MYOCARDIAL INFARCTION

MYOCARDIAL INFARCTION

Myocardial infarction occurs from prolonged myocardial ischaemia associated in most cases with coronary thrombosis at the site of atherosclerotic stenosis. The branches of coronary arteries which are usually occluded in order of frequency are.

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  1. Anterior descending branch of the left coronary artery-75%.
  2. Right coronary artery-20 %.
  3. Left circumflex branch-5%.

Infarction does not involve the right ventricle usually.

CAUSES

  1. Coronary thrombosis-the commonest cause.
  2. Prolonged coronary vasospasm.
  3. Prolonged hypotension with critical lowering of blood pressure.
  4. Coronary embolism.
  5. Vasculitis.
  6. Dissection of aortic root or coronary artery
  7. Aortitis.
  8. Cocaine addiction.

Whether coronary thrombosis or occlusion would produce an infarction that depends upon:

(i)Size of the vessel.

(ii ) Rapidity of onset.

(iii) Effective collateral circulation.

CLASSIFICATION OF MYOCARDIAL INFARCTION

Transmural

When there is classic electro-cardiographic elevation of ST-segment and development of Q-wave.

Non-transmural or Subendocardial

Associated with no Q-wave formation but ST-T changes are present. As Q-wave may even be absent in transmural infarction, now-a-days infarction is better classified as:

  1. Q-wave infarction.
  2. Non-Q-wave infarction.

PRECIPITATING FACTORS

These are present only in 50% of cases.

  1. Unaccustomed physical exertion.
  2. Emotional upset.
  3. Heavy meals.
  4. Sudden hypotension from surgical and non-surgical causes.
  5. Shovelling snow

CLINICAL FEATURES

Onset is acute, at any time of day and night, but commonly seen in the early hours of morning, after getting up from bed (circadian theory) between 6 AM to 10 AM due to increased catecholamine level during this time.

Premonitory symptoms

About 50%-75% of patients may have vague discomfort in the chest, little shortness of breath or weakness, days or week before the occurrence of myocardial infarction.

MYOCARDIAL INFARCTION

Symptoms due to Ischaemia

The typical retrosternal pain of angina pectoris is present but unlike angina pectoris it starts at rest, persists longer and is not relieved by coronary dilators. The site, character and  radiation of pain are same as in Angina Pectoris. In 20% of cases pain is either absent or less pronounced and is overshadowed by the associated complications (Painless infarction). Diabetes, high blood pressure or higher age may be associated with this type of silent myocardial infarction. In absence of pain, arrhythmia particularly severe life threatening arrhythmia, e.g. ventricular fibrillation may be associated with sudden death in 20% of cases.

Symptoms of Heart failure

Breathlessness, cough, frothy sometimes blood-tinged sputum may be present. Patient cannot lie down flat in bed because of pulmonary oedema and prefers to lie in a propped up position or erect position. Nausea and vomiting may also be present.

Symptoms due to Cardiogenic shock (when more than 40 % of myocardium is infarcted)

Sometimes the limbs are cold, severe sweating, restlessness and confusion may be present. Coma rarely develops. This is usually seen in 8%-14% of cases.

ON EXAMINATION

Patient is markedly anxious and restless.

Decubitus-propped up. BP is usually low and progressively declines (Zerisch Bezold’s reflex) when shock is present. It may be elevated in its absence at least initially. Systolic pressure is very much affected, so there is beheaded blood pressure. Pulse rate is high (there may be bradycardia sometimes in cases of inferior wall myocardial infarction), there may be pulsus alternans due to cardiac failure, sometimes pulse may be irregular due to development of cardiac arrhythmia. Congested jugular veins may be seen in patients with right ventricular infarction but when it develops later may indicate right-sided CCF.

MYOCARDIAL INFARCTION

Central cyanosis may be present, respiration rate is hurried. There may be subnormal temperature and limbs are cold. Temperature may be raised ranging from 37.8-39.4°C (100- 103°F) within 24 to 36 hours due to protein absorption from the necrotic cardiac muscle. This is associated with leucocytosis, high ESR, hyperglycaemia, glycosuria or albuminuria.

Paradoxical systolic expansile pulsation of the precordium may rarely be present due to dyskinesia of infarcted region Heart sounds are faint. First and second heart sounds may be indistinguishable and so-called tic-tac rhythm may develop. There may be gallop rhythm over the mitral area. Atrial gallop (S4) is very common but ventricular gallop (Sa) is less common and associated with severe left ventricular dysfunction. Reversed splitting of the second heart sound or fixed split may be present either due to LBBB or left ventricular dysfunction.Wide splitting width of S, components may develop in Acute RBBB. Soft systolic murmur due to papillary muscle dysfunction or loud systolic murmur due to rupture of interventricular septum or musical systolic murmur due to ruptured chordae tendinae may develop. Cardiac irregularities may be present due to tachy- or bradyarrhythmias. Pericardial friction sound may be present (20%) on 3rd to 4th day in transmural infarction. Lungs show moist sounds at both bases, presumably due to left heart failure. Clear lungs field is a good prognostic sign.

.MYOCARDIAL INFARCTION.