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Updated: Aug 12, 2025
Invasive Hemodynamic Monitoring of Aortic and Pulmonary Artery Hemodynamics in a Large Animal Model of ARDS
Published on: November 26, 2018
Longitudinal Validation of Right Ventricular Pressure Monitoring for the Assessment of Right Ventricular Systolic
Etienne J Couture1, Kevin Moses2, Manuel Ignacio Monge García3
1Department of Anesthesiology & Division of Intensive Care Medicine, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec, QC, Canada.
Abstract:
Right ventricular (RV) dysfunction is a major cause of morbidity and mortality in intensive care and cardiac surgery. Early detection of RV dysfunction may be facilitated by continuous monitoring of RV waveform obtained from a pulmonary artery catheter. The objective is to evaluate the extent to which RV pressure monitoring can detect changes in RV systolic performance assess by RV end-systolic elastance (Ees) following the development of an acute RV ischemic in a porcine model.
Hypothesis:
RV pressure monitoring can detect changes in RV systolic performance assess by RV Ees following the development of an acute RV ischemic model.
Methods And Models:
Acute ischemic RV dysfunction was induced by progressive embolization of microsphere in the right coronary artery to mimic RV dysfunction clinically experienced during cardiopulmonary bypass separation caused by air microemboli. RV hemodynamic performance was assessed using RV pressure waveform-derived parameters and RV Ees obtained using a conductance catheter during inferior vena cava occlusions.
Results:
Acute ischemia resulted in a significant reduction in RV Ees from 0.26 mm Hg/mL (interquartile range, 0.16-0.32 mm Hg/mL) to 0.14 mm Hg/mL (0.11-0.19 mm Hg/mL; p < 0.010), cardiac output from 6.3 L/min (5.7-7 L/min) to 4.5 (3.9-5.2 L/min; p = 0.007), mean systemic arterial pressure from 72 mm Hg (66-74 mm Hg) to 51 mm Hg (46-56 mm Hg; p < 0.001), and mixed venous oxygen saturation from 65% (57-72%) to 41% (35-45%; p < 0.001). Linear mixed-effect model analysis was used to assess the relationship between Ees and RV pressure-derived parameters. The reduction in RV Ees best correlated with a reduction in RV maximum first derivative of pressure during isovolumetric contraction (dP/dtmax) and single-beat RV Ees. Adjusting RV dP/dtmax for heart rate resulted in an improved surrogate of RV Ees.
Interpretation And Conclusions:
Stepwise decreases in RV Ees during acute ischemic RV dysfunction were accurately tracked by RV dP/dtmax derived from the RV pressure waveform.
