Pulmonary Vascular Resistance and Direct Ventricular Interaction during Mechanical Ventilation in an Oleic Acid Induced Acute Lung Injury Model: A Review
Jamie R. Mitchell*
Faculty of Medicine, Departments of Cardiac Sciences and Physiology & Pharmacology, The Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada
- *Corresponding Author:
- Jamie Mitchell, PhD
Departments of Cardiac Sciences and Physiology & Pharmacology
The Libin Cardiovascular Institute of Alberta
University of Calgary, GB37
Health Research Innovation Centre
3280 Hospital Dr NW, Calgary, AB, T2N 4Z6, Canada
E-mail: [email protected]
Received Date: September 09, 2011; Accepted Date: October 20, 2011; Published Date: October 24, 2011
Citation: Mitchell JR (2011) Pulmonary Vascular Resistance and Direct Ventricular Interaction during Mechanical Ventilation in an Oleic Acid Induced Acute Lung Injury Model: A Review. J Aller Ther S4:001. doi: 10.4172/2155-6121.S4-001
Copyright: © 2011 Mitchell JR. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Treatment of patients with Acute Lung Injury (ALI) can be challenging. Mechanical ventilation is often required and can have significant adverse cardiovascular effects. Clinicians and research scientists have been able to utilize an experimental model of ALI/Acute Respiratory Distress Syndrome (ARDS) that can mimic much of the clinical sequelae. This model has provided the opportunity to systematically test best care practices and clarify the important cardiopulmonary interaction during mechanical ventilation. During mechanical ventilation with positive end-expiratory pressure, increased pulmonary vascular resistance (PVR) may adversely affect right ventricular (RV) function, and therefore, left ventricular (LV) function. Thus, increased resistance to RV output can result in decreased LV preload by series interaction, but importantly, also by direct ventricular interaction (DVI) (leftward septal shift). Therefore, if the increase in PVR can be minimized, for example, by volume loading or nitric oxide, the adverse effects of mechanical ventilation on cardiac function may be limited. This paper will review the possible cardiac consequences of elevated PVR through DVI during mechanical ventilation in ALI, and suggest potential benefits of reducing PVR.