cad outline notes with arf dka

8/4/2019 CAD Outline Notes With ARF DKA

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Diagnostic Examinations

Non-invasive

Electrocardiogram (ECG)

1. Noninvasive ECG a graphic record of the electrical activity of the heart

2. Portable recorder (Holter monitor) provides continuous recording of ECG for up to 24 hrs. Three

electrodes are attached to the patient's chest and connected to a small portable EKG recorder by lead

wires.

Non-invasive: Types of Holter Monitor

1. Continuous recording - the EKG is recorded continuously during the entire testing period.

2. Event monitor, or loop recording - the EKG is recorded only when the patient starts the recording,when symptoms are felt.

Holter Monitor

Non-invasive-Hemodynamic Monitoring

Vital signs HR, BP, and RR

Arterial oxygen saturation

Transthoracic echocardiography

Invasive-Hemodynamic monitoring

Information obtained through hemodynamic monitoring:

Cardiovascular performance (right and left ventricular function)

Changes in hemodynamic status and organ perfusion

Pharmacologic and nonpharmacologic therapy

Prognosis


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Invasive-Hemodynamic monitoring

Indications:

Any deficit or loss of cardiac function: such as AMI, CHF, Cardiomyopathy

All types of shock; cardiogenic, neurogenic, or anaphylactic

Decreased urine output from dehydration, hemorrhage, G.I. bleed, burns, or surgery

Invasive-Hemodynamic Monitoring

Advantages:

Eliminates potential for error due to measurement technique

Assessment is not inhibited in low-flow states

Recommended for all ICU patients with cardiovascular instability

In 50% of shock patients non-invasive methods underestimate BP by > 30 mmHg

Invasive-Hemodynamic Monitoring

Swan Ganz Catheter/ Pulmonary Artery Catheter

Components of Swan-Ganz

Normally has four ports

Proximal port [Blue] used to measure central venous pressure/RAP and port for measurement of

cardiac output

Distal port [Yellow] used to measure pulmonary artery pressure

Balloon port [Red] used to determine pulmonary wedge pressure;1.5 special syringe is connected

Infusion port [White] used for fluid infusion

Components of the Monitoring System

Bedside monitor amplifier is located inside. The amplifier increases the size of signal


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Transducer changes the mechanical energy or pressures of pulse into electrical energy; should be level

with the phlebostatic axis you can estimate this by intersecting lines from the 4th ICS, mid axillary line

Recorder

PCWP

PCWP-Pulmonary Capillary Wedge Pressure

It is important to measure PCWP to diagnose the severity of left ventricular failure and to quantify the

degree of mitral valve stenosis

Above 20 mmHg - PULMONARY EDEMA

By measuring PCWP, the physician can titrate the dose of diuretic drugs and other drugs that are used to

reduce pulmonary venous and capillary pressure, and thereby reduce the pulmonary edema.

PCWP

Complete set -up

Nursing care to patients with Swan Ganz Catheter

1. a sterile dry dressing should be applied to site and changed every 24 hours; inspect site daily and

report signs of infection

2. if catheter is inserted via an extremity, immobilize extremity to prevent catheter dislodgment or

trauma

3.Observe catheter site for leakage.

Nursing care to patients with Swan Ganz Catheter

5. Continuously monitor PA systolic and diastolic pressures and report significant variations

6. Irrigate line before each reading of PCWP


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7. Maintain client in same position for each reading

8. Record PA systolic and diastolic readings at least every hour and PCWP as ordered.

CENTRAL VENOUS PRESSURE

Blood from the systemic veins flows into the right atrium.

The pressure in the right atrium is the CVP.

Purposes:

1. Reveals RA pressure,

2. to determine the venous return and intravascular volume of the right atrium

3. Provides an IV route for drawing blood samples, administering fluids or medication, and possibly

inserting a pacing catheter

CVP

CVP

Normal range is 4-10 cmH20;

elevation indicates hypervolemia,

decreased level indicates hypovolemia

CVP

Cardiac Catheterization

Cardiac Catheterization

Invasive

ABG

Perform Allens test to determine collateral circulation

Disorders


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Alterations in

Cardiovascular

Functions

TOPICS- CARDIAC DYSFUNCTIONS

CAD

Angina

Cardiac Failure

AMI

Incidence

Worldwide:

1 in every 5 deaths are

caused by Heart Attack

worldwide

Philippines:

#1 Killer

12 Million Filipinos are diagnosed with CAD

Every 7 minutes, a Filipino dies of Heart Attack

CORONARY ARTERY DISEASE (CAD)

A. General Information

refers to a variety of pathology that cause narrowing or obstruction of the coronary arteries, resulting in

decreased blood supply to the myocardium

affects the arteries that provide blood, oxygen, & nutrients to the myocardium


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Causes:

Atherosclerosis- fatty/ plaque deposition

Arteriosclerosis- hardening of arterial lumen

Stages of Development

If demand exceed supply = 02 deficit!!!!!!!!

Myocardial Injury

Myocardial Ischemia

when insufficient oxygen is supplied to meet the requirements of the myocardium

transient/reversible state

Myocardial Necrosis

when severe ischemia is prolonged & irreversible damage to tissue will result

Necrosis - tissue death

Normal vessels can dilate 5-6x normal

Stenotic diseased vessels cannot

Risk Factors- Modifiable

Diet- fats, cholesterol


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Exercise

Sedentary lifestyle

Stress

Cigarette Smoking

Diabetes Mellitus

Obesity

Contraceptive Pills

Type A personality: competitiveness, impatience, aggressiveness, time urgency

Uncontrolled Hypertension

Risk Factors- Non-Modifiable

Age- above 40 years old

Gender- male

Race- whites


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Heredity

Clinical Manifestations

CAD Surgical Management

Goal: Restore Blood Supply

1.Percutaneous transluminal coronary angioplasty (PTCA)

-balloon angioplasty flattens plaque against arterial walls

2.Coronary atherectomy - surgical removal of an atheroma (abnormal mass of fat or lipids) in a major

artery

3.Coronary artery stents a rod or threadlike device for supporting tubular structures during surgical

anastomosis (connection between 2 vessels )

PTCA

Candidates for PTCA:

Those with lesions that occlude at least 70% of the lumen of a major coronary artery

Those whose conditions do not respond to medical treatment and who meet criteria for CABG

Coronary Artery Disease

Angina


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chest pain from myocardial ischemia

caused by inadequate myocardial blood and 0xygen supply

s

4Es-Precipitating Factors

EXCESSIVE physical EXERTION

EXPOSURE to cold ENVIRONMENT

EXTREME EMOTIONAL response

EXCESSIVE intake of saturated food (EAT

Angina

Health History

1. Assess drug use amphetamines,

cocaine which cause excessive sympathetic

stimulation & cardiac work

2. Pt may describe S/s other than pain.

Ex-burning, aching, pressure, smothering

or indigestion

Angina

Pain Assessment

What precipitated pain

how do you describe pain

use scale 1-10 to rate

what relieves pain


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How long does pain last, how often does it occur

Do you carry NTG? Last taken, #tabs, relief

any other heart meds do you take

Limit ADLs?

Angina-S/s

Angina

ANGINA PECTORIS-MEDICAL MGMT

Drug therapy: nitrates, beta adrenergic blocking agents, and/or calcium blocking agents, lipid reducing

drugs if cholesterol is elevated

Cardiac Failure

Cardiac Output

CO = Stroke volume X heart rate

=70 ml X 60 beats/min

=4,200 ml/min.

Volume of blood ejected per minute

Each ventricle ejects approximately 70mL of blood/ beat

Averages between 4-8L/min

cardiac output (CO)- the amount of blood pumped in 1 minute.

stroke volume (SV),which is the amount of blood pumped out of the ventricle with each contraction.

Preload-stretching of the cardiac myocytes prior to contraction

Afterload- "load" that the heart must eject blood against

Heart Failure


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inability of the heart to maintain adequate circulation

to meet the metabolic needs of the body due to

impaired pumping ability

Etiology

It can be caused by :

Inappropriate work load (volume or pressure overload)

Restricted filling

Myocyte loss

Conditions that Precipitate and Exacerbate Heart Failure

Types of Heart Failure

Based on left ventricular functioning

Systolic heart failure- an alteration in ventricular contraction

Diastolic heart failure - an alteration in ventricular filling


Forward failure -diminished cardiac output, an inadequate output of the affected ventricle causes

decreased perfusion to vital organs

Backward failure- damming back of blood in the venous system ,blood backs up behind the left ventricle

causing increased pressure in the atrium


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Low output failure- not enough CO is available to meet the demands of the body

High output failure -occurs when a condition causes the heart to work harder to meet the demands of

the body


Left sided

Right sided

Biventricular

CLASSIFICATIONS- New York Heart Association (NYHA)Classification of Heart Failure

CONGESTIVE HEART FAILURE -

Diagnostic tests: RVF

- chest x-ray: reveals cardiac hypertrophy

-echocardiography: indicates size of

cardiac chambers

CVP, ALT(SGPT), PO2

Diagnostic tests: LVF

ECG, chest x-ray (cardiomegaly, pleural

effusion), echocardiography, cardiac catheterization, dec. PO2, inc. PCO2

- B-type natriuretic peptide


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CONGESTIVE HEART FAILURE

Medical Management:

1. determination and elimination/control of underlying cause

2. Drug therapy:

- Diuretics: Furosemide, Spironolactone

- Dilators: ACE inhibitors, nitrates

- Digitalis: digoxin

3. Diet: low salt, low cholesterol

If medical therapies unsuccessful, mechanical assist devices (intra-aortic balloon pump), cardiac

transplantation or mechanical hearts may be employed.

Diuretic Therapy

The most effective symptomatic relief

Mild symptoms

Block Na reabsorbtion in loop of henle and distal convoluted tubules

Thiazides are ineffective with GFR < 30 --/min

Side Effects

Pre-renal azotemia

Skin rashes

Neutropenia

Thrombocytopenia

Hyperglycemia

Uric Acid

Hepatic dysfunction


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Diuretics (cont.)

More severe heart failure loop diuretics

Lasix (20 320 mg QD), Furosemide

Bumex (Bumetanide 1-8mg)

Torsemide (20-200mg)

Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in

natriuresis, kaliuresis and metabolic alkalosis

Adverse reaction:

pre-renal azotemia

Hypokalemia

Skin rash

ototoxicity

K+ Sparing Agents

Triamterene & amilorideacts on distal tubules to K secretion

Spironolactone (Aldosterone inhibitor)

recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-

angiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis

Inhibitors of renin-angiotensin- aldosterone system

Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an

important role in the progression of the syndrome

Angiotensin converting enzyme inhibitors

Angiotensin receptors blockers

Spironolactone

Angiotensin Converting Enzyme Inhibitors


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They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II

vasodilation and Na retention

Ace Inhibitors were found to improve survival in CHF patients

Delay onset & progression of HF in pts with asymptomatic LV dysfunction

cardiac remodeling

Side effects of ACE inhibitors

Angioedema

Hypotension

Renal insuffiency

Rash

cough

Angiotensin II receptor blockers

Has comparable effect to ACE I

Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)

Digitalis

Mechanism of Action

+ve inotropic effect by intracellular Ca & enhancing actin-myosin cross bride formation (binds to the

Na-K ATPase inhibits Na pump intracellular Na Na-Ca exchange

Vagotonic effect

Arrhythmogenic effect

Effects of Cardiac Glycosides

Increased force of myocardial contraction

(+ INOTROPIC EFFECT)


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Increased renal perfusion

(DIURETIC EFFECT)

Slowed heart rate

(- CHRONOTROPIC EFFECT)

Decreased conduction velocity through the AV node

( -DROMOTROPIC EFFECT).

Nursing Responsibilities

Recognize signs and symptoms of digoxin toxicity

Cardiac

Sinoatrial arrest or block

Third-degree AV block (complete)

Ventricular arrhythmias

Bradycardia

Gastrointestinal

Abdominal pain

Anorexia

Diarrhea

Nausea

Vomiting

Nursing Responsibilities

Recognize signs and symptoms of digoxin toxicity

Neurologic

Blue-yellow color blindness

Blurred vision


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Colored dots in vision

Confusion

Depression

Disorientation

Flickering lights

Headache

Insomnia

White halos on dark objects

Nursing Management-CHF

Nursing Management

6. Monitor heart rate and presence of dysrhythmias by cardiac monitor.

7. Insert foley catheter as prescribed and monitor urine output.

8. MIO

9. Avoid unnecessary IV administration of fluids.

10. Monitor weight to determine response to treatment.

Nursing Management

Nursing Management

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

orthopnea, cough w/pink-tinged sputum


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TX: add morphine to relieve anxiety, slow respiratory rate, and decrease peripheral vascular resistance

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

Nursing Management

Monitor Intake and output

Maintain bed rest for the first 24-36 hours

Assess respiratory rate and characteristics. This may indicate heart failure.

Provide reassurance to the family and client.

CARDIAC SURGERIES

CORONARY ARTERY BYPASS SURGERY

A. General information:

A coronary artery bypass

graft is the surgery of choice

for clients with severe CAD

New supply of blood brought

to diseased/occluded

coronary artery by bypassing

the obstruction with a graft

that is attached to the aorta

proximally and to the

coronary artery distally.

Coronary Artery Bypass Grafting (CABG)

Candidates for CABG

Angina cannot be controlled by medical Rx


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Unstable angina

A positive exercise tolerance test & lesions or blockage that cannot be treated by PTCA

A left main coronary artery lesion or blockage of more than 70%

Individuals who have complications from unsuccessful PTCAs


B. Nursing interventions: preoperative

1. Explain anatomy of the heart, function of coronary arteries, effects of CAD

2. Explain events of the day of surgery

3. Orient to the critical and coronary care units and introduce to staff

4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc)

5. Demonstrate activity and exercise

6. Reassure availability of pain medications


C. Nursing interventions: post-operative

1. Maintain patent airway

2. Promote lung re-expansion-deep breathing & coughing, incentive spirometer

3. monitor cardiac status

4. maintain fluid and electrolyte balance/monitor drainage in chest tubes (report if 100-

150cc/hr)

5. maintain adequate cerebral circulation

6. provide pain relief-splinting,meds

7. prevent abdominal distension


8. Monitor for and prevent the ff. complications:

a. Thrombophlebitis / pulmonary embolism

b. Cardiac tamponade


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c. arrhythmias

d. CHF

9. Provide client teaching and discharge planning concerning:

a. limitation with progressive increase in activities


b. sexual intercourse can usually be resumed by 3rd or 4th week post-op

c. medical regimen

d. meal planning with prescribed modifications

e. wound cleansing daily and report for any signs of infection

f. Symptoms to be reported:

- fever, dyspnea, chest pain with minimal exertion

ALTERATION IN RESPIRATORY FUNCTION

VENTILATION & PERFUSION RATIO (V/Q)

PULMONARY/RESPIRATORY FAILURE

inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue

oxygenation and/or failure of CO2 homeostasis.

Classification

Respiratory Failure

Symptoms

CNS:

Headache


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Visual Disturbances

Anxiety

Confusion

Memory Loss

Weakness

Decreased Functional Performance

Respiratory Failure

Symptoms

Pulmonary:

Cough

Chest pains

Sputum production

Stridor

Dyspnea

Respiratory Failure

Symptoms

Cardiac:

Orthopnea

Peripheral edema

Chest pain

Other:

Fever, Abdominal pain, Anemia, Bleeding

Clinical

Respiratory compensation


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Sympathetic stimulation

Tissue hypoxia

Hemoglobin desaturation

Clinical


Tachypnoea RR > 35 Breath /min

Accessory muscles

Recesssion

Nasal flaring


Tissue hypoxia

Haemoglobin desaturation

Clinical



sweating

Tissue hypoxia


Clinical



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Tissue hypoxia

Altered mental state

(late)


Clinical

Altered mental state

PaO2 +PaCO2 acidosis dilatation of cerebral resistance vesseles ICP

Disorientation

Headache

coma

asterixis

personality changes

Clinical



Tissue hypoxia

Hemoglobin desaturation

cyanosis

Respiratory Failure

Laboratory Testing

Other tests

Hemoglobin


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Electrolytes, blood urea nitrogen, creatinine

Creatinine phosphokinase, aldolase

EKG, echocardiogram

Electromyography (EMG)

Nerve conduction study

Respiratory Failure

Laboratory Testing

Arterial blood gas

PaO2

PaCO2

PH

Chest imaging

Chest x-ray

CT sacn

Ultrasound

Ventilationperfusion scan

Respiratory failure:

Interventions

Supportive therapy

Specific therapy

Supportive therapy

Secure the airway

Pulse oximetry

Oxygen: by mask, nasal cannula, head box


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Proper positioning

Nebulization if indicated

Blood sampling: Routine, electrolytes, ABG

Secure IV line

CXR: upright AP & lateral views

Hypoxemic / Non - Hypercapnic respiratory failure

The major problem is PaO2.

If due to low V/Q mismatch; oxygen therapy.

If due to pulmonary intra-parenchymal shunts (ARDS), assisted ventilation with PEEP may be needed.

If due to intracardiac R-L shunt: O2 therapy is of limited benefit. Surgical t/t is needed.

Hypercapnic Respiratory failure

Key decision is whether mechanical ventilation is required or not.

In Acute respiratory acidosis: Mechanical ventilation must be strongly considered.

Chronic Resp acidosis: patient should be followed closely, mech ventilation is rarely required.

In acute-on-chronic respiratory failure, the trend of acidosis over time is a crucial factor.

Mechanical Ventilation: Indications

PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy.

Deteriorating respiratory status despite oxygen and Nebulization therapy

Anxious, sweaty lethargic child with deteriorating mental status.

Respiratory fatigue: for relief of metabolic stress of the work of breathing

Nursing Management


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Note changes suggesting increased work of breathing (tachypnea, diaphoresis, intercostal muscle

retraction, fatigue) or pulmonary edema (fine, coarse crackles or rales, frothy pink sputum).

Assess breath sounds.

Diminished or absent sounds indicate inability to ventilate the lungs sufficiently to prevent

Analyze ABG and compare with previous values

Determine hemodynamic status (blood pressure, pulmonary wedge pressure, cardiac output)

Nursing Management

Administer oxygen to maintain Pao2 of 60 mm Hg or Sao2 > 90% using devices that provide increased

oxygen concentrations (aerosol mask, partial rebreathing mask, nonrebreathing mask).

MIO

Provide measures to prevent atelectasis and promote chest expansion and secretion clearance, as

ordered (incentive spirometer, nebulization, head of bed elevated 30 degrees, turn frequently, out of

bed).

Perform chest physiotherapy to remove mucus. Teach slow, pursed-lip breathing to reduce airway

obstruction.

ARDS

clinical syndrome also called noncardiogenic pulmonary edema in which there is severe hypoxemia and

decreased compliance of the lungs, which leads to both oxygenation and ventilatory failure

Fulminant form of respiratory failure characterized by acute lung inflammationand diffuse

alveolocapillary injury

Sudden and life-threatening deterioration of the gas-exchange function of the lungs

S/S

Develop progressively as follows:


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Hyperventilation

Respiratory alkalosis

Dyspnea & Hypoxemia

Metabolic acidosis

Respiratory acidosis

Further hypoxemia

Hypotension, decreased cardiac output ,death

Diagnostic Evaluation

The hallmark sign for ARDS is a shunt; hypoxemia remains despite increasing oxygen therapy.

Decreased lung compliance; increasing pressure required to ventilate patient on mechanical ventilation.

Chest X-ray exhibits bilateral infiltrates.

Pulmonary artery catheter readings: pulmonary artery wedge pressure >18 mm Hg.

Histopathologic Changes

Diffuse alveolar damage is the descriptive term for the histopathologic findings encountered in acute

lung injury.

MEDICAL MANAGEMENT

Primary Focus in the management of ARDS includes:

Identification and treatment of the underlying condition.

Aggressive, supportive care must be provided to compensate for severe respiratory dysfunction

SUPPORTIVE THERAPY

Intubation

Mechanical ventilation


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Circulatory support

Adequate fluid volume

Nutritional support

Monitor ABGs, Pulse Oximetry, bedside Pulmonary Function Test

Positive End-Expiratory Pressure (PEEP) is a critical part of the treatment of ARDS.

Uses of PEEP-

PHARMACOLOGIC THERAPY (Under Investigation

Human Recombinant Interleukin-1 receptor antagonists

Neutrophil Inhibitors

Pulmonary-specific vasodilators

Surfactant Replacement Therapy

Antisepsis Agents

Antioxidant Therapy

Corticosteroids (late in the course of ARDS)

NUTRITIONAL THERAPY

Patients with ARDS require 35-45 Kcal/kg per day to meet caloric requirements.

Enteral Feeding is the first consideration; however TPN also may be required.

NURSING MANAGEMENT

General Measures

Close monitoring and frequent assessment


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Positioning is important to improve ventilation and perfusion in the lungs and enhance secretion

drainage.

Restrict fluid intake

Provide rest

Reassurance especially with neuromuscular blocking agents

Prepare for intubation and mechanical ventilation using PEEP

Definition Acute Renal failure (ARF)

Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes

Different to renal insufficiency where kidney function is deranged but can still support life

ARF

Occurs over hours/days

Lab definition

Increase in baseline creatinine of more than 50%

Decrease in creatinine clearance of more than 50%

Deterioration in renal function requiring dialysis

ARF

Pre renal (functional)

Renal-intrinsic (structural)

Post renal (obstruction)


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ACUTE RENAL FAILURE

Stages of ARF

OLIGURIC PHASE

urine output = < 400cc/day

Usually lasts 1-2 weeks

BUN, Creatinine, hyponatremia

DIURETIC PHASE

Gradual return to glomerular filtration

Excretion of fluid: 1-2 liters/ day- 4-5L

Usually lasts 2-3 weeks

BUN, Creatinine

RECOVERY PHASE

Returns to prerenal failure activity level

3-12 months

ACUTE RENAL FAILURE

Assessment

Urine output

Ultrasound

Azotemia (increased BUN and crea)

Hyperkalemia

Metabolic Acidosis

Anemia

Prevention


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Drugs taken by client

Nephrotoxic drugs

NSAIDs

ACUTE RENAL FAILURE

Medical Management

Fluid maintenance

Avoiding fluid excess

Dialysis

Pharmacologic treatment

Kayexalate (sodium polystyrene sulfonate)

Retention enema

Reduction of drug doses

Nutrition: protein- 1g/kg of weight; potassium restriction

ACUTE RENAL FAILURE

Maintaning fluid and electrolyte balance

High calorie, low protein diet

Reducing metabolic rate

Promoting pulmonary function

Infection prevention

Skin care

Emotional support


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Monro-Kellie Hypothesis

because of the limited space for expansion within the skull, an increase in any one of the components

causes a change in the volume of the others. (B&S, p. 2169)

What does this mean?

Decreased Cerebral Blood Flow

What happens to brain cells as blood flow decreases?

Early compensatory mechanism:

Vasomotor stimulation

What assessment findings indicate this?

Changes in concentration of CO2

causes cerebral vasodilation

causes vasoconstriction

Decreased cerebral outflow

Cerebral Perfusion Pressure

What is cerebral perfusion?

Steady cerebral perfusion can be maintained if arterial systolic pressure is 50 150 mm Hg and ICP is

below 40 mm Hg.

CPP = MAP ICP


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Normal CPP is 70 100 mm Hg

Increased ICP

Pathophysiology:

Acute neurologic condition alters the equilibrium of components within the cranial vault

Causes

Primary

Secondary

Regardless of cause, ICP decreases cerebral perfusion, stimulates further swelling, and may cause

herniation

Background Information

The brain is contained within and protected by the rigid cranial vault

The cranial vault also contains blood and CSF

These components are usually in a state of equilibrium and produce the ICP

Usually measured in the lateral ventricles

Normal pressure 10 to 20 mm Hg

Increased ICP and Cushings Response

Increased ICP: Clinical Manifestations

Early Indicators:

Subtle changes in LOC

Pupillary changes

Weakness of one extremity or one side

Constant headache increasing in intensity and aggravated by movement or straining

Late Indicators:

Continuing decrease in LOC progressing to coma

Bradypnea, bradycardia, hypertension and fever


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Altered respiratory pattern

Projectile vomiting

Hemiplegia, decorticate or decerebrate posturing

Loss of brain stem reflexes

Diagnostic Tests

CT

MRI

PET

SPECT

Transcranial Doppler

Electrophysiologic monitoring

Evoked potential monitoring

Contraindicated Diagnostic Test

Which diagnostic test is contraindicated in a patient with increased intracranial pressure?

Why?

Complications

Brain stem herniation

Diabetes insipidus

Syndrome of Inappropriate ADH (SIDAH)

What is the cause of these complications?

How will they be treated?

Medical Management


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Increased ICP is a true medical emergency

Treatment must be promptly initiated

Invasive monitoring of ICP

Manipulating one or more cranial vault component

Decrease cerebral edema

Maintain cerebral perfusion

Reduce CSF and intracranial blood volume

Controlling fever

Maintaining oxygenation

Reducing metabolic demands

Nursing Care

Maintaining a patent airway

Achieving an adequate breathing pattern

Optimizing cerebral tissue perfusion

Maintaining negative fluid balance

Preventing infection

Monitoring and managing potential complications

cEREBROvaSCULAR ACCIDENT

refers to a functional abnormality of the CNS that occurs when the normal blood supply to the brain is

disrupted

types

Ischemic stroke-little blood flow

Thrombotic


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Embolic

Hemorrhagic stroke-disrupted blood flow

Intracerebral

Subdural

types

Ischemic stroke-little blood flow

1. Thrombotic formation of a blood clot with coagulation the results in the narrowing of the lumen of a

blood vessel with eventual occlusion

2. Embolicocclusion of a cerebral artery by an embolus, resulting in necrosis and edema of the area

supplied by the involved vessel

types

Hemorrhagic stroke-disrupted blood flow

1. Intracerebral hemorrhage stroke-bleeding within the brain caused by a rupture of vessels

2. Subarachnoid hemorrhagic stroke-cause by aneurysm or AV malformation

cEREBROvaSCULAR ACCIDENT

Pathophysiology and Etiology

Cerebrovascular insufficiency is caused by atherosclerotic plaque or thrombosis, increased PCO2,

decreased PO2, decreased blood viscosity, hyperthermia/hypothermia, increased ICP.

Carotid arteries, vertebral arteries, major intracranial vessels, or microcirculation may be affected.


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Cardiac causes of emboli include atrial fibrillation, mitral valve prolapse, infectious endocarditis, and

prosthetic heart valve.

Development of CVA

1.Transient Ischemic attack-brief episodes of

neurologic manifestations which clear completely in

less than 24 hours

2. Reversible ischemic neurologic deficit-neurologic

deficits remain after 24 hours but leaves no residual

signs and symptoms after days to weeks

3. Stroke in-evolution-progressing stroke which

develops over a period of hours or days;

manifestations dont resolve and leave residual

neurologic effects

4. Completed stroke- when neurologic deficits remain

unchanged over 2-3 day period

Risk Factors

Prior ischemic episodes

Cardiac disease

DM

Atherosclerotic diseasae

Hypertension, hypercholesterolemia

Polycythemia

Smoking

Oral contraceptives


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Emotional stress

Obesity

Family history of stroke

Age

Assessment and diagnostic findings

Physical and neurologic exams (focus on airway patency and cough and gag reflex)

TIA (transient ischemic attack)

CT scan

ECG

Carotid ultra sound

Transesophageal echocardiography to rule out emboli from heart.

Tia s/s

History of intermittent neurologic deficit, sudden in onset, with maximal deficit within 5 minutes and

lasting less than 24 hours.

Carotid bruit

History of headaches of duration of days before ischemia.

Tia s/s

Carotid system involvement:

amaurosis fugax,

homonymous hemianopsia,

unilateral weakness, unilateral numbness or paresthesias,

aphasia

dysarthria.

Tia s/s


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Vertebrobasilar system involvement: vertigo, homonymous hemianopsia, diplopia, weakness that is

bilateral or alternates sides, dysarthria, dysphagia, ataxia, perioral numbness

Warning signs that may precede CVA

Paresthesia

Transient loss of speech

Hemiplegia

Severe occipital or nuchal headaches

Vertigo or syncope

Motor or sensory disturbances (tingling transient paralysis)

Epistaxis

Cva S/S

Cva S/S

Cva S/S

Treatment for Ischemic Stroke

tPA=Thrombolytic agent

Document time of symptom onset. (If awoke with symptoms, must go by time when last seen normal)

Immediate head CT (check for blood)

Evaluate for tPA administration (review exclusion/inclusion criteria)


If not a tPA candidate, ASA in ED. Rectal ASA if fails swallow eval. or if swallow eval. not complete.

Keep NPO, until a formal swallow eval. is done.

Admit as Inpatient and perform diagnostic testing: Carotid US, Echo, TEE, ECG monitoring for a-fib, MRI,

fasting Lipid, Clotting disorder blood work (Antiphospholipid, Factor V, Antithrombin III)


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Rehabilitation


Surgery carotid endarterectomy (removal of an atherosclerotic plaque or thrombus from the carotid

artery if with TIA symptoms)

tPA Administration Considerations

Must be started before 3 hours from onset

No blood on head CT

Review patients history for other risk factors

Accurate weight recorded

Foley catheter prior to tPA

tPA Cont

Consent explained and signed

(BP>185/110) treat with labetolol 10-20mg IV over 1-2 min. May repeat x1 or nitro paste 1-2 inches. If

treatment does not lower BP, do not give tPA

shows significant deficits to merit treatment.

tPA Contraindications

Any recent surgery185/110)

Seizure at the onset of stroke

Active internal bleeding (


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Use of anticoagulants with PT>15 or INR >1.7

Platelet count


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Improve Mobility and prevent joint deformities

Correctly position patient to prevent contractures

Place pillow under axilla

Hand is placed in slight supination- C

Change position every 2 hours

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

2. Enhance self-care

Carry out activities on the unaffected side

Prevent unilateral neglect

Keep environment organized

Use large mirror



3. Manage sensory-perceptual difficulties

Approach patient on the Unaffected side

Encourage to turn the head to the affected side to compensate for visual loss



4. Manage dysphagia

Place food on the UNAFFECTED side

Provide smaller bolus of food


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Manage tube feedings if prescribed

5. Help patient attain bowel and bladder control

Intermittent catheterization is done in the acute stage

Offer bedpan on a regular schedule

High fiber diet and prescribed fluid intake

CVA: Hemorrhagic Stroke

Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP

Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage


Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP

Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage


Sudden and severe headache

Same neurologic deficits as ischemic stroke

Loss of consciousness

Meningeal irritation

Visual disturbances

General manifestations


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Hemorrhagic Stroke Treatment

Do not give antithrombotics or anticoagulants

Monitor and treat blood pressure greater than 150/100

NPO, until swallow eval is completed

Anticipate Neurosurgical consult

Possible administration of blood products



1. Optimize cerebral tissue perfusion

2. relieve Sensory deprivation and anxiety

3. Monitor and manage potential complications


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Increased Intracranial pressure

Intracranial pressure more than 15 mmHg

Brunner= Normal intracranial pressure 10-20 mmHg

Causes:

Head injury

Stroke

Inflammatory lesions

Brain tumor

Surgical complications


Pathophysiology

The cranium only contains the brain substance, the CSF and the blood/blood vessels

MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of

the other

Any increase or alteration in these structures will cause increased ICP


Pathophysiology

Compensatory mechanisms:

1. Increased CSF absorption

2. Blood shunting

3. Decreased CSF production


Pathophysiology


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Decompensatory mechanisms:

1. Decreased cerebral perfusion

2. Decreased PO2 leading to brain hypoxia

3. Cerebral edema

4. Brain herniation

S/s Cushings triad

HPN

Bradycardia

Widening of pulse pressure

Decreased cerebral blood flow

Cerebral Edema

Abnormal accumulation of fluid in the intracellular space, extracellular space or both.

Herniation

Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down

on the brain stem

Cerebral response to increased ICP

Steady perfusion up to 40 mmHg

Cushings response

Vasomotor center triggers rise in BP to increase ICP

Sympathetic response is increased BP but the heart rate is SLOW

Respiration becomes SLOW



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CLINICAL MANIFESTATIONS

Early manifestations:

Changes in the LOC- usually the earliest

Pupillary changes- fixed, slowed response

Headache

vomiting


CLINICAL MANIFESTATIONS

late manifestations:

Cushing reflex- systolic hypertension, bradycardia and wide pulse pressure

bradypnea

Hyperthermia

Abnormal posturing


Nursing interventions:

Maintain patent airway

1. Elevate the head of the bed 15-30 degrees- to promote venous drainage

2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood


Nursing interventions

3. Administer prescribed medications- usually

Mannitol- to produce negative fluid balance

corticosteroid- to reduce edema


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anticonvulsants-p to prevent seizures



4. Reduce environmental stimuli

5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning



6. Keep head on a neutral position. ACOID- extreme flexion, valsalva

7. monitor for secondary complications

Diabetes insipidus- output of >200 mL/hr

SIADH

Altered level of consciousness

Consciousness

Requires:

1. Arousal: alertness; dependent upon

reticular activating system (RAS); system of

neurons in thalamus and upper brain stem


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2. Cognition: complex process, involving all

mental activities; controlled by cerebral

hemispheres

It is a function and symptom of multiple pathophysiologic phenomena

Causes: head injury, toxicity and metabolic derangement

Disruption in the neuronal transmission results to improper function


Assessment

Orientation to time, place and person

Motor function

Decerebrate

Decorticate

Sensory function


Patient is not oriented

Patient does not follow command

Patient needs persistent stimuli to be awake

COMA= clinical state of unconsciousness where patient is NOT aware of self and environment


Etiologic Factors

Head injury


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Stroke

Drug overdose

Alcoholic intoxication

Diabetic ketoacidosis

Hepatic failure


ASSESSMENT

Behavioral changes initially

Pupils are slowly reactive

Then , patient becomes unresponsive and pupils become fixed dilated

Glasgow Coma Scale is utilized


Nursing Intervention

1. Maintain patent airway

Elevate the head of the bed to 30 degrees

Suctioning

2. Protect the patient

Pad side rails

Prevent injury from equipments, restraints and etc.



3. Maintain fluid and nutritional balance

Input an output monitoring


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IVF therapy

Feeding through NGT

4. Provide mouth care

Cleansing and rinsing of mouth

Petrolatum on the lips



5. Maintain skin integrity

Regular turning every 2 hours

30 degrees bed elevation

Maintain correct body alignment by using trochanter rolls, foot board

6. Preserve corneal integrity

Use of artificial tears every 2 hours



7. Achieve thermoregulation

Minimum amount of beddings

Rectal or tympanic temperature

Administer acetaminophen as prescribed

8. Prevent urinary retention

Use of intermittent catheterization

Alteration In Metabolism

DKA

HHNK

TERMS


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Gluconeogenesis

is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon

substrates such as lactate, glycerol, and glucogenic amino acids.

Glycogenolysis

takes place in the muscle and liver tissues, where glycogen is stored, as a hormonal response to

epinephrine (e.g., adrenergic stimulation) and/or glucagon, a pancreatic peptide triggered by low blood

glucose concentrations, and produced in the alpha cells of the islets of Langerhans.

Lipolysis

is the breakdown of lipids and involves the hydrolysis of triglycerides into free fatty acids followed by

further degradation into acetyl units by beta oxidation. The process produces Ketones, which are found

in large quantities in ketosis, a metabolic state that occurs when the liver converts fat into fatty acids

and ketone bodies, which can be used by the body for energy.

Lipolysis testing strips such as Ketostix are used to recognize ketosis.

Role of Insulin

Required for transport of glucose into

Muscle

Adipose

Liver

Inhibits lipolysis

Absence of insulin

Glucose accumulates in the blood

Liver

Uses amino acids for gluconeogenesis

Converts fatty acids into ketone bodies

Acetone, Acetoacetate, -hydroxybutyrate

Increased counterregulatory hormones


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Diabetes Mellitus

group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia)

resulting from defects in insulin secretion, insulin action, or both ((American Diabetes Association )

Classification of Diabetes

DM1- IDDM - formerly insulin dependent diabetes mellitus

- near absolute/ absolute deficiency of insulin

- juvenile onset

-if insulin is not given,fats are metabolized ,resulting into ketonemia(acidosis)

DM2- NIDDM formerly non-insulin dependent DM - relative lack of insulin or

resistance to action of insulin

-usually sufficient to stabilize fat and protein metabolism ,but not to deal with carbohydrate metabolism

- adult-onset

Risk Factors

Family History

Diet

Obesity

Sedentary lifestyle

Age

Stress

4 Cardinal Signs

Polyuria

Polydipsia

Polyphagia


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Weight Loss

Diabetic Ketoacidosis

acute, life-threatening hyperglycemic crisis

Develops when severe/ absolute insulin deficiency occurs

Complication of DM 1

main characteristics:

hyperglycemia over 300 mg/dL (300-800)

low bicarbonate level (


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Medical Stress

Counterregulatory hormones

Oppose insulin

Stimulate glucagon release

Hypovolmemia

Increases glucagon and catecholamines

Decreased renal blood flow

Decreases glucagon degradation by the kidney

Diabetic Ketoacidosis

Due to:

Severe insulin deficiency

Excess counterregulatory hormones

Glucagon

Epinephrine

Cortisol

Growth hormone

3 Lines of defense against Acidosis

1st Line: Immediate buffering (converts H ions-CO2& H2O)

Lungs: excrete CO2

Kidneys: excrete acetoacetate in urine

2nd Line: Resp.: acetone & CO2 exhaled

depth & rate Kussmauls

fruity/ acetone breath


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3rd Line: Renal System: excretes 30-100g ketones/day

ammonia mechanism is activated

-excretion of excess hydrogen

Inadequate insulin

Clinical manifestations

Management

Goals:

Correct fluid & electrolyte imbalances-

Restore normal circulating blood volume

Shift from a state of fat catabolism to a state of carbohydrate catabolism by providing insulin

Identify and correct those factors that precipitated ketoacidosis

Management

Correct Fluid and Electrolyte Imbalances:


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Intravenous infusion of Isotonic saline (0.9% or 0.45% NaCl) started immediately

usually 1000 ml/first hour- then 2000-8000ml over the next 24 hours

Dextrose is added (D5NSS or D5 0.45 saline) when blood glucose level reaches 250-300 mg/dl

Clients with compromised cardiac function may require slower intravenous fluid replacement

Potassium Administration

Hypokalemia occurs Once Intervention begins due to re-entering of potassium back to the cells along

with insulin


Monitor Vital signs, neurovital signs ( ICP)

2. Assess weight, skin turgor, and hematocrit

3.Administer Oxygen therapy


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Start Intravenous line; (0.9% PNSS/ 0.45% NSS)

Client Education

Take insulin or oral antidiabetic medications as prescribed

Monitor blood glucose frequently

Monitor urine ketones when blood glucose levels rise (above 250mg/dl)

Schedule regular appointments with the physician for regular review of blood glucose tests, weight gain

or losses, and general health and well-being.

Recognize signs/symptoms of infection ( a major cause of DKA)

Call the physician/ seek consultation if any of the following develops:

Anorexia

Nausea, vomiting or diarrhea

Ketonuria persisting for more than 8 hours

A febrile illness or infection

Any sign or symptom of acidosis


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Hyperosmolar Nonketotic Syndrome

Extreme hyperglycemia and dehydration

Unable to excrete glucose as quickly as it enters the extracellular space

Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl

When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular

space.

HHNK

Hyperglycemic, HyperOsmolar, NonKetotic Coma

Occurs in DM2 (NIDDM)

Extreme hyperglycemia 800-2000 mg/dl

No ketosis and no acidosis

Polyphagia, polydipsia, glycosuria,hypotension, shock

Major difference of DKA and HHNK is

LACK of KETONURIA in HHNK

Treatment is similar with DKA

Hyperosmolar Nonketotic Syndrome

Extreme hyperglycemia and hyperosmolarity

High mortality (12-46%)

At risk

Older patients with intercurrent illness

Impaired ability to ingest fluids

Urine volume falls

Decreased glucose excretion


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Elevated glucose causes CNS dysfunction and fluid intake impaired

No ketones

Some insulin may be present

Extreme hyperglycemia inhibits lipolysis

Hyperosmolar Nonketotic Syndrome Presentation

Extreme dehydration

Supine or orthostatic hypotension

Confusion coma

Neurological findings

Seizures

Transient hemiparesis

Hyperreflexia

Generalized areflexia

Hyperosmolar Nonketotic Syndrome Presentation

Glucose >600 -1200mg/dl

Sodium

Normal, elevated or low

Potassium

Normal or elevated

Bicarbonate >15 mEq/L

Mental status changes

Seizures neurological deficts

Treatment of HHS

Hydration!!!


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Even more important than in DKA

Find underlying cause and treat!

Insulin drip

Should be started only once aggressive hydration has taken place.

Switch to subcutaneous regimen once glucose < 200 and patient eating.

Serial Electrolytes

Potassium replacement.

Hyperosmolar Nonketotic Syndrome Treatment

Fluid repletion

NS 2-3 liters rapidly

Total deficit = 10 liters

Replete in first 6 hours

Insulin

Make sure perfusion is adequate

Insulin drip 0.1U/kg/hr

Treat underlying precipitating illness

Clinical Errors

Fluid shift and shock

Giving insulin without sufficient fluids

Using hypertonic glucose solutions

Hyperkalemia

Premature potassium administration before insulin has begun to act

Hypokalemia

Failure to administer potassium once levels falling


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Recurrent ketoacidosis

Premature discontinuation of insulin and fluids when ketones still present

Hypoglycemia

Insufficient glucose administration

cad outline notes with arf dka

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