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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:
assessment
Implementation
Nsg interventions:
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
Intrinsic 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:
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
Renin-Angiotensin System
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
Types
Assessment
Immediate management
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
Assessment
hypotension
urine output less than 30 ml
cold clammy skin
poor peripheral pulses
tachycardia
pulmonary congestion
tachypnea
disorientation, restlessness and confusion
Implementation