Influence of tidal volume on pulse pressure variation and stroke volume variation during experimental intra-abdominal hypertension

Díaz et al. BMC Anesthesiology (2015) 15:127 DOI 10.1186/s12871-015-0105-x RESEARCH ARTICLE Open Access Influence of tidal volume on pulse pressure variation and stroke volume variation during experimental intra-abdominal hypertension F. Díaz1,2, B. Erranz3, A. Donoso4, T. Salomon2 and Pablo Cruces5,6* Abstract Background: Pulse pressure variation (PPV) and stroke volume variation (SVV) are frequently used to assess fluid responsiveness in critically ill patients on mechanical ventilation (MV). There are many factors, in addition to preload that influence the magnitude of these cyclic variations. We sought to investigate the effect of tidal volume (VT) on PPV and SVV, and prediction of fluid responsiveness in a model of intra-abdominal hypertension (IAH). Methods: Twelve anesthetized and mechanically ventilated piglets on continuous pulse contour cardiac output monitoring. Hypovolemia was ruled out with 2 consecutive fluid boluses after instrumentation. IAH was induced by intraperitoneal instillation of colloid solution with a goal of reducing respiratory system compliance by 50 %. Subjects were classified as fluid responders if stroke volume increased >15 % after each fluid challenge. SVV and PPV were recorded with tidal volumes (VT) of 6, 12 and 18 ml/kg before IAH after IAH induction and after a fluid challenge during IAH. Results: VT influenced PPV and SVV at baseline and during IAH, being significantly larger with higher VT. These differences were attenuated after fluid administration in both conditions. After IAH induction, there was a significant increase in SVV with the three-tested VT, but the magnitude of that change was larger with high VT: with 6 ml/kg from 3 % (3, 4) to 5 % (4, 6.25) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 11 % (8.75, 17) (p = 0.02) and 18 ml/kg from 5 % (4,7.5) to 15 % (8.75, 19.5) (p = 0.02). Similarly, PPV increased with all the tested VT after IAH induction, being this increase larger with high VT: with 6 ml/kg from 3 % (2, 4.25) to 6 % (4.75, 7) (p = 0.05), with 12 ml/kg from 5 % (4, 6) to 13.5 % (10.25, 15.5) (p = 0.02) and 18 ml/kg from 7 % (5.5, 8.5) to 24 % (13.5, 30.25) (p = 0.02). One third of subjects responded to fluid administration after IAH, but neither SVV nor PPV were able to identify the fluid responders with the tested VT. Conclusion: IAH induction in non-hypovolemic subjects significantly increased SVV and PPV with the three tested VT, but the magnitude of that change was higher with larger VT. This observation reveals the dependence of functional hemodynamic markers on intrathoracic as well intra-abdominal pressures, in addition to volemic status. Also, PPV and SVV were unable to predict fluid responsiveness after IAH induction. Future studies should take into consideration these findings when exploring relationships between dynamic preload indicators and fluid responsiveness during IAH. Background Functional hemodynamic monitoring has been demonstrated to be a powerful tool in critically ill patients. Careful selection of patients that will respond to fluid administration may help avoid fluid overload. Functional hemodynamic monitoring including stroke * Correspondence: 5 Centro de Investigación de Medicina Veterinaria, Escuela de Medicina Veterinaria, Facultad de Ecología y Recursos Naturales, Universidad Andres Bello, Santiago, Chile 6 Pediatric ICU, Hospital El Carmen de Maipú, Camino a Rinconada 1201, Maipú, Santiago, Chile Full list of author information is available at the end of the article volume variation (SVV) and pulse pressure variation (PPV), have been shown to be more accurate in predicting fluid responsiveness than classically used static parameters (central venous pressure (CVP) and pulmonary artery occlusion pressure) in mechanically ventilated patients without spontaneous breathing [1–3]. These dynamic indexes are based on cyclic transmission of airway pressure to the pleural and pericardial spaces, which induces changes in venous return and preload. Due to the complex relationship between intrathoracic structures (heart-lung interactions) numerous studies have demonstrated that functional hemodynamic © 2015 Díaz et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Díaz et al. BMC Anesthesiology (2015) 15:127 monitoring parameters do not only depend on preload and ventricular interdependence. Mechanical ventilation (MV) settings like tidal volume (VT), PEEP, driving pressure and respiratory rate (RR) as well as lung compliance are potential factors that may decrease the ability of functional hemodynamic monitoring parameters to predict fluid responsiveness [4–6]. Abdominal Compartment Syndrome (ACS) represents the final stage of a pathologic process caused by an increase in intra-abdominal pressure (IAP) to a degree that can compromise regional blood flow. It has significant morbidity, related to the ongoing inflammation due to ischemia and organ dysfunction, ultimately causing death [7, 8]. Judicious fluid administration plays a key role in the management of ACS. Early fluid therapy is fundamental during the initial resuscitation phase, but its liberal use is a known risk factor for ACS and excessive fluid administration may worsen IAP [7–12]. Therefore functional hemodynamic monitoring has been proposed to guide fluid therapy in patients at risk of ACS and during increased IAP [10, 13, 14]. Cyclic changes in SV and PP induced by positive pressure ventilation can be affected by extra thoracic modifications in compliance, such as ACS or contained laparotomy [15, 16]. Current literature has yielded conflicting data regarding the ability of PPV and SVV to predict fluid responsiveness in subjects with increased IAP [17–22]. This shows the complexity of the relationship between IAP and intrathoracic pressure; as well as the effect of pressure transmitted to intrathoracic vascular structures during MV [5, 7, 8, 23]. In addition protective ventilatory strategies [24, 25], specifically small VT, have been shown to modify functional hemodynamic monitoring parameters when lung compliance is reduced, like ARDS, due to low transmission of pressure from airway to pleura [4–6, 26, 27]. However the effect of different V T on functional hemodynamic monitoring in conditions of reduced respiratory system compliance due to extrapulmonary causes has not been studied. We sought to investigate the effect of different VT on PPV and SVV in a model of intra-abdominal hyperten (...truncated)