Effect of tidal volume, intrathoracic pressure, and cardiac contractility on variations in pulse pressure, stroke volume, and intrathoracic blood volume
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We evaluated the impact of increasing tidal volume (Vt), 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 (SVLV) 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 Vt of 5, 10, 15, and 25 ml/kg (n = 6). SVLV and right ventricular stroke volume (SVRV) 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 SVRV and SVLV.
Arterial PP and SVLV were tightly correlated during IPPV under all conditions (r2 = 0.85). Both PPV and SVV increased progressively as Vt increased and with thoraco-abdominal binding, and tended to decrease during AVF. SVRV phasically decreased during inspiration, whereas SVLV phasically decreased 2–3 beats later, such that ITBV decreased during inspiration and returned to apneic values during expiration. ITBV decrements increased with increasing Vt or with thoraco-abdominal binding, and decreased during AVF owing to variations in SVRV, such that both PPV and SVV tightly correlated with inspiration-associated changes in SVRV and ITBV.
Arterial PP and SVLV are tightly correlated during IPPV and their relation is not altered by selective changes in LV contractility, intrathoracic pressure, or Vt. However, contractility, intrathoracic pressure, and Vt directly alter the magnitude of PPV and SVV primarily by altering the inspiration-associated decreases in SVRV and ITBV.
KeywordsHemodynamic monitoring Fluid responsiveness Canine model Heart–lung interactions Mechanical ventilation
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