Effect of tidal volume, intrathoracic pressure, and cardiac contractility on variations in pulse pressure, stroke volume, and intrathoracic blood volume

Abstract

We evaluated the impact of increasing tidal volume (V (t)), decreased chest wall compliance, and left ventricular (LV) contractility during intermittent positive-pressure ventilation (IPPV) on the relation between pulse pressure (PP) and LV stroke volume (SV(LV)) variation (PPV and SVV, respectively), and intrathoracic blood volume (ITBV) changes. Sixteen pentobarbital-anesthetized thoracotomized mongrel dogs were studied both before and after propranolol-induced acute ventricular failure (AVF) (n=4), with and without chest and abdominal pneumatic binders to decrease chest wall compliance (n=6), and during V (t) of 5, 10, 15, and 25ml/kg (n=6). SV(LV) and right ventricular stroke volume (SV(RV)) were derived from electromagnetic flow probes around aortic and pulmonary artery roots. Arterial pressure was measured in the aorta using a fluid-filled catheter. Arterial PPV and SVV were calculated over three breaths as (max-min)/[(max+min)/2]. ITBV changes during ventilation were inferred from the beat-to-beat volume differences between SV(RV) and SV(LV). Arterial PP and SV(LV) were tightly correlated during IPPV under all conditions (r (2)=0.85). Both PPV and SVV increased progressively as V (t) increased and with thoraco-abdominal binding, and tended to decrease during AVF. SV(RV) phasically decreased during inspiration, whereas SV(LV) phasically decreased 2-3 beats later, such that ITBV decreased during inspiration and returned to apneic values during expiration. ITBV decrements increased with increasing V (t) or with thoraco-abdominal binding, and decreased during AVF owing to variations in SV(RV), such that both PPV and SVV tightly correlated with inspiration-associated changes in SV(RV) and ITBV. Arterial PP and SV(LV) are tightly correlated during IPPV and their relation is not altered by selective changes in LV contractility, intrathoracic pressure, or V (t). However, contractility, intrathoracic pressure, and V (t) directly alter the magnitude of PPV and SVV primarily by altering the inspiration-associated decreases in SV(RV) and ITBV.