Lung Resection and Pulmonary Hypertension

Introduction

Pulmonary hypertension (PH) has become an increasingly common diagnosis among patients presenting for surgery. With advances pertaining to the diagnosis and treatment of PH, these patients are now living longer with an improved quality of life. Although surgery still poses a significant risk, patients with PH can safely undergo noncardiac surgery. Patients with precapillary PH undergoing noncardiac surgery have a mortality rate ranging from 1% to 9.7% and a high perioperative morbidity rate range from 24% to 42% despite improvements in the quality of treatment and optimization. Common complications include respiratory failure (7%–28%), congestive heart failure and/or volume overload (10%–13.5%), arrhythmia (12%), hemodynamic instability (8%), acute kidney injury (7%–10%), and myocardial ischemia (4%). ^{, ,} Emergency procedures, particularly those with the potential for rapid blood loss, thoracic surgery, and laparoscopic surgery are all associated with highest risk. Changes in intrathoracic pressure, oxygenation, airway pressure, and the need for one-lung ventilation (OLV), all can acutely increase pulmonary vascular resistance (PVR) and suppress right ventricular (RV) function, which poses an increased risk to patients with PH patients undergoing thoracic surgery. However, with diligent preoperative optimization and careful intraoperative management, lung resections on patients with PH have been performed with no increase in morbidity or mortality. Successful intraoperative management of thoracic surgical patients with PH requires a thorough understanding of the disease process, assessment of the severity of the disease and comorbidities. Proper optimization, understanding the nature of the procedure being performed and a team approach to unified anesthetic plan considering the increased risk of cardiac and pulmonary complications is essential.

Definition

PH is defined as a persistent elevation of mean pulmonary artery pressure (MPAP) 25 mm Hg or more at rest measured by right heart catheterization. This definition was established at the World Symposium on PH organized by the World Health Organization. During the sixth World Symposium on PH in 2018, experts reconsidered MPAP of 20 mm Hg as the new cut off. PH is divided into five different groups ( Table 36.1 ) and can further be divided into three different categories based on the hemodynamic implications of the disease process ( Table 36.2 ). Anesthesiologists need to be aware of these classifications as they impact the available treatment and management strategies.

Classification/Pathophysiology

Group 1 pulmonary arterial hypertension (PAH) is associated with an alteration of pulmonary vasculature, including pulmonary arterial vasoconstriction smooth muscle hypertrophy, intimal and adventitial proliferation with eventual fibrosis, complex plexiform lesions, and thrombotic lesions. Endothelial dysfunction disrupts the balance between the production of vasodilators and vasoconstrictors. There are various sources stimulating endothelial dysfunction and include free radicals, hypoxia, inflammatory mediators, acidosis, stress from left-to-right intracardiac shunts, and fibrin from thromboembolism. Eventually this results in an overexpression of vasoconstrictor and proliferative substances, such as thromboxane A2 and endothelin-1 (ET-1). ET-1 is both a potent vasoconstrictor but also stimulates smooth muscle proliferation, resulting in smooth muscle hypertrophy of the pulmonary vasculature. On the other hand, there is a downregulation of vasodilator and antiproliferative substances, such as nitric oxide (NO) and prostacyclin. Platelets also take part in the pathogenesis of PAH by occluding vessels through the production of thrombotic lesions and vasoconstrictive mediators. These changes result in an elevation of MPAP and PVR with a normal pulmonary capillary wedge pressure (PCWP) and is known as precapillary PH ( Fig. 36.1 ).

Group 2 comprises PH caused by left heart disease. Hemodynamically, this group has elevated MPAP and PCWP with a normal PVR and is known as postcapillary PH. The elevation of MPAP is caused by passive back pressure from an elevation in left atrial pressure. Initially, the transpulmonary gradient is low but eventually with longstanding disease, the increase in MPAP is caused by the increase in left atrial pressure which results in vascular remodeling and pulmonary arterial vasoconstriction and consequently an increase in the transpulmonary pressure gradient. Careful consideration needs to be taken with the use of pulmonary vasodilators in this group of patients who are at risk of associated pulmonary edema from elevated pulmonary venous pressure.

Groups 3, 4, and 5 also fall under the category of precapillary PH. Group 3 represents PH secondary to lung disease. Hypoxia is the main driving factor causing pulmonary vasoconstriction. Hypoxia induces endothelial cell damage causing release of vasoconstrictors, such as ET-1, that lead to smooth muscle vasospasm and proliferation. Also there is eventually intimal thickening, medial, hypertrophy, and adventitial collagen deposition. Interestingly, although sleep disordered breathing is part of this group, relatively only a minority (17%) of patients with obstructive sleep apnea go on to develop PH. The likelihood however increases when the patient has associated underlying lung disease. Group 4 includes patients with thromboembolic obstruction of the pulmonary arteries. They may develop partial or complete occlusion of the pulmonary arteries through the formation of mural thrombi. These patients have an abnormal mechanism of fibrinolysis or have underlying hematologic or autoimmune disorders resulting in a hypercoagulable state. ^, Interestingly, vascular remodeling also occurs in vessel regions not affected by thrombi which may be related to sheer stress. Only a fraction of patients with acute pulmonary emboli develop chronic thromboembolic PH (CTEPH). Surgical intervention with pulmonary thromboendarterectomy is potentially curative. Anticoagulation is the main medical therapy for these patients. Finally, Group 5 is PH resulting from idiopathic or multifactorial mechanisms which include, sarcoidosis, splenectomy, and myeloproliferative disorders.