Pulmonary hypertension attenuates the dynamic preload indicators increase during experimental hypovolemia

Juan P Bouchacourt,Juan C Grignola,Juan Riva

doi:10.1186/s12871-017-0329-z

Juan P Bouchacourt, Juan C Grignola + Show 1 more

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https://doi.org/10.1186/s12871-017-0329-z

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Abstract

BackgroundPulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure. We hypothesized that RV afterload increase attenuates SVV and PPV during hypovolemia in a rabbit model of pulmonary embolism (PE) secondary to RV dysfunction.MethodsSeven anesthetized and mechanically ventilated rabbits were studied during four experimental conditions: normovolemia, blood withdrawal, pulmonary embolism and fluid loading of a colloidal solution. Central venous, RV and left ventricular (LV) pressures, and infra-diaphragmatic aortic blood flow (AoF) and pressure were measured. SV was estimated by the integral of systolic AoF. We analyzed RV and LV function through stroke work output curves. PPV and SVV were obtained by the variation of beat-to-beat PP and SV, respectively. We assessed RV and LV diastolic and systolic function by the time rate of relaxation (tau) and the ratio of the first derivative of ventricular pressure and the highest isovolumic developed pressure (dP/dt/DP), respectively. The vasomotor tone was estimated by the dynamic arterial elastance (Eadyn = PPV/SVV).ResultsPPV and SVV increased significantly during hemorrhage and returned to baseline values after PE which was associated to biventricular right-downward of the stroke work curves and a decrease of AoF and SV (P < 0.05). RV systo-diastolic function and LV systolic function were impaired. All the animals were nonresponders after volume expansion. Eadyn did not show any significant change during the different experimental conditions.ConclusionsThe dynamic preload indicators (SVV and PPV) were significantly reduced after a normotensive PE in hypovolemic animals, mainly by the systo-diastolic dysfunction of the RV associated with LV systolic impairment, which makes the animals nonresponsive to volume loading. This normalization of dynamic preload indices may prevent the detrimental consequence of fluid loading.

Highlights

Pulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure
pulmonary embolism (PE) determined a significant decrease in end-tidal pressure of CO2 (35 ± 3 vs. 27 ± 2 mm Hg) which denotes an increase of alveolar dead space
The increase of RV afterload during PE determined that Stroke volume variation (SVV) and pulse pressure variation (PPV) significantly decreased with respect on Blood withdrawal (BW), returning to baseline values in spite of the animals were hypovolemic (Fig. 2)

Summary

Introduction

Pulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure. Respiratory variation of stroke volume (SVV) or its surrogates, such as pulse pressure variation (PPV) have been demonstrated to predict preload responsiveness accurately in mechanically ventilated patients [4]. In the presence of RV failure, PPV and SVV are falsely elevated secondary to a RV stroke volume reduction during the inspiratory increase in RV afterload. In such cases, a high PPV or SVV could be a sign of RV afterload dependence rather than of fluid responsiveness. The effect of RV dysfunction on the dynamic preload indicators could be difficult to interpret depending on the study conditions (degree and type of PH, cause of the RV dysfunction), the study protocol (normo or hypovolemia before RV failure induction) and the definition of RV failure (RV ejection fraction, peak systolic velocity of tricuspid annular motion, systolic and/or diastolic dysfunction) [12, 14, 15]

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