OBJECTIVE: To examine whether the hemodynamic changes due to mechanical ventilation with positive end-expiratory pressure (PEEP) can be assessed by the respiratory-induced variations in the arterial pressure waveform during normovolemia and experimental acute ventricular failure. DESIGN: Prospective, controlled experimental study. SETTING: Institutional experimental laboratory. SUBJECTS: Adult mongrel dogs. INTERVENTIONS: Experimental acute ventricular failure was induced by the infusion of pentobarbital (a cardiodepressant) and methoxamine (a vasoconstrictor), combined with volume loading. Both the control and acute ventricular failure groups were subjected to ventilation with incremental levels of PEEP up to 20 cm H2O. MEASUREMENTS AND MAIN RESULTS: Cardiac function was evaluated by cardiac output and left and right ventricular change in pressure over time (dP/dt) measurements. Arterial pressure waveform analysis was performed by measuring the systolic pressure variation, which is the difference between the maximal and minimal systolic blood pressure values during one mechanical breath. The components of the systolic pressure variation, namely, dUp and dDown, which are the increase and decrease in the systolic pressure during the mechanical breath relative to the systolic pressure during apnea, were also measured at each PEEP level. PEEP caused significant reduction of cardiac output in normovolemic dogs, and was associated with significant increases in systolic pressure variation and dDown. Acute ventricular failure decreased the variations in the systolic pressure and caused the dDown component to disappear. The application of PEEP did not affect cardiac output in dogs with acute ventricular failure, nor did it change systolic pressure variation and the dDown. CONCLUSIONS: Analysis of arterial pressure waveforms during mechanical ventilation reflected the decrease in cardiac output in dogs with normal cardiac function subjected to incremental PEEP. In dogs with acute ventricular failure in which PEEP did not affect cardiac output, the systolic pressure variation was similarly unaffected by PEEP. In the absence of cardiac output measurement during mechanical ventilation with PEEP, the analysis of the respiratory variations in the arterial pressure waveform may be useful in assessing changes in cardiac output.
OBJECTIVE: To examine whether the hemodynamic changes due to mechanical ventilation with positive end-expiratory pressure (PEEP) can be assessed by the respiratory-induced variations in the arterial pressure waveform during normovolemia and experimental acute ventricular failure. DESIGN: Prospective, controlled experimental study. SETTING: Institutional experimental laboratory. SUBJECTS: Adult mongrel dogs. INTERVENTIONS: Experimental acute ventricular failure was induced by the infusion of pentobarbital (a cardiodepressant) and methoxamine (a vasoconstrictor), combined with volume loading. Both the control and acute ventricular failure groups were subjected to ventilation with incremental levels of PEEP up to 20 cm H2O. MEASUREMENTS AND MAIN RESULTS: Cardiac function was evaluated by cardiac output and left and right ventricular change in pressure over time (dP/dt) measurements. Arterial pressure waveform analysis was performed by measuring the systolic pressure variation, which is the difference between the maximal and minimal systolic blood pressure values during one mechanical breath. The components of the systolic pressure variation, namely, dUp and dDown, which are the increase and decrease in the systolic pressure during the mechanical breath relative to the systolic pressure during apnea, were also measured at each PEEP level. PEEP caused significant reduction of cardiac output in normovolemic dogs, and was associated with significant increases in systolic pressure variation and dDown. Acute ventricular failure decreased the variations in the systolic pressure and caused the dDown component to disappear. The application of PEEP did not affect cardiac output in dogs with acute ventricular failure, nor did it change systolic pressure variation and the dDown. CONCLUSIONS: Analysis of arterial pressure waveforms during mechanical ventilation reflected the decrease in cardiac output in dogs with normal cardiac function subjected to incremental PEEP. In dogs with acute ventricular failure in which PEEP did not affect cardiac output, the systolic pressure variation was similarly unaffected by PEEP. In the absence of cardiac output measurement during mechanical ventilation with PEEP, the analysis of the respiratory variations in the arterial pressure waveform may be useful in assessing changes in cardiac output.