Abstract
The cardiac status of hypertensive patients will influence not only the indications for and choice of antihypertensive agents but can also alter the effectiveness of antihypertensive therapy. The heart may interfere with adequate blood pressure control either because of marked increases in cardiac output or as result of decompensation activating various pressor mechanisms or through the generation of pressor reflexes. Reflex increases in cardiac output may blunt or even nullify the effect of reduction in peripheral resistance by vasodilators. Cardiac decompensation from incidental disease or secondary to some antihypertensive drugs can lead to hypertension rather than reduction in blood pressure. It is particularly liable to develop from excessive fluid retention, particularly when associated with reduction of cardioadrenergic support. Coronary insufficiency from either coexisting coronary disease or triggered by injudicious antihypertensive treatment can stimulate pressor reflexes leading to marked fluctuations in arterial pressure. Alterations in left ventricular relaxation and rapid filling have been reported with some antihypertensive drugs; these changes could conceivably influence blood pressure responses through their effect on reflexes from low pressure baroceptors.
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