Figure 73

Cardiac output. An increase in cardiac output has been suggested as a mechanism for hypertension, particularly in its early borderline phase [3,4]. Sodium and water retention have been theorized to be the initiating events. Sequential changes following salt loading are depicted [3]. The resultant high cardiac output perfuses the peripheral tissues in excess of their metabolic requirements, resulting in a normal autoregulatory (vasoconstrictor) pressure. The early phase of high cardiac output and normal peripheral vascular resistance gradually changes to the characteristic feature of the sustained hypertensive state: normal cardiac output and high peripheral vascular resistance. Shown here are segmental changes in the important cardiovascular hemodynamic variables in the first few weeks following the onset of short-term salt-loading hypertension. Note especially that the arterial pressure increases ahead of the increase in total peripheral resistance. (From Guyton and coworkers [3]; with permission.)

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