Hemodynamic effects of PEEP applied as a ramp in normo-, hyper-, and hypovolemia

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Abstract
Nonlinear hemodynamic responses on positive end-expiratory pressure (PEEP) have been attributed to a rise of mean central venous pressure (Pcv), to compensatory cardiovascular control mechanisms, and to the occurrence of a lung stretch depressor reflex above a threshold lung stretch. We tested the hypothesis that the contribution of each of these mechanisms is dependent on the preexisting volemic load. PEEP was applied as a continuous rise (ramp) in piglets in three different volemic loads. In the normovolemic circulation cardiac output (CO) decreased nonlinearly in three phases during the PEEP ramp up to 15 cmH2O. CO decreased gradually in phase I, followed by a sharp decrease in phase II between a PEEP of 3 and 9 cmH2O and again a more gradual decrease in phase III up to a PEEP of 15 cmH2O. Heart rate (HR) and mean aortic pressure (PaO) also decreased during phase II, indicating the predominance of a lung stretch depressor reflex. In the hypervolemic circulation (loading 15 ml . kg-1 dextran) only phases I and II were observed with the onset of phase II at a higher level of PEEP (6 cmH2O). More lung stretch appeared to be necessary to elicit the lung stretch depressor reflex. In the hypovolemic circulation (hemorrhage 15 ml . kg-1) CO decreased linearly, Pao was stable after an initial decrease, and HR increased continuously, indicating a predominance of cardiovascular compensatory mechanisms.