitis b

10%-15% - chronic carriers and are at higher risk for developing cirrhosis and liver Ca

 

Pathophyiology:

 

Transmitted sexually or through contact with blood or body fluids

 

Be transmitted to fetus by contact with vaginal  secretions and blood during delivery

 

Transmission:

ü  HAV is spread by droplets or hands

ü  Transmission to the fetus is rare BUT it can occur

ü  HBV can be transmitted to the fetus via placenta,

ü  BUT transmission  usually occurs when the infant is exposed to blood and genital secretions during

labor and delivery

 

 

 

Diagnosis:

For Hepatitis A:

Radioimmunoassay and enzyme-linked immunosorbent Assay methods – to detect HAV antibodies

 

*elevated IgM in the absence of IgG -  probable acute hepatitis

*elevated IgG in the absence of IgM - chronic stage of HAV

 

 

For Hepatitis B:

Hepatitis B surface antigen (HbsAg)

 

Serology to detect IgM antibody, bilirubin levels

 

VIRAL HEPATITIS

Management:

ü  Pregnant patients screen for  (HbsAg)

 

If the mother if (+)  for (HbsAg) – the neonate should receive within 12 hours:

Hepatitis immunoglobulin (HBIg)—provides immediate protection

 

Hepatitis B vaccine—provides long protection from infection

  Hepatitis A

ü  Treatment is supportive

ü  Condition limiting and does not result in chronic infection

 

Hepatitis B

ü  Bed rest

ü  High-protein, low-fat diet

ü  Increased fluids

 

HIV (Human Immunodeficiency Virus)

ü  leads to acquired immunodeficiency syndrome (AIDS)

ü  is the most serious of the STDs

 

The Infected Cell Produces New HIV

 

Pathophysiology

Retrovirus

ò

Infects T-lymphocytes

ò

Body’s ability to fight infection is disabled

Transmission (by blood or body fluids)

 

ü  Sexual intercourse

ü  Exposure to infected blood

ü  Vertical transmission across the placenta to the fetus at birth

ü  Breast milk to the newborn

 

Manifestations

ü  Weight loss

ü  Anemia

ü  Diarrhea and fatigue (AIDS-related complex); developing later on to “opportunistic infections”

(toxoplasmosis, candidiasis, GI illness, herpes simplex)

 

Diagnostics

ü  Serologic screening

ü  Antibody testing

 

Management

ü  Symptomatic, based on disease progression

 

Focus on prevention of HIV transmission

GROUP B BETA-HEMOLYTIC STREPTOCOCCI (GBS)

 

occurs at a higher incidence during pregnancy (10% to 30%)

 

Manifestations: Usually asymptomatic; symptoms of UTI

 

Transmission: Placental transfer; direct contact at birth

 

Effect on fetus: Pneumonia, meningitis

 

Diagnostics:  Cultures from anorectal and vaginal areas obtained at 36-37 weeks’ gestation

 

Management:  Penicillin or ampicillin during labor; if given earlier, recolonization may occur, with

subsequent infection of infant

 

v  Syphilis

Cause:

It is caused by a spirochete (spiral- or coil-shaped bacterium), Treponema pallidum.

crosses the placenta only after the 18th  week of pregnancy

Transmission:

It is transmitted sexual contact or through broken skin

Symptom:

Painless red pustule, appears within 2-6 weeks after exposure

Pathophysiology:

The pustule quickly erodes and develops a painless, bloodless ulcer called chancre

 

Because it is painless, the newly infected person may not notice the chancre

 

The chancre, which sheds infectious fluids

IF the pregnant woman becomes infected with Syphilis, the bacteria can cross the placenta causing

infection to the growing fetus

Manifestations dependent on stage

 

Primary:  a painless chancre (lesion or deep ulcer) seen generally on the genitalia, but may also be

present on the mouth or rectal area

 

Secondary (4 to 6 weeks after the chancre):  generalized maculopapular rash on palms and soles

 

Tertiary or latent:  neurologic symptoms such as mental confusion, slurred speech and lack of

coordination

 

Maternal effects:

Preterm birth, miscarriage, or stillbirth

 

If the woman carries the pregnancy to the age of viability, there is a 40% to 70% chance – infant will

be born infected

Fetal / Neonatal effects:

Birth defects such as: blindness, deafness or other deformities

 

Hutchinson’s triad- includes inflammation of the cornea, deafness notched teeth

 

Fetal / Neonatal effects:

 

Swollen lymph glands , spleen, and liver enlargement, jaundice , anemia, bone deformities, and

vesicular rash – contagious

Diagnosis:

VDRL slide test

Venereal Disease Research Laboratory

a routine blood test, performed for every pregnant woman in early pregnancy

Diagnosis:

FTA-ABS (fluorescent treponemal antibody absorption)

 

Management:

 Drug of choice:

Benzathine Penicillin G

 

 

 

v  Varicella and Herpes Zoster

Cause:

Herpes varicella virus

 

Incidence:

1-5 of 10,000 pregnancies

Transmission of Varicella Zoster:

respiratory droplet, highly contagious

 

the virus incubates for approximately 2 wks and is contagious 2 days before onset of the skin lesions

until the lesions crust over

 

generally 5 days after the initial onset

 

v  Herpes Zoster:

 

localized painful rash within a Dermatome - an area on the body surface supplied by a particular

sensorynerve.

 

*Anyone who has had chickenpox is at risk for developing Shingles*

Fetal / Neonatal effects:

Low birth weight, skin lesions

 

Contractures, damage to the ears, eyes

 

CNS leading to mental retardation, paralysis and seizures

 

Management:

ü  Serologic test – to detect varicella antibodies

ü  Varicella zoster immune globulin (VZIG) - given within 96 hours of exposure – to help prevent the

development of chickenpox.

ü  (VZIG) may also be given to the neonate IF the woman develops chickenpox 5 days before or within

48 hours after delivery

ü  Best is Prevention – vaccination

 

v  GONORRHEA

Cause:  gram-negative coccus Neisseria gonorrheae

Manifestations

Yellow-green vaginal discharge

Male partner:  severe pain on urination, purulent yellow penile discharge

Effect on fetus (esp. with vaginal delivery)

   destructive conjunctivitis (opthalmia neonatorum)

Diagnostics:  vaginal, rectal or urethral  cultures

Management:  Antibiotics, like

                        Ceftriaxone and Cefixime

 

v  Rubella

 

AKA German Measles / 3 Day Measles

Cause:  infection with the rubella virus

Transmission:  by droplet

RUBELLA German measles virus causing extensive fetal damage (teratogenic effects)

Greatest risk to embryo:  early pregnancy (organogenesis period)

Frequency of defects:  50% if infection occurs in first 8 weeks, 20% in the 9th – 16th week

Manifestations:  Rash, low grade fever, headache, lymphadenopathy

Effect on fetus:  Deafness, mental and motor retardation, cataracts, cardiac defects (PDA and

pulmonary stenosis), dental and facial clefts (cleft lip and palate)

Diagnostics:  Serum for antibody titers

Management:  No treatment available; vaccination of pregnant women not recommended because of

the risk of developing a rubella infection

Prevention

ü  Immunization; women of childbearing age who received vaccination advised to avoid getting

pregnant for 3 months’ time

Diagnosis: IgG antibodies to rubella are measured to determine the client’s rubella immunity

status:    

ü  A titer of 1:10 or greater indicates that the woman is immune to rubella. 

 

ü  A titer of 1:8 or less indicates minimal or no immunity

Effects

Maternal effects: Fever, rash and mild lymphedema

Fetal/neonatal effects: spontaneous abortion, stillbirth, congenital anomalies, and death

Risks: occurs if the woman develops rubella in the 1st trimester (first 11 weeks) = multiple anomalies

 

Management:

There is no cure for congenital rubella infection

Treatment are of symptoms and complications

Best tx.= prevention – rubella vaccine

 

Management:

Avoid anyone with flu-like symptoms or rash during the pregnancy

combination of MMR Vaccine (measles , mumps, rubella) == to children at 12-15 months,   2nd dose 

= 4-6 yrs before starting to school

 

v  Cytomegalovirus

Cause: exposure to the cytomegalovirus

Transmission: Can be transmitted through respiratory droplet (most common), semen, cervical and

vaginal secretions, breast milk, placental tissue, urine, feces and banked blood

At risk: workers in day care centers, institutions for the mentally retarded, health settings.

Manifestations:  Possibly asymptomatic

Effect on fetus:  Severe brain damage (hydrocephalus, microcephaly, spasticity); eye damage or

chronic liver disease. Child’s skin may be covered with large petechiae (“blueberry muffin” lesions)

Diagnostics

Serology:  positive viral titers

Management:  No treatment available in pregnancy or for the infected newborn

Diagnosis:

a viral culture is the most definitive tool

 CMV antibodies indicate a recent infection

a fourfold increase in CMV titer in paired sera drawn 10-14 days apart is usually indicative of an acute

infection

Maternal effects:

asymptomatic illness, cervical discharge, mononucleosis- like symptoms

Fetal/ neonatal effects:

Fetal death or severe generalized disease

     with hemolytic anemia and jaundice, hydrocephaly or microcephaly, Pneumonitis,

hepatosplenomegaly, deafness

Management:

Antiviral agents – Ganciclovir

Prevention:

Pregnant woman who have contact with small children should practice meticulous hand washing,

particularly after contact with saliva and urine

 

Proper disposal of the diapers, tissues, and other potentially infected items

Drinking glass and utensils should not be shared

 

Pregnant woman should practice universal precaution

Although CMV is passed through breast milk, breast feeding is not contraindicated – bec. CMV

infection contracted during birth or from breast-feeding rarely cause serious problems

 

v  Herpes Simplex virus (HSV)

Cause:  exposure to the herpes simplex virus

Transmission:

HSV type II is a sexually transmitted disease transmitted by exposure to vesicular lesions on the penis,

scrotum, vulva, perineum, perianal region, vagina, or cervix

Infant= infected during exposure to a  lesion in the birth canal, most at risk

Virus causing genital herpes infection

Transmission:  Placental transmission, or during vaginal delivery

Effects:  First trimester – severe congenital anomalies, spontaneous miscarriage; second trimester –

premature birth, IUGR

Method of delivery:  CS

Management:  Acyclovir (Zovirax)

Diagnosis:

Viral culture is used for definitive diagnosis; serologic test have a lower accuracy

Effects

Maternal effects: blisters, rash, fever, malaise,                   nausea and headache

Fetal/ neonatal effects:                                           miscarriage, preterm labor, stillbirth,

intrauterine growth retardation, mental retardation

Management:

Ante partum – cultures should be done when there is  active lesions during pregnancy to confirm

diagnosis

Management:

Neonatal treatment:

                                * Isolation

                                * Pharmacologic therapy                                                                        - the1st

line drug-Acyclovir

                                                - the 2nd line-  Vidarabine

                                * Feedings

 

STIs and Pregnancy

 

v  Syphilis

Associated with miscarriages, preterm labor, stillbirth and congenital anomalies

 

v  Herpes Simplex Virus Type 2

Associated with infection in the newborn

 

v  STIs and Pregnancy

v  Gonorrhea

Associated with severe eye infection and blindness

v  Human Papillomavirus

May obstruct birth canal

 

 

Nursing Process: A Woman Who Develops A Complication

 

Pregnancy Related Complications

Hemorrhagic Complications of Early Pregnancy

ü  Abortion

ü  Incompetent Cervical Os

ü  Ectopic Pregnancy

ü  Hydatidiform Mole

ü  Choriocarcinoma

ü  Hyperemesis Gravidarum

 

Hemorrhagic Disorders

Hemorrhagic disorders in pregnancy are medical emergencies

 

Maternal blood loss decreases oxygen-carrying capacity

Increased risk for hypovolemia, anemia, infection, preterm labor, and preterm birth

 

Hemorrhagic Disorders

Maternal blood loss decreases oxygen-carrying capacity

Adversely affects oxygen delivery to fetus

Fetal risks include blood loss or anemia, hypoxemia, hypoxia, anoxia, and preterm birth

Bleeding

ü  Development of shock

ü  Blood pressure

ü  Pulse

ü  Fetal heart

ü  Rate

ü  Treatment

 

 

1st Trimester Bleeding

ü  Spontaneous miscarriage

ü  Threatened

ü  Imminent

ü  Complete

ü  Missed

ü  Recurrent pregnancy loss

 

Complications of Miscarriage

ü  Hemorrhage

ü  Infection

ü  Septic abortion

ü  Isoimmunization

ü  Powerlessness or anxiety

 

1st Trimester Bleeding

ü  Ectopic pregnancy

-          Implantation occurs outside of the uterine cavity

ü  Abdominal pregnancy

 

Clinical manifestation

ü  Scant to dark brown vaginal bleeding

ü  Abdominal pain usually develop 3-5 weeks after a missed menstrual period

ü  PAIN is the predominant symptom of tubal rupture- localized on one side or felt over the entire

abdomen

 

CHARACTERISTIC of PAIN:

 

ü  Cramping or sharp, sudden, knifelike pain, often of extreme severity

ü  Shoulder tip pain- presence of intraperitoneal bleeding extending to the diaphragm (Phrenic nerve)

 

Ectopic pregnancy

Fertilized ovum implanted outside uterine cavity

95% occur in uterine (fallopian) tube

Most located on ampullar

Ectopic pregnancy

Other sites include:

Ovary (0.5%)

Abdominal cavity (1.5%)

Cervix (0.3%)

ECTOPIC PREGNANCY

 

Sites of Ectopic pregnancy

ü  Ampullar

ü  Isthmus

ü  Interstitial

ü  Cornual

ü  Cervical

ü  Abdominal

ü  Ovarian

 

2nd Trimester Bleeding

Gestational trophoblastic disease (hydatidform mole)

Abnormal proliferation and degeneration of the trophoblastic villi

 

HYDATIDIFORM MOLE

  a gestational trophoblastic neoplasm

 

Occurs when the chorionic villi abnormally increases & develop vesicles that resembles tiny

grapes

 

2 Types of Molar Growth

PARTIAL MOLE

ü  normal villi intermingled with hydropic villi

ü  some fetal material or an amnionic sac.

ü  Usually associated with one haploid maternal & two haploid paternal sets of chromosomes

ü  Triploid karyotype

 

COMPLETE MOLE

ü  large amount of edematous enlarge villi

ü  without a fetus or fetal membranes.

ü  Almost uniformly diploid w/ paternal chromosomal markers

 

Clinical Manifestation

ü  Pregnancy appears to be normal at first.

ü  1/3 to ½ of women with complete moles has a uterus larger than expected for gestational dates.

ü  Initial hCG levels are lower in patients with apartial mole than those with a complete mole.

ü  Bleeding may vary from brownish-red spotting to heavy bright red.

ü  Vomiting

ü  FHT is absent

ü  Pre –eclampsia may appear before the 20th week of gestation

ü  Those with partial moles typically have a clinical diagnosis of spontaneous or missed abortion.

Vesicles may be evident in the vaginal discharge or the abortus.

 

Causes

Exact cause is unknown

 

Partial moles – believed to originate from dispermic fertilization of a haploid ovum or fertilization of a

haploid ovum with a diploid sperm.

 

Complete moles – often result from fertilization of an empty egg by haploid sperm that reduplicates

 

Associated factors: age, multiparity, diet

 

Medical Diagnosis & Prognosis

ü  UTZ

With appropriate therapy, H-mole generally not associated with maternal mortality

 

Complete H-mole- has a higher incidence of malignant sequelae(10-30%);partial moles – 10%

 

Medical management

FIRST PHASE

Emptying the uterus through D & C.

Evaluation of the tissue by a pathologist

 

SECOND PHASE

hCG level surveillance by radioimmunoassay to detect any c               hanges suggestive of

trophoblastic malignancy.

 

Protocol for hCG monitoring/measurements

1 YEAR

Weekly until they are normal for 3 weeks

Then monthly until they are normal for 6 mos.

 

1 YEAR

 

Then q 2 mos for the next 6 months.

 

Negative hCG should be evident after 6 weeks of evacuation

 

Assessment

ü  Assessment of fundal height

ü  Careful auscultation for fetal heart sounds reveals no findings

ü  Positive pregnancy test

 

ü  Intense nausea & vomiting

 

ü  Check V/S; BP evaluation may reveal HPN before 20th week of pregnancy

 

ü  Blood should be assessed for clear, fluid vesicles.

 

ü  Lab tests: ↓Hgb,Hct and proteinuria.

 

Nursing Intervention

ü  Prepare the client for the evacuation of the uterus.

ü  Provide client education

ü  Family counseling to assist the woman in selecting desirable contraceptive

ü  Pregnancy should be avoided for at least 1 year, after which time conception is

permitted.

ü  Provide psychosocial support

ü  Encourage verbalization or expression of feelings.

 

2nd Trimester Bleeding

ü  Premature cervical dilatation

ü  Cannot hold the fetus until term

ü  Cervical cerclage

 

Incompetent Cervix

Incidence and etiology

 

Medical management

Conservative management of bed rest, progesterone, antiinflammatory drugs, and antibiotics

Shirodkar or McDonald procedure

Prophylactic cerclage is placed at 11 to 15 weeks of gestation

Nursing care and home care

also called cervical insufficiency.

premature opening (dilation) of the cervix usually in mid-pregnancy (18 to 22 weeks or 4 to 6 months

of pregnancy).

 

INCOMPETENT CERVICAL OS

 

Mechanical defect in the cervix that

cause it to   dilate prematurely

 

 occurs during

 midtrimester

 of pregnancy

 

Late habitual abortion or preterm labor

Incompetent Cervix

 

ccurs in about 1 out of every 100 pregnancies and may be responsible for 20 to 25 percent of second

trimester miscarriages.

 

Causes:

Congenital anomalies of the uterus or the cervix

Prior trauma

 

S/Sx:

ü  Painless dilatation

ü  Bloody show

ü  Premature rupture of the membranes

 

Treatment

ü  CERVICAL CERCLAGE

may be done at approx. 12 to 14 weeks gestation.

Removed @ 37 wee     gestation

 

 

 

2 Types of Cervical Cerclage

ü  SHIRODKAR TECHNIQUE

vaginal mucous membrane is elevated band of homologous fascia or a narrow strip of material is

carried around the internal os & tiedvaginal mucosa is restored to its original position & sutured.

 

ü  McDONALD TECHNIQUE

placement of a non absorbable suture around the cervix high on the cervical mucosa.

 

Nursing Management

ü  Monitor FHR.

ü  Observe for signs of rupture of the membranes or uterine contractions.

ü  If contractions ensue, place client on bed rest.

ü  Administer prescribed medicine to control contractions such as ritodrine hydrochloride.

 

PREGNANCT RELATED COMPLICATION

 Hemorrhagic complications  of  late pregnancy

ü  Placenta Previa

ü   Abruptio Placentae

 

3nd Trimester Bleeding

v  Placenta previa

ü   Low implantation of placenta

ü   Risk factors

ü   Assessment

ü   Management

 

PLACENTA PREVIA

 

 

   Is the development of the placenta in the lower uterine segment so that either partially

or wholly covers the

 region of the cervix.

Types of Placenta Previa

Total Placenta Previa – placenta completely covers the internal os.

Partial Placenta Previa – placenta partially covers the internal os.

Low implantation of the Placenta- placenta encroaches on the region of the internal os; can be

palpated by the AP; does not extend beyond the margin of internal os.

 

Clinical Manifestation

ü  Sudden onset of painless, bright-red vaginal bleeding

ü  The uterus usually remains soft

ü  FHR is stable & within normal limits

 

Causes

No known cause

 

PREDISPOSING FACTORS:

ü  Multiparity

ü  Advancing maternal age

ü  Multiple gestation

ü  previous Cesarean birth

ü  Uterine incisions

 

Medical Diagnosis &  Prognosis

ü  Transabdominal UTZ

ü  Internal examination (IE) in the operating room under UP”

 

Medical Management

Planned based on the location of the placenta, the amount of bleeding, and the gestational age of the

fetus.

 

Conservative management is appropriate  when the fetus is premature & bleeding is not excessive

 

Bedrest

 

Medical Management

ü  Administration of magnesium sulfate, terbutaline, or ritodrine.

 

ü  To confirm fetal maturity, amniocentesis is often performed

 

ü  Delivery must be performed irrespective of gestational age under emergency situation.

 

ü  Cesarean birth is the approach of choice for delivery

 

ü  Vaginal delivery may be accomplished with low implantation of the placenta, especially if the baby

is small & the cervix is partially dilated.

 

Nursing Assessment

Assessment include:

ü  Baseline V/S

ü  Amt, chartx of bleeding

ü  Uterine activity & condition( size, contour, irritability, relaxation)

ü  Pain or tenderness, especially in the abdomen;

ü  FHT & actvy

ü  LOC

 

Nursing Diagnosis

ü  Fluid Volume deficit; Hypovolemia r/t bleeding secondary to abnormal placental implantation

ü  Alteration in Tissue Perfusion r/t

ü  High RisK for Infection r/t

 

Nursing Intervention

Depends on whether conservative or active medical management

Home Care:

ü  Provide client & family education Importance of bedrest & restriction of activitiesInstruct the client

to save all perineal pads

ü  Advise client to report if she feels any fluid escaping from her vulva.

HOSPITAL CARE

ü  Periodically palpate the uterus gently to detect contractions suggesting onset of labor.

ü  Monitor for signs of shock.

ü  Monitor lab tests such as hgb, hct.Address emotional & psychosocial needs

ü  Prepare for possible transfusion of blood

 

3nd Trimester Bleeding

Abruptio Placentae

ü  Premature separation of placenta

ü  Occurs suddenly

ü  Most frequent cause of perinatal death

ü  Risk factors

ü  Assessment

ü  Management

 

ABRUPTIO PLACENTA

 

Premature separation of a normally implanted placenta after the 20th week of pregnancy

Clinical Manifestation

Clinical picture varies depending on the type of premature separation present;

 

Type of Abruptio Placentae

ü  COVERT or SEVERE ABRUPTIO

     PLACENTAE– characterized by central separation that entraps lost blood between the uterine wall &

the placenta concealed hemorrhage   masks the seriousness of the problem.

 

ü  OVERT or PARTIAL PLACENTAE – separation occurs at the margin, blood passes b/w the uterine wall

& fetal membranes creating an external hemorrhage.

 

ü  PLACENTAL PROLAPSE – involving complete or almost total separation.

 

Associated with massive vaginal bleeding.

 

Anomalies of Placenta and Cord

ü  Two-vessel cord

ü  Unusual cord length

 

Signs & Symptoms

 

ü  Vaginal bleeding that is dark

ü   abdominal pain( sudden, severe, knifelike)

ü  firm, tender uterus

ü  Signs of shock

ü  Fetal distress may be present

ü  Contraction is frequent, low-amplitude with an increase in resting tone.

Causes

Exact cause is unknown

 

PREDISPOSING FACTORS:

ü  Maternal hypertension

ü  Grand multiparity ( 5 or more pregnancies)

ü  Short umbilical cord

ü  Automobile accidents & trauma

ü  Multiple gestation

ü  hydramnios

 

Medical Diagnosis & Prognosis

ü  UTZ

ü  CAT scans

 

Perinatal mortality rates vary greatly with the type of abruptio, ranging from 15% to approaching

100% for infants experiencing nearly total or complete abruptions.

 

Medical Management

Treatment is dependent on the condition of the fetus & the mother at the time the diagnosis is made.

 

Prompt delivery either vaginal or cesarean depending on the condition of the fetus.

 

Disseminated Intravascular Coagulation (DIC)

ü  Disorder of blood clotting

Fibrinogen levels fall below effective limits

Symptoms

ü  Bruising or bleeding

 

Preterm Labor

Labor that occurs before the end of week 37 of gestation

9-11% of all pregnancies

2/3 of all infant deaths

 

Management

Preterm Labor

Drug administration

ü Antibiotics

ü Steroids

ü Magnesium sulfate

ü Beta sympathomimetics

                          Fetal Assessment

Fetal movement

Labor that cannot be stopped

ü  Assessment

ü  Management

 

Preterm Rupture of Membranes

Rupture of fetal membranes with a loss of amniotic fluid

ü  Before 37 weeks’ gestation

ü  Associated with chorioamnioitis

ü  Complications

ü  Assessment

ü  Management

 

Nursing Process: Pregnant Woman With Special Needs

 

Pregnant Adolescent

ü  Developmental tasks

ü  Prenatal assessment

Health history

Family profile

Day history

ü  Physical examination

ü  Prenatal health teaching

ü  Nutrition

ü  Activity and rest

ü  Pregnancy information

ü  Childbirth

 

Complications

ü  Pregnancy-induced hypertension

ü  Iron-deficiency anemia

ü  Preterm labor

 

 

Pregnant Adolescent

Complications and concerns of labor, birth and postpartum

ü  Cephalopelvic disproportion

ü  Postpartal hemorrhage

ü  Inability to adapt

ü  Lack of knowledge

 

Over Age 40

ü  Developmental tasks

ü  Prenatal assessment

Health history

Family profile

Day history

ü  Physical examination

ü  Chromosomal assessment

ü  Nutrition

ü  Prenatal classes

Complications

ü  Pregnancy-induced hypertension

 

Complications and concerns of labor, birth and postpartum

ü  Failure to progress

ü  Difficulty accepting event

ü  Postpartal hemorrhage

 

Physically or Cognitively Challenged

ü  Rights

ü  Modifications for pregnancy

ü  Safety

Emergency contacts

Transportation

Mobility

Elimination

Autonomic responses

 

ü  Prenatal care modifications

ü  Pregnancy education

ü  Labor and birth modifications

ü  Postpartum modifications

ü  Planning child care

 

 

 

 

Substance Dependent

Withdrawal symptoms following discontinuation of the substance

ü  Abandonment of important activities

ü  Spending increased time in activities related to substance use

ü  Using substance for a longer time than planned

 

Drugs commonly used during pregnancy

ü  Cocaine

ü  Amphetamines

ü  Marijuana and hashish

ü  Phencyclidine

ü  Narcotic agonists

ü  Inhalants

ü  Alcohol

 

Nursing Process: Labor or Birth Complications

 

Complications: Force of Labor

Ineffective uterine force

ü  Hypotonic contractions

ü  Hypertonic contractions

ü  Uncoordinated contractions

Dysfunctional Labor

ü  First stage

ü  Prolonged latent

ü  Protracted active

ü  Prolonged deceleration

ü  Secondary arrest of dilatation

ü  Second stage

ü  Prolonged descent

ü  Arrest of descent

 

Complications: Force of Labor

ü  Contraction rings

ü  Precipitate labor

ü  Uterine rupture

ü  Inversion of the uterus

ü  Amniotic fluid embolism

 

ABORTION

Termination of pregnancy at any time before the fetus has attained a stage of viability

 Before it is capable of   extrauterine existence

 

Occur in about 10%-20% of all pregnancies.

Causes

1. Fetal Factors

Defective embryologic development

Faulty ovum implantation

Rejection of the ovum by endometrium

Chromosomal abnormalities

2. Placental Factors

Premature separation of the normally implanted placenta

Abnormal placental implantation

Abnormal placental function

3. Maternal Factors

Infection

Severe malnutrition

Reproductive system abnormalities

   (eg, incompetent cervix)

Endocrine problems (eg, thyroid dysfunction)

Trauma, Drug ingestion

 

Pathophysiology

Fetal, placental defect & maternal condition

 

results in the disruption of blood flow, containing oxygen and nutrients, to the developing fetus.

 

The fetus is compromised

subsequently expelled from the uterus.

 

ABORTION VS. PRETERM DELIVERY

    ABORTION

Has not reached stage of viability (about 20 wks or less)

500g or less

 

PRETERM INFANT

born after the stage of viability has been reached but before it has the same chance for survival as a

full term infant

2500g or less

Division of Abortion

 

1. SPONTANEOUS ABORTION

 

1. INDUCED ABORTION

 

SPONTANEOUS ABORTION

  ONE IN WHICH THE PROCESS STARTS ON ITS OWN ACCORD THROUGH NATURAL CAUSES

Types of Spontaneous Abortion

 

INDUCED ABORTION

 ONE THAT IS ARTIFICIALLY INDUCED, WHETHER FOR THERAPEUTIC OR OTHER REASON

 

Clinical manifestations

ü  About 80% occur during first 12 weeks of pregnancy.

ü  15-20% terminate in spontaneous abortion

ü  Generally occur 1 to 3 weeks after the death of the embryo or fetus

 

SIGN & SYMPTOMS

ü  Bleeding

ü  Uterine cramps

ü  Softening and dilatation of the cervix

ü  Complete or incomplete expulsion of the

     products of conception

 

Medical diagnosis & Prognosis

ü  Internal Examination (IE)

ü  UTZ

 

Medical management

ü  Bed rest and sexual abstinence prescribed

ü  Sedatives

ü  Hospital confinement necessary If bleeding becomes copious & accompanied by cramps or uterine

contractions

ü  IVF/BT

ü  Oxytocin administration

ü  Surgical removal of the retained products

ü  Dilatation and curettage

ü  Vacuum extraction

ü  Forcep removal

ü  Administration of RhoD immune globulin (RhoGAM) within 72h after the abortion is indicated for Rh-

negative women

ü  Antibiotic therapy

 

Nursing Assessment

ü  Obtain a detailed, accurate hx.

ü  Ask client to describe the quantity of bleeding

ü  Assess characteristic of blood loss

ü  Assess for presence, nature, and location of accompanying discomforts such as cramping, dull or

sharp pain, and dizziness.

 

Nursing Diagnosis

ü  Knowledge deficit related to  physiological alterations in the reproductive system

ü  Fluid volume deficit

ü  High risk for infection

ü  Grieving r/t actual or threatened loss of pregnancy

 

Nursing Interventions

ü  Advise bed rest and eat a well  balanced diet.

ü  Provide information regarding the client’s condition.

ü  Counsel to save all perineal pads as well as all tissue and clots passed.

ü  Counsel to avoid coitus for 2 weeks following the last evidence of bleeding.

ü  Give psychosocial support.

ü  Encourage verbalization of feelings.

 

 EVALUATION

ü  Understands the physiological alteration occuring w/ her codition & r/t tx.

ü  Fluid volume corrected

ü  No signs of infection noted

ü  Appropriately progresses through the grieving process

 

Medical Management

ü  Early diagnosis of ectopic pregnancy based on health history, physical exam, diagnostic test.

 

DIAGNOSTIC TESTS:

ü  HCG level

ü  UTZ

ü  Lab tests: CBC (hgb, Hct↓, leukocytosis)

ü  Culdocentesis checks for abnormal fluid in the space that is just behind the vagina, the posterior cul-

de-sac.

 

v  Colpotomy

 

Surgical Management

ü  Laparoscopy

ü  Curettage

 

SALPINGECTOMY

   with or without  ipsilateral  oophorectomy.

 

Nursing Assessment

ü  Assess for the 3 main classic symptoms of ectopic pregnancy.

ü  Missed menstruation

ü  Abdominal pain

ü  Vaginal spotting

 

CHARACTERISTICS OF PAIN:“crampy”, “dull” or restricting to the

shoulder & back.

ü  Ask client about the use of IUD or history of previous tubal damage caused by dse or developmental

problems.

ü   Assess V/S

ü   Assess for signs of hypovolemic shock

Thready pulse

Tachypnea

Hypotension

ü  Check for cullen’s sign- blue tinge color in the umbilicus – indicative of peritoneal bleeding.

 

 

Nursing Interventions

ü  Explain various dxtc tests & provides support for the patient with a suspected ectopic pregnancy.

ü  Acurately record the perineal pad count.

ü  Prepare for surgery

ü  Adm.  IVF

ü  Monitor V/S

ü   Monitor I & O

ü  After surgery, early ambulation is encouraged.

ü  Administer antibiotic

ü   Provide emotional support and encourage verbalization of feelings

ü   Assist them in resolving feelings of guilt and self-blame.

 

 

 

Evaluation

ü  Understands the pathophysiology of her condition & treatment alternatives.

ü  No signs of infection or complications noted.

ü  Appropriately progresses through grieving process & accepts the loss of her child.

 

HYPEREMESIS GRAVIDARUM

also known as “Pernicious vomiting”

 

Severe & excessive nausea & vomiting during pregnancy, which leads to electrolyte, metabolic, and

nutritional imbalances in the absence of other medical problems.

 

Clinical manifestation

ü  Nausea on arising in the morning or may occur at other times of the day

ü  Persists for weeks & suddenly ceases may last 4 to 8 weeks or longer.

ü  Signs of dehydration & starvation

ü  ↓ urine output

ü  Dryness of the skin

ü  Hypovolemia w/ associated hypotension if dehydration is not corrected.

 

Causes

ü  exact cause is unknown.

ü  Endocrine imbalance caused by high level of hCG & estrogens

ü  Metabolic changes of normal gestation

ü  Fragments of chorionic villi entering the maternal circulation

ü  Diminished motility of the stomach

ü  psychological

 

Medical Diagnosis & Prognosis

ü  Diagnostic testing to detect underlying causes of nausea & vomiting

ü  Perinatal outcome may be improved through early tx to prevent significant lo weight loss

ü  Recovery is usually rapid once fluid & electrolyte balance are restored

ü  Directed toward preventing significant weight loss, correcting fluid & electrolyte imbalance, and

treating acidosis & alkalosis

ü  hospitalization if unable to remedy symptoms & hyperemesis

 

Goals of Intervention

1.  Treat the dehydration by liberal administration of parenteral fluids

     ( approx. 3000ml/24h)

 

        2.      Treat emotional component with an understand  in attitude.

 

1.  Reverse starvation by administration of glucose IV, thiamine chloride SQ, if necessary, feeding a high

caloric, high vitamin fluid diet through NGT or hyperalimentation method.

 

Nursing Diagnoses

ü  Altered Nutrition; less than body requirement r/t pernicious vomiting

ü   Risk for Impaired  Skin Integrity r/t excessive vomiting & dehydration

ü  Ineffective individual coping with the psychological tasks of pregnancy & motherhood

 

 

 

 

 

Nursing Assessment

ü  Assess the particular pattern of nausea & vomiting experience by the client

 

Review laboratory tests

ü  Elevated hgb, Hct

ü  ↓k, Na & Cl

 

Nursing Assessment

ü  Vit B deficiency

ü  Measure current weight, compare w/ her nonpregnant weight.

ü  Ask about ADL, lifestyle & attitude about herelf & pregnancy.

ü  Nutritional habits are assessed in detail & then compared w/ findings on P.E

ü   

Nursing Intervention

ü  Monitor I & O

ü  Restrict oral fluid intake until vomiting ceases.

ü  Start oral feeding once vomiting ceases.

Ex. small quantities of dry food may be given hourly alternating with small quantities of water then

progress slowly as tolerated.

ü  Provide a hygienic environment

ü  Provide psychological support

 

 

Surgery during Pregnancy

ü  Appendicitis

ü  Intestinal obstruction

ü  Gynecologic problems

ü  Trauma during Pregnancy

Significance

Special considerations for mother and fetus

Physiologic alterations of pregnancy

Presence of fetus

Special considerations for mother and fetus

Presence of fetus

Fetal survival depends on maternal survival

Pregnant woman must receive immediate stabilization and care for optimal fetal outcome

 

Effect of trauma on pregnancy influenced by:

Length of gestation

Type and severity of the trauma

Degree of disruption of uterine and fetal physiologic features

Maternal physiologic characteristics

Requires strategies adapted for appropriate resuscitation, fluid therapy, positioning, assessments, and

other interventions

Uterus and bladder positioning

Elevated levels of progesterone

Decreases tolerance for hypoxia and apnea

Cardiac output

Circulating blood volume

Fetal physiologic characteristics

Careful monitoring of fetal status assists greatly in maternal assessment

Fetal monitor tracing works as “oximeter” of internal maternal well-being

Mechanisms of trauma

Blunt abdominal trauma

Penetrating abdominal trauma

Thoracic trauma

Care management of trauma

Immediate stabilization

Primary survey

Secondary survey

Electronic fetal monitoring

Postmortem cesarean delivery

Discharge planning

Emergency Delivery

Precipitate Labor

Labor that lasts less than 3 hours with titanic-like contractions and rapid delivery.

 

Complications are uterine rupture, severe laceration of birth canal, hypotonic uterus after delivery with

profuse bleeding, and fetal hypoxia.

 

Nursing Diagnosis are pain and risk for injury.

 

Nursing Implementation: Safe delivery of infant between contractions using Ritgen’s maneuver;

Newborn care.

Preterm Labor

 Labor occurring after 20th Week but before 37th.

May cause fetal death if delivered with low birth weight. From 35th week onwards, there’s good

chance o survival.

Maternal complications requiring delivery of preterm infants

  placental separation with untrolled hemorrhage; Severe eclampsia or preeclampsia;

uncontrolled renal or CVD; Premature rupture of membrane; and Chorioamnionitis

.

Preterm Labor

Main Nursing Diagnosis: Fear.

 

Nursing Implications: Bedrest in less stimulating environ at lateral recumbent position;

Adequate hydration;  Use of steroids to prevent respiratory distress syndrome for infants;

Prepare for delivery; Administer tokolytic agents

  ( Vasodilan,  Ritodrine, Terbutaline, Magnesium Sulfate) as ordered, but prepare calcium

gluconate as an antidote.

Dystocia

Difficult labor and delivery due to problems with one of the “five P’s” leading to maternal exhaustion,

infection, trauma, and fetal injury and death.

 

Diagnostic exams include vaginal exam, pelvimetry, ultrasound, Leopold’s maneuver.

Dystocia

Defined as long, difficult, or abnormal labor

Dysfunctional labor from abnormal uterine contractions preventing normal progress of:

Cervical dilation

Effacement (primary powers)

Descent (secondary powers)

Increased risk for uterine dystocia includes:

Body build

Uterine abnormalities

Malpresentation and position of fetus

Overstimulation with oxytocin

Cephalopelvic disproportion (CPD)

Increased risk for dystocia includes: (cont’d)

Maternal fatigue, dehydration and electrolyte imbalance, and fear

Inappropriate timing of analgesic or anesthetic administration

Dysfunction of uterine contractions

Hypertonic or primary dysfunctional labor

Hypotonic or secondary uterine inertia

Secondary powers

Bearing-down efforts are compromised when large amounts of analgesia are given

Analgesics may also block the bearing-down reflex

Dystocia

Alterations in pelvic structure

Pelvic dystocia

Contractures of pelvic diameters that reduce the capacity of the bony pelvis, inlet, midpelvis, or outlet

Soft-tissue dystocia

Results from obstruction of the birth passage by an anatomic abnormality other than the bony pelvis

Dystocia

Fetal causes of dystocia

Anomalies

Cephalopelvic disproportion (CPD)

Malposition

Malpresentation

Multifetal pregnancy

Dystocia

Main Nursing Diagnosis are Pain and Anxiety

 

Management

    sedation for hypertonicity; Stimulation of labor for hypotonicity; C/S; Prophylaxis

antibiotic; Constant monitoring of fetal and maternal vital signs; Provide rest ; monitor

presence of cord prolapse or rupture of membrane; Regularly assess fatigue and pain.

 

Care Management

Assessment and nursing diagnoses

Diagnoses that might be identified in women experiencing dystocia

Expected outcomes of care

Plan of care and implementation

Nurses assume many caregiving roles when labor is complicated

Nurses also work collaboratively with other health care providers in providing care

Care Management

Plan of care and implementation

Version

External cephalic version (ECV)

Internal version

Trial of labor

Induction or augmentation with oxytocin

Cervical ripening methods

Chemical agents

Prostaglandin gel

Care Management

Plan of care and implementation

Cervical ripening methods

Mechanical methods

Amniotomy

Care Management

ü  Oxytocin

Hormone normally produced by posterior pituitary gland

Stimulates uterine contractions

Used to induce labor or to augment a labor progressing slowly because of inadequate uterine

contractions

Management of stimulation of labor is same regardless of indication

FDA has issued certain restrictions to its use

Indications

Contraindications

Special cautions

 

ü  Augmentation of labor

Stimulation of uterine contractions after labor has started but progress is unsatisfactory

Implemented for management of hypotonic uterine dysfunction

Common augmentation methods

Oxytocin infusion

Amniotomy

Nipple stimulation

ü  Obstetric Emergencies

ü  Prolapsed umbilical cord

When cord lies below presenting part of fetus

Contributing factors include:

Long cord (longer than 100 cm)

Malpresentation (breech)

Transverse lie

Unengaged presenting part

Cord Prolapse

Risk factors are breech presentation, multiple pregnancy, prematurity.

 

Assessment includes fetal hypoxia, irregular FHR, and Umbilical cord can be seen or felt.

 

Nursing Implication: Monitor FHR continuously; Elevate fetal presenting part to relieve pressure; Do not

push cord back to uterus; Prepare for immediate C/S.

 

ASSESSMENT

 

NURSING MANAGEMENT

 

Obstetric Emergencies

Rupture of the uterus

Very serious obstetric injury

Most frequent causes

Separation of scar of previous classic cesarean birth

Uterine trauma: accidents, surgery

Congenital uterine anomaly

Obstetric Emergencies

Rupture of the uterus

During labor and birth may be caused by:

Intense spontaneous uterine contractions

Labor stimulation: oxytocin, prostaglandin

Overdistended uterus: multifetal gestation

Malpresentation: external or internal version

Difficult forceps-assisted birth

More often in multigravidas than primigravidas

 

Rupture of Uterus

Rupture of uterus from stress of labor from uncontrolled titanic and hypertonic contractions, prolonged

labor, prior uterine surgey, fetal abnormalities and faulty use of forceps.

 

Clinical manifestation: sudden onset of sharp, stabbing abdominal pain during labor, shock syndrome,

cessation of uterine contraction with rigidity of abdomen.

Main Nursing diagnosis: Altered tissue perfusion and Pain.

 

Nursing care involves Close monitoring of labor and fetal and maternal vital signs ; preparation to

emergency surgery

Obstetric Emergencies

Amniotic fluid embolism (AFE)

Amniotic fluid containing particles of debris

Vernix, hair, skin cells, or meconium enters maternal circulation

Obstructs pulmonary vessels

Causes respiratory distress and circulatory collapse

Subinvolution

Retarded involution of puerperal uterus; With enlarged, boggy uterus, profuse and prolonged lochia

rubra, backache, pelvic discomfort,  and dragging sensation.

 

May be caused by poor uterine tone, retained placenta, endometritis, fibroids and tumors, and

displacement of uterus.

 

Main nursing diagnosis: Fluid volume deficit and high risk for infection.

 

Nursing care include: administration of antibiotics and oxytocin; ambulation; and health teachings.

 

Cystitis

Infection of bladder from trauma during delivery, catheterization, and temporary loss of bladder tone.

 

Manifested as urinary frequency, urgency and retention; Dysuria, nocturia, hematuria and tenderness,

fever.

 

Main nursing diagnosis: Pain and Knowledge deficit.

 

Nursing Care includes observing closely for bladder function; forcing fluids to 3000 mL per day;

antibiotics; Perineal care, Infection precautions.

 

Postpartum Hemorrhage

Bleeding of 500 mL or more following delivery; commonly caused by uterine atony.

 

Woman may experience copious amount of vaginal bleeding with or without bright or dark red clots;

boggy uterus; maternal shock.

 

Main Nursing Diagnosis: Fluid volume deficit

 

Nursing responsibility includes Monitoring bleeding, hemoglobin and hematocrit, V/S, I&O, fluid

replacement and Oxytocin administration; Maintaining asepsis; Iron supplements; follow up care.

Predisposing factors of  Postpartum Hemorrhage

Uterine Atony – loss of muscle tone in the uterus.

Over distention

Over massage

 

2. Laceration – of the birth canal

ü  1st degree –fourchette, perineal skin

ü  2nd degree - perineal muscles, vaginal muscles

ü  3rd degree – involves the anal sphincter, anus

ü  4th degree – includes the rectum and rectal muscles.

 

Pulmonary Disorders

Asthma

Therapy objectives

Relief of acute attack

Prevention or limitation of later attacks

Adequate maternal and fetal oxygenation

Cystic fibrosis

Infants of mothers with cystic fibrosis will be carriers of gene

With severe disease, pregnancy is often complicated by chronic hypoxia and frequent pulmonary

infections 

 

Gastrointestinal Disorders

Cholelithiasis (gallstones)

 

Cholecystitis

(inflammation of the gallbladder)

Inflammatory bowel disease

 

Integumentary Disorders

Dermatologic disorders induced by pregnancy include:

Melasma (chloasma)

Vascular “spiders”

Palmar erythema

Striae gravidarum

Skin problems aggravated by pregnancy

Acne vulgaris (in the first trimester)

Erythema multiforme

 

Herpetiform dermatitis

(fever blisters and genital herpes)

Granuloma inguinale (Donovan bodies)

Condylomata acuminata (genital warts)

Neurofibromatosis (von Recklinghausen disease)

Pemphigus

Neurologic Disorders

Epilepsy

Failure to take medications is common factor

Message that drugs are harmful to the fetus

Risks to the infant have been exaggerated

Multiple sclerosis (MS)

Bed rest and steroids used to treat acute exacerbations

Bell’s palsy

 

Autoimmune Disorders

Systemic lupus erythematosus (SLE)

Autoimmune antibody production affects skin, joints, kidneys, lungs, CNS, liver, and other body organs

Immunosuppressive medications not recommended during pregnancy

 

Systemic lupus erythematosus (SLE)

Myasthenia gravis (MG)

Women with MG usually tolerate labor well

Vacuum or forceps assistance for birth may be required due to muscle weakness

Oxytocin may be given

Magnesium sulfate is contraindicated

Narcotic analgesia should be avoided

Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome

 

Preconception counseling

Pregnancy risks

Women now fastest-growing population of individuals with HIV infection and AIDS

Perinatal transmission

90% of all pediatric AIDS cases are due to transmission of virus from mother to child

Obstetric complications

Human Immunodeficiency Virus and Acquired Immunodeficiency Syndrome

Care management

HIV-infected women should be treated with zidovudine during pregnancy

Opportunistic infections should be treated with medications specific for infection

Every effort should be made to decrease neonate’s exposure to blood and secretions 

Immediately after birth, infants should be wiped free of all body fluids and then bathed

All staff working with mother or infant must adhere strictly to infection control techniques

Observe Standard Precautions for blood and other body fluids 

Substance Abuse

Alcohol and other drugs easily pass from mother to baby through the placenta

Smoking during pregnancy has serious health risks including:

Bleeding complications

Miscarriage

Stillbirth

Prematurity

Placenta previa

Placental abruption

Low birth weight (LBW)

Sudden infant death syndrome

 

Substance Abuse

Barriers to treatment

Women fear losing custody of child and  criminal prosecution

Substance-abuse treatment programs do not address issues affecting pregnant women

Long waiting lists and lack of health insurance present further barriers to treatment

Legal considerations

Women who abuse substances may face criminal charges

Nurses who encourage prenatal care, counseling, and treatment are of greater benefit to mother and

child than prosecution

Care management

Women often deny or greatly underreport usage of drugs or alcohol consumption

Crucial for nurse to display nonjudgmental and matter-of-fact attitude to gain woman’s trust and elicit

reasonably accurate estimate

Michigan alcohol screening test (MAST)

CAGE

T-ACE and TWEAK specifically for alcohol use during pregnancy

 

Care management (cont’d)

Realistic goal may be to decrease substance use

Consequences of drug use should be clearly communicated and abstinence recommended

Women more receptive to making lifestyle changes during pregnancy than at any other time

Women for Sobriety

Methadone treatment for pregnant women

Cocaine use during pregnancy has increased dramatically

 

Care management (cont’d)

Breastfeeding definitely contraindicated in women who continue to use amphetamines, alcohol,

cocaine, heroin, or marijuana

Substance abusers difficult to care for  particularly during intrapartum and postpartum periods

Substance abuse is an illness; women deserve to be treated with patience, kindness, consistency, and

firmness

 

Care management (cont’d)

Before discharge

Home situation must be assessed for safe environment

 

Someone available to meet infant’s needs

if mother is unable

Family members or friends should become actively involved with mother before discharge

If infant’s well-being is questionable, case will be referred to child protective services agency

 

Management of Problems

 

Forceps Delivery

Forceps-assisted birth

Maternal indications

Shorten second stage in event of dystocia

Compensate for deficient expulsive efforts

Reverse a dangerous condition

Fetal indications

Distress or certain abnormal presentations

Arrest of rotation

Delivery of head in a breech presentation

 

Forceps delivery

 

Two double-crossed, spoon like articulated blades are used to assist in delivery of fetal head

 

Prerequisites: fully dilated cervix, engaged head, vertex or face presentation, absence of CPD, empty

bladder and bowel.

 

Types are:

High forceps à biparietal dimension of vertex above ischial spine.

 

Midforceps à vertex at ischial tuberosities.

 

Low forceps à vertex distending introitus, use to control and guide head, easiest to deliver.

 

  Low forceps à vertex distending introitus, use to control and guide head, easiest to deliver.

 

 Complications are perineal lacerations, damage to facial nerve of fetus, fetal death, postpartal

hemorrhage, cystocele, rectocele, or uterine prolapse.

 

 

  Low forceps à vertex distending introitus, use to control and guide head, easiest to deliver.

 

Main Nursing diagnosis: Fear and risks of injury to both fetus and mother.

 

Nursing Implications: Closely monitor both fetus and mother during delivery with continual

assessment.

 

Vacuum Delivery

Vacuum-assisted birth

Attachment of vacuum cup to fetal head, using negative pressure to assist birth of head

Prerequisites

Vertex presentation

Ruptured membranes

Absence of CPD

ASSESSMENT

 

NURSING MANAGEMENT

 

Cesarean Delivery

The birth through an abdominal incision into the uterus.

 

Indications are: CPD, severe PIH, genital herpes or papilloma, previous C/S History, placenta previa,

abruption placenta, tranvers fetal lie, breech presentation, extreme low birth weight, fetal distress,

large fetus

 

Types of C/S: Low transverse, Classic, Low vertical.

 

Preoperative care measures are Informed consent, overall hygiene, skin prep, GIT prep, MIO,

hydration, pre-op meds, role of support system.

 

TYPES OF CESAREAN DELIVERY

 

Postpartum Complications

Postpartum Hemorrhage

Definition and incidence

PPH traditionally defined as loss of more than:

500 ml of blood after vaginal birth

1000 ml after cesarean birth

Cause of maternal morbidity and mortality

Life-threatening with little warning

Often unrecognized until profound symptoms

Postpartum Hemorrhage

Etiology and risk factors

Uterine atony

Marked hypotonia of uterus

Leading cause of PPH, complicating approximately 1 in 20 births

Lacerations of genital tract

Retained placenta

Nondherent retained placenta

Adherent retained placenta

Postpartum Hemorrhage

Inversion of uterus

Subinvolution of uterus

Care Management

Assessment

Bleeding assessed for color and amount

Perineum inspected for signs of lacerations or hematomas to determine source of bleeding

Vital signs may not be reliable indicators because of postpartum adaptations

Measurements during first 2 hours may identify trends related to blood loss

Laboratory studies of hemoglobin and hematocrit levels

Care Management

Plan of care and implementation

Medical management

Hypotonic uterus

Bleeding with a contracted uterus

Uterine inversion

Subinvolution

Herbal remedies

Nursing interventions

Providing explanations about interventions and need to act quickly

Instructions in increasing dietary iron, protein intake, and iron supplementation

May need assistance with infant care and household activities until strength regained

Hemorrhagic (Hypovolemic) Shock

 

Medical management

 

Nursing interventions

Fluid or blood replacement therapy

Coagulopathies

Idiopathic thrombocytopenic purpura (ITP)

 

von Willebrand disease—type of hemophilia

 

Disseminated intravascular coagulation (DIC)

Pathologic clotting

Correction of underlying cause

Removal of fetus

Treatment for infection

Preeclampsia or eclampsia

Removal of placental abruption

 

Thromboembolic Disease

Results from blood clot caused by inflammation or partial obstruction of vessel

Incidence and etiology

ü  Venous stasis

ü  Hypercoagulation

 

Clinical manifestations

 

Medical management

 

Nursing interventions

 

Postpartum Infections

 

Puerperal sepsis: any infection of genital canal within 28 days after abortion or birth

 

Most common infecting agents are numerous streptococcal and anaerobic organisms

Endometritis, Wound infections

 

Urinary tract infections

 

Mastitis

 

Sequelae of Childbirth Trauma

 

Disorders of uterus and vagina related to pelvic relaxation and urinary incontinence, are often result of

childbearing

Uterine displacement and prolapse

Posterior displacement, or retroversion

Retroflexion and anteflexion

Prolapse a more serious displacementa

Cervix and body of uterus protrude through vagina and vagina is inverted

Sequelae of Childbirth Trauma

Cystocele and rectocele

Cystocele: protrusion of bladder downward into vagina when support structures in vesicovaginal

septum are injured

Rectocele is herniation of anterior rectal wall through relaxed or ruptured vaginal fascia and

rectovaginal septum

Urinary incontinence

Sequelae of Childbirth Trauma

Genital fistulas

May result from congenital anomaly, gynecologic surgery, obstetric trauma, cancer, radiation therapy,

gynecologic trauma, or infection

Vesicovaginal: between bladder and genital tract

Urethrovaginal: between urethra and vagina

Rectovaginal: between rectum or sigmoid colon and vagina

Postpartum Psychologic Complications

Mental health disorders in postpartum period have implications for mother, newborn, and entire family

Interfere with attachment to newborn and family integration

May threaten safety and well-being of mother, newborn, and other children

Postpartum Psychologic Complications

Postpartum depression without psychotic features

PPD: an intense and pervasive sadness with severe and labile mood swings

Treatment options

Antidepressants, anxiolytic agents, and electroconvulsive therapy

Psychotherapy focuses fears and concerns of new responsibilities and roles, and monitoring for suicidal

or homicidal thoughts

Postpartum Psychologic Complications

Postpartum depression with psychotic features

Postpartum psychosis: syndrome characterized by depression, delusions, and thoughts of harming

either infant or herself

Psychiatric emergency, and may require psychiatric hospitalization

Antipsychotics and mood stabilizers such as lithium are treatments of choice

Loss and Grief

Losses of what was hoped for, dreamed about, and/or planned

Any perception of loss of control during the birthing experience

Birth of a child with handicap

Maternal death

Fetal or neonatal death

Loss and Grief

Conceptual model of parental grief

Acute distress

Intense grief

Reorganization

Anticipatory grief

Loss and Grief

Plan of care and implementation

Communicating and care techniques

Actualize the loss

Provide time to grieve

Interpret normal feelings

Allow for individual differences

Cultural and spiritual needs of parents

Physical comfort

Loss and Grief

Plan of care and implementation

Options for parents

Seeing and holding

Bathing and dressing

Privacy

Visitations: other family members or friends

Religious rituals/funeral arrangements

Special memories

Pictures

Maternal Death

Rare for woman to die in childbirth

Families are at risk for developing complicated bereavement and altered parenting of surviving baby

and other children in family

Referral to social services can help combat potential problems before they develop

 

Equipments and Materials

Cardiac monitor, EKG machine, oxymeter

 

ventilatory support equipment, endotracheal tubes, tracheostomy tube

 

airway, BP apparatus, stethoscope, oxygen tank, O2 regulator, humidifier, monkey wrench, O2 tubings,

O2 cannula/catheter, O12

Equipments and Materials

masks, croupette, O2 tent, suction catheters, suction machine, cardiac

 

arrest board, gloves, peak flow meter, tongue depressor, microscope

 

glass slide, one-way/two-way/three-way water seal drainage, CVP

Equipments and Materials

manometer and tubing, peritoneal dialysis set, dialyzing solution

 

hemodialysis machine (optional), incubator, Billi light, Isolette

 

 Model for basic and advance life support