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Cardiac therapy by Michael R. Rosen, Brian F. Hoffman

By Michael R. Rosen, Brian F. Hoffman

Cardiac remedy has turn into ever extra advanced in past times area century. for instance, 25 years in the past, the treatment of cardiac failure used to be mostly restricted to digitalis, a really few diuretics, salt limit, and basic supportive measures. Antiarrhythmic treatment concerned - primarily - quinidine, procainamide, and digitalis, and questions corresponding to which arrhythmia to regard and the way to degree drug efficacy have been addressed in uncomplicated style purely. Cardiac surgical procedure was once restricted principally to congenital and valvular middle sickness; the parts of cardiac pacemaker remedy, defibrillation and other kinds of electric prognosis and treatment have been rudimentary. the growth of aid of cardiovascular examine through the nationwide Institutes of future health in addition to through institutional assets following global battle II has ended in significant successes in medical health and wellbeing care supply and better expertise made to be had to scientific investigators. In reviewing growth during the last 25 years, we now have been rather inspired by means of one remark: this can be the real interplay that has built among stories of pathophysiology and the supply of applicable cardiac therapy.

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In general the heart receives about 5% of the cardiac output, whereas the kidneys receive approximately 20-25% of the total cardiac output. Despite this difference, the heart consumes nearly twice as much oxygen as the kidneys. In general, coronary blood flow occurs primarily in diastole, since the wall tension developed by the 26 heart during systole tends to limit coronary flow during that period of the cardiac cycle, particularly to the left ventricle. There are powerful autoregulatory factors which control the arteriolar tone in coronary blood vessels [12].

Pressure overload of the left ventricle such as with severe aortic stenosis or end-stage hypertensive heart disease is a common cause of this phenomenon. Initially, the heart hypertrophies in an attempt to meet the increased pressure demands of an elevated aortic pressure. Gradually, however, irreversible changes occur in the myocardium which lead to a decrease in the intrinsic capacity of the heart muscle to develop pressure and shorten. These irreversible changes are accompanied by a decrease in ejection velocity and actomyosin ATPase activity.

In skeletal muscle, the half-time for this decline in tension is 20 min or more. During depolarization by the action potential, calcium both crosses the membrane and is released from internal storage sites to raise calcium to an appropriate level for contraction. Calcium attaches to troponin C on the actin filament which normally inhibits the active site of cross bridge formation. Calcium attachment to troponin reverses this repression and uncovers the active site, which then becomes available for attachment of the myosin cross bridge (Figure 2).

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