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Myocardial infarction

Myocardial infarction

Overview of anatomy and physiology
The heart is mainly made of special muscle (myocardium). The  heart pumps blood into arteries (blood vessels) which take the  lood to every part of the body. Like any other muscle, the heart muscle needs a good blood supply. The coronary arteries take blood to the heart muscle . The main coronary arteries branch off from the aorta (the large artery which takes oxygen‐rich blood from the heart chambers to the body.) The main coronary arteries divide into smaller branches which take blood to all parts of the heart muscle.
Pathophysiology
The most common cause of an MI is a blood clot (thrombosis) that forms inside a coronary artery, or one of its branches. This blocks the blood flow to a part of the heart. Blood clots do not usually form in normal arteries. However, a clot may form if there is some atheroma within the lining of the artery. Atheroma is like fatty patches or plaques that develop within the inside lining of arteries. (This is similar to water pipes that get furred up.) Plaques of atheroma may gradually form over a number of years in one or more places in the coronary arteries. Each plaque has an outer firm shell with a soft inner fatty core. In an MI (heart attack), a coronary artery or one of its smaller branches is suddenly blocked, which results in the damage of the myocardium (Figure 21.3). The part of the heart muscle supplied by this artery loses its blood (and oxygen) supply if the vessel is blocked. This part of the heart muscle is at risk of dying unless the blockage is quickly removed. When a part of the heart muscle is damaged it is said to be infarcted. The term myocardial infarction (MI) means damaged heart muscle. The area of infarct occurs in the distribution of the occluded vessel. Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. Where the infarct has taken place, a collagen scar forms in its place and the damaged muscle does not contract efficiently. Collagen is a bundle of inelastic fibres that do not stretch or contract effectively. Damaged heart tissue conducts electrical signals
much more slowly than normal heart tissue, which could result ininefficient contraction of the myocardium.

Signs and symptoms
A person having an acute myocardial infarction usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats and anxiety. Rapid,irregular pulse, hypotension and dyspnoea (shortness of breath) may all present as symptoms. The anxiety is often described as a
 sense of impending doom’. Dyspnoea occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary oedema.
Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms. These are called ‘silent’ myocardial infarctions.
Management
Patients suffering from an acute myocardial infarction will be maintained on bed rest to minimize cardiac work. Reassurance will be necessary for both the patient and relatives as they will be anxious. Pain relief is paramount, current guidelines recommend the use of morphine (5–10â•›mg) or diamorphine (2.5–5â•›mg) titrated to pain. A popular method of titrating pain relief is to make a 10â•›mg dose of morphine in 10â•›ml of water for injection and administer the morphine in 1â•›ml (1â•›mg) increments until pain relief is achieved. The benefit of opiate pain relief is that it also acts to relieve anxiety in the patient. However, as opiates are associated with nausea and vomiting it is advisable to administer an antiemetic at the same time. The patient is also attached to continuous cardiac monitoring as the risks of cardiac arrhythmias and even cardiac arrest are high. Some experts still recommend the use of sublingual nitrate spray in the patient suffering from myocardial infarction. If intravenous morphine is ineffective then the recommendation is for the use of intravenous nitrates or beta blocker drugs. Before the use of nitrates or beta blockers it is necessary to measure the patient’s blood pressure, as both nitrates and beta blockers can significantly reduce the blood pressure.


inefficient contraction of the myocardium.


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