Systemic and Pulmonary Arterial Hypertension

Systemic and pulmonary arterial hypertension represent two distinct pathophysiologic entities with dramatically different clinical implications for perioperative management. Systemic hypertension, redefined in 2017 by the ACC/AHA as sustained systolic pressure exceeding 130 mm Hg or diastolic pressure above 80 mm Hg, results from dysregulation of the autonomic nervous system, renin-angiotensin-aldosterone system, and imbalance between endogenous vasodilators and vasoconstrictors. Primary hypertension comprises most cases, while secondary hypertension arises from identifiable causes such as renal disease, aortic coarctation, hyperaldosteronism, thyroid dysfunction, obstructive sleep apnea, or pheochromocytoma. Chronic elevation drives vascular remodeling and end-organ damage. Treatment strategies include thiazide diuretics, calcium channel blockers, ACE inhibitors, and angiotensin receptor blockers as first-line agents, with perioperative management typically continuing home medications unless systolic pressure exceeds 180 mm Hg or diastolic exceeds 110 mm Hg with acute end-organ injury. Perioperative concerns include induction-related hypotension followed by severe hypertension during laryngoscopy and intubation, as well as acute postoperative hypertension occurring in approximately 2 percent of general surgical patients. Pulmonary arterial hypertension, defined as mean pulmonary artery pressure exceeding 20 mm Hg on right heart catheterization, encompasses five World Health Organization groups representing diverse etiologies from idiopathic and heritable causes to secondary mechanisms from left heart disease and chronic lung pathology. Pulmonary arterial hypertension specifically involves endothelial dysfunction, pathologic vascular proliferation, and in situ thrombosis obliterating small pulmonary arteries, requiring targeted vasodilator therapy through prostanoids, endothelin receptor antagonists, or nitric oxide pathway agents. The perioperative challenge with pulmonary arterial hypertension lies in maintaining mechanical coupling between the right ventricle and pulmonary circulation while avoiding triggers that increase pulmonary vascular resistance, including hypoxia, hypercarbia, acidosis, excessive positive end-expiratory pressure, and atelectasis. The hypertrophied right ventricle relies on diastolic coronary perfusion, making systemic hypotension potentially catastrophic and leading to right ventricular ischemia, dilation, septal displacement, and acute left-sided cardiac failure. High-risk surgeries for pulmonary arterial hypertension patients include orthopedic procedures with thromboembolism risk, laparoscopic operations increasing pulmonary vascular resistance through pneumoperitoneum and positioning, and thoracic surgery imposing severe stress through hypoxic pulmonary vasoconstriction during single-lung ventilation.