Key result
Acute ischemic RV dysfunction drops end-systolic elastance by ~46%, tracking with reduced RV dP/dt max.
Why the study?
Right ventricular dysfunction causes major morbidity and mortality in intensive care and cardiac surgery, but whether continuous right ventricular pressure monitoring can accurately detect changes in systolic performance remains to be evaluated.
Does RV pressure monitoring reliably detect changes in RV systolic performance assessed by Ees in a porcine model of acute RV ischemia?
Does RV pressure monitoring reliably detect changes in RV systolic performance assessed by Ees in a porcine model of acute RV ischemia?
Mean Difference: -0.08 (95% CI -0.22–-0.02)
Absolute Event Rate: 0.14% vs 0.26%
p-value: p=0.0102
Continuous monitoring of right ventricular dP/dt max provides a reliable, clinically accessible surrogate for RV end-systolic elastance during acute ischemic right ventricular dysfunction.
RV dP/dt max may surrogate Ees in acute porcine RV ischemia; hypothesis-generating, requires human validation before clinical use.
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 (E es ) 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 E es 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 E es obtained using a conductance catheter during inferior vena cava occlusions. RESULTS: Acute ischemia resulted in a significant reduction in RV E es 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 E es and RV pressure-derived parameters. The reduction in RV E es best correlated with a reduction in RV maximum first derivative of pressure during isovolumetric contraction (dP/dt max ) and single-beat RV E es . Adjusting RV dP/dt max for heart rate resulted in an improved surrogate of RV E es . INTERPRETATION AND CONCLUSIONS: Stepwise decreases in RV E es during acute ischemic RV dysfunction were accurately tracked by RV dP/dt max derived from the RV pressure waveform.
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Couture et al. (2023) studied Acute right ventricular ischemic dysfunction (n=10). Progressive microsphere embolization of the right coronary artery vs. Baseline (pre-ischemia) was evaluated on Right ventricular end-systolic elastance (Ees) (Mean difference -0.08, 95% CI -0.22 to -0.02, p=0.0102). In a porcine model of acute ischemic RV dysfunction, right ventricular end-systolic elastance (Ees) decreased significantly from 0.26 to 0.14 mm Hg/mL, which correlated with reductions in RV dP/dt max.
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