RN Expert Guides: Cardiovascular Care, 1st Edition (2008)

Chapter 8. Degenerative Disorders

ACUTE CORONARY SYNDROMES

Acute myocardial infarction (MI), including ST-segment elevation MI (STEMI) and non-ST-segment elevation MI (NSTEMI), and unstable angina are now recognized as part of a group of clinical diseases called acute coronary syndromes (ACS).

Rupture or erosion of plaque—an unstable and lipid-rich substance—initiates all coronary syndromes. The rupture and erosion result in platelet adhesions, fibrin clot formation, and activation of thrombin.

In cardiovascular disease—the leading cause of death in the United States and Western Europe—death usually results from cardiac damage after an MI. Each year, about 1 million people in the United States experience an MI. The incidence is higher in men younger than age 70. (Women have the protective effects of estrogen until menopause.) Mortality is high when treatment is delayed, and almost one-half of sudden deaths caused by an MI occur before hospitalization or within 1 hour of the onset of symptoms. The prognosis improves if vigorous treatment begins immediately.

Pathophysiology

ACS most commonly results when a thrombus progresses and occludes blood flow. The degree of blockage and the time that the affected vessel remains occluded determine the type of infarct that occurs. The underlying effect is an imbalance in myocardial oxygen supply and demand. (See Stages of myocardial ischemia, injury, and infarct, pages 382 and 383.)

For the patient with unstable angina, a thrombus full of platelets partially occludes a coronary vessel. The partially occluded vessel may have distal microthrombi that cause necrosis in some myocytes. The smaller vessels infarct, thus placing the patient at higher risk for NSTEMI. If a thrombus fully occludes the vessel for a prolonged time, a STEMI usually develops. (See What happens during an MI, and 385.) This type of MI involves a greater concentration of thrombin and fibrin. (SeeHow ACS affects the body, pages 386 and 387.)

STAGES OF MYOCARDIAL ISCHEMIA, INJURY, AND INFARCT

Ischemia

Ischemia is the first stage and indicates that blood flow and oxygen demand are out of balance. It can be resolved by improving flow or reducing oxygen needs. Electrocardiogram (ECG) changes reveal ST-segment depression or T-wave changes.

Injury

The second stage, injury, occurs when ischemia is prolonged enough to damage the area of the heart. ECG changes usually reveal ST-segment elevation (usually in two or more leads).

Infarct

Infarct is the third stage and occurs with actual death of myocardial cells. Scar tissue eventually replaces the dead tissue, and the damage caused is irreversible.

In the earliest stage of a myocardial infarction (MI), hyperacute or very tall and narrow T waves may be seen on the ECG. Within hours, the T waves become inverted and ST-segment elevation occurs in the leads facing the area of damage. The last change to occur in the evolution of an MI is the development of the pathologic Q wave, which is the only permanent ECG evidence of myocardial necrosis. Q waves are considered pathologic when they appear greater than or equal to 0.04 second wide and their height is greater than 25% of the R-wave height in that lead. Pathologic Q waves develop in over 90% of patients with ST-segment elevation MI. About 25% of patients with a non-STsegment elevation MI develop pathologic Q waves, and the remaining patients have a non-Q-wave MI.

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The location of the area of damage depends on the blood vessels involved.

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Anterior-wall MI occurs when the left anterior descending artery becomes occluded.

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Septal-wall MI typically accompanies an anterior wall MI because the ventricular septum is supplied by the left anterior descending artery as well.

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Lateral-wall MI is caused by a blockage in the left circumflex artery, and usually accompanies an anterior- or inferior-wall MI.

 

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Inferior-wall MI is caused by occlusion of the right coronary artery; it usually occurs alone or with a lateral-wall or right-ventricular MI.

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Posterior-wall MI is caused by occlusion of the right coronary artery or the left circumflex arteries.

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Right-ventricular MI follows occlusion of the right coronary artery; this type of an MI rarely occurs alone. (In 40% of patients, a right-ventricular MI accompanies an inferior-wall MI.)

Predisposing factors for ACS include:

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aging

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diabetes mellitus

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elevated triglyceride, low-density lipoprotein, and cholesterol levels, and decreased high-density lipoprotein levels

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excessive intake of saturated fats, carbohydrates, or salt

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hypertension

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obesity

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positive family history of coronary artery disease (CAD)

Up close

ff4-b01382759What happens during an MI

When blood supply to the myocardium is interrupted, the following events occur:

1. Injury to the endothelial lining of the coronary arteries causes platelets, white blood cells, fibrin, and lipids to converge at the injured site. Foam cells, or resident macrophages, congregate under the damaged lining and absorb oxidized cholesterol, forming a fatty streak that narrows the arterial lumen.

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2. Because the arterial lumen narrows gradually, collateral circulation develops and helps maintain myocardial perfusion distal to the obstruction. During this stage, the patient may have chest pain when myocardial oxygen demand increases.

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3. When myocardial demand for oxygen is more than the collateral circulation can supply, myocardial metabolism shifts from aerobic to anaerobic, producing lactic acid (A), which stimulates pain nerve endings. The patient experiences worsening angina that requires rest and medication for relief.

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Lacking oxygen, the myocardial cells die. This decreases contractility, stroke volume, and blood pressure. The patient experiences tachycardia, hypotension, diminished heart sounds, cyanosis, tachypnea, and poor perfusion to vital organs.

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5. Hypoperfusion stimulates baroreceptors, which in turn stimulate the adrenal glands to release epinephrine and norepinephrine. These catecholamines (C) increase heart rate and cause peripheral vasoconstriction, further increasing myocardial oxygen demand. The patient may experience tachyarrhythmias, changes in pulses, decreased level of consciousness, and cold, clammy skin.

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6. Damaged cell membranes in the infarcted area allow intracellular contents into the vascular circulation. Ventricular arrhythmias then develop with elevated serum levels of potassium (▪), creatine kinase (CK) and CK-MB (▲), and troponin (•).

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7. All myocardial cells are capable of spontaneous depolarization and repolarization, so the electrical conduction system may be affected by infarct, injury, and ischemia. The patient may have a fever, leukocytosis, tachycardia, and electrocardiogram signs of tissue ischemia (altered T waves), injured tissue (altered ST segment), and infarcted tissue (deep Q waves).

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8. Extensive damage to the left ventricle may impair its ability to pump, allowing blood to back up into the left atrium and, eventually, into the pulmonary veins and capillaries. When this occurs, the patient may be dyspneic, orthopneic, tachypneic, and cyanotic. Crackles may be heard in the lungs on auscultation. Pulmonary artery pressure and pulmonary artery wedge pressure are increased.

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9.2) and carbon dioxide (CO2). The patient experiences increasing respiratory distress, and arterial blood gas results may show decreased partial pressure of oxygen and arterial pH and increased partial pressure of carbon dioxide.

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sedentary lifestyle

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smoking

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stress or a type A personality (aggressive, competitive attitude, addiction to work, chronic impatience).

In addition, use of such drugs as amphetamines or cocaine can cause an MI.

Men are more susceptible to MIs than premenopausal women, although incidence is rising among women who smoke and take a hormonal contraceptive. The incidence in postmenopausal women resembles that in men.

Complications

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Arrhythmias

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Heart failure causing pulmonary edema

HOW ACS AFFECTS THE BODY

Acute coronary syndromes (ACS) can have far-reaching effects and requires a multi-disciplinary approach to care. Here's what happens in ACS:

Cardiovascular system

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An area of viable ischemic tissue surrounds the zone of injury.

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When the heart muscle is damaged, the integrity of the cell membrane is impaired.

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Intracellular contents, including cardiac enzymes (such as creatine kinase and aspartate aminotransferase) and proteins (such as troponin T, troponin I, and myoglobin) are released.

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Within 24 hours, the infarcted area becomes edematous and cyanotic.

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During the next several days, leukocytes infiltrate the necrotic area and begin to remove necrotic cells, thinning the ventricular wall.

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The scar tissue that forms on the necrotic area inhibits contractility.

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Compensatory mechanisms (vascular constriction, increased heart rate, and renal retention of sodium and water) try to maintain cardiac output.

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Ventricular dilation may also occur in a process called remodeling.

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Functionally, an MI may cause reduced contractility with abnormal wall motion, altered left ventricular compliance, reduced stroke volume, reduced ejection fraction, and elevated left ventricular end-diastolic pressure.

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Cardiogenic shock is caused by failure of the heart to perform as an effective pump and can result in low cardiac output, diminished peripheral perfusion, pulmonary congestion, and elevated systemic vascular resistance and pulmonary vascular pressures.

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Ineffective contractility of the heart leads to accumulation of blood in the venous circulation distal to the failing ventricle.

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Arrhythmias can occur in the patient with an acute MI as a result of autonomic nervous system imbalance, electrolyte disturbances, ischemia, and slowed conduction in zones of ischemic myocardium.

Neurologic system

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Hypoperfusion of the brain results in altered mental status, involving changes in the level of consciousness, restlessness, irritability, confusion, or disorientation.

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Stupor or coma may result if the decrease in cerebral perfusion continues.

Renal system

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Shock and hypoperfusion from an MI cause the kidney to respond by conserving salt and water.

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Poor perfusion results in diminished renal blood flow, and increased afferent arteriolar resistance occurs, causing a decreased glomerular filtration rate.

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Increased amounts of antidiuretic hormone and aldosterone are released to help maintain perfusion. Urine formation, however, is reduced.

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Depletion of renal adenosine triphosphate stores results from prolonged renal hypoperfusion, causing impaired renal function.

Respiratory system

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Cardiogenic shock with left-sided heart failure results in increased fluid in the lungs. This process can overwhelm the capacity of the pulmonary lymphatics, resulting in interstitial and alveolar edema.

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Lung edema occurs when pulmonary capillary pressure exceeds 18 mm Hg.

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Pulmonary alveolar edema develops when pressures exceed 24 mm Hg, impairing oxygen diffusion.

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Collaborative management

A cardiologist is consulted for initial assessment and treatment. A cardiothoracic surgeon may also be consulted if the patient requires invasive therapy. Other specialists may be required after initial therapy and treatment, such as a physical therapist for cardiac rehabilitation and a nutritionist for dietary and lifestyle changes.

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Cardiogenic shock

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Rupture of the atrial or ventricular septum, ventricular wall, or valves

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Pericarditis

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Ventricular aneurysms

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Dressler's syndrome (post-MI pericarditis) occurring days to weeks after an MI and causing residual pain, malaise, and fever (see Complications of an MI, pages 388 to 390)

ff1-b01382759AGE AWARE

Assessment findings

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COMPLICATIONS OF AN MI

COMPLICATION

ASSESSMENT

TREATMENT

Arrhythmias

• Electrocardiogram (ECG) shows premature ventricular contractions, ventricular tachycardia, or ventricular fibrillation; in an inferior myocardial infarction (MI), bradycardia and junctional rhythms or atrioventricular (AV) block; in an anterior MI, tachycardia or heart block.

• Antiarrhythmic, atropine, cardioversion, defibrillation, and pacemaker

Heart failure

• In left-sided heart failure, chest X-rays show venous congestion and cardiomegaly.

• Catheterization shows increases in pulmonary artery systolic and diastolic pressures, pulmonary artery wedge pressure (PAWP), central venous pressure, and systemic vascular resistance (SVR).

• Diuretic, angiotensin-converting enzyme inhibitor, beta-adrenergic receptor blocker, vasodilator, inotropic, and cardiac glycoside

Cardiogenic shock

• Catheterization shows decreased cardiac output, increased pulmonary artery systolic and diastolic pressures, decreased cardiac index, increased SVR, and increased PAWP.

• Signs are hypotension, tachycardia, decreased level of consciousness, decreased urine output, jugular vein distention, S3 and S4, and cool, pale skin.

• I.V. fluids, vasodilator, diuretic, cardiac glycoside, intra-aortic balloon pump (IABP), vasopressor, and beta-adrenergic receptor stimulant

Mitral insufficiency

• Auscultation reveals apical holosystolic murmur.

• Dyspnea is prominent.

• Catheterization shows increased pulmonary artery pressure (PAP) and PAWP.

• Nitroglycerin (Nitrostat), nitroprusside (Nitropress), IABP, and surgical replacement of the mitral valve; possible myocardial revascularization with significant coronary artery disease

Ventricular septal rupture

• Echocardiogram shows valve dysfunction.

• In left-to-right shunt, auscultation reveals a harsh holosystolic murmur and thrill.

• Catheterization shows increased PAP and PAWP.

• Increased oxygen saturation of right ventricle and pulmonary artery confirms the diagnosis.

• Color-flow and Doppler echocardiography demonstrate left-to-right blood flow across the septum.

• Surgical correction (may be postponed, but more patients have surgery immediately or up to 7 days after septal rupture), IABP, nitroglycerin, nitroprusside, low-dose inotropic (dopamine [Inocor]), and cardiac pacing when high-grade AV blocks occur

Pericarditis or Dressler's syndrome

• Auscultation reveals a pericardial friction rub.

• Chest pain is relieved in sitting position.

• Sharp pain is unlike previously experienced angina.

• Anti-inflammatory agent, such as aspirin (Ecotrin) or other nonsteroidal anti-inflammatory drug or corticosteroid

Ventricular aneurysm

• Chest X-rays may show cardiomegaly.

• ECG may show arrhythmias and persistent ST-segment elevation.

• Left ventriculography shows altered or paradoxical left ventricular motion.

• Cardiopulmonary resuscitation (CPR), cardioversion, defibrillation (if ventricular tachycardia or fibrillation occurs), antiarrhythmic, vasodilator, anticoagulant, cardiac glycoside, diuretic and, possibly, surgery

Cerebral or pulmonary embolism

• Dyspnea and chest pain or neurologic changes occur.

• Nuclear scan shows ventilation-perfusion mismatch in pulmonary embolism.

• Angiography shows arterial blockage.

• Oxygen and heparin

• CPR, epinephrine, or cardiac pacing

Ventricular rupture

• Cardiac tamponade occurs.

• Resuscitation as per Advanced Cardiac Life Support protocol

• Possible emergency surgical repair if CPR successful

 

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In some patients—particularly elderly patients or those with diabetes—pain may not occur; in others, it may be mild and confused with indigestion.

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Patients with CAD may report increasing anginal frequency, severity, or duration (especially when not precipitated by exertion, a heavy meal, or cold and wind).

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The patient may also report a feeling of impending doom, fatigue, nausea, vomiting, and shortness of breath. Sudden death, however, may be the first and only indication of an MI.

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- burning sensation or discomfort in the upper abdomen

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- difficulty breathing

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- nausea and vomiting

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- weakness or fatigue

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- profuse sweating

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- light-headedness and fainting.

Practitioners may also not recognize these signs and symptoms as cardiac related and may delay prompt diagnosis and treatment.

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Inspection may reveal an extremely anxious and restless patient with dyspnea and diaphoresis.

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If right-sided heart failure is present, you may note jugular vein distention.

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Within the first hour after an anterior MI, about 25% of patients exhibit sympathetic nervous system hyperactivity, such as tachycardia and hypertension.

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Up to 50% of patients with an inferior MI exhibit parasympathetic nervous system hyperactivity, such as bradycardia and hypotension.

 

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In patients who develop ventricular dysfunction, auscultation may disclose an S3, paradoxical splitting of S2, and decreased heart sounds. A systolic murmur of mitral insufficiency may be heard with papillary muscle dysfunction secondary to infarction. A pericardial friction rub may also be heard, especially in patients who have a transmural MI or have developed pericarditis.

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Fever is unusual at the onset of an MI, but a low-grade fever may develop during the next few days.

Diagnostic test results

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Serial 12-lead electrocardiogram (ECG) readings may be normal or inconclusive during the first few hours after an MI. Characteristic abnormalities include serial ST-segment depression in patients with a subendocardial MI, and ST-segment elevation and Q waves, representing scarring and necrosis, in those with a transmural MI. (SeeECG characteristics in ACS, page 392.)

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The creatine kinase (CK) level is elevated, especially the CK-MB isoenzyme, the cardiac muscle fraction of CK.

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White blood cell count usually appears elevated on the 2nd day and lasts 1 week.

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Myoglobin (the hemoprotein found in cardiac and skeletal muscle) is released with muscle damage and may be detected as soon as 2 hours after an MI.

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Troponin I, a structural protein found in cardiac muscle, is elevated only in patients with cardiac muscle damage. It's more specific than the CK-MB level. Troponin levels increase within 4 to 6 hours of myocardial injury and may remain elevated for 5 to 11 days.

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Echocardiography shows ventricular-wall dyskinesia with a transmural MI and helps evaluate the ejection fraction.

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Nuclear ventriculography (multiple gated acquisition scanning or radionuclide ventriculography) can identify acutely damaged muscle by picking up accumulations of radioactive nucleotide, which appears as a hot spot on the film. Myocardial perfusion imaging with thallium-201 or Cardiolite reveals a “cold spot” in most patients during the first few hours after a transmural MI.

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Elevated homocysteine and C-reactive protein levels have been found incidentally in patients with an MI and may indicate a newer risk factor. Folic acid supplementation is used to treat elevated homocysteine levels.

Treatment

The goals of treatment for patients with ACS include reducing the amount of myocardial necrosis in those with ongoing infarction, decreasing cardiac workload and increasing oxygen supply to the myocardium, preventing major adverse cardiac events, and providing for cardiopulmonary resuscitation and defibrillation when ventricular fibrillation or pulseless ventricular tachycardia (VT) is present. (See Treating an MI, pages 394 and 395.)

ECG CHARACTERISTICS IN ACS

The first step in assessing a patient complaining of chest pain is to obtain an electrocardiogram (ECG). This should be done within 10 minutes of being seen by a practitioner. It's crucial in determining the presence of myocardial ischemia, and the findings will direct the treatment plan.

Angina

Most patients with angina show ischemic changes on an ECG only during the attack. Because these changes may be fleeting, always obtain an order for and perform a 12-lead ECG as soon as the patient reports chest pain.

Myocardial infarction (MI)

According to the American Heart Association, patients should be classified as having ST-segment elevation or new left bundle-branch block (LBBB), ST-segment depression or dynamic T-wave inversion, or nondiagnostic or normal ECG.

ST-segment elevation or new LBBB

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Patients with an ST-segment elevation greater than 1 mm in two or more contiguous leads or with new LBBB need to be treated for an acute MI.

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More than 90% of patients with this presentation will develop new Q waves and have positive serum cardiac markers.

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Repeating the ECG may be helpful for patients who present with hyperacute T waves.

ST-segment depression or dynamic T-wave inversion

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Patients with ST-segment depression indicating a posterior MI benefit most when an acute MI is diagnosed.

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Ischemia should be suspected with findings of ST-segment depression greater than or equal to 0.5 mm, marked symmetrical T-wave inversion in multiple precordial leads, and dynamic ST-T changes with pain.

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Patients who display persistent symptoms and recurrent ischemia, diffuse or widespread ECG abnormalities, heart failure, and positive serum markers are considered high risk.

Nondiagnostic or normal ECG

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A normal ECG won't show ST-segment changes or arrhythmias.

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If the ECG is nondiagnostic, it may show an ST-segment depression of less than 0.5 mm or a T-wave inversion or flattening in leads with dominant R waves.

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Continue assessment of myocardial changes through use of serial ECGs, ST-segment monitoring, and serum cardiac markers.

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If further assessment is warranted, perform perfusion radionuclide imaging and stress echocardiography.

Initial treatment for the patient with ACS includes the following:

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Obtain a 12-lead ECG and cardiac markers to help confirm the diagnosis of an acute MI. Cardiac markers (especially troponin I and CK-MB) are used to distinguish unstable angina and NSTEMI.

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Use the memory aid “MONA,” which stands for morphine, oxygen, nitroglycerin, and aspirin, to treat any patient experiencing ischemic chest pain or suspected ACS. Administer:

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- morphine to relieve pain

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- oxygen to increase oxygenation of the blood

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- nitroglycerin sublingually to relieve chest pain (unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 beats/minute or greater than 100 beats/minute)

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- aspirin to inhibit platelet aggregation.

For the patient with unstable angina and NSTEMI, treatment includes the above initial measures, and:

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a beta-adrenergic receptor blocker to reduce the heart's workload and oxygen demands

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heparin and a glycoprotein IIb/IIIa inhibitor to minimize platelet aggregation and the danger of coronary occlusion with high-risk patients (patients with planned cardiac catheterization and positive troponin)

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nitroglycerin I.V. to dilate coronary arteries and relieve chest pain (unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 beats/minute or greater than 100 beats/minute)

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an antiarrhythmic, transcutaneous pacing (or transvenous pacemaker), or defibrillation if the patient has ventricular fibrillation or pulseless VT

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percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) surgery for obstructive lesions

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an antilipemic to reduce elevated cholesterol or triglyceride levels.

For the patient with STEMI, treatment includes the above initial measures and these additional measures:

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thrombolytic therapy (unless contraindicated) within 12 hours of onset of symptoms to restore vessel patency and minimize necrosis in STEMI

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I.V. heparin to promote patency in the affected coronary artery

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a beta-adrenergic receptor blocker to reduce myocardial workload

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an antiarrhythmic, transcutaneous pacing (or transvenous pacemaker), or defibrillation if the patient has ventricular fibrillation or pulseless VT

TREATING AN MI

This flowchart shows how treatments can be applied to a myocardial infarction (MI) at various stages of its development.

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an angiotensin-converting enzyme inhibitor to reduce afterload and preload and prevent remodeling (begin in STEMI 6 hours after admission or when the patient's condition is stable)

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interventional procedures (such as PTCA, stent placement, or surgical procedures such as CABG) may open blocked or narrowed arteries.

Nursing interventions

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Care for patients who have suffered an MI is directed toward detecting complications, preventing further myocardial damage, and promoting comfort, rest, and emotional well-being. Most patients receive treatment in the coronary care unit (CCU), where they're under constant observation for complications.

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Check the patient's blood pressure after giving nitroglycerin, especially the first dose.

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Frequently monitor the ECG to detect rate changes and arrhythmias. Analyze rhythm strips. Place a representative strip in the patient's chart if any new arrhythmias are documented, if chest pain occurs, at every shift change, or according to facility protocol.

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During episodes of chest pain, obtain a 12-lead ECG (before and after nitroglycerin therapy as well). Also obtain blood pressure and pulmonary artery catheter measurements, if applicable, to determine changes.

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Watch for crackles, cough, tachypnea, and edema, which may indicate impending left-sided heart failure. Carefully monitor daily weight, intake and output, respiratory rate, enzyme levels, ECG readings, and blood pressure. Auscultate for adventitious breath sounds periodically (patients on bed rest frequently have atelectatic crackles, which may disappear after coughing) and for S3 or S4 gallops.

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Organize patient care and activities to maximize periods of uninterrupted rest.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH ACS

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To promote compliance with the prescribed medication regimen and other treatment measures, thoroughly explain dosages and therapy. Inform the patient of the drug's adverse reactions, and advise him to watch for and report signs and symptoms of toxicity (for example, anorexia, nausea, vomiting, mental depression, vertigo, blurred vision, and yellow vision, if the patient is receiving a cardiac glycoside).

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Review dietary restrictions with the patient. If he must follow a low-sodium, low-fat, or low-cholesterol diet, provide a list of foods to avoid. Ask the dietitian to speak to the patient and his family.

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Encourage the patient to participate in a cardiac rehabilitation exercise program. The practitioner and the exercise physiologist should determine the level of exercise and then discuss it with the patient and secure his agreement to a stepped-care program.

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Counsel the patient to resume sexual activity progressively. He may need to take nitroglycerin before sexual intercourse to prevent chest pain from the increased activity.

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Advise the patient about appropriate responses to new or recurrent symptoms.

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Advise the patient to report typical or atypical chest pain. Post-myocardial infarction (MI) syndrome may develop, producing chest pain that must be differentiated from a recurrent MI, pulmonary infarction, and heart failure.

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Stress the need to stop smoking. If necessary, refer the patient to a support group.

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If the patient has a Holter monitor in place, explain its purpose and use.

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Review follow-up procedures, such as office visits and treadmill testing, with the patient.

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Ask the dietary department to provide a clear liquid diet until nausea subsides. A low-cholesterol, low-sodium diet, without caffeine, may be ordered. (See Teaching the patient with ACS)

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Provide a stool softener to prevent straining during defecation, which causes vagal stimulation and may slow heart rate.

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Allow the patient to use a bedside commode, and provide as much privacy as possible.

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Assist with range-of-motion exercises. If the patient is immobilized by a severe MI, turn him often. Antiembolism stockings help prevent venostasis and thrombophlebitis.

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Initiate a cardiac rehabilitation program, which typically includes education regarding heart disease, exercise, and emotional support for the patient and his family.

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Provide emotional support, and help reduce stress and anxiety; administer a tranquilizer if needed.

 

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If the patient has undergone PTCA, sheath care is necessary. Keep the sheath line open with a heparin drip. Observe the patient for generalized and site bleeding. Keep the leg with the sheath insertion site immobile. Maintain strict bed rest. Check peripheral pulses in the affected leg frequently. Provide an analgesic for back pain, if needed.

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After thrombolytic therapy, administer continuous heparin. Monitor the partial thromboplastin time every 6 hours, and monitor the patient for evidence of bleeding.

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Monitor ECG rhythm strips for reperfusion arrhythmias, and treat them according to facility protocol. If the artery reoccludes, the patient experiences the same symptoms as before. If this occurs, prepare the patient for return to the cardiac catheterization laboratory.

CORONARY ARTERY DISEASE

Coronary artery disease (CAD) results from the narrowing of the coronary arteries over time resulting from atherosclerosis. The foremost effect of CAD is the loss of oxygen and nutrients to myocardial tissue because of diminished coronary blood flow. As the population ages, the prevalence of CAD is increasing. About 13 million Americans have CAD, and it's more common in men, whites, and middle-aged and elderly people. With proper care, the prognosis for CAD is favorable.

Pathophysiology

Fatty, fibrous plaque progressively narrow the coronary artery lumina, reducing the volume of blood that can flow through them and leading to myocardial ischemia.

As atherosclerosis progresses, luminal narrowing is accompanied by vascular changes that impair the ability of the diseased vessel to dilate. This causes a precarious balance between myocardial oxygen supply and demand, threatening the myocardium beyond the lesion. When oxygen demand exceeds what the diseased vessel can supply, localized myocardial ischemia results.

Myocardial cells become ischemic within 10 seconds of a coronary artery occlusion. Transient ischemia causes reversible changes at the cellular and tissue levels, depressing myocardial function. Untreated, this can lead to tissue injury or necrosis. Within several minutes, oxygen deprivation forces the myocardium to shift from aerobic to anaerobic metabolism, leading to accumulation of lactic acid and reduction of cellular pH.

EXPLORING THE GENETIC LINK TO CAD

Researchers have identified more than 250 genes that may play a role in coronary artery disease (CAD). It commonly results from the combined effects of multiple genes, making it difficult to determine the impact of specific genes that can influence a person's risk of contracting the disease.

Some of the best understood genes linked to CAD include:

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low-density lipoprotein (LDL) receptor—a protein that removes LDL from the bloodstream; a mutation in this gene is responsible for familial hypercholesterolemia

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also affects blood levels of LDL

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apolipoprotein B-100—commonly called apo B-11, it's a component of LDL; mutations of the gene cause LDL to stay in the blood longer than normal, leading to high LDL levels

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apolipoprotein A—a glycoprotein that combines with LDL to form a particle called Lp(a); it appears as a part of plaque on blood vessels

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MTHFR—an enzyme that clears homocysteine from the blood; mutations in MTHFR genes may cause high homocysteine levels

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cystathionine B-synthase—also known as CBS, it's another enzyme involved in homocysteine metabolism; CBS mutations cause a condition known as homocystinuria (homocysteine levels are so high that homocysteine can be detected in urine).

The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular function. The strength of the contractions in the affected myocardial region is reduced as the fibers shorten inadequately, resulting in less force and velocity. Moreover, wall motion is abnormal in the ischemic area, resulting in less blood being ejected from the heart with each contraction. Restoring blood flow through the coronary arteries restores aerobic metabolism and contractility; however, if blood flow isn't restored, myocardial infarction (MI) results.

Atherosclerosis, the most common cause of CAD, has been linked to many risk factors. Some risk factors can't be controlled:

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age—Atherosclerosis usually occurs after age 40.

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sex—Men are eight times more susceptible than premenopausal women.

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heredity—A positive family history of CAD increases the risk. (See Exploring the genetic link to CAD.)

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race—White men are more susceptible than nonwhite men, and nonwhite women are more susceptible than white women.

The patient can modify the following risk factors with good medical care and appropriate lifestyle changes:

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high blood pressure—Systolic blood pressure that's higher than 160 mm Hg or diastolic blood pressure that's higher than 95 mm Hg increases the risk.

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high cholesterol levels—Increased low-density lipoprotein and decreased high-density lipoprotein levels substantially heighten the risk.

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smoking—Cigarette smokers are twice as likely to have an MI and four times as likely to experience sudden death. The risk dramatically drops within 1 year after smoking ceases.

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obesity—Added weight increases the risk of diabetes mellitus, hypertension, and elevated cholesterol levels.

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physical inactivity—Regular exercise reduces the risk.

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stress—Added stress or a type A personality increases the risk.

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diabetes mellitus—This disorder raises the risk, especially in women.

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other modifiable factors—Increased fibrinogen and uric acid levels, elevated hematocrit, reduced vital capacity; high resting heart rate, thyrotoxicosis, and use of a hormonal contraceptive heightens the risk.

Uncommon causes of reduced coronary artery blood flow include dissecting aneurysms, infectious vasculitis, syphilis, and congenital defects in the coronary vascular system. Coronary artery spasms may also impede blood flow. (See Understanding coronary artery spasm.)

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Arrhythmias

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Ischemic cardiomyopathy

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MI

Assessment findings

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The classic symptom of CAD is angina, the direct result of inadequate oxygen flow to the myocardium. The patient usually describes it as a burning, squeezing, or crushing tightness in the substernal or precordial chest that may radiate to the left arm, neck, jaw, or shoulder blade. Typically, the patient clenches his fist over his chest or rubs his left arm when describing the pain. Nausea, vomiting, fainting, sweating, and cool extremities may accompany the tightness.

Angina commonly occurs after physical exertion but may also follow emotional excitement, exposure to cold, or a large meal. Angina may also develop during sleep from which symptoms awaken the patient. (See Types of angina.)

UNDERSTANDING CORONARY ARTERY SPASM

In patients with coronary artery spasm, a spontaneous, sustained contraction of one or more coronary arteries causes ischemia and dysfunction of the heart muscle. This disorder may also cause Prinzmetal's angina and even a myocardial infarction (MI) in patients with nonoccluded coronary arteries.

Causes

The direct cause of coronary artery spasm is unknown, but possible contributing factors include:

·

altered influx of calcium across the cell membrane

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intimal hemorrhage into the medial layer of the blood vessel

·

 

·

an elevated catecholamine level

·

fatty buildup in the lumen.

Signs and symptoms

The major symptom of coronary artery spasm is angina. Unlike classic angina, this pain commonly occurs spontaneously and may be unrelated to physical exertion or emotional stress; it may, however, follow cocaine use. It's usually more severe than classic angina, lasts longer, and may be cyclic—recurring every day at the same time. Ischemic episodes may cause arrhythmias, altered heart rate, lower blood pressure and, occasionally, fainting caused by decreased cardiac output. Spasm in the left coronary artery may result in mitral valve prolapse, producing a loud systolic murmur and, possibly, pulmonary edema, with dyspnea, crackles, and hemoptysis. An MI and sudden death may occur.

Treatment

After diagnosis by coronary angiography and 12-lead electrocardiography, the patient may receive a calcium channel blocker (such as verapamil [Calan], nifedipine [Procardia], or diltiazem [Cardizem]) to reduce coronary artery spasm and to decrease vascular resistance, and a nitrate (such as nitroglycerin [Nitro-Bid] or isosorbide dinitrate [Isordil]) to relieve chest pain. During cardiac catheterization, the patient with clean arteries may receive ergotamine to induce the spasm and aid in the diagnosis.

Nursing interventions

When caring for a patient with coronary artery spasm, explain all necessary procedures and teach him how to take his drugs safely. For calcium antagonist therapy, monitor the patient's blood pressure, pulse rate, and cardiac rhythm strips to detect arrhythmias.

For nifedipine and verapamil therapy, monitor the digoxin (Lanoxin) level, and check for signs of digoxin toxicity. Because nifedipine may cause peripheral and periorbital edema, watch for fluid retention.

Because coronary artery spasm is sometimes associated with atherosclerotic disease, advise the patient to stop smoking, avoid overeating, minimize alcohol intake, and maintain a balance between exercise and rest.

TYPES OF ANGINA

There are four types of angina:

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Stable angina—pain is predictable in frequency and duration and is relieved by rest and nitroglycerin.

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Unstable angina—pain increases in frequency and duration and is more easily induced; it indicates a worsening of coronary artery disease that may progress to a myocardial infarction.

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Prinzmetal's, or variant, angina—pain is caused by spasm of the coronary arteries; it may occur spontaneously and may be unrelated to physical exercise or emotional stress.

·

Microvascular angina—impairment of vasodilator reserve causes angina-like chest pain in a person with normal coronary arteries.

 

·

Inspection may reveal evidence of atherosclerotic disease, such as xanthelasma and xanthoma.

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Ophthalmoscopic inspection may show increased light reflexes and arteriovenous nicking, suggesting hypertension, an important risk factor of CAD.

·

Palpation can uncover thickened or absent peripheral arteries, signs of cardiac enlargement, and abnormal contraction of the cardiac impulse, such as left ventricular akinesia or dyskinesia.

·

Auscultation may detect bruits, an S3, an S4, or a late systolic murmur (if mitral insufficiency is present).

ff1-b01382759AGE AWARE

In the older adult, CAD may be asymptomatic because of a decrease in sympathetic response. Dyspnea and fatigue are two key signals of ischemia in an active, older adult.

Diagnostic test results

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An electrocardiogram (ECG) during angina shows ischemia as demonstrated by T-wave inversion or ST-segment depression and possibly arrhythmias, such as premature ventricular contractions. ECG results may be normal during pain-free periods. Arrhythmias may occur without infarction, secondary to ischemia. A Holter monitor may be used to obtain continuous graphic tracing of the ECG as the patient performs daily activities.

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Treadmill or bicycle exercise testing may provoke chest pain and ECG signs of myocardial ischemia in response to physical exertion.

Monitoring electrical rhythm may demonstrate T-wave inversion or ST-segment depression in the ischemic areas.

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Coronary angiography reveals coronary artery stenosis or obstruction, collateral circulation, and the arteries' condition beyond the narrowing.

·

Myocardial perfusion imaging with thallium-201, Cardiolite, or Myoview during treadmill exercise helps detect ischemic areas of the myocardium, visualized as “cold spots.”

·

In pharmacologic myocardial perfusion imaging, a patent coronary artery vasodilator, such as adenosine (Adenocard) or dipyridamole (Persantine), is given and response is tested. This can be done along with stress testing. In normal arteries, coronary blood flow is increased to three to four times baseline. In arteries with stenosis, the decrease in blood flow is proportional to the percentage of occlusion.

·

 

·

Stress echocardiography may show wall motion abnormalities.

·

Electron-beam computed tomography identifies calcium within arterial plaque; the more calcium seen, the higher the likelihood of CAD.

Treatment

The goal of treatment in patients with angina is to reduce myocardial oxygen demand or increase the oxygen supply and reduce pain. Activity restrictions may be required to prevent onset of pain. Rather than eliminating activities, performing them more slowly can help avert pain. Stress-reduction techniques are also essential, especially if known stressors precipitate pain.

Pharmacologic therapy consists primarily of a nitrate, such as nitroglycerin, isosorbide dinitrate, or a beta-adrenergic receptor blocker or calcium channel blocker. A nitrate, such as nitroglycerin (Nitrostat) may be given to help reduce myocardial oxygen consumption. A beta-adrenergic receptor blocker is given to reduce the heart's workload and oxygen demands by reducing heart rate and peripheral resistance to blood flow. A calcium channel blocker is used to prevent coronary artery spasm. An antiplatelet drug helps to minimize platelet aggregation and the risk of coronary occlusion. A glycoprotein IIb/IIIa inhibitor, such as abciximab (ReoPro), eptifibatide (Integrilin), or tirofiban (Aggrastat), helps reduce the risk of blood clots. An antilipemic is given to reduce serum cholesterol or triglyceride levels. An antihypertensive is used to help control hypertension.

Obstructive lesions may necessitate atherectomy or coronary artery bypass graft (CABG) surgery, using vein grafts. A surgical technique available as an alternative to traditional CABG surgery is minimally invasive coronary artery bypass surgery, also known as  This procedure requires a shorter recovery period and has fewer postoperative complications. Instead of sawing open the patient's sternum and spreading the ribs apart, several small incisions are made in the torso through which small surgical instruments and fiberoptic cameras are inserted. This procedure was initially designed to correct blockages in just one or two easily reached arteries; it may be unsuitable for more complicated cases.

Percutaneous transluminal coronary angioplasty (PTCA) may be performed during cardiac catheterization to compress fatty deposits and relieve occlusion. In patients with calcification, PTCA may reduce the obstruction by fracturing the plaque. (See Relieving occlusions with angioplasty.)

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PTCA carries certain risks but causes fewer complications than surgery. Complications after PTCA can include circulatory insufficiency, death (rarely), an MI, restenosis of the vessels, retroperitoneal bleeding, sudden coronary occlusions, or vasovagal response and arrhythmias.

PTCA is a viable alternative to grafting in elderly patients or in those who otherwise can't tolerate cardiac surgery. However, patients with a left main coronary artery occlusion, lesions in extremely tortuous vessels, or occlusions older than 3 months aren't candidates for PTCA.

PTCA may be done along with coronary stenting, or stents may be placed alone. Stents provide a framework to hold an artery open by securing flaps of tunica media against an artery wall. Intravascular coronary stenting is done to reduce the incidence of restenosis. Prosthetic intravascular cylindrical stents made of stainless steel coil are positioned at the site of the occlusion. To be eligible for this procedure, the patient must be able to tolerate anticoagulant therapy and the vessel to be stented must be at least 1/8 (0.3 cm) in diameter. Some stents have a drug already placed in them that's released over time to help minimize the risk of in-stent restenosis. Coronary brachytherapy, which involves delivering beta or gamma radiation into the coronary arteries, may be used in patients who have undergone stent implantation in a coronary artery but then developed such problems as diffuse in-stent restenosis. Brachytherapy is a promising technique, but its use is restricted to the treatment of stent-related problems because of complications and the unknown long-term effects of the radiation. However, in some facilities, brachytherapy is being studied as a first-line treatment for coronary disease.

RELIEVING OCCLUSIONS WITH ANGIOPLASTY

For a patient with an occluded coronary artery, percutaneous transluminal coronary angioplasty can open the artery without opening the chest—an important advantage over bypass surgery.

First, coronary angioplasty must confirm the presence and location of the arterial occlusion. Then, a guide catheter is threaded through the patient's femoral artery into the coronary artery under fluoroscopic guidance.

When angiography shows the guide catheter positioned at the occlusion site, a smaller double-lumen balloon catheter is carefully inserted through the guide catheter and the balloon is directed through the occlusion (near right). A marked pressure gradient is obvious.

The balloon is alternately inflated and deflated until an angiogram verifies successful arterial dilation (far right) and that the pressure gradient has decreased.

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Laser angioplasty corrects occlusion by vaporizing fatty deposits with the excimer or hot-tip laser device. Percutaneous myocardial revascularization (PMR) is a procedure that uses a laser to create channels in the heart muscle to improve perfusion to the myocardium. A carbon dioxide laser is used to create transmural channels from the epicardial layer to the myocardium, extending into the left ventricle. This technique is also known as transmyocardial revascularization and appears to be up to 90% effective in treating severe symptoms.

Rotational ablation (or rotational atherectomy) removes atheromatous plaque with a high-speed, rotating burr covered with diamond crystals. Another method recently approved is an AngioJet system septa to remove clots in symptomatic coronary arteries and CABGs. It's an alternative to thrombolytic therapy and involves a jet stream of saline solution and a catheter to seek out clots. After the clot is removed, the patient can undergo angioplasty.

Nursing interventions

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During anginal episodes, monitor blood pressure and heart rate. Take a 12-lead ECG before administering nitroglycerin or other nitrates. Record the duration of pain, the amount of medication required to relieve it, and accompanying symptoms.

·

Ask the patient to grade the severity of his pain on a scale of 0 to 10. This allows him to give his individual assessment of pain as well as of the effectiveness of pain-relieving medications.

·

Keep nitroglycerin available for immediate use. Instruct the patient to call immediately whenever he feels chest, arm, or neck pain and before taking nitroglycerin.

·

Before cardiac catheterization, explain the procedure to the patient. Make sure he knows why it's necessary, understands the risks, and realizes that it may indicate a need for surgery.

·

During catheterization, monitor the patient for dye reactions. If symptoms, such as falling blood pressure, bradycardia, diaphoresis, and light-headedness appear, increase parenteral fluids as ordered, administer nasal oxygen, place the patient in the Trendelenburg position, and administer I.V. atropine if necessary.

·

After catheterization, review the expected course of treatment with the patient and his family. Monitor the catheter site for bleeding. Also, check for distal pulses. To counter the diuretic effect of the dye, increase I.V. fluids and make sure the patient drinks plenty of fluids. Assess potassium levels, and add potassium to the I.V. fluid if necessary.

·

After PTCA and intravascular stenting, maintain heparinization, observe the patient for bleeding systemically at the site, and keep the affected leg immobile. If the patient undergoes PMR, he must also remain immobile because the stents are left in the patient until his clotting time is less than 180 seconds. Precordial blood must be taken every 8 hours for 24 hours for cardiac enzyme levels. Complete blood count and electrolyte levels are monitored.

·

After rotational ablation, monitor the patient for chest pain, hypotension, coronary artery spasm, and bleeding from the catheter

site. Provide heparin and antibiotic therapy for 24 to 48 hours, as ordered.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH CAD

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Help the patient determine which activities precipitate episodes of pain. Help him identify and select more effective coping mechanisms to deal with stress. Occupational change may be needed to prevent symptoms, but many patients reject this alternative.

·

Stress the need to follow the ordered drug regimen.

·

Encourage the patient to maintain the ordered low-sodium diet and start a low-calorie diet as well.

·

Explain that recurrent angina symptoms after percutaneous transluminal coronary angioplasty or rotational ablation may signal reobstruction.

·

Encourage regular, moderate exercise. Refer the patient to a cardiac rehabilitation center or cardiovascular fitness program near his home or workplace. The staff can set up a program of exercise that best meets the patient's needs and limitations. Encourage other family members or a friend to join in the physical activity to encourage the patient's commitment to the exercise program.

·

Reassure the patient that he will be able to resume sexual activity and that modifications can allow for sexual fulfillment without fear of overexertion, pain, or reocclusion.

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Refer the patient to a program to stop smoking. Acknowledge that this will be difficult but that he should make every attempt to stop smoking immediately and never restart.

·

If the patient is scheduled for surgery, explain the procedure, provide a tour of the intensive care unit, introduce him to the staff, and discuss postoperative care.

·

After bypass surgery, provide care for the I.V. set, pulmonary artery catheter, and endotracheal tube. Monitor blood pressure, intake and output, breath sounds, chest tube drainage, and cardiac rhythm, watching for signs of ischemia and arrhythmias. I.V. epinephrine, nitroprusside (Nitropress), dopamine (Inocor), albumin, potassium, and blood products may be necessary. The patient may also need temporary epicardial pacing, especially if the surgery included replacement of the aortic valve.

·

Intra-aortic balloon pump insertion may be necessary until the patient's condition stabilizes. Also, watch for and treat chest pain. Perform vigorous chest physiotherapy, and guide the patient in pulmonary self-care.

·

Before discharge, stress the need to follow the prescribed drug regimen, exercise program, and diet. (See Teaching the patient with CAD.)

DILATED CARDIOMYOPATHY

Dilated cardiomyopathy—also called congestive cardiomyopathy—results from extensively damaged myocardial muscle fibers. It interferes with myocardial metabolism and grossly dilates every heart chamber, giving the heart a globular shape. When hypertrophy coexists with dilated cardiomyopathy, the heart ejects blood less efficiently than normal and a large volume of blood remains in the left ventricle after systole, causing signs of heart failure.

Dilated cardiomyopathy most commonly affects middle-aged men but can occur in any age-group. Because it isn't usually diagnosed until the advanced stages, the prognosis is generally poor. Most patients, especially those older than age 55, die within 2 years of symptom onset.

Pathophysiology

Dilated cardiomyopathy primarily affects systolic function. It results from extensively damaged myocardial muscle fibers. Consequently, contractility in the left ventricle decreases.

As systolic function declines, stroke volume, ejection fraction, and cardiac output decrease. As end-diastolic volumes increase, pulmonary congestion may occur. The elevated end-diastolic volume is a compensatory response to preserve stroke volume despite a reduced ejection fraction.

The sympathetic nervous system is also stimulated to increase heart rate and contractility. The kidneys are stimulated to retain sodium and water to maintain cardiac output, and vasoconstriction also occurs as the renin-angiotensin system is stimulated. When these compensatory mechanisms can no longer maintain cardiac output, the heart begins to fail. Left ventricular dilation occurs as venous return and systemic vascular resistance increase. Eventually, the atria also dilate, as more work is required to pump blood into the full ventricles. Blood pooling in the ventricles increases the risk of emboli.

The cause of most cardiomyopathies is unknown. Dilated cardiomyopathy can result from myocardial destruction by a toxic, infectious, or metabolic agent; an endocrine or electrolyte disorder; a nutritional deficiency; a muscle disorder (such as myasthenia gravis, muscular dystrophy, or myotonic dystrophy); an infiltrative disorder (such as hemochromatosis or amyloidosis); or sarcoidosis.

Cardiomyopathy may be associated with alcoholism, viral myocarditis (especially after infection with coxsackievirus B, poliovirus, or influenza virus), or acquired immunodeficiency syndrome.

Metabolic cardiomyopathies are related to endocrine and electrolyte disorders and nutritional deficiencies. Dilated cardiomyopathy may develop in patients with hyperthyroidism, pheochromocytoma, beriberi, or kwashiorkor. Cardiomyopathy may also result from rheumatic fever, especially among children with myocarditis.

Cardiomyopathy may develop during the last trimester of pregnancy or within months after delivery. Its cause is unknown, but it's most common in multiparous women older than age 30, particularly those with malnutrition or preeclampsia. In these patients, cardiomegaly and heart failure may reverse with treatment, allowing a subsequent normal pregnancy. If cardiomegaly persists despite treatment, the prognosis is poor.

Dilated cardiomyopathy has been linked to the use of doxorubicin (Adriamycin), cyclophosphamide (Cytoxan), cocaine, and fluorouracil (Fluoroplex). Also, familial forms of this disorder may exist, possibly with an X-linked inheritance pattern.

Complications

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Intractable heart failure, arrhythmias, and emboli, resulting from dilated cardiomyopathy

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Syncope and sudden death, resulting from ventricular arrhythmias

Assessment findings

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The patient may have a history of a disorder that can cause cardiomyopathy. He commonly reports a gradual onset of shortness of breath, orthopnea, exertional dyspnea, paroxysmal nocturnal dyspnea, fatigue, dry cough at night, palpitations, and vague chest pain.

·

Inspection may reveal peripheral edema, jugular vein distention, ascites, and peripheral cyanosis.

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Palpation of peripheral pulses may disclose tachycardia even at rest and alternating pulse in late stages. Palpation may also reveal hepatomegaly and splenomegaly.

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Percussion may detect hepatomegaly. Dullness is heard over lung areas that are fluid-filled.

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Blood pressure auscultation may show a narrow pulse pressure.

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Cardiac auscultation reveals irregular rhythms, diffuse apical impulses, pansystolic murmur (such as mitral and tricuspid insufficiency caused by cardiomegaly and weak papillary muscles), and

S3 and S4 gallop rhythms. Lung auscultation may reveal crackles and gurgles.

ASSESSMENT FINDINGS IN CARDIOMYOPATHIES

TYPE

ASSESSMENT FINDINGS

Dilated cardiomyopathy

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Generalized weakness, fatigue

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Chest pain, palpitations

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Syncope

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Tachycardia

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Narrow pulse pressure

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Pulmonary congestion, pleural effusions

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Jugular vein distention, peripheral edema

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Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion

Hypertrophic cardiomyopathy

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Angina, palpitations

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Syncope

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Orthopnea, exertional dyspnea

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Pulmonary congestion

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Loud systolic murmur

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Life-threatening arrhythmias

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Sudden cardiac arrest

Restrictive cardiomyopathy

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Generalized weakness, fatigue

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Bradycardia

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Dyspnea

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Jugular vein distention, peripheral edema

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Liver congestion, abdominal ascites

Dilated cardiomyopathy may need to be differentiated from other types of cardiomyopathy. (See Assessment findings in cardiomyopathies.)

Diagnostic test results

No single test confirms dilated cardiomyopathy. Diagnosis requires elimination of other possible causes of heart failure and arrhythmias.

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An electrocardiogram (ECG) and angiography can help rule out ischemic heart disease. The ECG may also show biventricular hypertrophy, sinus tachycardia, atrial enlargement, ST-segment and T-wave abnormalities and, in 20% of patients, atrial fibrillation or left bundle-branch block. QRS complexes are decreased in amplitude.

 

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Chest X-rays demonstrate moderate to marked cardiomegaly usually affecting all heart chambers, along with pulmonary congestion, pulmonary venous hypertension, and pleural effusion. Pericardial effusion may appear as a water-bottle shape.

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Echocardiography can help identify ventricular thrombi, global hypokinesis, and the degrees of left ventricular dilation and dysfunction.

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Cardiac catheterization can show left ventricular dilation and dysfunction, elevated left ventricular and (in some instances) right ventricular filling pressures, and diminished cardiac output.

·

Gallium scans may identify patients with dilated cardiomyopathy and myocarditis.

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Transvenous endomyocardial biopsy may be useful in some patients to determine the underlying disorder, such as amyloidosis or myocarditis.

Treatment

In patients with dilated cardiomyopathy, the goal of treatment is to correct the underlying causes and to improve the heart's pumping ability with a cardiac glycoside, a diuretic, oxygen, an anticoagulant, a vasodilator, and a low-sodium diet supplemented by vitamin therapy. An antiarrhythmic may be used to treat arrhythmias. If cardiomyopathy results from alcoholism, alcohol consumption must be stopped. A woman of childbearing age should avoid pregnancy.

Therapy may also include prolonged bed rest and selective use of a corticosteroid, particularly when myocardial inflammation is present.

A vasodilator can help reduce preload and afterload, thereby decreasing congestion and increasing cardiac output. Acute heart failure necessitates vasodilation with I.V. nitroprusside (Nitropress), I.V. nesiritide (Natrecor), or I.V. nitroglycerin (Nitrostat). Long-term treatment may include prazosin (Minipress), hydralazine (Apresoline), isosorbide dinitrate (Isordil), an angiotensin-converting enzyme inhibitor and, if the patient is on prolonged bed rest, an anticoagulant. Dopamine (Inocor), dobutamine (Dobutrex), and milrinone (Primacor) may be useful during the acute stage.

When these treatments fail, therapy may require heart transplantation for carefully selected patients.

Cardiomyoplasty may be used for those who aren't candidates for transplants and who are symptomatic at rest. During cardiomyoplasty, the latissimus dorsi muscle is wrapped around the ventricle, helping the ventricle to effectively pump blood. A cardiomyostimulator delivers bursts of electrical impulses during systole to contract the muscle.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH DILATED CARDIOMYOPATHY

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Before discharge, teach the patient about the illness and its treatment.

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Emphasize the need to restrict sodium intake, watch for weight gain, and take a cardiac glycoside, as ordered, and watch for a toxic reaction to it (such as anorexia, nausea, and vomiting).

·

Encourage family members to learn cardiopulmonary resuscitation because sudden cardiac arrest is possible.

Nursing interventions

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Alternate periods of rest with required activities of daily living and treatments. Provide personal care as needed to prevent fatigue.

·

Provide active or passive range-of-motion exercises to prevent muscle atrophy while the patient is on bed rest.

·

Consult with the dietitian to provide a low-sodium diet that the patient can accept.

·

Monitor the patient for signs of progressive failure (decreased arterial pulses, increased jugular vein distention) and compromised renal perfusion (oliguria, increased blood urea nitrogen and serum creatinine levels, and electrolyte imbalances). Weigh the patient daily.

·

Administer oxygen as needed.

·

If the patient is receiving a vasodilator, check his blood pressure and heart rate frequently. If he becomes hypotensive, stop the infusion and place him in a supine position with his legs elevated to increase venous return and ensure cerebral blood flow.

·

If the patient is receiving a diuretic, monitor him for signs of resolving congestion (decreased crackles and dyspnea) or toovigorous diuresis. Check his serum potassium level for hypokalemia, especially if therapy includes a cardiac glycoside.

·

Therapeutic restrictions and an uncertain prognosis usually cause profound anxiety and depression; offer support and let the patient express his feelings. Be flexible with visiting hours. If confinement to a facility is prolonged, try to obtain permission for the patient to spend occasional weekends at home. (See Teaching the patient with dilated cardiomyopathy.)

·

Allow the patient and his family to express their fears and concerns. As needed, help them identify effective coping strategies.

CLASSIFYING HEART FAILURE

Two sets of guidelines are available to classify heart failure. The New York Heart Association (NYHA) classification is based on functional capacity. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines are based on objective assessment. These guidelines are compared side-by-side below.

NYHA CLASSIFICATION

ACC/AHA GUIDELINES

 

Stage A.

Class I. Ordinary physical activity doesn't cause undue fatigue, palpitations, dyspnea, or angina.

Stage B. Structural heart disease, but without signs and symptoms of heart failure

Class II. Slight limitation of physical activity but asymptomatic at rest. Ordinary physical activity causes fatigue, palpitations, dyspnea, or angina.

Class III. Marked limitation of physical activity, but typically asymptomatic at rest. Less than ordinary physical activity causes fatigue, palpitations, dyspnea, or angina.

Stage C. Structural heart disease with prior or current signs and symptoms of heart failure

Class IV. Unable to perform any physical activity without discomfort; symptoms may be present at rest. Discomfort increases with physical activity.

Stage D. End-stage disease requiring specialized treatment strategies, such as mechanical circulatory support, continuous inotropic infusion, or heart transplant

HEART FAILURE

A syndrome rather than a disease, heart failure occurs when the heart can't pump enough blood to meet the body's metabolic needs. Heart failure results in intravascular and interstitial volume overload and poor tissue perfusion. An individual with heart failure experiences reduced exercise tolerance, a reduced quality of life, and a shortened life span. (See Classifying heart failure.)

Although the most common cause of heart failure is coronary artery disease, it also occurs in infants, children, and adults with congenital and acquired heart defects. The incidence of heart failure increases

with age. About 5 million people in the United States have heart failure. About 300,000 Americans die of heart failure each year. Mortality from heart failure is greater for males, blacks, and elderly people.

UP CLOSE

ff4-b01382759WHAT HAPPENS DURING HEART FAILURE

These illustrations show, step-by-step, what happens when myocardial damage leads to heart failure.

Left-sided heart failure

Increased workload and end-diastolic volume enlarge the left ventricle. Because of the lack of oxygen, however, the ventricle enlarges with stretched tissue rather than functional tissue. The patient may experience increased heart rate, pale and cool tingling in the extremities, decreased cardiac output, and arrhythmias.

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Diminished left ventricular function allows blood to pool in the ventricle and atrium and eventually back up into the pulmonary veins and capillaries. At this stage, the patient may experience exertional dyspnea, confusion, dizziness, orthostatic hypotension, decreased peripheral pulses and pulse pressure, cyanosis, and an S3

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As the pulmonary circulation becomes engorged, rising capillary pressure pushes sodium (Na) and water (H2O) into the interstitial space, causing pulmonary edema. Note coughing, subclavian retractions, crackles, tachypnea, elevated pulmonary artery pressure, diminished pulmonary compliance, and increased partial pressure of carbon dioxide.

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When the patient lies down, fluid in the extremities moves into the systemic circulation. Because the left ventricle can't handle the increased venous return, fluid pools in the pulmonary circulation, worsening pulmonary edema. You may note decreased breath sounds, dullness on percussion, crackles, and orthopnea.

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The right ventricle may now become stressed because it's pumping against greater pulmonary vascular resistance and left ventricular pressure. When this occurs, the patient's symptoms worsen.

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Right-sided heart failure

The stressed right ventricle hypertrophies with the formation of stretched tissue. Increasing conduction time and deviation of the heart from its normal axis can cause arrhythmias. If the patient doesn't already have left-sided heart failure, he may experience increased heart rate, cool skin, cyanosis, decreased cardiac output, palpitations, and dyspnea.

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Blood pools in the right ventricle and right atrium. The backed-up blood causes pressure and congestion in the vena cava and systemic circulation. The patient has elevated central venous pressure, jugular vein distention, and hepatojugular reflux.

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Backed-up blood also distends the visceral veins, especially the hepatic vein. As the liver and spleen become engorged, their function is impaired. The patient may develop anorexia, nausea, abdominal pain, palpable liver and spleen, weakness, and dyspnea secondary to abdominal distention.

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Increasing capillary pressure forces excess fluid from the capillaries into the interstitial space. This causes tissue edema, especially in the legs and abdomen. The patient may experience weight gain, pitting edema, and nocturia.

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For many patients, the symptoms of heart failure restrict the ability to perform activities of daily living, severely affecting quality of life. Advances in diagnostic and therapeutic techniques have greatly improved the outlook for these patients, but the prognosis still depends on the underlying cause and its response to treatment.

Pathophysiology

Heart failure may be classified according to the side of the heart it affects (left-sided or right-sided heart failure) or by the cardiac cycle involved (systolic or diastolic dysfunction). (See What happens during heart failure.)

Left-sided heart failure occurs as a result of ineffective left ventricular contractile function. As the pumping ability of the left ventricle fails, cardiac output falls. Blood is no longer effectively pumped out into the body; it backs up into the left atrium and then into the lungs, causing pulmonary congestion, dyspnea, and activity intolerance. If the condition persists, pulmonary edema and right-sided heart failure may result. Common causes include left ventricular infarctions, hypertension, and aortic and mitral valve stenosis.

RIGHT-SIDED HEART FAILURE

Right-sided heart failure results from ineffective right ventricular contractile function. Consequently, blood isn't pumped effectively through the right ventricle to the lungs, causing blood to back up into the right atrium and the peripheral circulation. The patient gains weight and develops peripheral edema and engorgement of the kidney and other organs. It may result from an acute right ventricular infarction, pulmonary hypertension, or a pulmonary embolus. However, the most common cause is profound backward blood flow due to left-sided heart failure.

SYSTOLIC DYSFUNCTION

Systolic dysfunction occurs when the left ventricle can't pump enough blood out to the systemic circulation during systole and the ejection fraction falls. Consequently, blood backs up into the pulmonary circulation and pressure increases in the pulmonary venous system. Cardiac output falls; weakness, fatigue, and shortness of breath may occur. Causes of systolic dysfunction include a myocardial infarction and dilated cardiomyopathy.

DIASTOLIC DYSFUNCTION

Diastolic dysfunction occurs when the ability of the left ventricle to relax and fill during diastole is reduced and the stroke volume falls. Therefore, higher volumes are needed in the ventricles to maintain cardiac output. Consequently, pulmonary congestion and peripheral edema develop. Diastolic dysfunction may occur as a result of left ventricular hypertrophy, hypertension, or restrictive cardiomyopathy. This type of heart failure is less common than systolic dysfunction, and its treatment isn't as clear.

All causes of heart failure eventually lead to reduced cardiac output, which triggers compensatory mechanisms, such as increased sympathetic activity, activation of the renin-angiotensin-aldosterone system, ventricular dilation, and hypertrophy. These mechanisms improve cardiac output at the expense of increased ventricular work.

Increased sympathetic activity—a response to decreased cardiac output and blood pressure—enhances peripheral vascular resistance, contractility, heart rate, and venous return. Signs of increased sympathetic activity, such as cool extremities and clamminess, may indicate impending heart failure.

Increased sympathetic activity also restricts blood flow to the kidneys, causing them to secrete renin, which in turn converts angiotensinogen to angiotensin I, which then becomes angiotensin II—a potent vasoconstrictor. Angiotensin causes the adrenal cortex to release aldosterone, leading to sodium and water retention and increased circulating blood volume. This renal mechanism is initially helpful; however, if it persists unchecked, it can aggravate heart failure as the heart struggles to pump against the increased volume.

In ventricular dilation, an increase in end-diastolic ventricular volume (preload) causes increased stroke work and stroke volume during contraction, stretching cardiac muscle fibers so that the ventricle can accept the intravascular volume. Eventually, the muscle becomes stretched beyond optimum limits and contractility declines.

In ventricular hypertrophy, an increase in ventricular muscle mass allows the heart to pump against increased resistance to the outflow of blood, improving cardiac output. However, this increased muscle mass also increases myocardial oxygen requirements. An increase in the ventricular diastolic pressure necessary to fill the enlarged ventricle may compromise diastolic coronary blood flow, limiting the oxygen supply to the ventricle and causing ischemia and impaired muscle contractility.

In heart failure, counterregulatory substances—prostaglandins and atrial natriuretic factor—are produced in an attempt to reduce the negative effects of volume overload and vasoconstriction caused by the compensatory mechanisms.

The kidneys release the prostaglandins, prostacyclin and prostaglandin E2, which are potent vasodilators. These vasodilators also act to reduce volume overload produced by the renin-angiotensin-aldosterone system by inhibiting sodium and water reabsorption by the kidneys.

Atrial natriuretic factor is a hormone secreted mainly by the atria in response to stimulation of the stretch receptors in the atria caused by excess fluid volume. B-type natriuretic factors work to counteract the negative effects of sympathetic nervous system stimulation and the renin-angiotensin-aldosterone system by producing vasodilation and diuresis. (See How heart failure affects the body.)

HOW HEART FAILURE AFFECTS THE BODY

This summary highlights how heart failure affects the major body systems and the multidisciplinary care required.

·

In left-sided heart failure, the pumping ability of the left ventricle fails and cardiac output falls. Blood backs up into the right atrium.

·

In right-sided heart failure, the right ventricle becomes stressed and hypertrophies, leading to increased conduction time and arrhythmias.

Respiratory system

·

As blood backs up into the right atrium (because the heart's pumping ability has failed), blood backs into the lungs, causing pulmonary congestion.

GI system

·

Congestion of the peripheral tissues leads to GI tract congestion and anorexia, GI distress, and weight loss.

·

Liver failure can occur as a result of blood backing up into the peripheral circulation and subsequent engorgement of organs.

Renal system

·

With right-sided heart failure, blood backs up into the right atrium and the peripheral circulation. The patient gains weight and develops peripheral edema and engorgement of the kidney and other organs.

Collaborative management

Multidisciplinary care is needed to determine the underlying cause and precipitating factors of heart failure, and may include the expertise of a respiratory therapist, dietitian, and physical therapist. Surgery may be indicated if the patient has coronary artery disease or is experiencing severe limitations or recurrent hospitalizations despite maximal medical treatment. Social services may be necessary to help the patient's transition to his home setting after the acute situation is resolved.

Complications

ACUTE

·

Acute renal failure

·

Arrhythmias

·

Pulmonary edema

CHRONIC

·

Activity intolerance

·

Cardiac cachexia

·

Metabolic impairment

 

·

Renal impairment

·

Thromboembolism

Assessment findings

·

The patient's history reveals a disorder or condition that can precipitate heart failure. The patient frequently reports shortness of breath, which in early stages occurs during activity and in late stages also occurs at rest. He may report that dyspnea worsens at night when he lies down. He may use two or three pillows to elevate his head to sleep or have to sleep sitting up in a chair. He may state that his shortness of breath awakens him shortly after he falls asleep, causing him to sit up to catch his breath. He may remain dyspneic, coughing, and wheezing even when he sits up. This is referred to as paroxysmal nocturnal dyspnea.

·

The patient may report that his shoes or rings have become too tight, a result of peripheral edema.

·

He may also report increasing fatigue, weakness, insomnia, anorexia, nausea, and a sense of abdominal fullness (particularly if he has right-sided heart failure).

·

 

·

The patient may have a cough that produces pink, frothy sputum. You may note cyanosis of the lips and nail beds, pale skin, diaphoresis, dependent peripheral and sacral edema, and jugular vein distention.

·

Ascites may also be present, especially in patients with right-sided heart failure.

·

If heart failure is chronic, the patient may appear cachectic.

·

 

·

Percussion reveals dullness over fluid-filled lung bases.

·

Auscultation of the blood pressure may detect decreased pulse pressure, reflecting reduced stroke volume. Heart auscultation may disclose an S3 and S4. Lung auscultation reveals moist, bibasilar crackles. If pulmonary edema is present, you hear crackles throughout the lung, accompanied by rhonchi and expiratory wheezing.

Diagnostic test results

·

Electrocardiography reflects heart strain or enlargement or ischemia. It may also reveal atrial enlargement, tachycardia, and extra systoles.

·

Chest X-rays show increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly.

·

Pulmonary artery pressure monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, left ventricular end-diastolic pressure in patients with left-sided heart failure, and elevated right atrial or central venous pressure in those with right-sided heart failure.

·

Echocardiography demonstrates left ventricular dysfunction with a reduced ejection fraction.

·

Brain natriuretic peptide (BNP) assay helps to detect abnormal hormone levels produced by failing ventricles.

·

 

Treatment

The goal of therapy is to improve pump function by reversing the compensatory mechanisms producing the clinical effects. Heart failure can usually be controlled quickly with treatment consisting of a diuretic (such as furosemide [Lasix], hydrochlorothiazide [HydroDIURIL], ethacrynic acid [Edecrin], bumetanide [Bumex], spironolactone [Aldactone], or triamterene [Dyrenium]) to reduce total blood volume and circulatory congestion; nesiritide (Natrecor), a recombinant form of human BNP, to increase diuresis and to decrease afterload; an angiotensin-converting enzyme (ACE) inhibitor to decrease peripheral vascular resistance; carvedilol (Coreg), a nonselective beta-adrenergic receptor blocker with alpha-receptor blockade to reduce mortality and improve quality of life; oxygen administration to increase oxygen delivery to the myocardium and other vital organ tissues; an inotropic drug, such as digoxin (Lanoxin), to strengthen myocardial contractility; a sympathomimetic, such as dopamine and dobutamine (Dobutrex), in acute situations; milrinone (Primacor), to increase contractility and cause arterial vasodilation; a vasodilator to increase cardiac output or an ACE inhibitor to decrease afterload; and antiembolism stockings to prevent venostasis and possible thromboembolism formation.

ff1-b01382759AGE AWARE

An elderly patient may require lower doses of an ACE inhibitor because of impaired renal clearance. Monitor him for severe hypotension, signifying a toxic effect.

Acute pulmonary edema requires morphine; nitroglycerin or nitroprusside (Nitropress) as a vasodilator to diminish blood return to the heart; dobutamine, dopamine, or milrinone to increase myocardial contractility and cardiac output; a diuretic to reduce fluid volume; supplemental oxygen; and high Fowler's position.

After recovery, the patient usually must continue taking a cardiac glycoside, a diuretic, and a potassium supplement and must remain under medical supervision. If the patient with valve dysfunction has recurrent acute heart failure, surgical replacement may be necessary.

The patient may also require lifestyle modifications (to reduce symptoms of heart failure), such as weight loss, limited sodium (3 g/day) and alcohol intake, reduced fat intake, smoking cessation, stress reduction, and development of an exercise program.

A biventricular pacemaker may be used to control ventricular dyssynchrony. If heart failure is due to coronary artery disease, the patient may require coronary artery bypass graft surgery or angioplasty. The patient may also require valve surgery to reshape and support the mitral valve and improve cardiac functioning. If heart failure is severe enough that the patient requires a heart transplant, he may have a left ventricular assist device placed to improve the pumping ability of the heart until transplantation can be performed.

Nursing interventions

·

Place the patient in Fowler's position and give him supplemental oxygen to help him breathe more easily. Organize all activity to provide maximum rest periods.

·

Weigh the patient daily (the best index of fluid retention), and check for peripheral edema. Also, monitor I.V. intake and urine output (especially if the patient is receiving a diuretic).

·

Assess vital signs (for increased respiratory and heart rates and for narrowing pulse pressure) and mental status. Auscultate the heart for abnormal sounds (S3 gallop) and the lungs for crackles or rhonchi. Report any changes immediately.

·

Frequently monitor blood urea nitrogen and serum creatinine, potassium, sodium, chloride, and magnesium levels.

·

Provide continuous cardiac monitoring during acute and advanced stages to identify and treat arrhythmias promptly.

DISCHARGE TEACHING

ff3-b01382759

·

Advise the patient to follow a lowsodium diet, if ordered. Identify lowsodium food substitutes and foods to avoid, and show how to read labels to assess sodium content. To evaluate compliance, analyze the patient's 24-hour dietary intake.

·

Show the patient how to take his own pulse by placing a finger on the radial artery and counting for 1 minute. Have him demonstrate the procedure.

·

Tell the patient to take digoxin at the same time each day, to check his pulse rate and rhythm before taking it, and to call the practitioner if the rate is less than 60 beats/minute or if the rhythm is irregular.

·

Teach the patient to report important signs and symptoms, such as dizziness, blurred vision, shortness of breath, persistent dry cough, palpitations, increased fatigue, paroxysmal nocturnal dyspnea, swollen ankles, and decreased urine output.

·

Advise the patient to weigh himself at least three times per week and to report an increase of 3 to 5 lb (1.4 to 2.3 kg) in 1 week.

·

Instruct the patient taking a potassium-wasting diuretic to eat high-potassium foods, such as bananas and orange juice.

·

Instruct the patient to avoid fatigue by scheduling his activities to allow for rest periods.

·

To prevent deep vein thrombosis from vascular congestion, help the patient with range-of-motion exercises. Apply antiembolism stockings as needed. Check for calf pain and tenderness.

·

Allow adequate rest periods. (See Teaching the patient with heart failure.)

HYPERTENSION

Hypertension is an intermittent or sustained elevation of diastolic or systolic blood pressure. The two major types are essential (also called primary or idiopathic) hypertension—the most common (90% to 95% of cases)—and secondary hypertension, which results from renal disease or another identifiable cause. Malignant hypertension is a severe, fulminant form of hypertension that typically arises from both types. Hypertension is a major cause of stroke, cardiac disease, and renal failure.

Hypertension affects about 50 million adults in the United States. The risk of hypertension increases with age and is higher for blacks than for whites and in those with less education and lower income. Men have a higher incidence of hypertension in young and early middle adulthood; thereafter, women have a higher incidence.

Essential hypertension usually begins insidiously as a benign disease, slowly progressing to an accelerated or malignant state. If untreated, even mild hypertension can cause significant complications and a high mortality. In many cases, however, treatment with stepped care offers patients an improved prognosis.

Pathophysiology

Arterial blood pressure is a product of total peripheral resistance and cardiac output. Cardiac output is increased by conditions that increase heart rate, stroke volume, or both. Peripheral resistance is increased by factors that increase blood viscosity or reduce the lumen size of vessels, especially the arterioles.

Several theories help to explain the development of hypertension, including:

·

changes in the arteriolar bed, causing increased peripheral vascular resistance

·

abnormally increased tone in the sympathetic nervous system that originates in the vasomotor system centers, causing increased peripheral vascular resistance

·

increased blood volume resulting from renal or hormonal dysfunction

·

an increase in arteriolar thickening caused by genetic factors, leading to increased peripheral vascular resistance

·

abnormal renin release, resulting in the formation of angiotensin II, which constricts the arteriole and increases blood volume. (See How hypertension develops, pages 424and .)

Prolonged hypertension increases the heart's workload as resistance to left ventricular ejection increases. To increase contractile force, the left ventricle hypertrophies, raising the heart's oxygen demands and workload. Cardiac dilation and failure may occur when hypertrophy can no longer maintain sufficient cardiac output. Because hypertension promotes coronary atherosclerosis, the heart may be further compromised by reduced blood flow to the myocardium, resulting in angina or a myocardial infarction (MI). Hypertension also causes vascular damage, leading to accelerated atherosclerosis and target organ damage, such as retinal injury, renal failure, stroke, and aortic aneurysm and dissection.

The pathophysiology of secondary hypertension is related to the underlying disease. For example:

UP CLOSE

ff4-b01382759HOW HYPERTENSION DEVELOPS

Increased blood volume, cardiac rate, and stroke volume or arteriolar vasoconstriction that increases peripheral resistance causes blood pressure to rise. Hypertension may also result from the breakdown or inappropriate response of the following intrinsic regulatory mechanisms.

Renin-angiotensin system

Autoregulation

Several intrinsic mechanisms work to change an artery's diameter to maintain tissue and organ perfusion, despite fluctuations in systemic blood pressure. Mechanisms include stress relaxation and capillary fluid shift. During stress relaxation, blood vessels gradually dilate when blood pressure rises to reduce peripheral resistance. During capillary fluid shift, plasma moves between vessels and extravascular spaces to maintain intravascular volume.

When blood pressure decreases, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla's vasomotor center. This action increases sympathetic stimulation of the heart by norepinephrine. This, in turn, increases cardiac output by strengthening the contractile force, increasing the heart rate, and augmenting peripheral resistance by vasoconstriction. Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance.

Blood vessel damage

Sustained hypertension damages blood vessels (as pictured below). Vascular injury begins with alternating areas of dilation and constriction in the arterioles. Increased intra-arterial pressure damages the endothelium (see illustration, below left). Independently, angiotensin induces endothelial wall contraction (see middle illustration below), allowing plasma to leak through interendothelial spaces. Eventually, plasma constituents deposited in the vessel wall cause medial necrosis (see illustration, below right).

 

c8-ff1

 

VASCULAR DAMAGE

·

The most common cause of secondary hypertension is chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal artery stenosis interferes with sodium excretion, the renin-angiotensin-aldosterone system, or renal perfusion, causing blood pressure to increase.

       

·

In Cushing's syndrome, increased cortisol levels raise blood pressure by increasing renal sodium retention, angiotensin II levels, and vascular response to norepinephrine.

·

In primary aldosteronism, increased intravascular volume, altered sodium concentrations in vessel walls, or high aldosterone levels cause vasoconstriction and increased resistance.

·

 

increases cardiac contractility and rate, whereas norepinephrine increases peripheral vascular resistance.

The cause of essential hypertension is unknown. Family history, race, stress, obesity, a diet high in sodium or saturated fat, use of tobacco or hormonal contraceptives, excess alcohol intake, smoking, sedentary lifestyle, and aging have all been studied to determine their role in the development of hypertension. Other causes may include excessive renin production, mineral deficiencies (especially calcium, potassium, and magnesium), obesity, sleep apnea, and increased stress.

ff1-b01382759AGE AWARE

Elderly people may have isolated systolic hypertension (ISH), in which just the systolic blood pressure is elevated, because atherosclerosis causes a loss of elasticity in large arteries. Previously, it was believed that ISH was a normal part of the aging process and shouldn't be treated. Results of the Systolic Hypertension in the Elderly Program, however, found that treating ISH with an antihypertensive lowered the incidence of stroke, coronary artery disease (CAD), and left-sided heart failure.

Secondary hypertension may result from renovascular disease; renal parenchymal disease; pheochromocytoma; primary hyperaldosteronism; Cushing's syndrome; diabetes mellitus; dysfunction of the thyroid, pituitary, or parathyroid gland; coarctation of the aorta; pregnancy; or a neurologic disorder. Use of a hormonal contraceptive may be the most common cause of secondary hypertension, probably because these drugs activate the renin-angiotensin-aldosterone system. Other medications contributing to secondary hypertension include glucocorticoids, mineralocorticoids, sympathomimetics, cyclosporine (Sandimmune), cocaine, and epoetin alfa.

Complications

·

Hypertensive crisis, peripheral arterial disease, dissecting aortic aneurysm, CAD, angina, MI, heart failure, arrhythmias, and sudden death (see What happens in hypertensive crisis)

·

Transient ischemic attacks, stroke, retinopathy, and hypertensive encephalopathy

·

Renal failure

Assessment findings

·

In many cases, the hypertensive patient has no symptoms, and the disorder is revealed incidentally during evaluation for another disorder or during a routine blood pressure screening program. When symptoms do occur, they reflect the effect of hypertension on the organ systems.

·

The patient may report awakening with a headache in the occipital region, which subsides spontaneously after a few hours. This symptom usually is associated with severe hypertension. He may also report dizziness, palpitations, fatigue, and impotence.

·

With vascular involvement, the patient may complain of nosebleeds, bloody urine, weakness, and blurred vision. Complaints of chest pain and dyspnea may indicate cardiac involvement.

·

Inspection may reveal peripheral edema in late stages when heart failure is present.

·

Ophthalmoscopic evaluation may reveal hemorrhages, exudates, and papilledema in late stages if hypertensive retinopathy is present.

·

Palpation of the carotid artery may disclose stenosis or occlusion.

WHAT HAPPENS IN HYPERTENSIVE CRISIS

c8-tt24

 

·

Palpation of the abdomen may reveal a pulsating mass, suggesting an abdominal aneurysm.

·

Enlarged kidneys may point to polycystic disease, a cause of secondary hypertension.

·

Systolic or diastolic pressure, or both, may be elevated. An increase in diastolic blood pressure from a sitting to a standing position suggests essential hypertension, whereas a fall in blood pressure from the sitting to the standing position indicates secondary hypertension.

·

Auscultation may reveal an abdominal bruit to the right or left of the umbilicus midline or in the flanks if renal artery stenosis is present. Bruits may also be heard over the abdominal aorta and the femoral or carotid arteries.

Diagnostic test results

The following tests may be used to find predisposing factors and help identify the cause of hypertension.

·

Serial blood pressure measurements may be useful. (See Classifying blood pressure readings.)

·

Urinalysis may show protein, red blood cells, or white blood cells, suggesting renal disease; glucose, suggesting diabetes mellitus; or presence of catecholamines associated with pheochromocytoma.

·

 

·

A serum potassium level less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).

·

A blood urea nitrogen level that's normal or elevated to more than 20 mg/dl and a serum creatinine level that's normal or elevated to more than 1.5 mg/dl suggest renal disease.

Other tests that help to detect cardiovascular damage and other complications include the following:

·

Electrocardiography may show left ventricular hypertrophy or ischemia, and chest X-rays may show cardiomegaly.

·

Ophthalmoscopy reveals arteriovenous nicking and, in patients with hypertensive encephalopathy, edema.

·

An oral captopril (Capoten) challenge may be done to test for renovascular hypertension. This functional diagnostic test depends on the abrupt inhibition of circulatory angiotensin II by an angiotensin-converting enzyme (ACE) inhibitor, removing the major support for perfusion through a stenotic kidney. The acutely ischemic

kidney immediately releases more renin and undergoes a marked decrease in glomerular filtration rate and renal blood flow.

CLASSIFYING BLOOD PRESSURE READINGS

In 2003, the National Institutes of Health issued The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (The JNC 7 Report). Updates since The JNC 6 report include a new category, prehypertension, and the combining of stages 2 and 3 hypertension. Categories now are normal, prehypertension, and stages 1 and 2 hypertension.

The revised categories are based on the average of two or more readings taken on separate visits after an initial screening. They apply to adults ages 18 and older. (If the systolic and diastolic pressures fall into different categories, use the higher of the two pressures to classify the reading. For example, a reading of 160/92 mm Hg should be classified as stage 2.)

Normal blood pressure with respect to cardiovascular risk is a systolic reading below 120 mm Hg and a diastolic reading below 80 mm Hg. Patients with prehypertension are at increased risk for developing hypertension and should follow healthpromoting lifestyle modifications to prevent cardiovascular disease.

In addition to classifying stages of hypertension based on average blood pressure readings, practitioners should also take note of target organ disease and additional risk factors, such as a patient with diabetes, left ventricular hypertrophy, and chronic renal disease. This additional information is important to obtain a true picture of the patient's cardiovascular health.

 

CATEGORY

SYSTOLIC

 

DIASTOLIC

 

NORMAL

< 120 mm Hg

and

 
 

PREHYPERTENSION

120 to 139 mm Hg

or

80 to 89 mm Hg

 

HYPERTENSION

     
 

Stage 1

140 to 159 mm Hg

or

90 to 99 mm Hg

 

Stage 2

160 mm Hg

or

100 mm Hg

·

Renal arteriography may show renal artery stenosis.

         

Treatment

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure of the National Institutes of Health, National Heart, Lung, and Blood Institute recommends:

·

Lifestyle modifications including weight reduction, use of a Dietary Approaches to Stop Hypertension (or DASH) diet (involves an increased

intake of fruits, vegetables, and low-fat dairy products and a decreased intake of saturated and total fat), reduction of dietary sodium intake, physical activity (regular aerobic activity such as brisk walking), and moderation of alcohol intake.

·

If the patient fails to achieve the desired blood pressure or make significant progress, continue lifestyle modifications and begin drug therapy.

·

For stage I hypertension in the absence of compelling indications (heart failure, post-MI, high coronary disease risk, diabetes, chronic kidney disease, or recurrent stroke), give most patients a thiazidetype diuretic. Consider using an ACE inhibitor, an angiotensin receptor blocker, a beta-adrenergic receptor blocker, a calcium channel blocker, or a combination.

·

 

·

If the patient has one or more compelling indications, base drug treatment on benefits from outcome studies or existing clinical guidelines. Treatment may include the following, depending on indication:

o

- heart failure—a diuretic, a beta-adrenergic receptor blocker, an ACE inhibitor, an angiotensin receptor blocker, or an aldosterone antagonist

o

- post-MI—a beta-adrenergic receptor blocker, an ACE inhibitor, or an aldosterone antagonist

o

- high CAD risk—a diuretic, a beta-adrenergic receptor blocker, an ACE inhibitor, or a calcium channel blocker

o

- diabetes—a diuretic, a beta-adrenergic receptor blocker, an ACE inhibitor, an angiotensin receptor blocker, or a calcium channel blocker

o

- chronic kidney disease—an ACE inhibitor or an angiotensin receptor blocker

o

- recurrent stroke prevention—a diuretic or an ACE inhibitor

o

- as needed—another antihypertensive.

Treatment for a patient with secondary hypertension includes correcting the underlying cause and controlling hypertensive effects.

Severely elevated blood pressure (hypertensive crisis) may be refractory to medications and may be fatal.

Hypertensive emergencies require parenteral administration of a vasodilator or an adrenergic inhibitor or oral administration of a selected drug (such as nifedipine [Procardia], captopril, clonidine [Catapres], or labetalol [Normodyne]), to rapidly reduce blood pressure.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH HYPERTENSION

·

Teach the patient to use a self-monitoring blood pressure cuff and to record the reading at least twice weekly in a journal for review by his practitioner at every office appointment. Tell the patient to take his blood pressure at the same hour each time with relatively the same type of activity preceding the measurement.

·

Tell the patient and his family to keep a record of drugs used in the past, noting especially which ones are or aren't effective. Suggest recording this information on a card so the patient can show it to his practitioner.

·

To encourage compliance with antihypertensive therapy, suggest establishing a daily routine for taking medication. Warn the patient that uncontrolled hypertension may cause stroke and heart attack. Tell him to report any adverse reactions to prescribed drugs. Advise him to avoid high-sodium antacids and over-the-counter cold and sinus medications containing harmful vasoconstrictors.

·

Help the patient examine and modify his lifestyle. Suggest stress-reduction techniques, dietary changes, and an exercise program, particularly aerobic walking, to improve cardiac status and reduce obesity and serum cholesterol levels.

·

Encourage a change in dietary habits. Help the obese patient plan a reducing diet. Tell him to avoid high-sodium foods (such as pickles, potato chips, canned soups, and cold cuts), table salt, and foods high in cholesterol and saturated fat.

The initial goal is to reduce mean arterial blood pressure by no more than 25% (within minutes to hours) and then to 160/110 within 2 hours while avoiding excessive falls in blood pressure that can precipitate renal, cerebral, or myocardial ischemia.

Examples of hypertensive emergencies include hypertensive encephalopathy, intracranial hemorrhage, acute left-sided heart failure with pulmonary edema, and dissecting aortic aneurysm. Hypertensive emergencies are also associated with eclampsia or severe gestational hypertension, unstable angina, and an acute MI.

Hypertension without accompanying symptoms or target-organ disease seldom requires emergency drug therapy.

Nursing interventions

·

If a patient is hospitalized with hypertension, find out if he was taking his prescribed antihypertensive. If he wasn't, ask why. If he can't afford the medication, refer him to the appropriate social service department. (See Teaching the patient with hypertension.)

 

·

When routine blood pressure screening reveals elevated pressure, make sure the sphygmomanometer cuff's size is appropriate for the patient's upper arm circumference. Take the pressure in both arms in lying, sitting, and standing positions. Ask the patient if he smoked, drank a beverage containing caffeine, or was emotionally upset before the test. Advise him to return for blood pressure testing at frequent and regular intervals.

·

To help identify hypertension and prevent untreated hypertension, participate in public education programs dealing with hypertension and ways to reduce risk factors. Encourage public participation in blood pressure screening programs. Routinely screen all patients, especially those at risk (blacks and those with family histories of hypertension, stroke, or heart attack).

HYPERTROPHIC CARDIOMYOPATHY

Hypertrophic cardiomyopathy—also known as idiopathic hypertrophic subaortic stenosis, hypertrophic obstructive cardiomyopathy, and muscular aortic stenosis—is a primary disease of cardiac muscle. It's characterized by left ventricular hypertrophy and disproportionate, asymmetrical thickening of the intraventricular septum and free wall of the left ventricle. In patients with hypertrophic cardiomyopathy, cardiac output may be low, normal, or high, depending on whether the stenosis is obstructive or nonobstructive. Eventually, left ventricular dysfunction—resulting from rigidity and decreased compliance—causes pump failure. If cardiac output is normal or high, stenosis may go undetected for years, but low cardiac output may lead to potentially fatal heart failure.

The course of this disorder varies. Some patients demonstrate progressive deterioration; others remain stable for several years.

The hypertrophied ventricle becomes stiff, noncompliant, and unable to relax during ventricular filling. Consequently, ventricular filling is reduced and left ventricular filling pressure rises, causing increases in left atrial and pulmonary venous pressures and leading to venous congestion and dyspnea.

Ventricular filling time is further reduced as a compensatory response to tachycardia. Reduced ventricular filling during diastole and obstruction of ventricular outflow lead to low cardiac output. If papillary muscles become hypertrophied and don't close completely during contraction, mitral insufficiency occurs. Moreover, intramural coronary arteries are abnormally small and may not be sufficient to supply the hypertrophied muscle with enough blood and oxygen to meet the increased needs to the hyperdynamic muscle.

About half of all cases of hypertrophic cardiomyopathy are transmitted as an autosomal dominant trait. Other causes aren't known.

Complications

·

Pulmonary hypertension

·

Heart failure

·

Sudden death

·

Ventricular arrhythmias, such as ventricular tachycardia and premature ventricular contractions

Assessment findings

·

Generally, clinical features don't appear until the disease is well advanced. Then atrial dilation and, sometimes, atrial fibrillation abruptly reduce blood flow to the left ventricle.

·

Most patients are asymptomatic but have a family history of hypertrophic cardiomyopathy.

ff1-b01382759

In some cases, death occurs suddenly, particularly in children and young adults.

·

Patients who have symptoms report exertional dyspnea (90% of patients) and orthopnea. They commonly have angina (75% of patients), fatigue, and syncope even at rest.

·

Inspection of the carotid artery may show a rapidly rising carotid arterial pulse.

·

Palpation of peripheral arteries reveals a characteristic double impulse (called pulsus biferiens).

·

Palpation of the chest reveals a double or triple apical impulse, which may be displaced laterally.

·

Percussion may reveal bibasilar crackles if heart failure is present.

·

Auscultation reveals a harsh systolic murmur, heard after S1 at the apex near the left sternal border. The murmur is intensified by standing and with Valsalva's maneuver. An S4 may also be audible.

Diagnostic test results

·

Echocardiography shows left ventricular hypertrophy and a thick, asymmetrical intraventricular septum in patients with obstructive hypertrophic cardiomyopathy, whereas hypertrophy affects various ventricular areas in those with nonobstructive hypertrophic cardiomyopathy. The septum may have a ground-glass appearance. Poor septal contraction, abnormal motion of the anterior mitral leaflet during systole, and narrowing or occlusion of the left ventricular

outflow tract may also be seen in obstructive hypertrophic cardiomyopathy. The left ventricular cavity appears small, with vigorous posterior-wall motion but reduced septal excursion.

·

 

·

Electrocardiography usually shows left ventricular hypertrophy; ST-segment and T-wave abnormalities; Q waves in leads II, III, aVF, and V4 to V6 (because of hypertrophy, not infarction); left anterior hemiblock; left-axis deviation; and ventricular and atrial arrhythmias.

·

Chest X-rays may show a mild to moderate increase in heart size, and a thallium scan usually reveals myocardial perfusion defects.

Treatment

The goals of treatment are to relax the ventricle and to relieve outflow tract obstruction. Propranolol (Inderal), a beta-adrenergic receptor blocker, is the drug of choice. It slows the heart rate and increases ventricular filling by relaxing the obstructing muscle, thereby reducing angina, syncope, dyspnea, and arrhythmias. However, propranolol may aggravate symptoms of cardiac decompensation.

Atrial fibrillation, a medical emergency with hypertrophic cardiomyopathy, necessitates cardioversion. It also calls for heparin administration before cardioversion and continuing until fibrillation subsides because of the high risk of systemic embolism. Calcium channel blockers (such as verapamil [Calan]) may improve diastolic dysfunction until fibrillation subsides.

If heart failure occurs, amiodarone (Cordarone) may be used, unless an atrioventricular block exists. This drug seems to be effective in reducing ventricular and supraventricular arrhythmias as well. Vasodilators (such as nitroglycerin [Nitro-Bid]), diuretics, and sympathetic stimulators (such as isoproterenol [Isuprel]) are contraindicated.

If drug therapy fails, surgery is indicated. Ventricular myotomy (resection of the hypertrophied septum) alone or combined with mitral valve replacement may ease outflow tract obstruction and relieve symptoms. However, ventricular myotomy is experimental and may cause complications, such as complete heart block and a ventricular septal defect. Dual-chamber pacing may prevent progression of hypertrophy and obstruction. An implantable defibrillator may be used in patients with malignant ventricular arrhythmias.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH HYPERTROPHIC CARDIOMYOPATHY

·

Remind the patient and his family that propranolol may cause depression. Notify the practitioner if symptoms occur.

·

Instruct the patient to take his drugs as ordered. Tell him to notify any practitioner caring for him that he shouldn't be given nitroglycerin, a cardiac glycoside, or a diuretic because these drugs can worsen an obstruction.

·

Inform the patient that before dental work or surgery, he needs antibiotic prophylaxis to prevent subacute bacterial endocarditis.

Nursing interventions

·

Alternate periods of rest with required activities of daily living and treatments. Provide personal care, as needed, to prevent fatigue.

·

Provide active or passive range-of-motion exercises to prevent muscle atrophy if the patient must maintain bed rest.

·

If propranolol is discontinued, don't stop the drug abruptly; doing so may cause rebound effects, resulting in a myocardial infarction or sudden death. To determine the patient's tolerance for an increased dose of propranolol, take his pulse to check for bradycardia, and have him stand and walk around slowly to check for orthostatic hypotension.

·

Therapeutic restrictions and an uncertain prognosis usually cause profound anxiety and depression; offer support and let the patient express his feelings. Be flexible with visiting hours. If confinement to a facility is prolonged, try to obtain permission for the patient to spend occasional weekends at home.

·

Allow the patient and his family to express their fears and concerns. As needed, help them identify effective coping strategies. (See Teaching the patient with hypertrophic cardiomyopathy.)

ff2-b01382759RED FLAG

Warn the patient against strenuous activity, which may precipitate syncope or sudden death. Also, advise him to avoid Valsalva's maneuver or sudden position changes; both may worsen an obstruction. Urge his family to learn cardiopulmonary resuscitation.

Pulmonary hypertension occurs when pulmonary artery pressure (PAP) rises above normal for reasons other than aging or altitude. No definitive set of values is used to diagnose pulmonary hypertension, but the National Institutes of Health requires a mean PAP of 25 mm Hg or more.

Primary or idiopathic pulmonary hypertension is characterized by increased PAP and increased pulmonary vascular resistance, both without an obvious cause. This form is most common in females ages 20 to 40 and is usually fatal within 4 years.

ff2-b01382759RED FLAG

Mortality is highest in pregnant women.

Secondary pulmonary hypertension results from existing cardiac or pulmonary disease or both. The prognosis in secondary pulmonary hypertension depends on the severity of the underlying disorder.

Pathophysiology

In primary pulmonary hypertension, the smooth muscle in the pulmonary artery wall hypertrophies for no reason, narrowing the small pulmonary artery (arterioles) or obliterating it completely. Fibrous lesions also form around vessels, impairing distensibility and increasing vascular resistance. Pressures in the left ventricle, which receives blood from the lungs, remain normal. However, the increased pressures generated in the lungs are transmitted to the right ventricle, which supplies the pulmonary artery. Eventually, the right ventricle fails (cor pulmonale). Although oxygenation isn't severely affected initially, hypoxia and cyanosis eventually occur. Death results from cor pulmonale.

Alveolar hypoventilation can result from diseases caused by alveolar destruction or from disorders that prevent the chest wall from expanding sufficiently to allow air into the alveoli. The resulting decreased ventilation increases pulmonary vascular resistance. Hypoxemia resulting from this ventilation-perfusion mismatch also causes vasoconstriction, further increasing vascular resistance and resulting in pulmonary hypertension.

Coronary artery disease or mitral valvular disease causing increased left ventricular filling pressures may cause secondary pulmonary hypertension. Ventricular septal defect (VSD) and patent ductus arteriosus (PDA) cause secondary hypertension by increasing blood flow through the pulmonary circulation through left-to-right shunting. Pulmonary emboli and chronic destruction of alveolar walls, as in emphysema, cause secondary pulmonary hypertension by obliterating or obstructing the pulmonary vascular bed. Secondary pulmonary hypertension can also occur by vasoconstriction of the vascular bed, such as through hypoxemia, acidosis, or both. Conditions resulting in vascular obstruction can also cause pulmonary hypertension because blood isn't allowed to flow appropriately through the vessels.

Secondary pulmonary hypertension can be reversed if the disorder is resolved. If hypertension persists, hypertrophy occurs in the medial smooth-muscle layer of the arterioles. The larger arteries stiffen, and hypertension progresses. Pulmonary pressure begins to equal systemic blood pressure, causing right ventricular hypertrophy and, eventually, cor pulmonale.

Primary cardiac disease may be congenital or acquired. Congenital defects cause a left-to-right shunting, rerouting blood through the lungs twice and causing pulmonary hypertension. Acquired cardiac diseases, such as rheumatic valvular disease and mitral stenosis, result in left-sided heart failure that diminishes the flow of oxygenated blood from the lungs. This increases pulmonary vascular resistance and right ventricular pressure.

The causes of primary pulmonary hypertension are unknown but are thought to include altered immune mechanisms and hereditary factors.

Secondary pulmonary hypertension results from hypoxemia caused by various conditions, including acquired cardiac disease, such as mitral stenosis and rheumatic valvular disease; alveolar hypoventilation resulting from chronic obstructive pulmonary disorders, diffuse interstitial pneumonia, kyphoscoliosis, malignant metastases, obesity, sarcoidosis, or scleroderma; primary cardiac disease resulting from atrial septal defect, PDA, or VSD; and vascular obstruction resulting from fibrosing mediastinitis, idiopathic veno-occlusive disease, left atrial myxoma, mediastinal neoplasm, pulmonary embolism, and vasculitis.

Complications

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Cor pulmonale

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Cardiac failure

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Assessment findings

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The patient with primary pulmonary hypertension may have no signs or symptoms until lung damage becomes severe. (In fact, the disorder may not be diagnosed until autopsy.)

 

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Usually, a patient with pulmonary hypertension complains of increasing dyspnea on exertion, weakness, syncope, and fatigue. He may also have difficulty breathing, feel short of breath, and report that breathing causes pain. Such signs may result from left-sided heart failure.

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Inspection may show signs of right-sided heart failure, including ascites and jugular vein distention.

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The patient may appear restless and agitated and have a decreased level of consciousness (LOC). He may be confused and have memory loss.

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You may observe decreased diaphragmatic excursion and respiration, and the point of maximal impulse may be displaced beyond the midclavicular line.

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On palpation, you may also note signs of right-sided heart failure such as peripheral edema. The patient typically has an easily palpable right ventricular lift and a reduced carotid pulse. He may also have a palpable and tender liver and tachycardia.

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Auscultation findings are specific to the underlying disorder but may include a systolic ejection murmur, a widely split S23 and S4 sounds. You may also hear decreased breath sounds and loud tubular sounds.

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Breath sounds are commonly decreased because of fluid in the lungs, or loud tubular sounds may be heard.

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The patient may have decreased blood pressure.

Diagnostic test results

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Arterial blood gas (ABG) analysis reveals hypoxemia (decreased partial pressure of arterial oxygen).

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Electrocardiography, in right ventricular hypertrophy, shows right axis deviation and tall or peaked P waves in inferior leads.

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Cardiac catheterization discloses increased PAP, with a systolic pressure greater than 30 mm Hg. It may also show an increased pulmonary artery wedge pressure (PAWP) if the underlying cause is left atrial myxoma, mitral stenosis, or left-sided heart failure; otherwise, PAWP is normal.

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Pulmonary angiography reveals filling defects in the pulmonary vasculature such as those that develop with pulmonary emboli.

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Pulmonary function tests show decreased flow rates and increased residual volume in underlying obstructive disease; in underlying restrictive disease, they may show reduced total lung capacity.

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Radionuclide imaging allows assessment of right and left ventricular function.

 

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Open lung biopsy may determine the type of disorder.

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Echocardiography allows the assessment of ventricular wall motion and possible valvular dysfunction. It can also demonstrate right ventricular enlargement, abnormal septal configuration consistent with right ventricular pressure overload, and a reduction in left ventricular cavity size.

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Perfusion lung scan may produce normal or abnormal results, with multiple patchy and diffuse filling defects that don't suggest pulmonary thromboembolism.

Treatment

Oxygen therapy decreases hypoxemia and resulting pulmonary vascular resistance. For patients with right-sided heart failure, treatment also includes fluid restriction, cardiac glycosides to increase cardiac output, and diuretics to decrease intravascular volume and extravascular fluid accumulation. Vasodilators and calcium channel blockers can reduce myocardial workload and oxygen consumption. Bronchodilators and beta-adrenergic agents may also be prescribed. A patient with primary pulmonary hypertension usually responds to epoprostenol (PGI2) as a continuous home infusion.

For a patient with secondary pulmonary hypertension, treatment must also aim to correct the underlying cause. If that isn't possible and the disease progresses, the patient may need a heart-lung transplant.

Nursing interventions

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Give oxygen therapy, and observe the patient's response. Report signs of increasing dyspnea so the practitioner can adjust treatment accordingly.

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Monitor ABG levels for acidosis and hypoxemia. Report a change in the patient's LOC immediately.

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When caring for a patient with right-sided heart failure, especially one receiving diuretics, record weight daily, carefully measure intake and output, and explain all medications and diet restrictions. Check for increasing jugular vein distention, which may signal fluid overload.

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Monitor the patient's vital signs, especially his blood pressure and heart rate. If hypotension or tachycardia develops, notify the practitioner. If the patient has a pulmonary artery catheter, monitor his PAP and PAWP as ordered and report changes.

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Make sure the patient alternates periods of rest and activity to reduce the body's oxygen demand and prevent fatigue.

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Arrange for diversional activities. The type of activity—whether active or passive—depends on the patient's physical condition.

DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH PULMONARY HYPERTENSION

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Teach the patient which signs and symptoms to report to his practitioner (increasing shortness of breath, swelling, increasing weight gain, increasing fatigue).

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Fully explain the drug regimen.

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If necessary, go over diet restrictions the patient should follow to maintain a low-sodium diet.

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Teach the patient taking a potassiumwasting diuretic which foods are high in potassium.

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Warn the patient not to overexert himself, and suggest frequent rest periods between activities.

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If the patient needs special equipment for home use, such as oxygen equipment, refer him to the social services department.

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Before discharge, help the patient adjust to the limitations imposed by this disorder. (See .)

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Listen to the patient's fears and concerns, and remain with him during periods of extreme stress and anxiety.

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Answer questions the patient has as best as you can. Encourage him to identify care measures and activities that make him comfortable and relaxed. Perform these measures, and encourage the patient to do so as well.

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Include the patient in care decisions, and include family members in all phases of his care.

RESTRICTIVE CARDIOMYOPATHY

Restrictive cardiomyopathy, a disorder of the myocardial musculature, is characterized by restricted ventricular filling (the result of left ventricular hypertrophy) and endocardial fibrosis and thickening. If severe, it's irreversible.

Pathophysiology

An extremely rare disorder, the cause of primary restrictive cardiomyopathy is unknown. However, restrictive cardiomyopathy syndrome, a manifestation of amyloidosis, results from infiltration of amyloid into the intracellular spaces in the myocardium, endocardium, and subendocardium.

In both forms of restrictive cardiomyopathy, the myocardium becomes rigid, with poor distention during diastole, inhibiting complete ventricular filling, and fails to contract completely during systole, resulting in low cardiac output.

Restrictive cardiomyopathy is rare. It's most common in children and young adults. There's no racial predilection, but people living in Africa, South America, and India are at increased risk.

Complications

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Heart failure

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Arrhythmias

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Systemic or pulmonary embolization

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Sudden death

Assessment findings

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Fatigue, dyspnea, orthopnea, chest pain, edema, liver engorgement, peripheral cyanosis, pallor, and S3 or S4 gallop rhythms due to heart failure

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Systolic murmurs caused by mitral and tricuspid insufficiency

Diagnostic test results

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In advanced stages of this disease, chest X-ray shows massive cardiomegaly, affecting all four chambers of the heart; pericardial effusion; and pulmonary congestion.

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Echocardiography, computed tomography scan, or magnetic resonance imaging rules out constrictive pericarditis as the cause of restricted filling by detecting increased left ventricular muscle mass and differences in end-diastolic pressures between the ventricles.

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Electrocardiography may show low-voltage complexes, hypertrophy, atrioventricular conduction defects, or arrhythmias.

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Arterial pulsation reveals blunt carotid upstroke with small volume.

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Cardiac catheterization shows increased left ventricular end-diastolic pressure and rules out constrictive pericarditis as the cause of restricted filling.

Restrictive cardiomyopathy may be difficult to differentiate from constrictive pericarditis. A biopsy of heart muscle may be used to confirm the diagnosis. Cardiac catheterization can also help differentiate the type of cardiomyopathy through simultaneous left- and right-heart catheterization. In some cases, surgical exploration and biopsies are the only means to distinguish the type of cardiomyopathy or to differentiate it from pericarditis.

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DISCHARGE TEACHING

ff3-b01382759TEACHING THE PATIENT WITH RESTRICTIVE CARDIOMYOPATHY

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Teach the patient to watch for and report signs and symptoms of digoxin toxicity (anorexia, nausea, vomiting, and yellow vision); to record and report weight gain; and, if sodium restriction is ordered, to avoid canned foods, pickles, smoked meats, and use of table salt.

Treatment

Although no therapy exists for restricted ventricular filling, a cardiac glycoside, a diuretic, and a restricted sodium diet are beneficial by easing the symptoms of heart failure.

An oral vasodilator—such as isosorbide dinitrate (Isordil), prazosin (Minipress), or hydralazine (Apresoline)—may control intractable heart failure. Anticoagulant therapy may be necessary to prevent thrombophlebitis in the patient on prolonged bed rest. A steroid or chemotherapy may help with underlying disease. A heart transplant may be considered in those with poor myocardial functioning.

Nursing interventions

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In the acute phase, monitor heart rate and rhythm, blood pressure, urine output, and pulmonary artery pressure readings to help guide treatment.

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Give psychological support. Provide appropriate diversionary activities for the patient restricted to prolonged bed rest. Because a poor prognosis may cause profound anxiety and depression, be especially supportive and understanding, and encourage the patient to express his fears. Refer him for psychosocial counseling, as necessary, for assistance in coping with his restricted lifestyle. Be flexible with visiting hours whenever possible. (See Teaching the patient with restrictive cardiomyopathy.)