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CARDIOMYOPATHY

 subacute or chronic disorder of heart muscle


 common in excessive alcohol intake, pregnant women, clients with systemic hypertension
 treatment is only palliative

Types

1. Dilated cardiomyopathy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy

Dilated Cardiomyopathy

 most common
 Excessive ingestion of alcohol, pregnancy, HPN and infections
 Ventricular dilation, contractile dysfunction and heart failure
 Idiopathic, viral myocarditis, infections, toxins, pregnancy

PATHOPHYSIOLOGY:

 Left and right ventricles dilate


 Myocardial fibers degenerate
 Fibrotic tissue replaces viable tissue
 Reduced contractility decreased stroke volume low cardiac output
 Increase in HR
 Heart failure with ventricular dysrhythmias
 Risk of blood pooling within the heart
 Clot formation

assessment

 symptoms of Left ventricular failure


 weakness and fatigue
 activity intolerance
 chest pain
 dysrhythmias
 right sided heart failure

Implementation

 treatment for heart failure


 Diuretics (furosemide) , cardiac glycosides (digoxin) and vasodilator
 antidysrhythmics
 avoid alcohol
 heart transplant

Nsg interventions:

 Avoid poorly tolerated activities


 Emotional and physical stress will exacerbate disease
 + severe activity intolerance

Hypertrophic Cardiomyopathy
 Disproportionate thickening of the interventricular septum
 Wall rigidity
 Resistance to blood flow from the left atrium
 Obstruction of left ventricular outflow
 Encroaches on L ventricular chamber
 Small elongated L ventricle
Assessment
 exertional dyspnea
 syncope
 chest pain at rest but unrelated to exertion
 dysrhythmias

implementation

 symptomatic treatment
 conversion of atrial fibrillation
 Instruct to report dizziness or fainting
 instruct to avoid alcohol
 beta blockers and calcium antagonist:↓ outflow obstruction and heart rate
 vasodilator and cardiac glycosides are contraindicated (NTG, digoxin)
 ventriculomyotomy or muscle resection with mitral valve replacement/myotomy

Restrictive Cardiomyopathy

 Least common
 Diastolic dysfunction = main abnormality
 Any infiltrative process of the heart that results in fibrosis and thickening can cause
restrictive cardiomyopathy
 Fibrotic infiltration to the myocardium, endocardium and subendocardium
 Ventricles lose ability to stretch
 Rigid ventricular walls
 Impair filling during diastole (contraction during systole = normal)
 Increase Filling pressure
 Decrease cardiac output
 Cardiac failure and mild ventricular hypertrophy occur
 restriction of the filling of ventricles
 associated with amyloidosis: deposition of eosinophifibrous protein in the heart

Assessment

 exertional dyspnea
 weakness

implementation

 symptomatic treatment
 exercise restriction
 Give diuretics, cardiac glycosides and vasodilator as ordered
 Instruct to report dizziness or fainting
 avoid alcohol

HEART FAILURE

 inability of the heart to maintain adequate circulation


 diminished cardiac output and inadequate perfusion of peripheral tissue
 congestion of lungs may occur
 Physiologic state where heart cant pump enough blood to meet metabolic needs
 Not a disease in itself
 Manifestations: volume overload (leading to pulmonary and systemic venous
congestion), inadequate tissue perfusion, and poor exercise tolerance

ETIOLOGY AND RISK FACTORS:

Intrinsic Factors

 CAD (common cause)


 MI
 Valve disease
 Cardiomyopathy
 Dysrhythmias
 Cardiac Tamponade
 Constrictive Pericarditis

ETIOLOGY AND RISK FACTORS:

Extrinsic Factors:

 Abnormal loading (pressure or volume of blood increase in ventricles) can alter contractility
 Overload happens due to inability of blood to leave ventricles during contraction
 PRELOAD – length of cardiac muscle fiber before contraction cause by amounts of blood in
chamber
 Frank – Starling mechanism
 AFTERLOAD – amount of tension the heart must generate to overcome systemic pressure
 High peripheral vascular resistance and high blood pressure causes ventricle to work harder
to eject blood
 Ventricles will eventually fail

PATHOPHYSIOLOGY:

 Cardiac reserve allows heart to meet increase demands


 When CO is not enough = compensatory mechanisms

Compensatory mechanisms:

 Ventricular dilation
 Increased sympathetic stimulation
 Activation of renin-angiotensin system

Ventricular Dilation
 Lengthening of muscle fibers increasing the volume of heart chambers
 Increase in preload
 Increase in CO
 If stretched beyond will become ineffective
 Dilated heart needs more O2
 Normal coronary flow + inc O2 demands = hypoxia

Increased Sympathetic Stimulation

 Vasoconstriction, tachycardia, increased myocardial contractility = increase CO


 Increase in peripheral vascular resistance (afterload)
 Increase in myocardial workload
 Stimulates renin-angiotensin system

Renin-Angiotensin System

 Decreased renal perfusion


 Renin is released
 Renin interacts with angiotensin = angiotensin I
 Angiotensin I contacts ACE in lungs = Angiotensin II
 Angiotensin II = vasoconstriction, release of norepinephrine, release of aldosterone

 Plasma volume expand and increase in preload


 When compensatory mechanism is prolonged it leads to changes in myocardial cells
 Heart cannot maintain adequate circulation
 When compensatory mech. Fails = blood remaining in left ventricle after contraction
increases
 Decreases ability of L ventricle to receive blood from L atrium
 L atrium dilates and hypertrophies
 L atrium unable to receive full amt of incoming blood from pulmonary vein
 Pulmonary Edema
 LEFT SIDED FAILURE

 Right ventricle will dilate and hypertrophy due to increase pressure in the lung vessels
 Right ventricle fails
 Backflow of blood to venous systems
 Congestion in GI, liver, kidneys, legs
 Edema = main manifestation
 RIGHT VENTRICULAR FAILURE

Classification: acute or chronic

 Types

1. Right side heart failure/left sided heart failure

 represents 2 different pumping system


 heart failure begins with left ventricular failure then both
 acute pulmonary edema occurs: medical emergency
2. Forward failure/backward failure

 inadequate output in affected ventricles


 decrease perfusion of vital organs
 blood backs up behind the affected ventricle→ increase pressure in the atria

3. low output/ high output heart failure

 low output: low cardiac output


 high output: heart increase in activity to meet demands of the body

4. systolic failure/ diastolic failure

 diastolic failure: problem in relaxing and filling of blood


 systolic failure: problem of contraction and ejection of blood

Assessment

 right-sided heart failure

 signs in systemic circulation


 pitting , dependent edema
 ascitis due to portal hypertension
 tenderness of right upper quadrant
 distended neck veins
 pulsus alterans
 abdominal pain, bloating
 anorexia, nausea
 fatigue
 weight gain

 Left- sided heart failure

 signs of pulmonary system


 cough: can become frothy and productive
 dyspnea upon exertion
 orthopnea
 paroxysmal nocturnal dyspnea
 (+) rales and crackles
 tachycardia
 pulsus alterans
 fatigue
 pallor
 cyanosis
 confusion and disorientation
 signs of cerebral anoxia
 nocturnal diuresis

 Acute pulmonary edema

 severe dyspnea and orthopnea


 pallor
 tachycardia
 expectoration of blood tinged, frothy sputum
 wheezing and rales
 bubbling respiration
 profuse sweating and cold clammy perspiration
 cyanosis
 nasal flaring and use of accessory muscle of respiration
 tachypnea

Immediate management

 High fowlers position


 O2 administration: high concentration
 prepare for intubation and ventilator support
 suction as needed
 assess LOC
 monitor VS
 Monitor for hypotension
 Assess edema on dependent areas
 Insert Foley catheter after diuretic administration
 monitor I and O
 avoid unnecessary IV
 administer morphine sulfate
 Administer diuretics
 administer digitalis
 Administer bronchodilators for bronchospasm
 administer additional inotropic meds( dopamine or dobutamine)
 administer vasodilators
 monitor weight
 assess for hepatomegaly and ascitis
 analyze ABG result
 monitor potassium level

 Management after acute episode

 let patient verbalize regarding lifestyle changes


 instruct patient regarding medication and to report adverse effect of the drugs
 Instruct patient to avoid caffeine
 Diet: low sodium, low fat and low cholesterol diet
 increase intake of potassium
 instruct patient to report signs of fluid retention

CARDIAC TAMPONADE

 pericardial effusion: fluid filled space between visceral and parietal layer of
pericardium
 restrict ventricular filling and cardiac outputs drops
 Acute type: 20-50 ml of fluid accumulates
 assessment

 pulsus paradoxus
 increased CVP
 jugular vein distention
 distant heart sounds
 decreased cardiac output

 implementation

 administer IVF
 chest x ray or echocardiogram
 pericardiocentesis
 if recurrent tamponade: pericardial window or pericardiectomy
 Pericardiocentesis

CARDIOGENIC SHOCK

 failure of the heart to pump adequately causing decrease cardiac output


 necrosis of more than 40% of the left ventricle due to blood vessel occlusion
 goal of treatment: maintain tissue oxygenation and perfusion and improve pumping
ability of the heart

 Assessment

 hypotension
 urine output less than 30 ml
 cold clammy skin
 poor peripheral pulses
 tachycardia
 pulmonary congestion
 tachypnea
 disorientation, restlessness and confusion

Implementation

 administer IV morphine sulfate


 Administer O2
 administer diuretics and nitrates
 administer vasopressor and positive inotropics
 prepare for insertion of intraaortic balloon pump: facilitate draining of left ventricle
 monitor ABG
 monitor Urine output
 assist in insertion of Swan Ganz catheter
 Intra-Aortic Balloon Pump
 Swan Ganz Catheter
THE END