Submitted on September 15, 2008
Revised on November 7, 2008
Accepted on November 16, 2008
Effects of Head and Body Cooling on Hemodynamics During Immersed Prone Exercise at 1 ATA
Tracy Elizabeth Wester1, Anne D. Cherry1, Neal W. Pollock2, John J. Freiberger1, Michael J. Natoli1, Eric A. Schinazi1, Pelzer O. Doar1, Albert E. Boso1, Eric L. Alford1, Aaron J. Walker1, Donna Uguccioni2, Dawn Kernagis3, and Richard Edward Moon1*
1 Duke University
2 Duke University/Divers Alert Network
3 Duke University Medical Center
* To whom correspondence should be addressed. E-mail: richard.moon{at}duke.edu.
Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters, and studied at 1 ATA during dry and immersed rest and exercise in thermoneutral (29-31°C) and cold (18-20°C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (p
0.004). Resting MPAP and PAWP values were 20±2.9/13±3.9 mmHg, mean±SD (cold body/cold head), 21±3.1/14±5.2 (cold/warm), 14±1.5/10±2.2 (warm/warm), 15±1.6/10±2.6 (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (p<0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE.
