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, pages 384 and 385.) This type of MI involves a greater concentration of thrombin and fibrin. (See How ACS affects the body, pages 386 and 387.)
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, pages 384 and 385.) This type of MI involves a greater concentration of thrombin and fibrin. (See How 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.
Anterior-wall MI occurs when the left anterior descending artery becomes occluded.
Septal-wall MI typically accompanies an anterior wall MI because the ventricular septum is supplied by the left anterior descending artery as well.
Lateral-wall MI is caused by a blockage in the left circumflex artery, and usually accompanies an anterior- or inferior-wall MI.
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.
Posterior-wall MI is caused by occlusion of the right coronary artery or the left circumflex arteries.
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:
aging
diabetes mellitus
elevated triglyceride, low-density lipoprotein, and cholesterol levels, and decreased high-density lipoprotein levels
excessive intake of saturated fats, carbohydrates, or salt
hypertension
obesity
positive family history of coronary artery disease (CAD)
Up close
What happens during an MIWhen 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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4. 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. As back pressure increases, fluid crosses the alveolar-capillary membrane, impeding diffusion of oxygen (O2) 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
smoking
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
Arrhythmias
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
An area of viable ischemic tissue surrounds the zone of injury.
When the heart muscle is damaged, the integrity of the cell membrane is impaired.
Intracellular contents, including cardiac enzymes (such as creatine kinase and aspartate aminotransferase) and proteins (such as troponin T, troponin I, and myoglobin) are released.
Within 24 hours, the infarcted area becomes edematous and cyanotic.
During the next several days, leukocytes infiltrate the necrotic area and begin to remove necrotic cells, thinning the ventricular wall.
Scar formation begins by the 3rd week after a myocardial infarction (MI); by the 6th week, scar tissue is well established.
The scar tissue that forms on the necrotic area inhibits contractility.
Compensatory mechanisms (vascular constriction, increased heart rate, and renal retention of sodium and water) try to maintain cardiac output.
Ventricular dilation may also occur in a process called remodeling.
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.
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.
Ineffective contractility of the heart leads to accumulation of blood in the venous circulation distal to the failing ventricle.
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
Hypoperfusion of the brain results in altered mental status, involving changes in the level of consciousness, restlessness, irritability, confusion, or disorientation.
Stupor or coma may result if the decrease in cerebral perfusion continues.
Renal system
Shock and hypoperfusion from an MI cause the kidney to respond by conserving salt and water.
Poor perfusion results in diminished renal blood flow, and increased afferent arteriolar resistance occurs, causing a decreased glomerular filtration rate.
Increased amounts of antidiuretic hormone and aldosterone are released to help maintain perfusion. Urine formation, however, is reduced.
Depletion of renal adenosine triphosphate stores results from prolonged renal hypoperfusion, causing impaired renal function.
Respiratory system
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.
Lung edema occurs when pulmonary capillary pressure exceeds 18 mm Hg.
Pulmonary alveolar edema develops when pressures exceed 24 mm Hg, impairing oxygen diffusion.
Increased interstitial and intraalveolar fluid causes progressive reduction in lung compliance, increasing the work of ventilation and increasing perfusion of poorly ventilated alveoli.
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.
Cardiogenic shock
Rupture of the atrial or ventricular septum, ventricular wall, or valves
Pericarditis
Ventricular aneurysms
Mural thrombi causing cerebral or pulmonary emboli
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)
AGE AWAREAn elderly patient is more prone to complications and death. Psychological problems can also occur, either from the patient’s fear of another MI or from an organic brain disorder caused by tissue hypoxia. Occasionally, a patient may have a personality change.
Assessment findings
Typically, the patient reports the cardinal symptom of an MI: persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, and shoulder blades. He commonly describes the pain as heavy, squeezing, or crushing, and it may persist for 12 or more hours.
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. • Arrhythmias, such as ventricular tachycardia and ventricular fibrillation, occur or sudden death results. | • Resuscitation as per Advanced Cardiac Life Support protocol • Possible emergency surgical repair if CPR successful |
In some patients—particularly elderly patients or those with diabetes—pain may not occur; in others, it may be mild and confused with indigestion.
Patients with CAD may report increasing anginal frequency, severity, or duration (especially when not precipitated by exertion, a heavy meal, or cold and wind).
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.
Women may experience atypical signs and symptoms of an MI, which may go unnoticed. These include:
– burning sensation or discomfort in the upper abdomen
– difficulty breathing
– nausea and vomiting
– weakness or fatigue
– profuse sweating
– light-headedness and fainting.
Practitioners may also not recognize these signs and symptoms as cardiac related and may delay prompt diagnosis and treatment.
Inspection may reveal an extremely anxious and restless patient with dyspnea and diaphoresis.
If right-sided heart failure is present, you may note jugular vein distention.
Within the first hour after an anterior MI, about 25% of patients exhibit sympathetic nervous system hyperactivity, such as tachycardia and hypertension.
Up to 50% of patients with an inferior MI exhibit parasympathetic nervous system hyperactivity, such as bradycardia and hypotension.
In patients who develop ventricular dysfunction, auscultation may disclose an S4, 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.
Fever is unusual at the onset of an MI, but a low-grade fever may develop during the next few days.
Diagnostic test results
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. (See ECG characteristics in ACS, page 392.)
The creatine kinase (CK) level is elevated, especially the CK-MB isoenzyme, the cardiac muscle fraction of CK.
White blood cell count usually appears elevated on the 2nd day and lasts 1 week.
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.
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.
Echocardiography shows ventricular-wall dyskinesia with a transmural MI and helps evaluate the ejection fraction.
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.
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.)
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
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.
More than 90% of patients with this presentation will develop new Q waves and have positive serum cardiac markers.
Repeating the ECG may be helpful for patients who present with hyperacute T waves.
ST-segment depression or dynamic T-wave inversion
Patients with ST-segment depression indicating a posterior MI benefit most when an acute MI is diagnosed.
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.
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
A normal ECG won’t show ST-segment changes or arrhythmias.
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.
Continue assessment of myocardial changes through use of serial ECGs, ST-segment monitoring, and serum cardiac markers.
If further assessment is warranted, perform perfusion radionuclide imaging and stress echocardiography.
Initial treatment for the patient with ACS includes the following:
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.
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:
– morphine to relieve pain
– oxygen to increase oxygenation of the blood
– 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)
– aspirin to inhibit platelet aggregation.
For the patient with unstable angina and NSTEMI, treatment includes the above initial measures, and:
a beta-adrenergic receptor blocker to reduce the heart’s workload and oxygen demands
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)
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)
an antiarrhythmic, transcutaneous pacing (or transvenous pacemaker), or defibrillation if the patient has ventricular fibrillation or pulseless VT
percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG) surgery for obstructive lesions
an antilipemic to reduce elevated cholesterol or triglyceride levels.
For the patient with STEMI, treatment includes the above initial measures and these additional measures:
thrombolytic therapy (unless contraindicated) within 12 hours of onset of symptoms to restore vessel patency and minimize necrosis in STEMI
I.V. heparin to promote patency in the affected coronary artery
a beta-adrenergic receptor blocker to reduce myocardial workload
an antiarrhythmic, transcutaneous pacing (or transvenous pacemaker), or defibrillation if the patient has ventricular fibrillation or pulseless VT
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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)
interventional procedures (such as PTCA, stent placement, or surgical procedures such as CABG) may open blocked or narrowed arteries.
Nursing interventions
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.
On admission to the CCU, monitor and record the patient’s ECG readings, blood pressure, temperature, and heart and breath sounds.
Assess pain and give an analgesic. Record the severity, location, type, and duration of pain. Don’t give I.M. injections because absorption from the muscle is unpredictable, the CK level may be falsely elevated, and I.V. administration gives more rapid relief of signs and symptoms.
Check the patient’s blood pressure after giving nitroglycerin, especially the first dose.
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.
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.
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.
Organize patient care and activities to maximize periods of uninterrupted rest.
DISCHARGE TEACHING
TEACHING THE PATIENT WITH ACS
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).
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.
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.
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.
Advise the patient about appropriate responses to new or recurrent symptoms.
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.
Stress the need to stop smoking. If necessary, refer the patient to a support group.
If the patient has a Holter monitor in place, explain its purpose and use.
Review follow-up procedures, such as office visits and treadmill testing, with the patient.
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.)
Provide a stool softener to prevent straining during defecation, which causes vagal stimulation and may slow heart rate.
Allow the patient to use a bedside commode, and provide as much privacy as possible.
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.
Initiate a cardiac rehabilitation program, which typically includes education regarding heart disease, exercise, and emotional support for the patient and his family.
Provide emotional support, and help reduce stress and anxiety; administer a tranquilizer if needed.
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.
After thrombolytic therapy, administer continuous heparin. Monitor the partial thromboplastin time every 6 hours, and monitor the patient for evidence of bleeding.
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:
low-density lipoprotein (LDL) receptor—a protein that removes LDL from the bloodstream; a mutation in this gene is responsible for familial hypercholesterolemia
apolipoprotein E—mutations in this gene, commonly called apo E, also affects blood levels of LDL
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
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
MTHFR—an enzyme that clears homocysteine from the blood; mutations in MTHFR genes may cause high homocysteine levels
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:
age—Atherosclerosis usually occurs after age 40.
sex—Men are eight times more susceptible than premenopausal women.
heredity—A positive family history of CAD increases the risk. (See Exploring the genetic link to CAD.)
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:
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.
high cholesterol levels—Increased low-density lipoprotein and decreased high-density lipoprotein levels substantially heighten the risk.
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.
obesity—Added weight increases the risk of diabetes mellitus, hypertension, and elevated cholesterol levels.
physical inactivity—Regular exercise reduces the risk.
stress—Added stress or a type A personality increases the risk.
diabetes mellitus—This disorder raises the risk, especially in women.
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.)
Complications
Arrhythmias
Ischemic cardiomyopathy
MI
Assessment findings
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.)
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
intimal hemorrhage into the medial layer of the blood vessel
hyperventilation
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:
Stable angina—pain is predictable in frequency and duration and is relieved by rest and nitroglycerin.
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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