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Contrasting effects of isocapnic and hypocapnic hyperventilation on orthostatic circulatory control

¹Department of Neurology and Clinical Neurophysiology, Leiden University Medical Center, Leiden; ²Department of Pulmonary Medicine, Medical Centre Alkmaar, Alkmaar; and ³Medium Care Unit, Department of Internal Medicine, Academic Medical Centre, Amsterdam, The Netherlands

Submitted 2 January 2008 ; accepted in final form 8 July 2008

The effects of hyperventilation (HV) on mean arterial pressure (MAP) are variable. To identify factors affecting the MAP response to HV, we dissected the effects of hypocapnic HV (HHV) and isocapnic HV (IHV) and evaluated the effects of acute vs. prolonged HHV. In 11 healthy subjects the cardio- and cerebrovascular effects of HHV and IHV vs. normal ventilation were examined for 15 min in the supine position and also for 15 min during 60° head-up tilt. The end-tidal CO₂ of the HHV condition was set at 15–20 mmHg. With HHV in the supine position, mean cerebral blood flow velocity (mCBFV) declined [95% confidence interval (CI) –43 to –34%], heart rate (HR) increased (95% CI 7 to 16 beats/min), but MAP did not change (95% CI –1 to 6 mmHg). However, an augmentation of the supine MAP was observed in the last 10 min of HHV compared with the first 5 min of HHV (95% CI 2 to 12 mmHg). During HHV in the tilted position mCBFV declined (95% CI –28 to –12%) and MAP increased (95% CI 3 to 11 mmHg) without changes in HR. With supine IHV, mCBFV decreased (95% CI –14 to –4%) and MAP increased (95% CI 1 to 13 mmHg) without changes in HR. During IHV in the tilted position MAP was further augmented (95% CI 11 to 20 mmHg) without changes in CBFV or HR. Preventing hypocapnia during HV resulted in a higher MAP, suggesting two contrasting effects of HV on MAP: hypocapnia causing vasodepression and hyperpnea without hypocapnia acting as a vasopressor.

blood pressure; cerebral perfusion