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* From the Intensive Care Unit (Dr. Nakos) and Department of Pulmonary Medicine (Dr. Costantopoulos), Ioannina University Hospital, Ioannina, Greece; and the Department of Intensive Care Unit (Dr. Lahana), Athens Veterans Hospital, Athens, Greece.
Correspondence to: George Nakos, MD, FCCP, Director, Intensive Care Unit, Ioannina University Hospital, 45500 Ioannina, Greece; e-mail: gnakos{at}cc.uoi.gr
Study objectives: To investigate the local cardiovascular response to hypoxemia and hypercapnia in a simulated central apnea model in which the central autonomic regulation was absent.
Design: Experimental study.
Setting: A university hospital.
Interventions: A simulated central apnea model achieved by a particular setting of the mechanical ventilator in 10 brain-dead patients.
Measurements: Hemodynamic studies using right-heart catheterization and continuous monitoring of arterial blood gas levels.
Results: Hypercapnic hypoxic apneas were associated with no change in heart rate, fall in mean systemic arterial pressure and systemic vascular resistance (from 83 ± 9 to 68 ± 7 mm Hg and 1,115 ± 82 to 768 ± 58 dyne·s·cm5, respectively; each p < 0.05), and rise in mean pulmonary artery pressure, pulmonary vascular resistance, and pulmonary capillary wedge pressure (PCWP) [from 17 ± 1.5 to 26 ± 3 mm Hg, 102 ± 27 to 166 ± 43 dyne·s·cm5, and 10 ± 1 to 14 ± 2 mm Hg, respectively; each p < 0.05].
Conclusion: Our results suggest that in the absence of central autonomic regulation in humans, apnea-induced hypoxemia and/or hypercapnia are associated with peripheral vasodilatation and pulmonary vasoconstriction, which are probably local in origin, as well as a significant increase in PCWP indicating cardiac dysfunction.
Key Words: acute cardiovascular response brain death central apnea hypercapnia hypoxemia
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