14658676 cardio nursing course audit 21

7/31/2019 14658676 Cardio Nursing Course Audit 21

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Cardiovascular

System

By:

Ms. Irene M. Magbanua


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FOUR STAGES OF LIFE


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CARDIOVASCULAR SYSTEM

IMPORTANT FUNCTION:

- provide oxygen in everytissue in the body which

is essential in performingits function

CONSISTS of:

HEART

BLOOD VESSEL

BLOOD


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HEART Hollow, muscular

4-chambered

Located in middle of thoracic cavitybetween lungs in space calledmediastinum(The space between the

lungs, which includes the heart,pericardium, aorta and vena cava)

Inverted cone


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The Cardiovascular System

HEART

Normal Anatomy: Microscopic

Consists of Three layers- epicardium,myocardium and endocardium


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The epicardiumcovers the outer surfaceof the heart

The myocardium is the middle muscularlayer of the heart

The endocardium lines the chambers andthe valves


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The layer that covers the heart is the

PERICARDIUM

There are two parts- parietal and visceralpericardium

The space between the two pericardial

layers is the pericardial space


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PERICARDIAL EFFUSION


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Normal Anatomy: Gross

The heart is located in the LEFT side of

the mediastinum


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The heart chambers are guarded byvalves

The Atrio-ventricular valves-

The Semilunar valves-


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BLOOD VESSELS

Great vessels:

large veins and

arteries leadingdirectly to and

away from heart SUPERIOR VENA CAVA

AND INFERIOR VENACAVA

PULMONARY ARTERY

PULMONARY VEIN

AORTA


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LAUGH BREAK

BOY: Isang babaeng siopao nga!

LEA: Babaeng siopao?

BOY: Oo, yung may saping papel, may

napkin!

LEA: Ah ganun ba? Mayrun kaming

siopao na bading

BOY: Bading na siopao?

LEA: May sapin din, pero may itlog sa

loob!


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LAUGH BREAK

AMO: Day, gamitin mo sa pader itongchalk pamatay ng ipis.MAID: Yis ati!

NEXT DAY... nagulat ang amo, nakasulat sa pader:EPES MAMATAY KAYUNG LAHAT!

SYET! PAKYO!


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LAUGH BREAK

PASYENTE: Dok bakit pag tuwingumiinm ako ng alak sumasakit ang tyanko? Pero pag libre, di naman?

DKTOR: Normal yan, manipis kasi ataymo. Tapos makapal mukha mo!


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LAUGH BREAK

BUS HINOLDAP!Holdaper: Re-reypin ko lahat ng babaedito!

Prosti: Ako na lang po, maawa kayo saiba..

Lola: Sinabi na ngang LAHAT eh!Sasagot pa!


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CORONARY ARTERIES

The Blood supply ofthe heart comesfrom the Coronary

arteries1. Right coronary

artery

2. Left coronaryartery


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Cardiophysiology

Conduction system

Cardiac (heart) sounds

Heart rate and Blood pressure Cardiac cycle


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CHARACTERISTICS OF THE

CARDIAC MUSCLE

Inherent abilities of cardiac muscle cells:

AutomaticityConductivity

Excitability

Refractoriness


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The CONDUCTING SYSTEM OF THEHEART

Consists of the

1. SA node- the pacemaker 2. AV node- slowest conduction

3. Bundle of Hisbranches into the

Right and the Left bundle branch 4. Purkinje fibers- fastest conduction


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LAUGH BREAK

HONEYMOON:

Wife: Hon wag mo ako bibiglain ha?I'm still a virginHusband: You mean ako ang una?Wife: Yes, do it na please!

Husband: I did it na, kanina pa!!Wife: Ah ganon ba? Aray pala, shit!!!


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Heart rate

Normal range is 60-100 beats per minute

Tachycardia is greater than 100 bpm Bradycardia is less than 60 bpm

Sympathetic system INCREASES HR

Parasympathetic system (Vagus)DECREASES HR


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The Heart: Physiology

The amount of blood the heart pumpsout in each beat is called the STROKEVOLUME

When this volume is multiplied by thenumber of heart beat in a minute (heartrate), it becomes the CARDIACOUTPUT

When the Cardiac Output is multipliedby the Total Peripheral Resistance, itbecomes the BLOOD PRESSURE


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Blood pressure is:Cardiac output X peripheral

resistance


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Cardiac Output Regulation

The heart pumps approximately 5 L of

blood every minute

The heart rate increases with exercise;

therefore cardiac output increases

The cardiac output will vary according to

the amount of venous return.


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Blood pressure

Control is neural (central and

peripheral) and hormonal Baroreceptors in the carotid and aorta

Hormones- ADH, Adrenergic hormones,

Aldosterone and ANF


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Blood pressure Hormones- ADH, Adrenergic hormones,

Aldosterone and ANF

ADH increases water retention

Aldosterone increases sodium retentionand water retention secondarily

Epinephrine and NE increase HR and BP ANF= causes sodium excretion


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LAUGH BREAK

Bakla at Macho nagkasabay sa CR...

Bakla: Ang laki naman nyan sayo...

Macho: Wala na tong silbi kasi iniwanna ako ng GF ko... puputulin ko nalang at ipapakain ko sa aso!

Bakla: aw! aw! aw!


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The Heart: Physiology

The PRELOAD is the degree ofstretching of the heart muscle

when it is filled-up with blood

The AFTERLOAD is the resistance

to which the heart must pump toeject the blood


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Anatomy & PhysiologyTerminologyChronotropic

effect

Dromotropiceffect

Inotropiceffect

Refers to a change in heart rate

A positive chronotropic effect refers to anincrease in heart rate A negative chronotropic effect refers to a

decrease in heart rate

Refers to a change in the speed of conduction

through the AV junction A positive dromotropic effect results in an

increase in AV conduction velocity A negative dromotropic effect results in a

decrease in AV conduction velocity

Refers to a change in myocardial contractility A postive inotropic effect results in an

increase in myocardial contractility A negative inotropic effect results in a

decrease in myocardial contractility


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LAUGH BREAK

PATIENT: Nurse bakit TAE ko may

kasamang plema?

NURSE: Ok lang yan! Mas delikado kung

pag singa mo may kasamang TAE!


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Factors regulating StrokeVolume

1. Degree of stretch of the cardiac musclebefore contraction (Starling s Law);determined by the volume of blood in theventricle at the end of diastole or diastolicfilling.

2. Contactility: ability of the myocardium

to contract; contractility is increased bycirculating catecholamines andmedications like digitalis


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3. Preload : the filling of the ventricles atthe end of diastole. The more the

ventricles fill, the more the cardiacmuscles are stretched, and the greater the

force of the contraction during systole

(Starlings Law). If there is a decrease in

contractility and in cardiac output.


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4. Afterload: the pressure in the aorta thatthe ventricles must overcome to pump

blood into the systemic circulation.

A decrease in the afterload causes a

decrease in the workload of the ventricles;

this in turn will assist to increase the stroke

volume and the cardiac output


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Factors that increasemyocardial oxygen demands

Increased heart rate

Increased force of contractions

Increased afterload


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Cardiac compensatory

mechanisms When the normal compensatory

mechanisms cannot maintain cardiac

output to meet body needs, the client isin a state ofcardiacdecompensation.


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SUKO SA MISTER:

Misis 1: Suko na ako sa mister ko, lagina lang ako binubugbog bagoniroromansa. ..

Misis 2: Mas grabe yung mister ko.

Binubugbog ako tapos si Inday angniroromansa.


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The vascular system consists of thearteries, veins and capillaries

The arteries are vessels that carry blood

away from the heart to the periphery The veins are the vessels that carry blood

to the heart

The capillaries are lined with squamouscells, they connect the veins and arteries


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The lymphatic system also is part of the

vascular system and the function of this

system is to collect the extravasated fluid

from the tissues and returns it to the blood


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Differences Between Blood VesselTypes

Slide 11.26

Walls of arteries are the thickest

Lumens of veins are larger

Skeletal muscle milks blood in veinstoward the heart

Walls of capillaries are only one celllayer thick to allow for exchangesbetween blood and tissue


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Movement of Blood ThroughVessels

Slide 11.27

Most arterial blood is

pumped by the heart Veins use the milking

action of muscles to

help move blood

Figure 11.9


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Tutpik!

Kustomer: Ano ba naman itongtutpik nyo, iisa na nga lang, angdali pang mabali!

Waiter (inis): Alam nyo, sir, ang

dami nang gumamit nyan, perokayo lang nakabali!


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Major Arteries of Systemic Circulation

Slide 11.30

Figure 11.11


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Blood Supply to:

Bone Haversian canal and Volkmann s canal Blood Vessel vasa vasorum Heart coronary arteries Brain common carotid artery external and

internal carotid artery,anterior, middle and posterior cerebral artery(Circle of Willis)

Upper Extremities basillic cephalic brachial radial and ulnar

Lower Extremitiesiliac femoral poplitealsaphenous tibial


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Blood Supply to:

Eyes choroids (between sclera and retina)cornea gets 02 from the atmosphere

Kidneys renal artery interlobar arteryarcuate artery interlobular artery afferentarteriole glomerulus efferent arteriole - vasarecta back to the heart

Liver celiac artery hepatic artery and hepaticportal vein (food laden) - liver sinusoids (mixedblood) hepatic cells extract 02, nutrients anddetoxify toxic substances.

Organs of the GIT celiac trunk Lungs bronchial arteries


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Major Veins of Systemic Circulation

Slide 11.31

Figure 11.12


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Arterial Supply of the Brain

Slide 11.32

Figure 11.13


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Hepatic Portal Circulation

Slide 11.33

Figure 11.14

Circulation to the Fetus


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Circulation to the Fetus

Slide 11.34


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LAUGH BREAK

DALAWANG MADRE NIREREYP:

MADRE 1: Jusko! Patawarin nyo po

sya, di po nya alam ang ginagawanya!

MADRE 2: Sister yung akin

marunong!!!! Whooooo! Yeeaahhh!!!

Bl d P


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Blood Pressure

Measure of force exerted by blood against

the wall

Blood moves through vessels because of

blood pressure

Measured by listening for Korotkoff sounds

produced by turbulent flow in arteries as

pressure released from blood pressurecuff


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Blood Pressure: Effects of Factors

Slide 11.39b

Temperature

Heat has a vasodilation effect

Cold has a vasoconstricting effect

Chemicals

Various substances can cause increases ordecreases

Diet

F t D t i i Bl d P


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Factors Determining Blood Pressure

Slide 11.40

Figure 11.19

P l


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Pulse

Slide 11.35

Pulse pressure waveof blood

Monitored atpressurepoints wherepulse is easilypalpated

Figure 11.16

P l P


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Pulse Pressure

Difference betweensystolic and diastolicpressures

Increases whenstroke volumeincreases or vascularcompliancedecreases

Pulse pressure can

be used to take apulse to determineheart rate andrhythmicity

V i ti i Bl d P


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Variations in Blood Pressure

Slide 11.41

Human normal range is variable

Normal

140110 mm Hg systolic

8075 mm Hg diastolic

Hypotension

Low systolic (below 110 mm HG)

Often associated with illness

HypertensionHigh systolic (above 140 mm HG)

Can be dangerous if it is chronic

Effects of Aging on the


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Effects of Aging on theHeart

Gradual changes in heart function,minor under resting condition, more

significant during exercise

Hypertrophy of left ventricle Maximum heart rate decreases

Increased tendency for valves to

function abnormally and arrhythmias tooccur

Increased oxygen consumption required

to pump same amount of blood


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CardiacAssessment


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Cardiac History Interview

Focused assessment


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CARDIAC ASSESSMENT

Health HistoryObtain description of

present illness and the chiefcomplaintChest pain, DOB, Edema,

etc.Assess risk factors


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CARDIAC ASSESSMENT

Physical examinationVital signs- BP, PP,

Inspection of the skin Inspection of the thoraxPalpation of the PMI, pulsesAuscultation of the heart

sounds


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Fig. 13.23


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WHY NURSING?

Do you know why I took up nursing? Itwas in 4th year high school that I saw avision of a great woman bearing a light

in her right hand wearing a long gownand a headress calling me to serveher.

STATUE OF LIBERTY


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STATUE OF LIBERTY


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CARDIAC ASSESSMENT

Laboratory and diagnosticstudies CBC

Cardiac catheterization

Lipid profile

Arteriography

Cardiac enzymes and proteins

CXR

CVP

ECG

Holter monitoring

Exercise ECG


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Laboratory Test Rationale

1. To assist in diagnosing MI

2. To identify abnormalities

3. To assess inflammation


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Laboratory Test Rationale

4. To determine baseline value

5. To monitor serum level ofmedications

6. To assess the effects ofmedications


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LABORATORY PROCEDURES

CARDIAC Proteins and enzymes

CK- MB ( creatine kinase)

Elevates in MI within 4hours, peaks in 18 hoursand then declines till 3days


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CK- MB ( creatine kinase)

Normal value is 0-7 U/L



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Lactic Dehydrogenase (LDH)

Elevates in MI in 24 hours,peaks in 48-72 hours


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Lactic Dehydrogenase (LDH)

Normal value is 70-200 IU/L



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Myoglobin

Rises within 1-3 hoursPeaks in 4-12 hours

Returns to normal in a day



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Troponin I and TTroponin I is usually utilized for

MI

Elevates within 3-4 hours, peaks

in 4-24 hours and persists for 7

days to 3 weeks!Normal value for Troponin I is

less than 0 6 ng/mL


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Troponin I and T

REMEMBER to AVOID IM

injections before obtainingblood sample!

Early and late diagnosis can bemade!


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Myoglobin

Not seen alone in cardiacproblems

Muscular and RENAL disease

can have elevated myoglobin


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SERUM LIPIDSLipid profile measures the

serum cholesterol,triglycerides and lipoproteinlevels

Cholesterol=


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SERUM LIPIDS

LDL- 130 mg/dL

HDL- 30-70- mg/dL

NPO post midnight(usually 12 hours)

AFTER THE WEDDING


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AFTER THE WEDDING:

Husband: Sinungaling ka, sabi movirgin ka! Bakit kagabi maluwag

na!

Wife: Ulol ka! Dahil lasing ka,katabi mo kagabi si mama!



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ELECTROCARDIOGRAM(ECG)

A non-invasive procedurethat evaluates the electricalactivity of the heart

Electrodes and wires areattached to the patient



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ELECTROCARDIOGRAM(ECG)

Tell the patient that there isno risk of electrocution

Avoid muscularcontraction/movement


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Holter MonitoringA non-invasive test in

which the client wears aHolter monitor and an

ECG tracing recordedcontinuously over aperiod of 24 hours


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Stress TestA non-invasive test that

studies the heart duringactivity and detects andevaluates CAD

Exercise test,pharmacologic test andemotional test



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yLABORATORY PROCEDURES

Stress TestTreadmill testing is the most

commonly used stress testUsed to determine CAD,

Chest pain causes, drugeffects and dysrhythmias inexercise



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Stress TestPre-test: consent may be

required, adequate rest, eata light meal or fast for 4hours and avoid smoking,alcohol and caffeine



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Post-test: instruct client tonotify the physician if any

chest pain, dizziness orshortness of breath

Instruct client to avoid takinga hot shower for 10-12 hoursafter the test



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Pharmacological stress test

Use of dipyridamole

Maximally dilates coronaryartery

Side-effect: flushing of face


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Pharmacological stresstest

Pre-test: 4 hours fasting,avoid alcohol, caffeine

Post test: report symptomsof chest pain


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CARDIAC catheterization Insertion of a catheter into

the heart and surroundingvessels

Determines the structure and

performance of the heartvalves and surroundingvessels



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CARDIAC catheterizationUsed to diagnose CAD,

assess coronary arterypatency and determine

extent of atherosclerosis


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Pretest: Ensure Consent,assess for allergy to

seafood and iodine, NPO,document weight andheight, baseline VS, bloodtests and document theperipheral pulses



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Pretest: Fast for 8-12hours, teachings,medications to allayanxiety


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Post-test: Monitor VS and cardiac rhythm

Monitor peripheral pulses, color andwarmth and sensation of theextremity distal to insertion site

Maintain sandbag to the insertionsite if required to maintain pressure

Monitor for bleeding and hematomaformation



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Maintain strict bed rest for 6-12 hours Client may turn from side to side but

bed should not be elevated more than

30 degrees and legs always straight Encourage fluid intake to flush out the

dye

Immobilize the arm if the antecubitalvein is used

Monitor for dye allergy


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CVPThe CVP is the pressure

within the SVCReflects the pressure

under which blood isreturned to the SVC andright atrium


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CVPNormal CVP is 0 to 8 mmHg/

4-10 cm H2O


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CVPElevated CVP indicates

increase in blood volume,excessive IVF or heart/renalfailure


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CVPLow CVP may indicate

hypovolemia, hemorrhageand severe vasodilatation



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Measuring CVP 1. Position the client supine with

bed elevated at 45 degrees (CBQ)

2. Position the zero point of theCVP line at the level of the rightatrium. Usually this is at the MAL,4th ICS

3. Instruct the client to be relaxedand avoid coughing and straining.


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CARDIAC IMPLEMENTATION


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1. Assess the cardio-pulmonarystatus

VS, BP, Cardiac assessment

2. Enhance cardiac output

Establish IV line to administerfluids



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3. Promote gas exchange

Administer O2

Position client in SEMI-Fowler sEncourage coughing and deep

breathing exercises



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4. Increase client activity tolerance

Balance rest and activity

periodsAssist in daily activities

Provide strict bed rest if

indicatedSoft foods

Assistance in self-care



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5. Promote client comfortAssess the client s description

of pain and chest discomfort

Administer medication asprescribed

Morphine for MINitroglycerine for Angina

Diuretics to relieve congestion

(CHF)



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6. Promote adequate sleep7. Prevent infection

Monitor skin integrity of lower

extremitiesAssess skin site for edema,

redness and warmth

Monitor for fever

Change position frequently



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8. Minimize patient anxiety

Encourage verbalization offeelings, fears and concerns

Answer client questions.

Provide information aboutprocedures and medications

ActivityIntolerance

Monitor TPR and BPSpace activities in the dayPermit rest periods before activityLimit activity 1 hour before meals


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Limit activity 1 hour before mealsTeach energy conservation measures like bed rest

Edema Instruct patient to avoid constricting garmentsInstruct to elevate edematous areasInstruct patient to avoid dependent positionsTeach patient to prepare low sodium meals

Apply anti-embolic stockings

Pain Instruct patient to stop activity when pain occursAdminister nitroglycerine for anginaPace activities within patient s limitsInstruct patient to avoid cold temperatures andsmokingInstruct to report unrelieved pain immediately

CARDIAC DISEASES


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CARDIAC DISEASES

Coronary Artery DiseaseMyocardial Infarction

Congestive Heart FailureInfective Endocarditis

Cardiac TamponadeCardiogenic Shock

VASCULAR DISEASES


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VASCULAR DISEASES

Hypertension

Buerger s disease

Aneurysm

Varicose veins

Deep vein thrombosis

CAD


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CORONARY ARTERY DSEresults from the focal

narrowing of the large andmedium-sized coronaryarteries due to deposition of

atheromatous plaque in thevessel wall


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CAD


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RISK FACTORS

Most important MODIFIABLEfactors:

SmokingHypertension

Diabetes

Cholesterol abnormalities


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CAD


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Pathophysiology

There is decreased perfusion ofmyocardial tissue and inadequatemyocardial oxygen supply

If 50% of the left coronary arteriallumen is reduced or 75% of theother coronary artery, this

becomes significant

CAD


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Pathophysiology Potential for Thrombosis and

embolism

Angina Pectoris


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Angina Pectoris

Chest pain resulting fromcoronary atherosclerosis

or myocardial ischemia

Angina Pectoris: Clinical Syndromes


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THREE COMMON TYPES OF ANGINA

1. STABLE ANGINAThe typical angina that

occurs during exertion,relieved by rest and drugsand the severity does not

change

Angina Pectoris: Clinical Syndromes


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Three Common Types of ANGINA

2. Unstable angina

Occurs unpredictably

during exertion andemotion, severity increases

with timeand pain may notbe relieved by rest and drug

Angina Pectoris: ClinicalSyndromes


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Syndromes

Three Common Types of ANGINA

3. Variant angina

Prinzmetal angina, resultsfrom coronary arteryVASOSPASMS, may occur

at rest

Angina Pectoris


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ASSESSMENT FINDINGS1. Chest pain- ANGINA

The most characteristic symptom

PAIN is described as mild tosevere retrosternal pain,

squeezing, tightness or burningsensation

Radiates to the jawand left arm


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Angina Pectoris


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ASSESSMENT FINDINGS2. Diaphoresis

3. Nausea and vomiting4. Cold clammy skin

5. Sense of apprehension and

doom6. Dizziness and syncope


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Angina Pectoris


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LABORATORY FINDINGS2. Cardiac catheterizationProvides the MOST DEFINITIVE

source of diagnosis by showing thepresence of the atheroscleroticlesions

Angina Pectoris


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NURSING DIAGNOSES:Decreased cardiac output

Impaired gas exchange

Activity intolerance

Anxiety


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Angina Pectoris


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2. Teach the patient management ofanginal attacks

Advise patient to stop all activities

Put one nitroglycerin tablet under the

tongue Wait for 5 minutes

If not relieved, take another tablet and wait

for 5 minutes Another tablet can be taken (third tablet)

If unrelieved after THREE tablets seekmedical attention

Angina Pectoris


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3. Obtain a 12-lead ECG

Angina Pectoris


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4. Promote myocardial perfusion Instruct patient to maintain bed rest

Administer O2 @ 3 lpm

Advise to avoid valsalva maneuvers

Provide laxatives or high fiber dietto lessen constipation

Encourage to avoid increasedphysical activities

Angina Pectoris


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5. Assist in possible treatmentmodalities

PTCA- percutaneous transluminalcoronary angioplasty

To compress the plaque against thevessel wall, increasing the arteriallumen

CABG- coronary artery bypass graftTo improve the blood flow to the

myocardial tissue


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Angina Pectoris


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6. Provide information to familymembers to minimize anxietyand promote family

cooperation7. Assist client to identify risk

factors that can be modified

8. Refer patient to properagencies

Myocardial infarction


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Death of myocardialtissue in regions of the

heart with abruptinterruptionof coronary

blood supply


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ETIOLOGY and Risk factors1. CAD

2. Coronary vasospasm3. Coronary artery occlusion by

embolus and thrombus

4. Conditions that decreaseperfusion- hemorrhage, shock



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Risk factors 1. Hypercholesterolemia

2. Smoking

3. Hypertension

4. Obesity

5. Stress 6. Sedentary lifestyle



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PATHOPHYSIOLOGY Interrupted coronary blood flow

myocardial ischemia anaerobic

myocardial metabolism for severalhours myocardial death depressed cardiac function

triggers autonomic nervoussystem response furtherimbalance of myocardial O2demand and supply



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ASSESSMENT findings1. CHEST PAIN

Chest pain is described assevere, persistent, crushingsubsternal discomfort

Radiates to the neck, arm, jawand back


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Laboratory findings1. ECG- the ST segment is

ELEVATED, T wave inversion,presence of Q wave

2. Myocardial enzymes-elevated CK-MB, LDH andTroponin levels


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Laboratory findings3. CBC- may show elevated

WBC count

4. Test after the acute stage-Exercise tolerance test,

thallium scans, cardiaccatheterization



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Pain

Decreased cardiac output

Impaired gas exchangeActivity intolerance

Altered tissue perfusion

Constipation


Nursing Interventions


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1. Provide Oxygen at 2 lpm, Semi-fowler s

2. Administer medications

Morphine to relieve pain

Nitrates, thrombolytics, aspirinand anticoagulants

Stool softener and hypolipidemics



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Nursing Interventions3. Minimize patient anxiety

Provide information as to

procedures and drug therapyAllow verbalization of feelings

Morphine can be administered



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4. Provide adequate rest periods

Bed rest during acute stage

5. Minimize metabolic demandsProvide soft diet

Provide a low-sodium, low

cholesterol and low fat diet



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6. Assist in treatment modalitiessuch as PTCA and CABG

7. Monitor for complications of MI-

especially dysrhythmias, sinceventricular tachycardia can happenin the first few hours after MI

8. Provide client teaching

MI


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Medical Management1. ANALGESIC

The choice is MORPHINE It reduces pain and anxiety

Relaxes bronchioles to enhance

oxygenation

MI


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Medical Management2. ACE inhibitors

Prevents formation ofangiotensin II

Limits the area of infarction


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NURSING INTERVENTIONS AFTER ACUTEEPISODE

1. Maintain bed rest for the first 3

days 2. Provide passive ROM exercises

3. Progress with dangling of the feetat side of bed



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NURSING INTERVENTIONS AFTERACUTE EPISODE

4. Proceed with sitting out of bed,

on the chair for 30 minutes TID5. Proceed with ambulation in the

room toilet hallway TID


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CARDIOMYOPATHIES


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Heart muscle diseaseassociated with cardiac

dysfunction

CARDIOMYOPATHIES


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1. Dilated Cardiomyopathy2. Hypertrophic

Cardiomyopathy3. Restrictive cardiomyopathy

DILATED CARDIOMYOPATHY


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ASSOCIATED FACTORS1. Heavy alcohol intake

2. Pregnancy3. Viral infection

4. Idiopathic

DILATED CARDIOMYOPATHY

PATHOPHYSIOLOGY


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PATHOPHYSIOLOGY

Diminished contractile proteinspoor contraction decreased

blood ejection

increased bloodremaining in the ventricleventricular stretching and

dilatation.SYSTOLIC DYSFUNCTION

HYPERTROPHICCARDIOMYOPATHY


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Associated factors:1. Genetic

2. Idiopathic


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RESTRICTIVECARDIOMYOPATHY


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PathophysiologyRigid ventricular wall

impaired stretch and diastolicfilling decreased output

Diastolic dysfunction

CARDIOMYOPATHIES


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Assessment findings 1. PND

2. Orthopnea

3. Edema

4. Chest pain

5. Palpitations 6. dizziness

7. Syncope with exertion


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CARDIOMYOPATHIES


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Nursing Management1. Improve cardiac output

Adequate restOxygen therapy

Low sodium diet

CARDIOMYOPATHIES


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Nursing Management2. Increase patient tolerance

Schedule activities with restperiods in between

CARDIOMYOPATHIES


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Nursing Management3. Reduce patient anxiety

Support patientOffer information about

transplantations

Support family in anticipatorygrieving


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Infective endocarditis


181/320

Can be acute, sub-acuteor chronic



182/320

Etiologic factors1. Bacteria- Organism

depends on several factors2. Fungi


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Infective endocarditisPathophysiology


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Pathophysiology

Direct invasion of microbes

microbes adhere to damaged valve surface

and proliferate

damage attracts platelets causing clot

formation

erosion of valvular leaflets and the clot and

ve etation can embolize



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Assessment findings1. Intermittent high grade fever

2. anorexia, weight loss3. cough, back pain and joint

pain

4. splinter hemorrhages undernails



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Assessment findings5. Osler s nodes- painful

nodules on fingerpads6. Roth s spots- pale

hemorrhages in the retina



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Assessment findings7. Heart murmurs

8. Heart failure= usuallyacute heart failure



188/320

PreventionAntibiotic prophylaxis if

patient is undergoingprocedures like dentalextractions, bronchoscopy,surgery, etc.



189/320

PreventionAny invasive procedure that is

associated with transientbacteremia may cause themicrorganism to lodge in thedamaged, irregular valves



190/320

LABORATORY EXAMBlood Cultures to determine

the exact organismUsually, 3 culture specimensare obtained and antibioticsensitivity done


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192/320



193/320

Medical management2. Surgery

Valvular replacement

CHF


194/320

A syndrome of congestionof both pulmonary andsystemic circulation caused

by inadequate cardiacfunction and inadequate

cardiac output to meet themetabolic demands oftissues

CHF


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Inability of the heart topump sufficiently

The heart is unable tomaintain adequatecirculation to meet the

metabolic needs of thebody

CHF


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This can happen acutely orchronically

Acute in Myocardial infarction

Chronic cardiomyopathies

CHF


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Classified according to themajor ventriculardysfunction:

1. Left Ventricular failure

2. Right ventricular failure


198/320


199/320

New York Heart Association


200/320

Class 1Ordinary physical activity does

NOT cause chest pain and

fatigueNo pulmonary congestion

AsymptomaticNO limitation of ADLs



201/320

Class 2SLIGHT limitation of ADLs

NO symptom at rest

Symptoms with INCREASEDactivity

Basilar crackles and S3



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Class 3Markedly limitation on ADLs

Comfortable at rest BUTsymptoms present in LESS

than ordinary activity



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Class 4SYMPTOMS are present at

rest


204/320

CHF


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PATHOPHYSIOLOGYLEFT ventricular failure

Decreased cardiac outputDecreased perfusion to the brain,

kidney and other tissues

Cerebral anoxia, fatigue, oliguria,dizziness

CHF


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PATHOPHYSIOLOGYRIGHT ventricular failure

blood pooling in the venouscirculation

increased hydrostatic pressure

peripheral edema

CHF


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PATHOPHYSIOLOGYRIGHT ventricular failure

Venous blood pooling

venous congestion in the kidney,liver and GIT


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RIGHT SIDED CHFASSESSMENT FINDINGS


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1. Peripheral dependent,pitting edema

2. Weight gain

3. Distended neck vein

4. hepatomegaly

5. Ascites

RIGHT SIDED CHFASSESSMENT FINDINGS


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6. Body weakness 7. Anorexia, nausea 8. Pulsus alternans

9. Nocturia= urination at night atfrequent intervals as the bloodmoves from interstitial space tothe intravascular space and isexcreted

CHF


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LABORATORY FINDINGS1. CXR may reveal

cardiomegaly2. ECG may identify Cardiac

hypertrophy

3. Echocardiogram may showhypokinetic heart


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CHF


214/320

NURSING INTERVENTIONS1. Assess patient's cardio-

pulmonary status2. Assess VS, CVP and

PCWP. Weigh patient daily tomonitor fluid retention

CHF

NURSING INTERVENTIONS


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3. Administer medications-usually cardiac glycosides aregiven- DIGOXIN or DIGITOXIN,Diuretics, vasodilators andhypolipidemics are prescribed

CHFCardiotonics

Positive inotropic

To increase cardiac

contractility


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Positive inotropic

agents

y

Diuretics To decrease the

intravascular volume in thecirculation

Low Sodium Diet To minimize water retention

Hypolipidemics To decrease the lipid levels

of high risk patients


217/320

CHF



218/320

Digoxin Health teaching

Withhold the drug if apical

pulse is less than 60Note for early signs of toxicity:

NAVDA

Provide potassiumsupplements

CHF


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NURSING INTERVENTIONS4. Provide a LOW sodium diet.

Limit fluid intake as necessary

5. Provide adequate restperiods to prevent fatigue

CHF


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NURSING INTERVENTIONS6. Position on semi-fowler s to

fowler s for adequate chest

expansion7. Prevent complications of

immobility

CHF


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NURSING INTERVENTION AFTER THEACUTE STAGE

1. Provide opportunities for

verbalization of feelings 2. Instruct the patient about the

medication regimen- digitalis,vasodilators and diuretics

3. Instruct to avoid OTC drugs,Stimulants, smoking and alcohol

CHF


222/320


4. Provide a LOW fat and LOW

sodium diet5. Provide potassium

supplements

6. Instruct about fluid restriction

CHF


223/320


7. Provide adequate rest periods

and schedule activities8. Monitor daily weight and report

signs of fluid retention

CARDIOGENIC SHOCK


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Heart fails to pumpadequately resulting to adecreased cardiac output

and decreased tissueperfusion

CARDIOGENIC SHOCK


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ETIOLOGY 1. Massive MI

2. Severe CHF

3. Cardiomyopathy 4. Cardiac trauma

5. Cardiac tamponade

CARDIOGENIC SHOCKASSESSMENT FINDINGS


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1. HYPOTENSION 2. Oliguria (less than 30 ml/hour)

3. Tachycardia

4. Narrow pulse pressure 5. weak peripheral pulses

6. cold clammy skin

7. changes in sensorium/LOC 8. pulmonary congestion


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CARDIOGENIC SHOCK


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NURSING INTERVENTIONS 1. Place patient in a modified

Trendelenburg (shock ) position

2. Administer IVF, vasopressors andinotropics such as DOPAMINE and

DOBUTAMINE

CARDIOGENIC SHOCK


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NURSING INTERVENTIONS 3. Administer O2

4. Morphine is administered todecreased pulmonary congestion

and to relieve pain, relieveanxiety

CARDIOGENIC SHOCK


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5. Assist in intubation,mechanical ventilation, PTCA,CABG, insertion of Swan-Ganz

cath and IABP 6. Monitor urinary output, BP and

pulses

7. cautiously administer diureticsand nitrates

CARDIAC TAMPONADE


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A condition where the heartis unable to pump blood

due to accumulation of fluidin the pericardial sac(pericardial effusion)


232/320

CARDIAC TAMPONADE


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This condition restrictsventricular filling resulting todecreased cardiac output

Acute tamponade may happenwhen there is a suddenaccumulation of more than 50

ml fluid in the pericardial sac

CARDIAC TAMPONADE


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ASSESSMENT FINDINGS 1. BECK s Triad- Jugular vein

distention, hypotension and

distant/muffled heart sound

2. Pulsus paradoxus

3. Increased CVP 4. Decreased cardiac output

CARDIAC TAMPONADE


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ASSESSMENT FINDINGS 5. Syncope

6. Anxiety

7. Dyspnea

8. Percussion- Flatness across

the anterior chest

CARDIAC TAMPONADE


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Laboratory FINDINGS1. Echocardiogram= shows

accumulated fluid in thepericardial sac

2. Chest X-ray

CARDIAC TAMPONADE


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NURSING INTERVENTIONS 1. Assist in

PERICARDIOCENTESIS

2. Administer IVF

3. Monitor ECG, urine output and

BP 4. Monitor for recurrence of

tamponade

Pericardiocentesis


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Patient is monitored by ECGMaintain emergency equipments

Elevate head of bed 45-60degrees

Monitor for complications-

coronary artery rupture,dysrhythmias, pleural lacerationand myocardial trauma

General Measures to ImprovePeripheral Circulation


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1. Implement Regular Physical Activity to facilitate movement of venous blood

2. Eliminate cigarette smoking- toprevent vasoconstriction

3. Control hyperlipidemia and cholesterollevels- to prevent the progression ofatherosclerosis

HYPERTENSION


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A systolic BP greater than140 mmHg and a diastolicpressure greater than 90mmHg over a sustainedperiod, based on two or more

BP measurements.


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HYPERTENSION


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PATHOPHYSIOLOGYMulti-factorial etiology

BP= CO (SV X HR) x TPR

Any increase in the aboveparameters will increase BP


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244/320


245/320

HYPERTENSION

PATHOPHYSIOLOGY

A i i h b


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Any increase in the above parameterswill increase BP

3. Increased activity of the RAAS 4. Increased vasoconstriction of the

peripheral vessels

5. Insulin resistance

HYPERTENSION

ASSESSMENT FINDINGS


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ASSESSMENT FINDINGS1. Headache

2. Visual changes3. chest pain

4. dizziness

5. N/V

HYPERTENSION

DIAGNOSTIC STUDIES


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DIAGNOSTIC STUDIES 1. Health history and PE

2. Routine laboratory- urinalysis,ECG, lipid profile, BUN, serumcreatinine , FBS

3. Other lab- CXR, creatinineclearance, 24-huour urine protein

HYPERTENSION

MEDICAL MANAGEMENT


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MEDICAL MANAGEMENT1. Lifestyle modification

2. Diet therapy3. Drug therapy

HYPERTENSION

MEDICAL MANAGEMENT


250/320

Drug therapy Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers

Vasodilators

HYPERTENSION



251/320

NURSING INTERVENTIONS1. Provide health teaching topatient

Teach about the diseaseprocess

Elaborate on lifestyle changes

Assist in meal planning to loseweight

HYPERTENSION



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1. Provide health teaching to thepatient

Provide list of LOW fat , LOWsodium diet of less than 2-3grams of Na/day

Limit alcohol intake to 30 ml/dayRegular aerobic exerciseAdvise to completely stop

smoking

HYPERTENSION



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2. Provide information about anti-hypertensive drugs

Instruct proper compliance and notabrupt cessation of drugs even if ptbecomes asymptomatic/ improvedcondition

Instruct to avoid over-the-counterdrugs that may interfere with thecurrent medication

HYPERTENSION

N i I t ti


254/320

Nursing Intervention3. Promote Home care management

Instruct regular monitoring of BP

Involve family members in care

Instruct regular follow-up

HYPERTENSION

N i I t ti


255/320

Nursing Intervention4. Manage hypertensive emergency

and urgency properly

ANEURYSM

Dil ti i l i t


256/320

Dilation involving an arteryformed at a weak point inthe vessel wall


257/320

ANEURYSM

RISK FACTORS


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RISK FACTORS1. Atherosclerosis

2. Infection= syphilis

3. Connective tissue disorder

4. Genetic disorder= Marfan s

Syndrome

ANEURYSM

PATHOPHYSIOLOGY


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PATHOPHYSIOLOGYDamage to the intima and media

weakness outpouching of vessel

wall

Dissecting aneurysm tear in the

intima and media with dissectionof blood through the layers


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ANEURYSM

LABORATORY:


261/320

LABORATORY: CT scan

Ultrasound

X-ray

Aortography

ANEURYSM

Medical Management


262/320

Medical Management: Anti-hypertensives

Synthetic graft

ANEURYSM

Nursing Management:


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Nursing Management: Administer medications

Emphasize the need to avoid

increased abdominal pressure No deep abdominal palpation

Remind patient the need for serialultrasound to detect diameterchanges

PERIPHERAL ARTERIALOCCLUSIVE DISEASE

Refers to arterial insufficiency of


264/320

Refers to arterial insufficiency ofthe extremities usuallysecondary to peripheral

atherosclerosis.Usually found in males age 50

and above

The legs are most often affected


265/320

ARTERIOSCLEROSIS

OF THE EXTREMITIES


266/320

OF THE EXTREMITIES

Arteriosclerosis of the extremities is a disease of the peripheral blood vesselsthat is characterized by narrowing and hardening of the arteries that supply the

legs and feet. The narrowing of the arteries causes a decrease in blood flow.

Symptoms include leg pain, numbness, cold legs or feet and muscle pain in the

thighs, calves or feet.


Risk factors for Peripheral Arterial


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Risk factors for Peripheral Arterialocclusive disease

Non-Modifiable

1. Age

2. gender

3. family predisposition


Risk factors for Peripheral Arterialocclusive disease


268/320

occlusive disease

Modifiable

1. Smoking

2. HPN

3. Obesity

4. Sedentary lifestyle 5. DM

6. Stress

WALANGORIGINA-LITY!HHMMPP!


269/320

HHMMPP!


ASSESSMENT FINDINGS


270/320

ASSESSMENT FINDINGS 1. INTERMITTENT

CLAUDICATION-the hallmark of

PAOD This is PAIN described as

aching, cramping or fatiguing

discomfort consistentlyreproduced with the same degreeof exercise or activity


ASSESSMENT FINDINGS

1 INTERMITTENT


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1. INTERMITTENTCLAUDICATION-the hallmark of

PAODThis pain is RELIEVED by REST

This commonly affects the

muscle group below the arterialocclusion


Assessment Findings


272/320

Assessment Findings2. Progressive pain on the

extremity as the disease

advances

3. Sensation of cold andnumbness of the extremities

ARTERIOSCLEROSIS OF THE EXTREMITIES


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Assessment FindingsS


274/320

Assessment Findings 4. Skin is pale when elevated

and cyanotic and ruddy when

placed on a dependent position

5. Muscle atrophy, leg ulceration

and gangrene


275/320


Diagnostic Findings


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Diagnostic Findings1. Unequal pulses between the

extremities

2. Duplex ultrasonography

3. Doppler flow studies

PAODMedical Management

1 Drug therapy


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1. Drug therapy Pentoxyfylline (Trental) reduces

blood viscosity and improves

supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet

aggregation and increases

vasodilatation2. Surgery- Bypass graft and

anastomoses



1 Maintain Circulation to the extremity


278/320

1. Maintain Circulation to the extremity

Evaluate regularly peripheral pulses,temperature, sensation, motor functionand capillary refill time

Administer post-operative care to patientwho underwent surgery

Administer heat modalities to the legcautiously to promote vasodilatation



2 M it d


279/320

2. Monitor and managecomplications

Note for bleeding, hematoma, anddecreased urine output

Elevate the legs to diminish edema

Encourage exercise of the extremitywhile on bed

Teach patient to avoid leg-crossing




280/320

Nursing Interventions3. Promote Home management

Encourage lifestyle changes Instruct to AVOID smoking

Instruct to avoid leg crossing

BUERGER S DISEASE

Thromboangiitis obliterans


281/320

Thromboangiitis obliteransA disease characterized by

recurring inflammation of the

medium and small arteries andveinsof the lower extremities

BUERGER S DISEASE

Thromboangiitis obliterans


282/320

Thromboangiitis obliteransOccurs in MEN ages 20-35

RISK FACTOR: SMOKING!


283/320

BUERGER S DISEASE

ASSESSMENT FINDINGS

1 Leg PAIN


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1. Leg PAIN

Foot cramps in the arch

(INSTEP CLAUDICATION) afterexercise

Relieved by rest

Aggravated by smoking, emotionaldisturbance and cold chilling

BUERGER S DISEASE

ASSESSMENT FINDINGS

2 Digit l t i t h g d b


285/320

2. Digital rest pain not changed byactivity or rest

BUERGER S DISEASE

ASSESSMENT FINDINGS3 I RUBOR ( ddi h bl


286/320

ASSESSMENT FINDINGS 3. Intense RUBOR(reddish-blue

discoloration), progresses to

CYANOSIS as disease advances

4. Paresthesias

BUERGER S DISEASE

Diagnostic Studies


287/320

Diagnostic Studies1. Duplex ultrasonography

2. Contrast angiography

BUERGER S DISEASE


1 Assist in the medical and s rgical


288/320

1. Assist in the medical and surgicalmanagement

Bypass graft amputation

2. Strongly advise to AVOID smoking

3. Manage complicationsappropriately

BUERGER S DISEASE


Post-operative care: after amputation


289/320

Post-operative care: after amputation

Elevate stump for the FIRST 24 HOURSto minimize edema and promote venous

return Place patient on PRONE position after 24

hours several times a day

Assess skin for bleeding and hematoma Wrap the extremity with elastic bandage

RAYNAUD S DISEASE

A form of intermittent arteriolarVASOCONSTRICTION that results in


290/320

VASOCONSTRICTION that results incoldness, pain and pallor of thefingertips or toes

RAYNAUD S DISEASE

Cause : UNKNOWN


291/320

Cause : UNKNOWN

Most commonly affects WOMEN,

16- 40 years old

RAYNAUD S DISEASE

ASSESSMENT FINDINGS1 R d h


292/320

ASSESSMENT FINDINGS1. Raynaud s phenomenon

A localized episode of

vasoconstriction of the smallarteries of the hands and feetthat causes color andtemperature changes

RAYNAUD S DISEASE

W-B-R is the acronym for the colorchange


293/320

W B R is the acronym for the colorchange

Pallor- due to vasoconstriction,

then Blue- due to pooling of

Deoxygenated blood

Red- due to exaggerated reflow orhyperemia

RAYNAUD S DISEASE

ASSESSMENT FINDINGS2 Tingling sensation


294/320

ASSESSMENT FINDINGS2. Tingling sensation

3. Burning pain on the hands and

feet

RAYNAUD S DISEASE

Medical management


295/320

Medical managementDrug therapy with the use of

CALCIUM channel blockers

To prevent vasospasms

RAYNAUD S DISEASE


1. instruct patient to avoid situations thatb f l


296/320

pmay be stressful

2. instruct to avoid exposure to cold and

remain indoors when the climate is cold 3. instruct to avoid all kinds of nicotine

4. instruct about safety. Careful handling

of sharp objects

LAUGH BREAK

Bisaya 1: " Gara ng kutsi, siguro kay Miyur


297/320

y g , g y y

iyan."!

Bisaya 2: " Dili bay!"

Bisaya 1: " Kay Hipi?"Bisaya 2: " Tuntu ka man. Kay

FATHER iyan. Gisulat niya sa

likud o,"'SAFARI'."

VARICOSE VEINS

THESE are dilated veinsll i h l


298/320

THESE are dilated veinsusually in the lower

extremities


299/320

VARICOSE VEINS

Predisposing FactorsPregnancy


300/320

PregnancyProlonged standing or

sittingIncompetent venous valves

VARICOSE VEINS

Pathophysiology


301/320

PathophysiologyFactors venous

stasis increasedhydrostatic pressure edema

VARICOSE VEINS

Assessment findings


302/320

Assessment findingsTortuous superficial veins

on the legsLeg pain and Heaviness

Dependent edema

VARICOSE VEINS

Laboratory findings


303/320

Laboratory findingsVenography

Duplex scanpletysmography

VARICOSE VEINS

Medical management


304/320

Medical managementPharmacological therapy

Leg vein stripping andligation

Anti-embolic stockings


305/320

VARICOSE VEINS

Nursing management1 Advise patient to elevate


306/320

Nursing management1. Advise patient to elevate

the legs with pillow to

increase venous return2. Caution patient to avoid

prolonged standing orsitting

VARICOSE VEINS

Nursing management3 P id hi h fib f d


307/320

Nursing management3. Provide high-fiber foods

to prevent constipation4. Teach simple exercise to

promote venous return

VARICOSE VEINS

Nursing management


308/320

Nursing management5. Caution patient to

avoid constrictiveclothing

VARICOSE VEINS

Nursing management6 A l ti b li


309/320

Nursing management6. Apply anti-embolic

stockings as directed7. Avoid massage on theaffected area

DVT- Deep Vein Thrombosis

Inflammation of the deepveins of the lower


310/320

a at o o t e deepveins of the lowerextremities and the pelvicveins

The inflammation results to

formation of blood clots inthe area


Predisposing factorsProlonged immobility


311/320

g y

Varicosities

Traumatic procedures

Increased age

Malignancy

Estrogen therapySmoking


Complication


312/320

ComplicationPULMONARY

thromboembolism


Assessment findings


313/320

Assessment findingsLeg tenderness

Leg pain and edemaPositive HOMAN s SIGN


HOMAN s SIGNTh f t i FLEXED d


314/320

HOMAN s SIGN The foot is FLEXED upward

(dorsiflexed) , there is a sharp pain

felt in the calf of the leg indicative of venous inflammation


Laboratory findings


315/320

Laboratory findingsVenography

Duplex scan


Medical managementA i l l i i


316/320

ed ca a age e tAntiplatelets- aspirin

AnticoagulantsVein stripping and

graftingAnti-embolic stockings


Nursing management1 Provide measures to avoid


317/320

g g1. Provide measures to avoid

prolonged immobility

Repositioning Q2

Provide passive ROMEarly ambulation


Nursing management2 Provide skin care to


318/320

g g2. Provide skin care toprevent the complication of

leg ulcers

3. Provide anti-embolicstockings


Nursing management

4. Administer anticoagulants as


319/320

4. Administer anticoagulants asprescribed

5. Monitor for signs ofpulmonary embolism sudden respiratory distress

The End


320/320

The End

Thank You!

14658676 cardio nursing course audit 21

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