Description

Coronary artery disease (CAD) is a condition involving the arteries supplying the myocardium (heart muscle) (see Figure 10-7). The arteries become narrowed by atherosclerotic deposits over time, causing temporary cardiac ischemia and eventually MI (myocardial infarction, or heart attack).

Symptoms and Signs

Patients are asymptomatic initially, with the first symptom being the pain of angina pectoris (see “Angina Pectoris” section). In advanced disease, the severe pain of MI is described as burning, squeezing, crushing, and radiating to the arm, neck, or jaw (see “Myocardial Infarction” section) and is due to diminished blood flow and lower oxygen saturation. Nausea, vomiting, and weakness also can be experienced. Changes in the electrocardiogram (ECG) are often but not always recognized. Many patients may be asymptomatic up until an MI or sudden death event; this is why noninvasive screening of high-risk patients is imperative.

Patient Screening

Severe chest pain of sudden onset with or without previous diagnosis of angina is considered to be a cardiac event and has the potential for being catastrophic; therefore the patient should immediately be entered into the emergency medical system.

Etiology

Deposits of fat-containing substances called plaque in the lumen (opening) of the coronary arteries result in atherosclerosis and subsequent narrowing of the lumen of the arteries (Figure 10-8). The myocardium must have an adequate blood supply to function. The coronary arteries supply the cardiac muscle with blood but become constricted by atherosclerosis (Figure 10-9).

Arteriosclerosis, commonly called “hardening of the arteries,” is associated with the elderly and diabetics. The arteries eventually lose elasticity and become hard and narrow, resulting in cardiac ischemia. The cells in the myocardium gradually weaken and die. Replacement scar tissue forms, interfering with the heart’s ability to pump, resulting in heart failure.

People at higher risk for CAD are those who have a genetic predisposition to the disease, those older than 40 years of age, men (slightly more than women), postmenopausal women, and Caucasians. Other factors contributing to increased risk of the disease include a history of smoking; residence in an urban society; the presence of hypertension, diabetes, or obesity; and a history of elevated serum cholesterol or reduced serum high-density lipoprotein (HDL) levels. Lack of exercise (a sedentary lifestyle) and stress are additional risk factors.

Diagnosis

The patient usually does not experience chest pain from atherosclerosis until the coronary arteries are about 75% occluded. Collateral circulation often develops to supply the tissue with needed oxygen and nutrients (Figure 10-10). An ECG shows ischemia (caused by a lack of blood supply) and possibly arrhythmias. Treadmill testing, thallium or Cardiolite scan, CT scans, stress echocardiograms, cardiac catheterization, E10-1, and angiograms are other tools of cardiac status evaluation used to detect insufficient oxygen supply and to confirm the diagnosis. Electron beam computerized testing, a noninvasive assessment identifying calcium buildup in arteries, is another means of risk evaluation.

Treatment

Treatment consists of measures to restore adequate blood flow to the myocardium. Vasodilators and other types of medicines are prescribed. Angioplasty with a balloon or stenting is attempted in some instances to open the constricted arteries (Figure 10-11). Claims of reduction of the plaque buildup with hypolipidemic drugs are being confirmed in some cases. First line drug therapy for the prevention of CAD may include angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), thiazide diuretics, or vasodilators. Beta-blockers and anticoagulants are used to prevent blood clots from breaking off and lodging in cerebral arteries. When the blockage is severe or does not respond to drug therapy or angioplasty, coronary artery bypass surgery may be indicated to restore circulation to the affected myocardium (Figure 10-12).

Experimental gene therapy uses injections of DNA directly into cardiac muscle to stimulate new growth of blood vessels; this is still very preliminary.

Prognosis

The prognosis varies and depends on the patient’s response to the treatment, whether prescribed drug therapy, angioplasty, or coronary bypass surgery. An additional factor affecting the prognosis of smokers is the effect of smoking on the coronary arteries and whether they cease smoking.

Prevention

Measures to prevent CAD include a diet that is low in salt, fat, and cholesterol, combined with exercise. E10-2 Patients are encouraged to reduce stress and, if they smoke, to stop or reduce smoking.

Patient Teaching

Give patients information about symptoms of impending myocardial infarction and encourage them to seek immediate emergency medical care at the first sign of any related symptoms. Offer printed information to all patients about the prevention or control of CAD and emphasize the importance of a low-fat diet, weight control, exercise, and cessation of smoking. Encourage follow-up cholesterol blood tests.

Description

Angina pectoris, chest pain due to ischemia during or shortly after exertion, is the result of reduced oxygen supply to the myocardium.

Symptoms and Signs

The patient has a sudden onset of left-sided chest pain during or shortly after exertion. The pain may radiate to the left arm or back (Figure 10-13). The patient also may experience dyspnea. The pain usually is relieved by ceasing the strenuous activity and placing nitroglycerin tablets sublingually or using nitroglycerin spray also sublingually (under the tongue). The blood pressure may increase during the attack, and arrhythmias may occur.

Patient Screening

Patients experiencing symptoms of angina for the first time require immediate assessment. The sudden onset of chest pain could represent a life-threatening condition, and acute myocardial infarction must be ruled out. Those who have been diagnosed with angina pectoris, and in whom cessation of activity and use of vasodilating medications does not provide relief from the pain within 20 minutes, require immediate medical intervention through the emergency medical system.

Etiology

Atherosclerosis causes a narrowing of the coronary arteries, compromising the blood flow to the myocardium. Exertion requires increased blood flow to supply more oxygen, but the vessels cannot supply it. Spasms of the coronary arteries also may be a causative factor. Severe prolonged tachycardia, anemias, and respiratory disease also can cause cardiac ischemia.

Diagnosis

The patient history reveals a previous exertional chest pain. An ECG taken during the anginal episode may show ischemia; it is important to realize that a normal ECG does not preclude the diagnosis of angina. Other diagnostic measures, such as those described for CAD, are performed.

Treatment

Treatment consists of cessation of the strenuous activity and the placing of nitroglycerin tablets under the tongue. Transdermal nitroglycerin helps in preventing angina. When angina persists after treatment or for more than 20 minutes, immediate medical attention is indicated.

Prognosis

The prognosis varies and depends on the extent of the arterial involvement. When patients can stop the pain by ceasing strenuous activities and using vasodilating medications, the angina usually will diminish or disappear. The patient’s ability to modify his or her lifestyle may improve the prognosis.

Prevention

Prevention is similar to that recommended for coronary artery disease. Recommendations focus on lifestyle modification, including appropriate exercise; a diet low in fat, cholesterol, and salt; control of hypertension; weight loss; and smoking cessation. Patients are encouraged to reduce stress.

Patient Teaching

Patients and families should be given dietary information and suggestions for menu planning within the appropriate diet. Emphasize the importance of compliance with prescribed drug therapy. Help the patient and family locate and contact community services and support groups.

Patients should be instructed to carry the nitroglycerin tablets with them at all times. Additionally, patients and their families should be instructed that the tablets should not be exposed to light or air and therefore the tablets should be kept in the original light-resistant bottle with a cap that can be tightened.

Description

Myocardial infarction is death of myocardial tissue caused by the development of ischemia.

Symptoms and Signs

An occlusion of a coronary artery resulting in ischemia and infarct (death) of the myocardium causes sudden, severe substernal or left-sided chest pain (Figure 10-14). The pain may be crushing, causing a feeling of massive constriction of the chest, may be burning, or may just be a vague discomfort. This pain may radiate to the left or right arm, back, or jaw and is not relieved by rest or the administration of nitroglycerin. Irregular heartbeat, dyspnea, and diaphoresis often accompany the pain, and the patient usually exhibits denial and experiences severe anxiety, sometimes with the feeling of impending doom (Figure 10-15). MI occasionally is clinically silent, especially in diabetics.

Patient Screening

Early and immediate intervention improves the chance for survival and minimizes irreversible injury to the myocardium. Recent recommendations include calling 911 for entrance into the emergency medical system and chewing one 5 grain/325 mg aspirin tablet. Emergency intervention must be initiated immediately to control pain, stabilize heart rhythm, and minimize damage to the heart muscle. Most deaths caused by an MI result from primary ventricular fibrillation. Thus immediate ECG monitoring and possible defibrillation are of primary concern. The American Heart Association and the American Red Cross currently recommend defibrillation training for all certified first responders. The latest technology in AEDs affords auditory instructions to the rescuer, making the use safe for victim and rescuer.

Etiology

Myocardial infarction (MI) results from insufficient oxygen supply, such as occurs when a coronary artery is occluded by atherosclerotic plaque, thrombus, or myocardial muscle spasm (Figure 10-16). The pain is caused by ischemia, and if ischemia is not reversed within about 6 hours, the cardiac muscle dies. Coronary thrombosis is the most common cause of MI.

Diagnosis

The diagnosis includes a thorough history, electrocardiogram (ECG), chest radiographic studies, and laboratory tests for cardiac enzyme levels. Changes in enzyme levels indicate the death of cardiac tissue and include (1) creatine phosphokinase (CPK) and troponin, which are elevated in the first 6 to 24 hours after MI; (2) lactic dehydrogenase (LDH), which peaks at 48 hours after MI; and (3) aspartate aminotransferase (AST). When an elevation of these enzymes is detected, a study of cardiac isoenzymes is ordered to confirm the diagnosis. ECG changes in the P–R and QRS complexes and in the ST segment correspond to the ischemic areas. Diagnostic confirmation is assisted by elevated cardiac enzyme levels and altered isoenzyme levels identified through blood tests.

Treatment

Oxygen is administered, and morphine is given for pain. Aspirin is given as soon as possible to reduce the risk of additional damage to the heart and tissue by ischemia. Vasodilation is attempted by nitroglycerin drip. Lidocaine or amiodarone given by an intravenous drip, after a loading bolus, helps to control arrhythmias. Thrombolytic drugs, including tissue plasminogen activator (TPA), streptokinase, or alteplase (Activase) may be administered as soon as possible after the diagnosis, unless there are contraindications. Within the 6-hour window before permanent damage, an attempt may be made to open the occlusion and to restore blood flow to the area by angioplasty (see Figure 10-11), the administration of thrombolytic drugs, or by coronary artery bypass surgery (Figure 10-17). Currently, the standard of care is to try to emergently open the artery with a stent (Figure 10-18), preferably within 60 to 90 minutes of arrival; this has been demonstrated to more effectively decrease heart damage than IV thrombolytic drugs. E10-2

Prognosis

About 65% of deaths caused by MI occur in the first hour. The prognosis is determined by immediate defibrillation for ventricular fibrillation. Late mortality depends on the extent of damage to the heart muscle and the occurrence of complications. Most late cardiac death is sudden, caused by the onset of a fatal arrhythmia.

Prevention

The prevention is similar to that recommended for coronary artery disease. Recommendations focus on lifestyle modification, including appropriate exercise; a diet low in fat, cholesterol, and salt; control of hypertension; weight loss; and smoking cessation. Patients are encouraged to reduce stress. Those surviving an MI are urged to take a daily aspirin dose and a beta-blocker or ACE inhibitor for life. Lipid-lowering medications are also recommended.

Patient Teaching

Give patients and families dietary information and suggestions for menu planning within the appropriate diet. Emphasize the importance of compliance with prescribed drug therapy. Help the patient and family find and contact community services and support groups.

Description

Cardiac arrest is the sudden, unexpected cessation of cardiac activity.

Symptoms and Signs

The patient is unresponsive, with no respiratory effort and no palpable pulse.

Patient Screening

Cardiac arrest is a true life-threatening emergency. Immediate intervention with instantaneous initiation of CPR and defibrillation by means of an automated external defibrillator (AED) may successfully restore contraction of the heart (Figure 10-19). The American Heart Association or American Red Cross protocol for caregivers in the field requires immediate contact of the emergency medical system by calling 911. Inpatient facilities use the “Code, Dr. Blue” message to alert personnel.

Etiology

Cardiac arrest results from anoxia (absence of oxygen to the tissue) or interruption of the electrical stimuli to the heart. It can be caused by respiratory arrest, arrhythmia, or MI. Electrocution, drowning, severe trauma, massive hemorrhage, or drug overdose also can cause cardiac arrest.

Diagnosis

The diagnosis is based on the absence of respiratory effort and lack of palpable pulse. The ECG shows ventricular fibrillation or asystole.

Treatment

Cardiopulmonary resuscitation (CPR) must be instituted within 4 to 6 minutes of the cardiac arrest. Until recently, cardiac defibrillation was only attempted by trained, advanced life-support personnel. AEDs are now available for use by anyone who observes a cardiac arrest. The latest technology implemented in these devices talks the rescuer through the defibrillation process (see Figure 10-19). The rescuer should be familiar with the device he/she is attempting to use. Cardiac drugs are administered, including epinephrine (Adrenalin) and isoproterenol (Isuprel) or dobutamine to stimulate the heart. Antiarrhythmic drugs, including lidocaine and amiodarone, also may be administered.

Prognosis

The prognosis varies depending on the length of time the individual has been in cardiac arrest. The earlier in the event that CPR and defibrillation are instituted, the greater possibility there is for survival. Within 1 to 2 minutes after cessation of cardiac activity, respiratory efforts will cease. At 4 to 6 minutes after the cessation of cardiac activity, brain cells will begin to die. At 10 minutes after the cardiac activity has ceased with no intervention, the brain will die and death is inevitable. Many public venues and emergency vehicles now have portable defibrillators to allow more rapid resumption of cardiac function.

Successful resuscitation depends on immediate and complete intervention. Other factors that affect the final outcome of the event include the general health and age of the patient and the cause of the arrest. Successful interventions in cold water near-drowning and electrical shock have been recorded.

Prevention

Prevention of the catastrophic event of cardiac arrest is problematic. However, as in CAD and myocardial infarction, the same lifestyle modifications can reduce risk. One cannot predict near-drowning or electrical shock accidents, but the prudent individual will try to avoid situations that carry this risk. Recently, in high-risk patients with a history of abnormal heart rhythms or weak heart muscle, the implanting of defibrillators has been shown to decrease the risk of sudden cardiac death.

Patient Teaching

Encourage all possible candidates for CPR training to become certified. Help families of patients who do not survive cardiac arrest to find and contact support groups in the community. Emphasize safety guidelines to prevent drowning and electrical shock.

Encourage survivors of cardiac arrest to comply with the prescribed regimen of activities and drug therapy. Survivors also may need help in finding and contacting support groups for survivors of cardiac arrest.

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