Pulmonary Hypertension and RV Failure

Introduction: Pulmonary hypertension (PH) and the associated RV dysfunction is increasingly being encountered in the perioperative period. Managing these patients is challenging, but a thorough understanding of the pathophysiology of PH and the associated RV dysfunction allows the practioner to anticipate, prevent and successfully manage many of the perioperative risks. The normal systolic, diastolic, and mean pulmonary artery pressure (PAP) is 25 mmHg, 10 mmHg, and 15 mmHg, respectively; the normal range for pulmonary vascular resistance (PVR) is 0.9 to 1.4 Wood units (or 90 to 120 dynes · s · cm). The PVR is the quotient represented by PVR = (ΔP)/flow, where ΔP represents the mean PAP (mPAP) minus the left atrial pressure (LAP). This gradient commonly is referred to as the transpulmonary gradient (TPG). If the TPG is elevated, there is an increase in the PVR. On the contrary, if the TPG is not elevated, the increase in PAP is caused by an elevated LAP (implicating elevated LA pressure as a result of cardiac pathology). Flow is the blood flow through the pulmonary circulation i.e. cardiac output (CO). Thus, PVR = (mPAP LAP) ÷ CO, or mPAP = LAP + (CO X PVR). Therefore, only 3 physiological factors increase in mPAP: (1) increase in LAP (due to cardiac pathology), (2) an increase in CO (congenital heart disease [CHD] with left-to right shunt, fluid overload, and hyperdynamic states), and (3) an increase in PVR (pulmonary parenchymal/airway disease, hypoxia, interstitial lung disease, thromboembolic disease, and idiopathic pulmonary artery hypertension). Because of pulmonary vascular remodeling, even factors 1 and 2 eventually leads to an increased PVR, and the associated increased mPAP will reflect both an increased LA pressure as well as increased PVR. For example, a patient with mitral valve stenosis who has an increased mPAP solely because of an increased LAP (without increased PVR, i.e., “reversible” PH). These patients, mitral valve replacement is usually uncomplicated and has little risk of RV failure. In comparison, patients with mitral stenosis and increased mPAP because of increased LAP as well as increased PVR (secondary to pulmonary vascular remodeling, i.e., “fixed” PH), may have severe RV failure after mitral valve replacement and difficulty in weaning from CPB. Acute–on-chronic increases in PVR are common the perioperative period, and can lead to acute decompensation in RV function. These factors include, amongst others, hypoxia, hypercarbia, acidosis, hypothermia (shivering), increased sympathetic tone (pain, anxiety), and exogenous or endogenous pulmonary vasoconstrictors such as catecholamines, serotonin, thromboxane, and endothelin. Early recognition and reversal of these causes of acute deterioration could be lifesaving.