Pulmonary Arterial Compliance and Pulmonary Vascular Resistance as a Predictor of Survival in Acute Respiratory Distress Syndrome: More Questions Than Answers

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We read with great enthusiasm the article published in a recent issue of Critical Care Medicine by Metkus et al (1), which showed an inverse relationship between pulmonary arterial compliance (CPA) and pulmonary vascular resistance (PVR). Furthermore, this article suggested CPA and PVR as predictors of survival in patients with acute respiratory distress syndrome (ARDS). The authors also observed that an increase in the pulmonary artery occlusion pressure (PAOP) lowers CPA independent of PVR. The rise in PAOP is not expected to increase the transpulmonary gradient, and therefore, mean pulmonary artery pressure must rise to overcome the increase in PAOP. In addition, PVR rarely changes in response to rise in PAOP (2). An increased mean pulmonary artery pressure would impose after load burden on the right ventricle irrespective of CPA. An elevated PAOP must have lowered the CPA either by a decrease in stroke volume or increase in pulmonary artery pulse pressure or disproportionate changes in both. Transpulmonary gradient is a flow-independent variable and PVR may decrease with increase in stroke volume or flow (3). Therefore, an explanation must be provided for the observed change in CPA with an increase in PAOP. The plots should have been drawn to establish the relationship between PAOP, transpulmonary gradient, and mean pulmonary artery pressure. Furthermore, a relationship between stroke volume, pulmonary artery pulse pressure, and the CPA should also have been established before arriving at definitive conclusions.
There are innumerable variables that can influence CPA and PVR in this subset of patients. In this study, survival had higher positive end-expiratory pressure (PEEP), stroke volume, PaO2, PaO2/FIO2 ratio, and CPA, whereas nonsurvival had higher vasopressor use, fluid balances, and PVR. There is an intricate relationship between PEEP, functional residual capacity (FRC), and PVR. The optimization of PEEP in the survival group could have achieved an optimal FRC to keep PVR at its lowest ebb. In addition, higher PaO2 in the survival group could have lowered the PVR. The PEEP-induced right ventricular after load is counteracted by improvement in systemic oxygenation. Furthermore, vasopressors could have also influenced PVR and CPA in the nonsurvival group. Noradrenaline and vasopressin behave in divergent ways. Vasopressin has shown to produce pulmonary vasodilation (4). The lower stroke volume in the nonsurvival group, due to intrinsic right ventricular dysfunction unrelated to high PVR, was possibly the main culprit behind lower CPA. The relationship between pulmonary artery pulse pressure, stroke volume, and PVR should be established at baseline and with increasing fluid balance to further strengthen the predictability of CPA for ARDS outcomes. Like PVR, CPA also appears to be flow dependent, and it improves with increasing stroke volume unrelated to changes in lung dynamics. Therefore, we need to find out the hemodynamic variables that can show consistent response with improvement in lung parenchymal function in patients with ARDS.
Drs. A. K. Jha and N. Jha helped in writing the article. The authors have disclosed that they do not have any potential conflicts of interest.

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