Longitudinal Validation of Right Ventricular Pressure Monitoring for the Assessment of Right Ventricular Systolic Dysfunction in a Large Animal Ischemic Model

Author:

Couture Etienne J.1,Moses Kevin2,Monge García Manuel Ignacio3,Potes Cristhian2,Haddad Francois4,Grønlykke Lars5,Garcia Fernando2,Paster Eden2,Pibarot Philippe6,Denault André Y.7

Affiliation:

1. Department of Anesthesiology & Division of Intensive Care Medicine, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec, QC, Canada.

2. Edwards Lifesciences, Irvine, CA.

3. Department of Intensive Care Medicine, Hospital Universitario SAS de Jerez, Jerez de la Frontera, Spain.

4. Department of Cardiovascular Medicine, Stanford University, Stanford, CA.

5. Department of Cardiothoracic Anaesthesiology, Copenhagen University Hospital, Copenhagen, Denmark.

6. Research Center, Institut Universitaire de Cardiologie et de Pneumologie de Québec, Québec, QC, Canada.

7. Department of Anesthesiology & Division of Intensive Care Medicine, Montreal Heart Institute, Université de Montréal, Montreal, QC, Canada.

Abstract

CONTEXT: 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Critical Care and Intensive Care Medicine

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