Cardiac responses to hypoxia were analyzed as a continuous function of Pa02 in 5 conscious, tracheostomized dogs chronically instrumented with aortic blood flow transducers, left atrial and arterial catheters, and solid state left ventricular (LV) pressure transducers. The dogs rebreathed air from a 40 L Douglas bag with a CO2 absorber. This resulted in a gradual decline in Pa02 from 72 mm Hg (±1.5SE) to 28 mm Hg (±1.0) over a period of 31 min (±2.5). Heart rate and LV dP/dt max were elevated significantly above control values at a Pa02 of 55 mm Hg (p<0.05). Aortic blood flow was increased significantly at a Pa02 level of 40 mm Hg (p<0.05), while mean aortic and LV systolic pressures were elevated significantly at a Pa02 level of 35 mm Hg (p<0.05). Systemic vascular resistance declined significantly at a Pa02 level of 32.5 mm Hg (p<0.05). Stroke volume and LV end-diastolic pressure did not change in significant fashion. The cardiac and systemic hemodynamic responses observed at the lowest Pa02 (28 mm Hg) were similar to those the authors have previously described in dogs breathing 7% FIO2 (Fed. Proc. 35(3), 1976). These results indicate that although improved ventricular contractile performance is detected at a Pa02 of 55 mm Hg, lower Pa02 levels (40 mm Hg) are required to elicit well-defined increases in cardiac output.
|Original language||English (US)|
|Pages (from-to)||No. 898|
|State||Published - Jan 1 1977|
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