Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation (V'(E)) that follows abrupt cessation of voluntary hyperventilation. 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 with essential hypertension, in whom the increase in CO as a result of various stimuli is less pronounced. Twenty male hypertensives (mean arterial blood pressure±SEM: 178/107±3/1 mmHg), and 12 age-matched male healthy subjects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). V'(E), CO, end- tidal CO2 and O2 tensions were measured, and the time constant (τ) of the V'(E) decay during recovery calculated. The V'(E) decay was faster in hypertensives (τ: 0-8.4 s) than in healthy subjects (τ: 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 healthy subjects (12.9±1.1 L·min-1; p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to τ (r=0.646; n=20; p=0.002). The less pronounced rise in cardiac output during hyperventilation in hypertensives could account for the shorter duration of posthyperventilation hyperpnoea.
- Cardiac output
- Cardiovascular-respiratory interactions
- Control of breathing
- Essential hypertension
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine