Research

The effect of open lung ventilation on right ventricular and left ventricular function in lung-lavaged pigs

Dinis Reis Miranda¹ , Lennart Klompe² , Filippo Cademartiri³ , Jack J Haitsma¹ , Alessandro Palumbo³ , Johanna JM Takkenberg² , Burkhard Lachmann¹ , Ad JJC Bogers² and Diederik Gommers¹

¹Department of Anesthesiology, Erasmus MC, Rotterdam, The Netherlands

²Department of Cardio-Thoracic Surgery, Erasmus MC, Rotterdam, The Netherlands

³Department of Radiology, Erasmus MC, Rotterdam, The Netherlands

author email corresponding author email

Critical Care 2006, 10:R86doi:10.1186/cc4944

Published:	8 June 2006

Abstract

Introduction

Ventilation according to the open lung concept (OLC) consists of recruitment maneuvers, followed by low tidal volume and high positive end-expiratory pressure, aiming at minimizing atelectasis. The minimization of atelectasis reduces the right ventricular (RV) afterload, but the increased intrathoracic pressures used by OLC ventilation could increase the RV afterload. We hypothesize that when atelectasis is minimized by OLC ventilation, cardiac function is not affected despite the higher mean airway pressure.

Methods

After repeated lung lavage, each pig (n = 10) was conventionally ventilated and was ventilated according to OLC in a randomized cross-over setting. Conventional mechanical ventilation (CMV) consisted of volume-controlled ventilation with 5 cmH₂O positive end-expiratory pressure and a tidal volume of 8–10 ml/kg. No recruitment maneuvers were performed. During OLC ventilation, recruitment maneuvers were applied until PaO₂/FiO₂ > 60 kPa. The peak inspiratory pressure was set to obtain a tidal volume of 6–8 ml/kg. The cardiac output (CO), the RV preload, the contractility and the afterload were measured with a volumetric pulmonary artery catheter. A high-resolution computed tomography scan measured the whole lung density and left ventricular (LV) volumes.

Results

The RV end-systolic pressure–volume relationship, representing RV afterload, during steady-state OLC ventilation (2.7 ± 1.2 mmHg/ml) was not significantly different compared with CMV (3.6 ± 2.5 mmHg/ml). Pulmonary vascular resistance (OLC, 137 ± 49 dynes/s/cm⁵ versus CMV, 130 ± 34 dynes/s/cm⁵) was comparable between groups. OLC led to a significantly lower amount of atelectasis (13 ± 2% of the lung area) compared with CMV (52 ± 3% of the lung area). Atelectasis was not correlated with pulmonary vascular resistance or end-systolic pressure–volume relationship.

The LV contractility and afterload during OLC was not significantly different compared with CMV. Compared with baseline, the LV end-diastolic volume (66 ± 4 ml) decreased significantly during OLC (56 ± 5 ml) ventilation and not during CMV (61 ± 3 ml). Also, CO was significantly lower during OLC ventilation (OLC, 4.1 ± 0.3 l/minute versus CMV, 4.9 ± 0.3 l/minute).

Conclusion

In this experimental study, OLC resulted in significantly improved lung aeration. Despite the use of elevated airway pressures, no evidence was found for a negative effect of OLC on RV afterload or LV afterload, which might be associated with a loss of hypoxic pulmonary vasoconstriction due to alveolar recruitment. The reductions in the CO and in the mean pulmonary artery pressure were consequences of a reduced preload.