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Cardiogenic shock may be defined as the clinical state resulting from inability of the heart to pump sufficient blood for the perfusion need of the vital organs. The most common cause of cardiogenic shock is acute myocardial infarction. Oligaemic shock is not included in this definition.
Clinical Signs and Pathogenesis of Cardiogenic Shock:
Insufficient blood flow through the skin, skeletal muscles, kidneys and brain and excess secretion of catecholamines give the clinical signs of shock. The skin is pale cold and moist because of Vasoconstriction and sweating under the influence of excess catecholamines. There is profound muscular weakness as enough blood does not flow through the skeletal muscles. The resulting metabolic acidosis causes ‘air hunger’.
There is oliguria or anuria renal blood flow. Mental confusion or coma result from cerebral hypoxia. Excess secretion of catecholamines causes anxiety and fear of death. If the patient survives the acute episode, results of hypoxic damage of the kidney, lung, liver and brain may manifest as acute renal tubular necrosis, ‘shock-lung’, jaundice and cerebral oedema respectively.
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In acute myocardial infarction, cardiac output goes down. To compensate for this peripheral vasoconstriction and tachycardia occur under the influence of catecholammes. Blood pressure generally falls after acute myocardial infarction. Occasionally, there is disproportionate vasoconstriction and there is transient rise of blood pressure.
In a few cases there is bradycardia instead of tachycardia. This is attributed to vagotonia. One should not therefore insist on finding low blood pressure and tachycardia before making a diagnosis of shock. If there are clinical signs of tissues under perfusion as detailed above, the patient may be said to be in shock.
It is to be noted that nowadays emphasis has shifted from blood pressure to blood flow. The aim of circulation is to maintain tissue perfusion and not any specific normal blood pressure. Therefore, if the patient’s skin is warm, his urinary secretion is normal and he is mentally clear, one does not need to give any vasoconstrictor drugs even if the blood pressure falls to 80 or 90 mm Hg systolic and 50-60 mm Hg diastolic. If the blood pressure falls below these figures, coronary and renal circulation may suffer.
Management of Cardiogenic Shock:
(a) Intravenous Line:
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The first step is to establish a good intravenous line and to secure it well. Percutaneous introduction of a cannula into a major vein is preferable to a venesection in a small peripheral vein.
(b) Intravenous Fluids:
Most cases are in negative fluid balance because of sweating vomiting restricted fluid intake and loss of fluid into interstitial space. Even those not in a negative balance seems to improve with I.V. fluids because of increased filling pressure which improves cardiac output. Glucose 5% is the most commonly used fluid and is usually readily available Dextran plasma or even blood may be given and these are preferable because they stay longer in the vascular 9ompartment.
Fluid is given in increments of 100 ml at a fairly rapid rate while effects of circulatory improvement are observed, e.g. rise of blood pressure, fall of heart rate skin becoming warm and resumption of urine output. Careful watch is kept on signs of overhydration, i.e. increase in respiratory rate, onset of cough and appearance of moist sounds in lungs Jugular venous pressure may be allowed to rise to 5-7 on above sternal angle. Monitoring of left atrial filling pressure (‘wedge’ pressure) is desirable but is usually not feasible in general practice.
(c) Inotropic Drugs:
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If the administration of fluid results in appearance of signs of overhydration without improvement of circulatory state, one should slow down the drip rate to a minimum and give drugs which will strengthen myocardial contractility. Dopamine in a dose of 2-5 microgram/ kg/min (200 mg in 500 ml of 5% glucose given @ 5-12 drops/min) given as an intravenous drip increases myocardial contractility and increases renal blood flow. Drip rate should be carefully adjusted by repeated blood pressure readings and a careful record of urine output which is best measured by putting in an in-dwelling catheter.
Isoproterenol was in use before dopamine became available. It causes increase of myocardial contractility and heart-rate and peripheral vasodilatation. It may cause cardiac arrhythmias and increased myocardial oxygen consumption. Increase of vascular bed capacity necessitates administration of more I.V. fluids.
Digoxin is a potent inotropic drug but its action is too slow in onset for use in this acute emergency. Cardiac arrhythmias may arise because the myocardium is ischaemic.
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(d) Vasodilator Drugs:
Vasodilator drugs like sodium nitroprusside, glyceryl trinitrate and hydralazine have been used in well-equipped hospitals with facilities for continuous monitoring of arterial central venous and pulmonary capillary, pressures. Their use in the setting outside a hospital does not appear practical.
(e) Vasoconstrictor Drugs:
Vasoconstrictor drugs like noradrenaline and mephentine have been going out of favour because they increase peripheral vascular resistance and thus the mechanical work of the heart. Tissue perfusion may actually go down, with resultant metabolic acidosis.
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These drugs tend to cause cardiac arrhythmias. They may however be needed if blood pressure falls below critical pressure levels. These drugs should be given as an intravenous drip, the drip-rate being titrated to maintain the systolic pressure at about 90 mm Hg. They should not be given as a bolus.
(f) Sedatives:
Sedatives like morphine should be given in minimal doses, just enough to relieve pain and restlessness. Morphine 2-5 mg I.V. may achieve this without causing respiratory depression. Drugs given intramuscularly are absorbed erratically in patients in shock.
(g) Oxygen:
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Oxygen should be administered to these patients as it may help to relieve pain and to reduce infarct size.
(h) Antiarrhythmic Drugs:
Ectopic beats do not produce effective forward flow and consume scarce oxygen. On the other hand, most antiarrhythmic drugs have a depressant action on the myocardium. Ectopic beats up to 5/min need not be treated. More frequent ectopic beats should be treated with xylocaine drip. This drug causes minimal myocardial depression. Marked bradycardia (below 50 beats/min) should be treated with atropine.
Prognosis of Cardiogenic Shock:
Mortality rate remains very high in cardiogenic shock in spite of all treatment. Tissue hypoxia for any length of time encourages irreversible circulatory failure. Energetic treatment should therefore be started as soon as signs of shock are recognizable. Those who survive the acute attack may succumb to acute renal tubular necrosis, shock lung or cerebral oedema. As the condition carries a high mortality rate, the patient should be admitted to a hospital as soon as feasible.
