Heart-lung interactions in acute respiratory distress syndrome: pathophysiology, detection and management strategies

Abstract

Acute respiratory distress syndrome (ARDS) is the most severe form of acute respiratory failure characterized by diffuse alveolar and endothelial damage. The severe pathophysiological changes in lung parenchyma and pulmonary circulation together with the effects of positive pressure ventilation profoundly affect heart lung interactions in ARDS. The term pulmonary vascular dysfunction (PVD) refers to the specific involvement of the vascular compartment in ARDS and is expressed clinically by an increase in pulmonary arterial (PA) pressure and pulmonary vascular resistance both affecting right ventricular (RV) afterload. When severe, PVD can lead to RV failure which is associated to an increased mortality. The effect of PVD on RV function is not only a consequence of increased pulmonary vascular resistance as afterload is a much more complex phenomenon that includes all factors that oppose efficient ventricular ejection. Impaired pulmonary vascular mechanics including increased arterial elastance and augmented wave-reflection phenomena are commonly seen in ARDS and can additionally affect RV afterload. The use of selective pulmonary vasodilators and lung protective mechanical ventilation strategies are therapeutic interventions that can ameliorate PVD. Prone positioning and the open lung approach (OLA) are especially attractive strategies to improve PVD due to their effects on increasing functional lung volume. In this review we will describe some pathophysiological aspects of heart-lung interactions during the ventilatory support of ARDS, its clinical assessment and discuss therapeutic interventions to prevent the occurrence and progression of PVD and RV failure.

Keywords: Acute respiratory distress syndrome (ARDS); lung protective ventilation; open lung approach (OLA); positive end-expiratory pressure (PEEP); prone positioning; pulmonary vascular dysfunction (PVD); pulmonary vascular mechanics; pulmonary vascular resistance (PVR).

Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1

Pulmonary vascular dysfunction in ARDS. PAH, pulmonary artery hypertension; RV, right ventricular; MOD, multi-organ dysfunction; ARDS, acute respiratory distress syndrome.

Figure 2

Correlates of functional lung volume and pulmonary vascular mechanics. A sequence of 3 different levels of PEEP performed during a decremental PEEP trial in an experimental porcine model of ARDS is presented. The sequence corresponds to the same animal in different moments of the protocol. For each PEEP level the corresponding CT image and the pulmonary arterial (PA) waveform are displayed. This example illustrates how the size of the functional (aerated) lung has a profound impact on pulmonary vascular mechanics: on the absolute pressure values (SPAP, systolic PA pressure), the pulmonary arterial pulse pressure (PAP), the effect of wave-reflection presented as the site of the incidence of the reflected wave seen as a distinctive notching in the systolic portion (Pi) and the augmented pressure due to the effect of the backward reflected pressure wave represented as ΔP. This augmented pressure is an additional load component that the RV must overcome during ejection due to wave reflection phenomena. Note that despite the lower levels of PEEP, RV afterload is greatly increased as shown by the higher PA values, higher PA pulse pressure and higher augmented pressure. PEEP, positive end-expiratory pressure; ARDS, acute respiratory distress syndrome; RV, right ventricular.

Figure 3

Example of changes in airway, transpulmonary and pulmonary arterial pressure in response to lung recruitment. This example presents the simultaneous recording of airway, transpulmonary and pulmonary arterial pressures in a patient during cardiac surgery in which two consecutive maneuvers were performed. Clear systolic and pulse PA pressure changes occur after each maneuver. The circles highlight the condition reached after recruitment when final protective ventilator settings were adjusted with a PEEP level of 10 and a reduced driving pressure which corresponds to a reduced transpulmonary driving pressure and pulmonary artery pulse pressure. Also note that expiratory transpulmonary pressure remains positive after the first recruitment suggesting an open lung condition. In the lower panel selected individual PA waveforms from different moments of the sequence are presented. Note the different morphology and amplitude. PEEP, positive end-expiratory pressure; PA, pulmonary arterial.