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In cardiac failure, cardiac output is reduced. This means initially that with exercise the organs and tissues do not have an adequate blood supply. As the condition progresses the supply may not be sufficient even at rest. Cardiac failure can result if the myocardium is damaged by ischaemia, if the heart is inefficient due to valve disease or because of excessive peripheral vascular resistance and hypertension.

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The pulmonary and aortic valves close while the atria contract; the tricuspid and bicuspid valves close while the ventricles contract. This prevents backflow of blood. The contraction phase is known as systole and the relaxation phase of the heart is known as diastole. Cardiac output is the volume of blood pumped out of the left ventricle every minute and is a function of the stroke volume and heart rate. Stroke volume is the amount of blood ejected by the left ventricle during one contraction and the heart rate is the number of beats per minute.

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Both thiazides and loop diuretics also produce vasodilation, which reduces peripheral vascular resistance and helps reduce blood pressure. Thiazide diuretics are recommended as an alternative to calcium channel blockers as first choice drugs in hypertensive patients over the age of Adverse effects of diuretics are excessive potassium and hydrogen ion loss leading to hypokalaemia and metabolic alkalosis. Hypokalaemia enhances the toxic effects of cardiac glycosides. Normally potassium ions compete with cardiac glycosides for their site of action, which is the NaK ATPase pump in the cardiac muscle cell membrane. If potassium ion concentration is reduced, the inhibitory effects of digoxin are increased.

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Authored by Dr. Amit M. Patel, MD, DABA, DABAPM

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