Heart Attack Medicine heart attack , also called myocardial infarction , death of a section of the myocardium, the muscle of the hear...
heart attack, also called myocardial infarction, death of a section of the myocardium, the muscle of the heart, caused by an interruption of blood flow to the area. A heart attack results from obstruction of the coronary arteries. The most common cause is a blood clot (thrombus) that lodges in an area of a coronary artery thickened with cholesterol-containing plaque due to atherosclerosis.
Factors that contribute to the risk of atherosclerosis include high blood pressure (hypertension), diabetes mellitus, increased blood levels of low-density lipoprotein (LDL) cholesterol, smoking, and a family history of the disease. Particularly vulnerable to atherosclerosis are middle-aged men and individuals with the hereditary disease hypercholesterolemia. In the early 21st century, heart attacks were becoming increasingly common among women under age 55. Although the reason for this increase was unclear, increased rates of diabetes, hypertension, and obesity in women likely played a role.
Most heart attacks occur in the morning, a phenomenon that researchers have linked to circadian rhythm. In the morning hours, increasing circadian-driven secretion of certain hormones, particularly epinephrine, norepinephrine, and cortisol, triggers subsequent increases in oxygen demand and blood pressure. These factors in turn increase circulatory activity. In addition, the production of endothelial progenitor cells, which appear to play a crucial role in repairing the lining of blood vessels, also follows a circadian pattern, with fewer cells present in the circulation in the early morning. Decreased levels of these cells results in depressed endothelial maintenance, which scientists suspect may facilitate the onset of a heart attack upon waking.
Typically, a person experiencing a heart attack has severe chest pain, described as crushing, squeezing, or heavy, that is unremitting for 30 to 60 minutes and sometimes is experienced for longer periods. It often radiates to the arms, neck, and back. The pain is similar to that of angina pectoris, but it is of longer duration. Other common symptoms include shortness of breath; sweating; nausea; rapid heartbeat, often complicated by one or more arrhythmias (irregular heartbeats); and reduced blood pressure. The intensity of the symptoms depends on the size of the area of muscle affected by the heart attack. A small percentage of individuals do not experience pain; in these cases heart attack may be diagnosed from a routine electrocardiogram (ECG).
The focus of treatment is to limit the size of the area of tissue lost from lack of blood (infarct) and to prevent and treat complications, such as arrhythmia. Thus, the sooner the heart rate can be monitored by an ECG and the more promptly the arrhythmia is reversed by defibrillation with either antiarrhythmic drugs or electrical shock, the greater the chance of survival. Pain is treated with analgesics such as morphine, and rest and sedation are required. Other drugs that may be administered include beta-adrenergic-blocking drugs (beta-blockers) to relax the heart muscle, anticoagulants (e.g., heparin) to prevent clotting, fibrinolytic drugs to dissolve existing clots, and nitroglycerin to improve blood flow to the heart. Coronary thrombolysis therapy is widely used; it involves the administration of drugs such as streptokinase or tissue plasminogen activator (tPA) to prevent further blood clots from forming. Angioplasty or coronary artery bypass surgery are additional measures for patients requiring further treatment.
The prognosis for patients. who survive a heart attack depends largely on the degree of injury to the heart and the associated decline in heart function. Reduced heart function following an attack is caused by the formation of scar tissue that interferes with the normal electrical activity of the heart, leading to reduced heart muscle contractility, progressive weakening of the heart, and heart failure. To prevent such outcomes, scientists are investigating stem cell-based regenerative therapies, which aim to replace scar tissue with new heart muscle cells.
Antiplatelet drug
antiplatelet drug, any drug that interferes with the aggregation of platelets and formation of a clot (thrombus) in a blood vessel. Clot formation in coronary arteries may cut off the blood supply to a region of the heart and cause a myocardial infarction (heart attack). When administered during a heart attack, antiplatelet drugs can reduce the extent of damage to the heart muscle and the incidence of immediate reinfarction and death.
Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit an enzyme (cyclooxygenase) involved in the production of thromboxane A2 in platelets and of prostacyclin in the endothelial cells that line the heart cavities and walls of the blood vessels. Cyclooxygenase is synthesized by endothelial cells but not by platelets. The goal of NSAID therapy is to neutralize cyclooxygenase only in platelets, which inhibits thromboxane A2 synthesis and therefore platelet aggregation, but to continue the production of cyclooxygenase and prostacyclin in endothelial cells. The occurrence of coronary embolization (when a clot detaches from a blood vessel and becomes lodged in a coronary artery) and the incidence of acute myocardial infarction and death also are reduced with the administration of low-dose aspirin therapy.
Dipyridamole, which widens (dilates) the coronary arteries, decreases platelet adhesiveness to damaged endothelium. The drug prevents platelet aggregation and release by increasing the concentration of platelet cyclic adenosine monophosphate (cAMP) in two ways: by inhibiting an enzyme (phosphodiesterase) that degrades cAMP and by increasing the stimulating effect of prostacyclin on an enzyme (adenylate cyclase) that synthesizes cAMP. Dipyridamole alone does not reduce the incidence of death following myocardial infarction, but it works effectively in combination with other inhibitors of platelet function or with anticoagulants.
Other antiplatelet drugs, including ticlopidine, abciximab, eptifibatide, and tirofiban, bind to various receptors found on the surface of platelets that must be stimulated to activate platelets, thus inhibiting platelet aggregation.
cardiopulmonary resuscitation
cardiopulmonary resuscitation (CPR), emergency procedure for providing artificial respiration and blood circulation when normal breathing and circulation have stopped, usually as a result of trauma such as heart attack or near drowning. CPR buys time for the trauma victim by supplying life-sustaining oxygen to the brain and other vital organs until fully equipped emergency medical personnel arrive on the scene.
While training is required for conventional CPR, a modern form, known as “hands-only” CPR, may be performed by individuals who have not received formal training. According to the American Heart Association (AHA), hands-only CPR, which is recommended solely for use on adults who have suddenly collapsed, requires just “two steps to save a life.” First, the person who acts (the rescuer) takes steps to summon emergency medical personnel to the scene. Second, the rescuer begins to push hard and fast in the centre of the victim’s chest, forcing the chest down 4–5 cm (1.5–2 inches) with each press. Chest presses should continue uninterrupted, at a rate of 100 presses per minute, until medical personnel arrive. Hands-only CPR performed on adults who have suddenly collapsed is just as effective as conventional CPR; however, the AHA recommends only conventional CPR be used on children and infants.
The first step in conventional CPR is to establish unconsciousness. If the victim is unconscious, the rescuer summons help and then prepares to administer CPR. The sequence of steps may be summarized as the ABCs of CPR—A referring to airway, B to breathing, and C to circulation.
The rescuer opens the victim’s airway by placing him on his back, tilting the head back, and lifting the chin. Then the rescuer should check for signs of breathing.
If the victim is not breathing, the rescuer must perform mouth-to-mouth resuscitation. In this procedure he makes an airtight seal with his mouth over the victim’s mouth while at the same time pinching the victim’s nostrils shut. The rescuer breathes twice into the victim’s mouth, causing the victim’s chest to rise visibly each time and allowing it to deflate naturally. Artificial respiration is performed at a rate of about 12 times per minute.
The rescuer next looks for signs of circulation; the recommended method is to check for a pulse in the carotid artery of the neck. If a pulse is not felt after 10 seconds of careful searching, the rescuer proceeds to deliver chest compressions. The rescuer places the heels of his hands, overlapping, on the lower half of the victim’s breastbone, or sternum. With his elbows locked, arms straight, and shoulders directly over the victim, the rescuer uses his upper body to apply a perpendicularly directed force onto the victim’s sternum. The chest is depressed approximately 4–5 cm (1.5–2 inches) at a brisk rate of about 100 compressions per minute. At the end of each compression, pressure is released and the chest allowed to rebound completely, though the rescuer’s hands are not removed. After 30 compressions, the rescuer delivers two full breaths, then another 30 compressions, and so on. CPR continues uninterrupted until spontaneous breathing and circulation are restored or until professional medical assistance is obtained. The procedure is modified somewhat for infants and children and under special circumstances (such as multiple injuries).
Before the introduction of modern CPR techniques, attempts to revive victims of cardiac or respiratory arrest were sporadic and rarely successful. In 1958 Peter Safar and James Elam, anesthesiologists at Johns Hopkins Hospital in Baltimore, Maryland, described an emergency ventilation technique that involved tipping the victim’s head back and pulling the jaw forward in order to clear the air passage and then blowing air into the victim’s lungs through a mouth-to-mouth connection. Safar’s technique was the basis of what became the first two letters (for airway and breathing) in the ABCs of CPR. The basis of the third letter (for circulation) was provided by electrical engineer William B. Kouwenhoven and colleagues, also at Johns Hopkins, who in 1960 described the “closed-chest cardiac massage,” a method of restoring circulation in a heart-attack victim by pushing down rhythmically on the sternum. The combination of Kouwenhoven’s technique with Safar’s ventilation technique evolved into the basic method of CPR. In the mid-1990s a group of researchers at the University of Arizona Sarver Heart Center discovered that continual chest presses kept blood circulating in adult victims of cardiac arrest better than conventional CPR techniques. They found that mouth-to-mouth breaths required too much time, resulting in slowed or stopped circulation before compressions were resumed. In 2008 the researchers’ “hands-only” method for adult victims, which uses only continuous chest presses, was adopted by the AHA.
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