Вы находитесь на странице: 1из 2

CARDIOMYOPATHY

Heart muscle disease associated w/ cardiac dysfunction


Pathophysiology: series of events that culminate in impaired CO. Decreased
SV stimulates the sympathetic nervous system & the renin-angiotensingaldosterone response, resulting in increased systemic vascular resistance &
increased Na & fluid retention.
Classified according to the structural & functional abnormalities of the heart
muscle:
- Dilated Cardiomyopathy (DCM) most common. Significant dilation of
the ventricles without simultaneous hypertrophy & systolic dysfunction.
Causes may include: pregnancy, heavy alcohol intake, viral infection &
Chagas disease. Poor systolic function. Structural changes decrease the
amount of blood remaining in the ventricle after contraction. Less blood is
then able to enter the ventricle during diastole, increasing end-diastolic
pressure. Altered valve function, usually regusgitarion can result from an
enlarged stretched ventricle.
- Hypertrophic Cardiomyopathy (HCM) heart muscle asymmetrically
increases in size & mass, especially along the septum. The increased
thickness of the heart muscle reduces the size of the ventricular cavities &
causes the ventricles to take a longer time to relax after systole.
Structural changes that result in the smaller-than-normal ventricular
cavity also create a high-velocity flow of bloof out of the L ventricle into
the aorta. May cause significant diastolic dysfunction, but systolic function
is usually normal or high, resulting in a higher-than-normal ejection
fraction. Doppler echocardiography us used to detect the HCM & blood
flow alterations
- Restrictive Cardiomyopathy (RCM) characterized by diastolic
dysfunction caused by regid ventricular walls that impair diastolic filling &
ventricular stretch. Systolic function is usually normal. Signs & symptoms:
dyspnea, nonproductive cough, chest pain. CVPs, CT & MRI usually show
normal thickness of the pericardium.
Clinical Manifestations: Pt may remain stable and without symptoms for yrs.
1st symptoms may be those of HF(dyspnea on exertion, fatigue), PND
(paroxysmal nocturnal dyspnea), cough, orthopnea, fluid retention, peripheral
edema, nausea, chest pain, palpitations, dizziness, syncope with exertion. In
young people, cardiac arrest may be the initial manifestation.
Assessment & Diagnostic Findings: physical examination in the early stage
may reveal tachycardia & extra heart sounds. Pts with DCM may have
diastolic murmurs, & pts with DCM & HCM may have systolic murmurs. With
disease progression, examination also reveals s/s of HF (crackles, JVD, pitting
edema, enlarged liver).Echocardiogram, ECG (to observe dysrhythmias),
chest x-ray (reveals hearts enlargement). Cardiac catheterization is
sometimes used to rule out CAD. Endomyocardial biopsy may be performed.

Medical Management: directed toward determining & managing possible


underlying or precipitating causes; correcting the HF w/ medications, a lowsodium diet, & exercise/rest regimen; & controlling dysrhythmias w/
antiarrhythmic medications & possibly w/ an implanted electronic device,
such as an implantable cardiovertes defibrillator. Infective endocarditis
prophylaxis & systemic anticoagulation to prevent thromboembolic events
are usually recommended. If pt has s/s of congestion, fluid intake may be
limited to 2L each day. Pts with HCM may need beta blockers & avoid
dehydration.
Pts with HCM or RCM may need to limit physical activity to avoid lifethreatening dysrhythmia.
Pacemaker may be implanted to alter electrical stimulation of the muscle &
prevent forceful hyperdynamic contraction that occur w/ HCM.
Nonsurgical septal reduction therapy: percutaneous catheter positioned in 1
or more of the septal coronary arteries. Once position is verified, 2-5 mL of
ethanol (ethyl alcohol) is injected to kill myocardial cells.
Nursing Process P. 931