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

Abstract

Purpose: 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.

Methods: 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 25 ml/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).

Results: 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.

Conclusion: 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.

Fig. 1

Paired pulse pressure (PP) and left ventricular stroke volume (SV) on a beat-to-beat basis during control 10 ml/kg tidal volume IPPV for one animal

Fig. 2

Pulse pressure variation (PPV) (gray bars) and left ventricular stroke volume variation (black bars) for different tidal volumes. Data presented as mean ± SD (n = 4)

Fig. 3

A strip chart recording of one animal during positive-pressure ventilation (10 ml/kg) under control, control-binder, and acute ventricular failure conditions. See text for discussion. SV_RV right ventricular stroke volume, SV_LV left ventricular stroke volume, P_a arterial pressure, P_latm left atrial transmural pressure, P_patm pulmonary artery transmural pressure, P_ratm right atrial transmural pressure, P_aw airway pressure, P_pl pleural pressure. Transmural pressure is vascular pressure relative to P_pl. Note that pressure scaling for P_ratm, P_aw, and P_pl vary across conditions

Fig. 4

Effect of different tidal volumes (V_t) on the dynamic changes in intrathoracic blood volume estimated as the differences in paired right ventricular stroke volume (SV_RV) to left ventricular stroke volume (SV_LV) for a single breath for one animal