By Vibhu Sharma, MD
Associate Professor of Medicine, University of Colorado, Denver
SYNOPSIS: In this experimental study, increasing tidal volume increased right ventricular afterload.
SOURCE: Slobod D, Assanangkornchai N, Alhazza M, et al. Right ventricular loading by lung inflation during controlled mechanical ventilation. Am J Respir Crit Care Med 2022;205:1311-1319.
The authors described 51 patients who were being passively ventilated after cardiac surgery in whom they assessed the effect of increasing tidal volume (Vt) on right ventricular (RV) parameters. The investigators are affiliated with McGill University, where a pulmonary artery (PA) catheter is placed routinely in patients undergoing cardiac surgery. Esophageal pressure (Peso), a surrogate of pleural pressure (Ppl) was measured using an esophageal balloon inserted in the immediate post-operative period. Vt was increased briefly from 2 mL/kg ideal body weight up to 12 mL/kg in 2 mL increments. Tidal volumes in this range were applied randomly. The study was terminated if there were any spontaneous breaths. Transesophageal echocardiography was performed in a subset of patients in which the same measurements were performed.
Outcome variables assessed at different Vt included end-inspiratory isovolumetric contraction pressure, calculated as the difference between the diastolic pulmonary artery pressure (PADP) and the right ventricular end diastolic pressure (RVEDP), pulmonary artery pulse pressure (PAP), which is a surrogate for RV stroke volume, and transmural RVEDP (RVEDP-Peso). Echocardiographic markers of RV stroke volume included the pulmonary artery velocity time integral (VTI), expiratory to inspiratory change in peak PA flow velocity, and changes in PA acceleration time. Predictor variables included Vt, plateau pressure (Pplat), transpulmonary pressure (Pplat-Peso), and end-expiratory PA occlusion pressure (PAOP) or wedge pressure.
With lung inflation and an applied positive pressure breath comes an increase in left atrial pressure (LAP), as blood is squeezed out of the capillary bed and into the left atrium. This pressure also is transmitted to the pleura and is reflected as an increase in Peso. Typically, the increase in LAP (measured via its surrogate PAOP) exceeds the increase in Peso by approximately 2 mmHg. This reflects transmission of alveolar pressure (Palv) to the left atrium (which also is transmitted to the pleura), and the increase in blood volume in the left atrium. With increasing pressure inflating the lung, pressure increases in the PAOP begin to represent more direct transmission of alveolar pressure to the balloon occluded PA segment rather than the LAP. This leads to a greater than 2 mmHg difference in PAOP and Peso and represents a change to West Lung non-Zone 3 conditions where Pa > Palv > Pv (West Lung Zone 2) or Palv > Pa > Pv (West Lung Zone 1). The authors found that increasing Vt reduced PA pulse pressure, increased RV isovolumetric contraction pressures (reflecting increased afterload), and reduced estimates of RV stroke volume (PA-VTI/PAAT). Interestingly, even at a tidal volume of 6 mL/kg, the presence of West Lung non-Zone 3 conditions was > 50%. Mean driving pressure at this Vt was approximately 11.5 cm H2O.
COMMENTARY
This elegant study puts into numerical perspective what is intuitively obvious: An increase in inflating pressures increases measures of RV afterload and induces a reduction in echocardiographic measures of RV stroke volume. In this study, > 50% of patients developed non-Zone 3 conditions with Vt of 6 mL/kg, a relatively “normal” tidal volume, and in the setting of relatively “normal” driving pressures (mean ~ 11.5 cm H2O) These changes were linearly associated with changes in transpulmonary pressures. Increases in RV afterload can affect RV systolic function adversely when it matters. Sepsis-induced cardiomyopathy and post-cardiac surgery RV dysfunction are two common scenarios where inflation pressures to deliver relatively “normal” Vt may result in a detrimental increase in RV afterload. This study recruited post-cardiac surgery patients with normal lungs, but implications extend to patients with acute respiratory distress syndrome (ARDS) wherein PAP may be elevated due to the disease process itself, with an added increase in afterload related to positive end-expiratory pressure (PEEP) needed to maintain ventilation/perfusion matching. While adding PEEP may allow for reductions in driving pressure, the opposite is expected in non-recruitable lung, and cor pulmonale may occur with driving pressures as low as 18 cm H2O.1 It is impractical to place an esophageal balloon in every patient with ARDS. Transthoracic echo is well-suited to acquire markers of RV stroke volume and in the right setting, assessing the response of the RV to changes in driving pressure (even when < 15 cm H2O) may provide useful, actionable information.
REFERENCE
1. Mekontso Dessap A, Boissier F, Charron C, et al. Acute cor pulmonale during protective ventilation for acute respiratory distress syndrome: Prevalence, predictors, and clinical impact. Intensive Care Med 2016;42:862-870.
In this experimental study, rising tidal volume increased right ventricular afterload.
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