Myocardial infarction
With myocardial infarction (MI), also known as heart attack, reduced blood flow through one of the coronary arteries results in myocardial ischemia and necrosis. With cardiovascular disease, the leading cause of death in the United States and western Europe, death usually results from the cardiac damage or complications of an MI.
Mortality is high when treatment is delayed; almost half of all sudden deaths due to an MI occur before hospitalization, within 1 hour of the onset of symptoms. The prognosis improves if vigorous treatment begins immediately.
Causes
Predisposing factors include:
❑ positive family history
❑ hypertension
❑ smoking
❑ elevated levels of serum triglycerides, total cholesterol, and low-density lipoproteins
❑ diabetes mellitus
❑ obesity or excessive intake of saturated fats, carbohydrates, or salt
❑ sedentary lifestyle
❑ aging
❑ stress or a type A personality (aggressive, ambitious, competitive, addicted to work, chronically impatient)
❑ drug use, especially cocaine.
Men and postmenopausal women are more susceptible to an MI than premenopausal women, although incidence is rising among females, especially those who smoke and take a hormonal contraceptive. (See MI in women.)
The site of the MI depends on the vessels involved. Occlusion of the circumflex branch of the left coronary artery causes a lateral wall infarction; occlusion of the anterior descending branch of the left coronary artery, an anterior wall infarction.
True posterior or inferior wall infarctions generally result from occlusion of the right coronary artery or one of its branches. Right ventricular infarctions can also result from right coronary artery occlusion, can accompany inferior infarctions, and may cause right-sided heart failure. With a transmural MI, tissue damage extends through all myocardial layers; with a subendocardial MI, only in the innermost and possibly the middle layers.
Signs and symptoms
The cardinal symptom of an MI is persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, or shoulder blades. Such pain is typically described as heavy, squeezing, or crushing and may persist for 12 hours or more. However, in some MI patients — particularly older adults or diabetics — pain may not occur at all; in others, it may be mild and confused with indigestion.
In patients with coronary artery disease, angina of increasing frequency, severity, or duration (especially if not provoked by exertion, a heavy meal, or cold and wind) may signal impending infarction.
Other features
Other signs and symptoms include a feeling of impending doom, fatigue, nausea, vomiting, and shortness of breath. Some patients may have no symptoms. The patient may experience catecholamine responses, such as coolness in the extremities, perspiration, anxiety, and restlessness. Fever is unusual at the onset of an MI, but a low-grade fever may develop during the next few days. Blood pressure varies; hypotension or hypertension may be present.
Complications
The most common post-MI complications include recurrent or persistent chest pain, arrhythmias, left ventricular failure (resulting in heart failure or acute pulmonary edema), and cardiogenic shock. Unusual but potentially lethal complications that may develop soon after infarction include thromboembolism; papillary muscle dysfunction or rupture, causing mitral insufficiency; rupture of the ventricular septum, causing ventricular septal defect; rupture of the myocardium; and ventricular aneurysm.
Up to several months after infarction, Dressler’s syndrome may develop (pericarditis, pericardial friction rub, chest pain, fever, leukocytosis and, possibly, pleurisy or pneumonitis). (See Complications of myocardial infarction.)
Diagnosis
Persistent chest pain, ST-segment changes on the electrocardiogram (ECG), and elevated levels of total creatine kinase (CK) and the CK-MB isoenzyme over a 72-hour period usually confirm an MI. Cardiac troponins are useful in differentiating an MI from skeletal muscle injury, or when CK-MB measurements are low and a small MI has actually occurred. Auscultation may reveal diminished heart sounds, gallops and, in papillary dysfunction, the apical systolic murmur of mitral insufficiency over the mitral valve area.
When signs and symptoms are equivocal, assume that the patient has had an MI until tests rule it out. Diagnostic test results include the following:
❑ serial 12-lead ECG: ECG abnormalities may be absent or inconclusive during the first few hours following an MI. When present, characteristic abnormalities include serial ST-segment depression in subendocardial MI and ST-segment elevation in a transmural MI.
❑ coronary angiography: Visualization reveals which vessels have been affected and the extent of damage.
❑ serial serum enzyme levels: CK levels are elevated; specifically, CK-MB or troponin levels.
❑ myoglobin: Because myoglobin always rises within 3 to 6 hours after an MI, lack of an increase within 6 hours indicates that an MI hasn’t occurred.
❑ echocardiography: Echocardiography may show ventricular-wall motion abnormalities in patients with a transmural MI.
❑ nuclear ventriculography (multigated acquisition scan or radionuclide ventriculography) scanning: Nuclear scanning can identify acutely damaged muscle by picking up radioactive nucleotide, which appears as a “hot spot” on the film. It’s useful in localizing a recent MI.
Elevated homocysteine and C-reactive protein levels have been found incidentally in MI and may indicate a newer risk factor. The practical value of these tests remains unknown. Folic acid supplementation is used as treatment for elevated homocysteine levels.
Treatment
The goals of treatment are to relieve chest pain, to stabilize heart rhythm, to reduce cardiac workload, to revascularize the coronary artery, and to preserve myocardial tissue. Arrhythmias, the predominant problem during the first 48 hours after the infarction, may require an antiarrhythmic, possibly a pacemaker and, rarely, cardioversion.
To preserve myocardial tissue, I.V. thrombolytic therapy should be started within 6 hours after the onset of symptoms (unless contraindications exist). Thrombolytic therapy includes either streptokinase or recombinant tissue plasminogen activator and is usually followed by I.V. infusion of heparin.
Percutaneous transluminal coronary angioplasty (PTCA) may be another option. If PTCA is performed soon after the onset of symptoms, the thrombolytic agent may be administered directly into the coronary artery. Emergency coronary artery bypass surgery may be necessary in some cases.
Other treatments include:
❑ antiplatelet drugs, such as aspirin, to inhibit platelet aggregation (should be initiated within 24 hours after onset of symptoms)
❑ sublingual or I.V. nitrates, such as nitroglycerin, to relieve pain by redistributing blood to ischemic areas of the myocardium, thus increasing cardiac output and reducing myocardial workload
❑ morphine I.V. for pain and sedation
❑ bed rest with bedside commode to decrease cardiac workload
❑ oxygen administration at a modest flow rate for 3 to 6 hours (a lower concentration is necessary if the patient has chronic obstructive pulmonary disease)
❑ drugs to increase myocardial contractility or blood pressure
❑ pulmonary artery catheterization to detect left- or right-sided heart failure and to monitor the patient’s response to treatment
❑ angiotensin-converting enzyme inhibitors to improve survival rate in a low ejection fraction (a large anterior-wall MI).
Other medications, such as antiarrhythmics, diuretics, glycoprotein IIb/IIIa inhibitors, beta-adrenergic blockers, and calcium channel blockers, are used as needed.
Special considerations
❑ 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 MI patients receive treatment in the coronary care unit (CCU), where they’re under constant observation for complications.
❑ On admission to the CCU, record the patient’s blood pressure, temperature, and heart and breath sounds, and monitor them regularly. Also, obtain an ECG.
❑ Assess and record the severity and duration of pain; administer an analgesic. Avoid I.M. injections; absorption from the muscle is unpredictable.
❑ Check the patient’s blood pressure after giving nitroglycerin, especially the first dose.
❑ Frequently monitor the ECG to detect rate changes or arrhythmias. Place rhythm strips in the patient’s chart periodically for evaluation.
❑ During episodes of chest pain, obtain ECG, blood pressure, and pulmonary artery catheter measurements for changes.
❑ Watch for signs and symptoms of fluid retention (crackles, cough, tachypnea, and edema), which may indicate impending heart failure. Carefully monitor daily weight, intake and output, respirations, serum enzyme levels, and blood pressure.
❑ Auscultate for adventitious breath sounds periodically (patients on bed rest frequently have atelectatic crackles, which may disappear after coughing) and for third or fourth heart sounds.
❑ Organize patient care and activities to maximize periods of uninterrupted rest.
❑ Ask the dietary department to provide a clear liquid diet until nausea subsides. A low-cholesterol, low-sodium, caffeine-free diet may be ordered.
❑ Provide a stool softener to prevent straining during defecation, which causes vagal stimulation and may slow the heart rate. Allow use of a bedside commode, and provide as much privacy as possible.
❑ Assist with range-of-motion exercises. If the patient is completely immobilized by a severe MI, turn him often. Antiembolism stockings help prevent venostasis and thrombophlebitis.
❑ Provide emotional support, and help reduce stress and anxiety; administer a tranquilizer, if needed.
❑ Explain procedures, and answer questions. Explaining the CCU environment and routine can ease anxiety. Involve the patient’s family in his care as much as possible.
To prepare the patient for discharge:
❑ Promote adherence measures by thoroughly explaining the prescribed medication regimen and other treatment measures.
❑ Warn the patient about adverse reactions to drugs, and advise him to watch for and report signs and symptoms of toxic reaction (anorexia, nausea, vomiting, and yellow vision, for example, if the patient is receiving digoxin).
❑ Review dietary restrictions with the patient. If he must follow a low-sodium or low-fat and low-cholesterol diet, provide a list of foods that he should avoid. Ask the dietitian to speak to the patient and his family.
❑ Counsel the patient to resume sexual activity progressively.
CLINICAL TIP: Advise the patient to report typical or atypical chest pain. Postinfarction syndrome may develop, producing chest pain that must be differentiated from a recurrent MI, pulmonary infarct, or heart failure.
❑ If the patient has a Holter monitor in place, explain its purpose and use.
❑ Stress the need to stop smoking.
❑ Encourage participation in a cardiac rehabilitation program.
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright Details: Handbook of Diseases, Copyright © 2008 Williams & Wilkins.
More About Causes of Chest symptoms
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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Chest injuries, blunt (Handbook of Diseases)
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