CARDIOGENIC SHOCK
CARDIOGENIC SHOCK: Etiology:Cardiogenic shock is one of the most dreaded cardiovascular emergencies, carrying a mortality of 50-80 -percent. It is most frequently the result of acute myocardial infarction but may also occur in cases of massive pulmonary embolism, acute cardiac tamponade, tension pneumothorax and in severe left heart failure. The description that follows refers primarily to cases of cardiogenic shock due to acute myocardial infarction.
The frequency of shock in cases °LAW is directly related to extent of myocardial necrosis. It usually occurs only when acute infarcts involve 40% of the total ventricular mass, and is th-e-i—v-fore most—oTten seen with anteiitkAkyocardial infarction since left anterior descending artery supplies the largest area of myocardium. Cardiogenic shock is uncommon with inferior myocardial infarction unless there is associated infarction of the right ven-tricle.
It may be the presenting feature in a case of AMI, but more often appears 24-72 hours after the onset of infarction since ischaemic injury is progressive over time and its full impact on haemodynamic disturbances may evolve over several hours or even a few days. Occasionally, it is ushered in by other serious complications of acute infarction such as acute pulmonary oedema, tachy or bradyarrhythmias, pulmonary embolism, A-V blocks, acute papillary muscle dysfunction or rupture of inter-ventricular septum, The basic disturbance in cases of cardiogenic shock is an acute and marked reduction in cardiac output due to severe myocardial damage. The blood volume is essentially normal and it is this feature which distinguishes cardiogenic shock from majority of other cases of shock (see Chapter :11). However, in a small proportion of cases of cardiogenic shock, hypovolaemia may play a central role, being either due to excessive fluid loss (resulting from vomiting, profuse perspiratiOn, use of diuretic•coupled with diminished fluid intake) or the result of pooling of blood in the peripheral veins with consequent diminished venous return. The prognosis in these cases is considerably better than when shock is due entirely to myocardial damage.
Clinical Features: While some degree of fall in blood pressure after myocardial infarction is not unusual, a state Of true shock presents a typical clinical picture resulting from impaired blood supply to certain vital organs, and intense compensatory peripheral vasoconstriction dile to sympathetic overactivity. The patient is often restless and confused but may. be apathetic and even drowsy. He feels extremely weak and exhauSted, appears pale and is cyanosed. There is profuse perspiration and skin is cold and clammy especially in the peripheral regions. The systolic pressure falls progressively, is usually below 80 mm Hg (or lower by 50 mm Hg than former levels in hypertensive subjects), pulse is rapid, weak and thready, and respiration may be rapid and shallow, especially if there is associated left heart failure. The urinary output is reduced to less than 20 ml per hour.
Tags: bradyarrhythmias, Cardiogenic Shock, hypovolaemia, oedema, pulmonary embolism, tachy
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