ABSTRACT
INTRODUCTION An early cross-sectional study of mild hypertension reported that the predominant hemodynamic feature was a high cardiac output [1], and this observation has been confirmed consistently since. Although not invariably so, the high cardiac output is accompanied by an increased heart rate, and several studies have demonstrated that when oxygen consumption is measured, both cardiac output and this parameter are raised [2]. In the mild early stages of essential hypertension, the peripheral resistance is low, although the crucial point is that it remains appropriately high for the corresponding cardiac output. A 20-year longitudinal study of the hemodynamics of essential hypertension confirmed the finding of initially increased cardiac index, heart rate, oxygen consumption, and blood pressure with normal peripheral resistance [3]. However, over this period, the high cardiac index and normal total peripheral resistance (TPR) pattern changes to a low cardiac index and high resistance pattern. Again, the inappropriately high level of vascular resistance for the increase in cardiac output is a hallmark of early hypertension. Such a hemodynamic profile could be ascribed to a high sympathetic nervous tone with the resulting increased drive to the heart, peripheral circulation, and metabolic receptors, which would then promote enhanced oxygen consumption. Other studies demonstrated that autonomic blockade of the heart in mild hypertensive patients restored cardiac output to normal, and there was a combination of increased sympathetic tone and decreased parasympathetic activity in such individuals [4,5]. This combination of increased sympathetic discharge coupled with a reduced parasympathetic activity suggests that the abnormality in essential hypertension is one of integrated function in the medulla oblongata.
