Arterial hypertension is caused by a decreased compliance of the large arteries, an increased resistance of the systemic arterioles, or an increased cardiac output.

Isolated systolic hypertension occurs with normal arterial compliance and a large stroke volume, as occurs in marked bradycardia, severe aortic incompetence, a large patent ductus arteriosus or arteriovenous fistula, or peripheral vasodilatation from heat, anemia, or thyrotoxicosis. It also occurs beyond middle age, when the compliance of large arteries may decrease.

In both of these situations, ejection leads to excessively high systolic pressures, but diastolic pressures are normal or reduced, and the pulse pressure is wide.

For other forms of hypertension, increased diastolic and systolic pressures can be understood by realizing that blood pressure is the product of cardiac output and peripheral resistance. An increase in either of these will raise blood pressure as long as the other variable does not decrease. Thus, a high cardiac output in anemia does not cause hypertension because peripheral resistance falls, but it does raise blood pressure with anxiety, in which peripheral resistance is high.

Mechanisms of increased cardiac output and peripheral resistance are given in

Table 22-21.