The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension

Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation ((VE)-E-1) that follows abrupt cessation of voluntary hyperven tilation, It has been hypothesized that the increase in cardiac output (CO) during hyperventilation could contribute to the duration of PHVH. This hypothesis was tested by measuring the duration of PHVH in patients wi th essential hypertension, in whom the increase in CO as a result of variou s stimuli is less pronounced. Twenty male hypertensives (mean arterial bloo d pressurer+/-SEM: 178/107+/-3/1 mmNg), and 12 age-matched male healthy sub jects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). (VE)-E-1, CO, end -tidal CO2 and O-2 tensions were measured, and the time constant (tau) of t he (VE)-E-1 decay during recovery calculated. The (VE)-E-1 decay was faster in hypertensives (tau: 0-8.4 s) than in healt h!, subjects (tau: 12-59 s; p<0.01), During voluntary hyperventilation, CO increased to a lesser extent in hypertensives (6.8+0.7 L.min(-1)) than in h ealthy subjects (129+/-1.1 L.min(-1); p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to tau(r=0 .646; n=20; p=0.002). The less pronounced rise in cardiac output during hyp erventilation in hypertensives could account for the shorter duration of po sthyperventilation hyperpnoea.