Structural, Inflammatory, and Infectious Conditions

- Cardiomyopathy is disease of the heart muscle that is associated with cardiac dysfunction.
o Ischemic cardiomyopathy – enlarged heart caused by coronary artery disease
 primary cardiomyopathies (genetic, nongenetic, and acquired)
 secondary cardiomyopathies, which show myocardial involvement secondary
to the influence of a vast list of disease processes (amyloidosis, Fabry disease,
sarcoidosis, and scleroderma).

- Dilated Cardiomyopathy (DCM) – most common form of cardiomyopathy, significant dilation of

the ventricles without simultaneous hypertrophy and systolic dysfunction.
o Conditions and diseases may cause DCM
o including pregnancy, hypertension, heavy alcohol intake, viral infection,
chemotherapeutic medications, thyrotoxicosis, myxedema, persistent tachycardia, and
Chagas disease.
 Diminished contractile elements (actin and myosin filaments) of the muscle
fibers and diffuse necrosis of myocardial cells.
 The result is poor systolic function
 decrease the amount of blood ejected from the ventricle
 increasing 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
 increasing pulmonary and systemic venous pressures.
 Altered valve function, usually regurgitation, can result from an enlarged
stretched ventricle.
- Hypertrophic Cardiomyopathy (HCM) – autosomal dominant genetic disorder that leads to
increased heart muscle size and mass, especially along the septum
o 12-lead ECGs, physical examinations, and echocardiograms are used to screen for the
disease.
 Hypertrophied cardiac muscle cells are disorganized
 Decreasing the effectiveness of contractions
 Coronary arteriole walls are thickened
 Decrease the internal diameter of the arterioles
 Narrow arterioles restrict the blood supply to the myocardium
  Numerous small areas of ischemia and necrosis
 Myocardium ultimately fibrose and scar, further impeding ventricular
contraction
 Increased thickness of the heart muscle
 Reduction of ventricular cavities
 Ventricles to take a longer time to relax after systole
 More difficult for the ventricles to fill with blood
- Restrictive Cardiomyopathy (RCM) – the least common type of cardiomyopathy, diastolic
dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch
o An infiltrative disease that may cause RCM is amyloidosis, in which amyloid, a
misfolded protein, is deposited between cardiomyocytes.
o Signs and symptoms are similar to constrictive pericarditis and include dyspnea,
nonproductive cough, and chest pain.
- Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D) – uncommon form of
inherited heart muscle disease, occurs when the myocardium is progressively infiltrated and
replaced by fibrous scar and adipose tissue.
o Infiltration of fibrous and adipose tissue leads to ventricle dilatation, poor
contractility, and arrhythmias.
o Genetic disorder
- Unclassified cardiomyopathies – caused by fibroelastosis, noncompacted myocardium, systolic
dysfunction with minimal dilation, and mitochondrial diseases
o Clinical Manifestations – dilated or restrictive cardiomyopathy is first diagnosed when
the patient presents with signs and symptoms of heart failure
 orthopnea, peripheral edema, early satiety, nausea
- Medical Management – correcting the heart failure with medications, a low sodium diet, and
an exercise/rest regimen
o Controlling arrhythmias with antiarrhythmic medications
o HCM should avoid dehydration and may need beta-blockers to maintain cardiac
output and minimize the risk of LVOT (Left Ventricular Outflow Obstructions)
obstruction during systole.

INFECTIOUS DISEASES OF THE HEART

- Rheumatic Endocarditis – Acute rheumatic fever, caused by group A beta-hemolytic

streptococcal pharyngitis.
o Patients with rheumatic fever may develop rheumatic heart disease as evidenced by a
new heart murmur, cardiomegaly, pericarditis, and heart failure.
o Prompt and effective treatment of “strep” throat with antibiotics can prevent
development of rheumatic fever.
- Infective Endocarditis – microbial infection of the endothelial surface of the heart
o It usually develops in older adults, or in people with prosthetic heart valves or cardiac
devices.
o Pathophysiology
 A deformity or injury of the endocardium leads to accumulation of fibrin and
platelets (clot formation) on the endocardium.
  Staphylococci or streptococci, invade the clot and endocardial lesion.
 Infection most frequently results in platelets, fibrin, blood cells, and
microorganisms that cluster as vegetations on the endocardium.
 Vegetations may embolize to other vessels throughout the body.
 Infecting organism is covered by new clot and concealed from the body’s
normal defenses.
 Infection may erode through the endocardium into underlying structures
o Clinical Manifestations
 Primary presenting symptoms – fever and a heart murmur
 Clusters of petechiae
 Small, painful nodules (Osler nodes)
 Irregular, red or purple, painless flat macules (Janeway lesions), present on
palms, fingers, hands, soles, and toes.
 Hemorrhages with pale centers (Roth spots)
 Splinter hemorrhages (reddish-brown lines and streaks), under the proximal
half of fingernails and toenails
 Heart failure
o Medical Management
 Antibiotic therapy usually is given intravenously for 2 to 6 weeks.
 Parenteral therapy is given in doses that produce a high serum concentration
for a significant period to ensure eradication of the dormant bacteria within
dense vegetations.
 Serum levels of the antibiotic and blood cultures are monitored to gauge
effectiveness of therapy.
o Surgical Management
 Surgical interventions include:
 valve repair and replacement, débridement of vegetations,
débridement and closure of an abscess, and closure of a fistula.
o Nursing Management
 monitors the patient’s temperature at regular intervals, because the course of
fever is one indication of treatment effectiveness.
 administers antibiotic, antifungal, or antiviral medication as prescribed.
 Timing of antimicrobial medication administration is critical to maintain
therapeutic drug levels.
 NSAIDs may be prescribed
- Myocarditis – an inflammatory process involving the myocardium, can cause heart dilation,
thrombi on the heart wall (mural thrombi), infiltration of circulating blood cells around the
coronary vessels and between the muscle fibers, and degeneration of the muscle fibers
themselves
o Medical Management
 Bed rest also helps decrease myocardial damage and the complications of
myocarditis.
 NSAIDs should not be used for pain control.
o Nursing Management
  Patients with arrhythmias should have continuous cardiac monitoring with
personnel and equipment readily available to treat life-threatening
arrhythmias.
- Pericarditis – inflammation of the pericardium, which is the membranous sac enveloping the
heart
o Pathophysiology
 Frequent or prolonged episodes of pericarditis
 Thickening and decreased elasticity of the pericardium, or scarring may fuse
the visceral and parietal pericardium.
 Restrict the heart’s ability to fill with blood
o Causes of Pericarditis
 Idiopathic or nonspecific causes
 Infection
 Autoimmune disorders
o Medical Management
 Analgesic medications and NSAIDs (aspirin, indomethacin, or ibuprofen) may be
prescribed for pain relief during the acute phase.
 Corticosteroids (prednisone) can be used as an alternative when NSAIDs are
contraindicated (kidney disease).
 Colchicine may be prescribed if the pericarditis is severe as an additive therapy
to NSAIDs
o Nursing Management
 acute pericarditis requires pain management with antispasmodic agents,
assistance with positioning, and psychological support.
 Pain may be relieved with a forward-leaning or sitting position.
o Patients with pericarditis must be alert to signs and symptoms of cardiac tamponade