Myocardial Infarction Heart Condition Biology Essay

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Myocardial infarction, more commonly known as a heart attack, is a life-threatening and sudden heart condition. A MI occurs when a part of the heart muscle is obstructed or injured, and may die due to total interruption of blood flow (ischemia) and therefore an arrest of life-sustaining oxygen. This critical medical emergency demands both immediate attention and emergency medical services (EMS).

The term myocardial infarction comes from "myo" meaning muscle, "cardium" referring to the heart, and "infarction" meaning tissue death. Therefore, myocardial infarction is tissue death to the heart muscle (usually caused by an obstruction of blood flow). The phrase "heart attack" is often misused and could also refer to heart problems other than a myocardial infarction, such as unstable angina pectoris, which is chest pain.

The underlying mechanism of a heart attack is the death of heart muscle cells due to a lack of oxygen. If these cells are not supplied with sufficient oxygen to meet their metabolic requirements, they die by a process called infarction. The decrease in blood supply causes the following:

Heart muscle which has lost blood flow long enough (10-15 minutes) ends up dying (a process called necrosis) and is irreversible. Thus, the heart ends up permanently impaired as a pump for the remainder of the individual's life.

Injured heart muscle conducts the electrical impulses which initiate each heart beat much more slowly due to the tissue damage. The speed can slow to the point that the spreading impulse is preserved long enough for the uninjured muscle to complete contraction. The now slowed electrical signal, still traveling within the injured area, can re-enter and trigger the healthy muscle to beat again too soon for the heart to relax long enough and refill from venous return. This causes the heart to increase substantially. This sustained heart rate (200 to over 400 BPM) is termed ventricular tachycardia (V-Tach) or ventricular fibrillation (V-Fib). The rapid heart rate effectively stops heart pumping, after which the heart will flutter or quiver.

Cardiac output and blood pressure descend rapidly to nearly zero and the individual can quickly die. This is the most common mechanism of the sudden death that can result from a myocardial infarction. The cardiac defibrillator device was specifically designed for halting and correcting these rapid heart rates. If used properly, it stimulates the entire heart muscle to contract all in synchrony. This will hopefully stop continuation of the re-entry process and re-start the heart. If used within minutes of the onset of V-Tach or V-Fib, the defibrillator has a high success rate in stopping these often fatal arrhythmias and allowing a functional heart rhythm to return (Buckberg 1977).

Acute myocardial infarction is usually characterized by varying degrees of chest pain or discomfort, weakness, nausea/vomiting, sweating, and arrhythmias, anxiety, and sometimes loss of consciousness. Chest pain is the most common symptom of acute myocardial infarction and it is often described as constriction, tightness, or pressure. Pain may then move to the jaw, neck, arms, and back, most often to the left side of the body. Approximately one quarter of all myocardial infarctions are silent and without symptoms. Patients may complain of atypical symptoms like fatigue, syncope, or weakness. Approximately half of all MI patients have experienced warning symptoms prior to the infarct.

Myocardial infarctions can vary substantially in severity. Most familiar cases of myocardial infarction are identifiable by ambulance staff, emergency room doctors and cardiac specialist nurse practitioners as soon as they come into contact with the patient. Yet many myocardial infarctions (smaller or less painful) are not recognized by victims, never receive medical attention, and possibly result in either death or increasing heart weakness. For a more thorough diagnosis, medical history, combined with ECG results and blood tests for heart muscle damage on the cellular level, are necessary. Electrocardiogram (ECG) findings suggestive of MI are elevations of the ST segment and changes in the T wave. After a myocardial infarction, changes can often be seen on the ECG Q waves, representing scarred heart tissue. The ST segment elevation distinguishes between STEMI and NSTEMI (myocardial infarction without ST elevation). The latter is diagnosed when cardiac enzymes are elevated (Buckberg, 1987).

Cardiac enzymes are proteins from cardiac tissue found in the blood that can be used in diagnosis of MI. Before the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury, after which disproportional elevation of a subtype of the enzyme creatine phosphokinase (CPK) was found to be very specific for myocardial injury. Currently, troponin isoenzymes I or T, which are thought to rise before permanent injury develops, are considered the gold standard. APositive troponin accompanying chest pain may accurately predict a high likelihood of a myocardial infarction in the near future. The diagnosis of myocardial infarction used to require all three components (history, ECG, and enzymes) to accurately test positive for MI. To date, enzyme tests have become reliable to the point that enzyme elevations alone are considered reliable measures of cardiac injury, with ECG serving to determine the location that the damage has occurred and medical history serving to screen patients for further testing (Nicholas, 2004).

In more obscure cases or in situations where intervention to restore blood flow is possible, an angiogram can be done. Using a catheter inserted into an artery, usually the femoral artery, obstructed or narrowed vessels can be identified, and angioplasty applied. Angiography requires extensive skill (usually performed by cardiologists), especially in emergency settings, and may not be immediately available after established hospital hours. There is a risk of plaque and vessel rupture on balloon inflation and should this occur, emergency open-chest surgery may be required.

Histopathological examination of the heart shows that there is a circumscribed area of ischemic necrosis. In the first few days, the myocardial fibers are still delineated but lose their transversal striations and nucleus. The interstitial space may be full of red blood cells giving the concentrated pink cytoplasm. After healing has begun (a week to two weeks) the area shows myocardial fibers with preservation of their contour, but the transverse striations and nuclei are lost. The interstitium of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, in order to clear the myocyte debris by phagocytosis. The necrotic area is surrounded and progressively taken over by granulation tissue, which will replace the damaged tissue with fibrous scar tissue.

The most common cause of heart attack is atherosclerosis (a gradual buildup of cholesterol and fibrous tissue in plaques in the arterial wall) typically over many years. However these can become unstable, rupture, and additionally promote a thrombus (blood clot) that completely blocks the artery, which can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction. All risk factors for atherosclerosis are also modifiable risk factors for ischemic heart disease (including myocardial infarction): older age, smoking, hypercholesterolemia (high low density lipoprotein (LDL) and low high density lipoprotein (HDL), diabetes (with/without insulin resistance) and obesity.

Heart attacks are associated with higher levels of intense exertion, stress or physical exertion, especially if the exertion is more intense than the individual usually performs. Quantitatively, the period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate for people who are physically very fit. For those in poor physical condition, the rate differential from intense exercise and subsequent recovery is over 35-times higher. One observed mechanism for this phenomenon is the increased arterial pulse pressure stretching and relaxation of arteries with each heart beat which increases mechanical "shear stress" on atheromas and the likelihood of plaque rupture. Increased spasm/contraction of coronary arteries in association with cocaine abuse can also trigger myocardial infarction (Absolute astronomy, 2000).

As myocardial infarction is a common medical emergency, the signs are often part of first aid courses. General management in the immediate setting is:

calling for help as soon as possible

giving aspirin (162-325 mg), which inhibits formation of further blood clots

giving the patient nitroglycerine under the tongue if the patient is carrying tablets or liquid spray

being prepared to administer cardiopulmonary resuscitation (CPR) in case of arrhythmia or cardiac arrest (Nicolas, 2004).

Since the publication of data showing that the ease and rapid response of automated external defibrillators (AEDs) in public places may significantly increase chances of survival, many of these have been installed in public buildings, public transport facilities and in non-ambulance emergency vehicles (e.g. police cars and fire engines). AEDs analyze the rhythm and determine whether the arrhythmia is amenable to defibrillation. A heart attack, especially because of cardiac arrhythmias, is often a life-threatening medical emergency which demands both immediate attention and activation of the emergency medical services. Immediate termination of arrhythmias and transport by ambulance to a hospital where advanced cardiac life support (ACLS) is available can greatly improve both chances for survival and recovery. The more time that passes, the more severe/permanent the damage will be and the more likely the occurrence of both life threatening arrhythmias and death.

Once in the hospital, oxygen, aspirin, nitroglycerin and analgesia, usually morphine, are given as soon as possible, if this has not already been administered during transit. The goal of hospital personnel in the first phases of care is to salvage as much myocardial tissue as possible and restore the function of heart chambers and their remaining tissue. This is achieved primarily with thrombolytic drugs, such as streptokinase, urokinase, alteplase (recombinant tissue plasminogen activator, rtPA) or reteplase (Nicholas, 2004). Angioplasty as a first-line measure is probably not the first option available due to the availability of an experienced interventional cardiologist on-site, or the availability of rapid transport to a specialized center. Coronary artery bypass surgery is an option, although primary angioplasty’s development makes it a more viable option. The same limitations apply in that exceptional cardiothoracic surgery services are not available in many hospitals. Recent studies have shown benefit of the initiation of a statin (e.g. simvastatin) even in patients without known hypercholesterolemia. Patients are discouraged from working, strenuous activity, and sexual activity for about two months, while they undergo cardiac rehabilitation training. Local laws may also place limitations on driving motorized vehicles. It will be determined if the patient suffers from angina, especially pectoris, during a follow-up or before discharge. If so, treadmill testing, thallium scintigraphy or coronary angiography are often performed to identify treatable causes, as this will decrease the risk of future myocardial infarction (Cannon, 2007).

Cardiovascular endurance will obviously be radically reduced and along with that, muscular endurance and strength, and body composition as they walk hand in hand with heart functioning capacity. Flexibility could possibly be maintained as long as the individual did not exert him/herself. All six of the skill related physical fitness components would be vastly affected. Speed, agility, reaction time, and power will be substantially reduced while balance and coordination could be kept again, as long as the patient didn’t exert post surgery.

Cardiac rehab is absolutely paramount post myocardial infarction not only to limit the damage caused, but to also control risk for subsequent cardiovascular diseases. Ideally, cardiovascular endurance, muscular strength, and muscular endurance should be introduced gradually post-infarction. Flexibility should be incorporated as a warm-up and cool-down method. Not only will this possibly halt if not slow the damage already done, but it will steel the patient from further CVD. If anything it could be a wakeup call to a sedentary or unhealthy individual to change.

Any of the treadmill tests could be used post-infarction to see capacity and whether the patient should worry about other episodes of CVD. Obviously, a physician would need to be present and the protocol would need to be modified to start at extremely light workloads. Cardiac rehab programs are typically broken down into four phases:

Phase 1: during hospitalization

Phase II: generally during the first 3 months after hospitalization or convalescent period, usually conducted in supervised outpatient medical facilities

Phase III: a late outpatient supervised community-based or home-based phase

Phase IV: the community-based, generally unsupervised, lifetime maintenance phase (Leone, 2000)

During/after phase IV, activities such as walking if not jogging are attainable goals. The paramount objective here is to not overstress and overwork the system before it is ready.