Clinical utility of pulmonary artery catheter derived hemodynamic parameters: a prospective clinical study

Background. Induction of anesthesia and mechanical ventilation frequently lead to arterial hypotension whose nature can be elucidated through analysis of volumetric and pressure-derived hemodynamic parameters. These include measured or calculated, including indexed, indicators of the left and right cardiac chambers (left ventricular stroke work index, right ventricular stroke work index), peripheral (indexed total peripheral vascular resistance — iTPVR) and pulmonary (indexed pulmonary vascular resistance — iPVR) vascular resistance. Informative value of these indicators remains a subject of debate. Objective. To evaluate utility of pulmonary artery catheter derived hemodynamic parameters at induction of anesthesia and initiation of mechanical ventilation in patients with various heart failure phenotypes scheduled for CABG. Material and methods. We studied 100 patients with coronary artery disease at induction of anesthesia and initiation of mechanical ventilation immediately before myocardial revascularization. Group 1 (n=50) consisted of patients with preserved left ventricular ejection fraction (LVEF ≥50%); group 2 (n=50) — reduced LVEF (41–49%). Hemodynamic assessment included pressure-derived parameters (pulmonary artery catheter) and volumetric measurements (transesophageal echocardiography, TEE). Measurements were performed at four stages: (1) before induction of anesthesia (“baseline”); (2) after induction of anesthesia, prior to administration of muscle relaxants (“spontaneous breathing phase”); (3) 10 min after initiation of mechanical ventilation (“post-MV”); and (4) 3 min after Trendelenburg positioning (30° head-down tilt). Results. Anesthesia induction resulted in arterial hypotension in both groups without impairment of myocardial contractility. This indicated vasoplegia as predominant mechanism. Initiation of mechanical ventilation and subsequent Trendelenburg positioning increased central venous pressure (CVP) and pulmonary artery pressures (mean PAP) by 20% and 60%, respectively (p<0.05). According to TEE data, these changes were not attributable to preload augmentation, but rather reflected the influence of elevated intrathoracic pressure. Under MV, interpretation of pulmonary artery catheter derived parameters was hindered by unpredictable effects of increased intrathoracic pressure. This questioned clinical significance of calculated indices of cardiac performance and vascular resistance. Dynamics of iPVR and iTPVR depended on balance between myocardial performance and pressure gradients (mean PAP — pulmonary capillary wedge pressure and mean arterial pressure — CVP, respectively). This dynamics did not provide additional insights into ventricular preload or afterload. TEE is essential to understand hemodynamic profile of a particular patient. Conclusion. PAC derived hemodynamic parameters such as LVSWI, RVSWI, iPVR and iTPVR do not provide additional clinically meaningful information about hemodynamic profile of patients.