By Ed Sutton, MD
As anesthesia providers, it’s important that we understand the physiology and pharmacology involved in cardiac assessment and can converse with other medical providers as we consider anesthetic management and patient assessment. Pulmonary artery/venous hypertension has historically been difficult to manage in the acute setting of anesthesia, often complicated by sudden decompensation that doesn’t respond to normal resuscitation efforts and medications. The thin-walled right ventricle is more susceptible to failure with acute or chronic increases in pulmonary vascular afterload. Reductions in right ventricular ejection fraction result in diminished left ventricular filling and hypotension, as well as inadequate alveolar gas exchange and resultant hypoxia. Hypoxia acutely increases pulmonary pressures, leading to a rapid worsening of the situation.
As anesthesia providers, we are well trained to manage acute decreases in left ventricular function with inotropes and chronotropes. However, these same medications, in the setting of many types of pulmonary hypertension, have the potential to increase pulmonary vascular resistance (PVR), worsening right-sided heart failure and hypotension.
The World Health Organization (WHO) classifies pulmonary hypertension into five groups based on underlying causes (e.g., thromboembolic disease, left heart disease, idiopathic, heritable) and conditions. In anesthesia management, we must primarily consider two types with distinct treatment requirements: precapillary arterial pulmonary hypertension and postcapillary venous pulmonary hypertension.
Postcapillary pulmonary hypertension, or pulmonary venous hypertension, is more commonly encountered and treated by anesthesia providers. It occurs with increased pressure in the left ventricle and pulmonary veins and is most commonly caused by reductions in left ventricular function due to ischemic heart disease, left-sided valvular disease, or severe systemic hypertension. Chronic left-sided heart failure with postcapillary hypertension—whether with reduced or preserved ejection fraction (CHFrEF, CHFpEF)—is typically managed with fluid restriction and afterload reduction.
In acute postcapillary hypertension, an increasing number of anesthesia providers rely on point-of-care ultrasound (POCUS) to guide inotropic therapy and fluid management. Pulmonary artery catheters (Swan-Ganz), once the gold standard for complex intraoperative management, are increasingly being replaced by transesophageal echocardiography (TEE).
Precapillary pulmonary hypertension, regardless of etiology, can rapidly lead to hemodynamic instability that is refractory to standard resuscitation medications, resulting in right-sided heart failure. Oxygen is a direct pulmonary vasodilator and should always be the first-line therapy. Precapillary pulmonary hypertension may be caused by thromboembolic disease, congenital heart disease, connective tissue disorders, or idiopathic and heritable conditions, many of which are progressive and may ultimately require lung transplantation.
Management is significantly more complex than postcapillary disease and involves endothelin receptor antagonists, prostacyclin receptor agonists, and nitric oxide pathways. IV epoprostenol, IV or inhaled milrinone, and inhaled nitric oxide may be required for severe instability, but these therapies often take hours to arrange and are typically unavailable in noncardiac operating rooms.
Chronic stable patients may be treated with phosphodiesterase-5 inhibitors (e.g., sildenafil, tadalafil), which increase nitric oxide-mediated pulmonary vasodilation. Non-intubated unstable patients may be treated with nitroglycerin delivered via jet nebulization, which is converted to nitric oxide. This involves dissolving 2 mg of nitroglycerin (five 0.4 mg tablets) in 3 mL of normal saline and administering it via a standard nebulizer.
Patients with moderate to severe precapillary pulmonary hypertension should not be considered candidates for outpatient procedures involving anesthesia. Hypoxia and hypercarbia can rapidly worsen pulmonary pressures and lead to refractory right-sided heart failure. Management of these patients exceeds the capabilities of ambulatory surgical centers.
