Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a systematic literature review

Abstract

Introduction: Pulmonary vascular dysfunction, pulmonary hypertension (PH), and resulting right ventricular (RV) failure occur in many critical illnesses and may be associated with a worse prognosis. PH and RV failure may be difficult to manage: principles include maintenance of appropriate RV preload, augmentation of RV function, and reduction of RV afterload by lowering pulmonary vascular resistance (PVR). We therefore provide a detailed update on the management of PH and RV failure in adult critical care.

Methods: A systematic review was performed, based on a search of the literature from 1980 to 2010, by using prespecified search terms. Relevant studies were subjected to analysis based on the GRADE method.

Results: Clinical studies of intensive care management of pulmonary vascular dysfunction were identified, describing volume therapy, vasopressors, sympathetic inotropes, inodilators, levosimendan, pulmonary vasodilators, and mechanical devices. The following GRADE recommendations (evidence level) are made in patients with pulmonary vascular dysfunction: 1) A weak recommendation (very-low-quality evidence) is made that close monitoring of the RV is advised as volume loading may worsen RV performance; 2) A weak recommendation (low-quality evidence) is made that low-dose norepinephrine is an effective pressor in these patients; and that 3) low-dose vasopressin may be useful to manage patients with resistant vasodilatory shock. 4) A weak recommendation (low-moderate quality evidence) is made that low-dose dobutamine improves RV function in pulmonary vascular dysfunction. 5) A strong recommendation (moderate-quality evidence) is made that phosphodiesterase type III inhibitors reduce PVR and improve RV function, although hypotension is frequent. 6) A weak recommendation (low-quality evidence) is made that levosimendan may be useful for short-term improvements in RV performance. 7) A strong recommendation (moderate-quality evidence) is made that pulmonary vasodilators reduce PVR and improve RV function, notably in pulmonary vascular dysfunction after cardiac surgery, and that the side-effect profile is reduced by using inhaled rather than systemic agents. 8) A weak recommendation (very-low-quality evidence) is made that mechanical therapies may be useful rescue therapies in some settings of pulmonary vascular dysfunction awaiting definitive therapy.

Conclusions: This systematic review highlights that although some recommendations can be made to guide the critical care management of pulmonary vascular and right ventricular dysfunction, within the limitations of this review and the GRADE methodology, the quality of the evidence base is generally low, and further high-quality research is needed.

Figure 1

Short-axis view of a transthoracic echocardiogram in a normal subject (a) and a patient with an acutely dilated right ventricle (RV) in the setting of high pulmonary vascular resistance (b). The intraventricular septum (IVS) is D-shaped in (b), reflecting the acute RV pressure overload in this patient, and marked enlargement of the RV in (b) compared with (a). Courtesy of Dr Susanna Price, Royal Brompton Hospital, London, UK.

Figure 2

Pathophysiology of right ventricular failure in the setting of high PVR. CO, cardiac output; LV, left ventricle; MAP, mean arterial pressure; PVR, pulmonary vascular resistance; RV, right ventricle.

Figure 3

Calculation of pulmonary vascular resistance. Normal range, 155-255 dynes/sec/cm⁵. CO, cardiac output; mPAP, mean pulmonary artery pressure; PAOP, pulmonary arterial occlusion pressure.

Figure 4

Increased PVR at extremes of lung volumes. This figure represents measurements made in an animal-lobe preparation in which the transmural pressure of the capillaries is held constant. It illustrates that at low lung volumes (as may occur with atelectasis), extraalveolar vessels become narrow, and smooth muscle and elastic fibers in these collapsed vessels increase PVR. At high lung volumes, as alveolar volumes are increased and walls are thinned, capillaries are stretched, reducing their caliber and also increasing PVR. (Adapted from John West's Essential Physiology, 10^th edition, Philadelphia: Lippincott & Williams, with permission).