Anesthesia for Patients With Pulmonary Hypertension or Right Heart Failure

Function

A detailed preoperative evaluation plays a pivotal role in managing patients with known or suspected pulmonary hypertension, guiding risk stratification, anesthetic planning, and perioperative optimization. Given the high morbidity and mortality associated with pulmonary hypertension during surgery, comprehensive assessment enables clinicians to minimize complications and make informed decisions regarding the timing, setting, and conduct of the procedure. Consequently, effective management of pulmonary hypertension requires individualized, interprofessional collaboration to optimize outcomes and minimize perioperative risk.

Clinical Features of Pulmonary Hypertension

Evaluation begins with a meticulous history and physical examination. Pulmonary hypertension frequently remains underdiagnosed, and some patients present for surgery without a confirmed diagnosis. The condition affects up to 1% of the global population and approximately 10% of individuals older than 65.[10] Diagnostic delays remain common, averaging more than 1 year from symptom onset, and exceeding 3 years in about 20% of cases. Furthermore, approximately 40% of patients consult 4 or more healthcare practitioners before being diagnosed.[10]

Symptoms depend on disease severity. Mild cases often present with fatigue or exercise intolerance, whereas advanced disease may cause exertional dyspnea, chest pain, presyncope, or syncope.[7][11][12] These nonspecific manifestations often overlap with other comorbidities, particularly in older adults. Physical examination findings suggesting right ventricular dysfunction include elevated jugular venous pressure, hepatomegaly, ascites, peripheral edema, a tricuspid regurgitation murmur, and a right-sided S3 gallop.[11][12]

On the day of surgery, new or worsening symptoms, eg, resting dyspnea, syncope, or hypoxemia, warrant postponement of elective procedures unless emergent. These findings may signal decompensated right heart failure or an evolving pulmonary hypertension crisis, prompting further diagnostic workup.[7] In patients with severe pulmonary hypertension or new evidence of right ventricular dysfunction without recent evaluation, right heart catheterization is recommended to confirm disease severity and guide perioperative management.[7][12]

Preoperative Evaluation

A comprehensive preoperative evaluation must include a review of previous echocardiograms to assess biventricular function, along with recent right heart catheterization data—specifically, mean pulmonary arterial pressure, pulmonary vascular resistance (PVR), and pulmonary arterial wedge pressure (PAWP)—to determine the hemodynamic classification and severity. Functional assessments, eg, the New York Heart Association (NYHA) classification or the 6-minute walk test, provide additional insight into disease burden and exercise tolerance. Screening for secondary causes—including left heart disease, chronic lung disease, or chronic thromboembolic pulmonary hypertension—further refines management. An interprofessional approach involving anesthesiology, cardiology, or pulmonary hypertension specialists, as well as the surgical team, ensures a coordinated and individualized perioperative risk mitigation strategy.[7][12]

Preoperative laboratory testing and imaging also contribute to optimal planning. Essential studies include laboratory assessments eg, hemoglobin and hematocrit and complete metabolic panel, to assess renal and hepatic function, and additional diagnostic testing eg, a 12-lead electrocardiogram (ECG), echocardiogram, and chest radiograph.[8] For patients with uncertain or newly suspected disease, pulmonary function testing and arterial blood gas (ABG) analysis may help evaluate respiratory reserve and gas exchange.[7]  Pulmonary vasodilator therapy may require escalation or adjustment, eg, transitioning to intravenous formulations or adding inhaled prostanoids, and must continue uninterrupted throughout the perioperative period.[6]

Operative Physiological Stressors

Additionally, the anesthesiologist must remain familiar with procedure-specific physiological stressors. For example, laparoscopic surgery increases intra-abdominal pressure, potentially reducing lung compliance, impairing venous return, and inducing respiratory acidosis, conditions that may necessitate ventilatory adjustments or interventions, eg, sodium bicarbonate to maintain acid-base balance and prevent decompensation in vulnerable patients.[9] Orthopedic procedures using bone cement may trigger severe hypotension requiring immediate intervention. These procedures also have an increased risk of fat or cement emboli.[7]  In nonemergent cases, the surgical team should weigh procedural risks against benefits, and the anesthesiologist must confirm the availability of resources to manage acute right ventricular failure.[9] Preoperative medical optimization to reduce PVR and strengthen right ventricular performance is strongly advised.

Furthermore, anesthesia profoundly affects outcomes in patients with pulmonary hypertension or right heart failure. Both regional and general anesthesia can destabilize cardiovascular function in these patients due to their limited tolerance of hemodynamic fluctuations. The anesthetic approach should ideally ensure effective analgesia, stable hemodynamics, optimal oxygenation, and minimized postoperative complications. Therefore, individualized technique selection based on comprehensive preoperative evaluation enhances outcomes in this high-risk population.[13]

Anesthesia Monitoring Recommendations

Anesthesia guidelines by the American Society of Anesthesiologists (ASA) recommend that standardized monitoring include pulse oximetry, ECG, noninvasive blood pressure, and temperature measurement. Patients with pulmonary hypertension, however, often require enhanced intraoperative monitoring. An indwelling arterial catheter enables continuous blood pressure monitoring and frequent ABG analysis for rapid correction of instability.[3] Invasive monitoring should commence before the procedure begins, after optimizing pulmonary hypertension therapy, to bring parameters, eg, mean pulmonary artery pressure and PVR, as close to baseline as possible.[14]

Advanced hemodynamic monitoring provides additional benefits in high-risk cases of pulmonary hypertension or right heart failure. Placement of a central venous catheter with a pulmonary artery catheter allows for continuous monitoring of central venous pressure, pulmonary artery pressures, cardiac output, and PVR, enabling targeted use of vasopressors, vasodilators, and fluid therapy.[15] Transesophageal echocardiography is a valuable adjunct for intraoperative assessment of right ventricular function and volume status. The mid-esophageal 4-chamber view provides clear visualization of right ventricular size and shape. In cases of volume overload, the interventricular septum shifts leftward during diastole, giving the left ventricle a “D-shaped” appearance. In contrast, pressure overload causes septal shift during systole.[12] Transesophageal echocardiography can also assist in estimating pulmonary artery pressures and guiding real-time clinical decisions.[8][9]

Anesthesia Induction

General anesthesia is a common approach for patients with pulmonary hypertension. Before induction, patients should be preoxygenated with 100% oxygen to increase functional residual capacity and reduce the risk of hypoxemia. Intravenous or nebulized pulmonary vasodilators (eg, prostanoids or nitric oxide) may be administered to blunt pulmonary hypertensive responses to laryngoscopy and intubation.[9] 

A balanced induction using moderate to high-dose opioids (eg, fentanyl 2–7 μg/kg) is considered reliable for limiting tachycardia and systemic vascular resistance (SVR) decreases, though recovery time may be prolonged. Propofol remains widely used but should be coadministered with vasopressors to mitigate hypotension. Etomidate provides hemodynamic stability but is less favored in most centers due to its adrenal suppressive effects. Moreover, certain drugs, including ketamine, nitrous oxide, and protamine, can increase PVR. However, the effect of ketamine on PVR is generally minimal and can be offset by its sympathetic stimulation, which enhances right ventricular performance and helps maintain SVR.[6] 

Adding a benzodiazepine or an opioid during induction further attenuates the sympathetic response.[9] Volatile anesthetics exert minimal direct effects on the pulmonary arteries at clinical concentrations but may impair right ventricular contractility.[1] The overall hemodynamic goals are to avoid abrupt changes in preload, SVR, and right ventricular contractility to preserve cardiac output.[5] For perioperative pain management, peripheral nerve blocks and epidurals are useful, as uncontrolled pain can precipitate pulmonary hypertension crises. However, spinal anesthesia should be avoided because of its rapid onset and profound sympatholytic effects.[9] A rapid sequence induction, performed by an experienced clinician, is recommended. Importantly, laryngoscopy attempted before achieving an adequate depth of anesthesia can trigger intense sympathetic stimulation and exacerbate pulmonary hypertension.[7] 

Neuraxial techniques may help mitigate the hemodynamic instability associated with general anesthesia in patients with pulmonary hypertension, but the evidence is limited. Spinal or epidural anesthesia can cause hypotension, impairing right ventricular perfusion and worsening shunting in Eisenmenger syndrome or with a patent foramen ovale. Low-dose spinal or combined spinal–epidural approaches may be safer, particularly for elective cesarean section in pulmonary hypertension patients.[6]

Additionally, supplemental oxygen prevents hypoxemia, and meticulous de-airing of intravenous lines minimizes the risk of embolism, especially in the presence of a patent foramen ovale. Measures to prevent hypothermia, eg, warming blankets, heat–moisture exchangers, and warmed IV fluids, are also important, as hypothermia can impair hypoxic pulmonary vasoconstriction and worsen ventilation–perfusion mismatch.[1]

Ventilation Techniques

Even with careful pharmacological induction, tracheal intubation can trigger hemodynamic instability due to sedation, hypoxemia, sympathetic stimulation, changes in intrathoracic pressure, and hypoventilation. These factors can transiently increase PVR and place additional stress on the right ventricle. During mechanical ventilation, high plateau and peak airway pressures should be avoided, as they can further elevate PVR and compromise right ventricular function. Lung-protective strategies using low tidal volumes (5–7 mL/kg) and low levels of PEEP are recommended to optimize gas exchange while minimizing ventilator-induced lung injury.[6] 

After securing the airway, ventilator management should begin with tidal volumes of approximately 6 mL/kg and peak airway pressures maintained below 30 mm Hg.[9] Oxygen supplementation is crucial, with higher fractions of inspired oxygen preferred over increasing PEEP to improve oxygenation, as excessive PEEP can reduce venous return, decrease preload, and precipitate systemic hypotension. Mild hyperventilation may be used to maintain an exhaled CO2 level between 30 and 35 mm Hg, helping to prevent acidosis and its potential effect on pulmonary vasoconstriction.[7] 

Volatile inhaled anesthetics can be used to maintain anesthesia; at clinically relevant concentrations, they have minimal direct effect on pulmonary arteries but may impair right ventricular contractility, necessitating careful hemodynamic monitoring. Generally, 1-lung ventilation should be avoided, as blood flow redistribution to the ventilated lung can trigger acute pulmonary hypertensive crises via hypoxic pulmonary vasoconstriction.[9] Overall, the ventilatory strategy should aim to maintain oxygenation and normocapnia while minimizing increases in PVR and preserving right ventricular function.

Pharmacologic Therapies

Pharmacologic therapies for pulmonary hypertension continue to evolve, targeting vasodilation, reducing vascular remodeling, and improving right ventricular function. The major pharmacologic classes include prostanoids, endothelin receptor antagonists, nitric oxide, and phosphodiesterase (PDE-5) inhibitors.[16] 

Prostanoids mimic endogenous prostacyclin, promoting vasodilation, inhibiting platelet aggregation, and reducing smooth muscle proliferation. Among these, intravenous epoprostenol has demonstrated a survival benefit in pulmonary arterial hypertension and remains a cornerstone of advanced therapy.[17] Endothelin is a potent vasoconstrictor and mitogen; therefore, endothelin receptor antagonists not only facilitate vasodilation but also exhibit anti-inflammatory and antiproliferative effects, with oral agents improving hemodynamics and exercise capacity.[17] Nitric oxide induces pulmonary vasodilation by activating soluble guanylate cyclase and increasing cyclic GMP, but its short half-life limits sustained use; hence, continuously inhaled nitric oxide is particularly valuable in the perioperative period to blunt acute rises in PVR.[18] 

PDE-5 inhibitors (eg, sildenafil and tadalafil) act by preventing cGMP breakdown, prolonging nitric oxide–mediated vasodilation. These agents have demonstrated benefit in pulmonary arterial hypertension and in pulmonary hypertension secondary to left heart disease. However, their efficacy is limited in pulmonary hypertension related to chronic lung disease or chronic thromboembolic disease.[19][20] In select patients, especially those newly diagnosed, preoperative sildenafil may be considered to reduce the risk of perioperative exacerbation.[5][20] Notably, while pulmonary arterial hypertension-targeted drugs—including endothelin receptor antagonists, PDE-5 inhibitors, soluble guanylate cyclase stimulators, and systemic prostanoids—are effective in group 1 pulmonary arterial hypertension, they have not demonstrated consistent benefit in pulmonary hypertension associated with chronic lung disease and may even be harmful by worsening ventilation–perfusion mismatch. The exception is inhaled treprostinil, which has been shown to improve exercise capacity and functional status in patients with interstitial lung disease–associated pulmonary hypertension, marking a significant step forward in this subgroup.[21]

Interventional Therapies

Pulmonary endarterectomy remains the gold-standard treatment for chronic thromboembolic pulmonary hypertension, significantly improving hemodynamics and survival. Optimal outcomes require referral to high-volume centers and careful patient selection based on operability, clot distribution, and comorbidities..[22] Early and long-term results in severe chronic thromboembolic pulmonary hypertension are excellent despite higher postoperative risk, and extracorporeal membrane oxygenation (ECMO) can serve as a bridge to recovery when needed.[23] 

In patients who are not surgical candidates—whether due to advanced age, comorbidity burden, or patient preference—balloon pulmonary angioplasty has emerged as an effective alternative. Balloon pulmonary angioplasty can improve pulmonary hemodynamics, functional class, and exercise tolerance, though prospective head-to-head data comparing balloon pulmonary angioplasty with pulmonary endarterectomy are still lacking.[22]

Issues of Concern

The anesthesiologist needs to balance blood pressure, fluid management, oxygenation, and acid-base physiology throughout the procedure. Unfortunately, even with the best efforts, complications may arise. These can include acute right heart failure, arrhythmias, systemic hypotension, and even death. With right heart failure, the right heart is not adequately pumping blood through the pulmonary vasculature and the left heart, decreasing cardiac output. Right heart failure is managed by fluid administration, afterload reduction, and improved contractility.

If the patient has depleted intravascular volume due to excessive blood loss or insensible losses, the heart cannot maintain cardiac output because of inadequate right-sided filling pressures. In this situation, fluid administration would be appropriate to increase filling pressures and thus cardiac output. To reduce the right ventricle afterload, any hypercapnia, hypoxia, or acidemia present should be corrected. If no improvement is noted despite correction of these issues, then pulmonary vasodilators should be added. Lastly, improving right ventricular contractility with inotropic agents, eg, norepinephrine, may be beneficial.[24] The most dangerous intraoperative complication from a pulmonary hypertension exacerbation is right ventricular failure, causing persistent systemic hypotension.

Systemic hypotension is not well tolerated in these patients and needs to be aggressively treated with vasoconstrictors, eg, vasopressin or phenylephrine (an alpha-1 agonist). To avoid exacerbations, treatment with inhaled vasodilators, eg, nitric oxide or iloprost (a synthetic analog of prostacyclin PGI2), may be beneficial.[5] The most common arrhythmias are supraventricular tachycardia, and they can trigger right heart decompensation. The therapeutic goal is to restore a sinus rhythm using either electrical cardioversion, radiofrequency ablation, or drug therapy (eg, amiodarone). If the patient undergoes a cardioversion or ablation without success, then rate control with beta-blockers or calcium channel blockers must be considered.[16]

Clinical Significance

Pulmonary hypertension, similar to chronic obstructive pulmonary disease, is a chronic and progressive disease that usually causes a delay in diagnosis and, therefore, treatment.[11] The incidence of patients presenting for surgery with treated or untreated pulmonary hypertension continues to increase worldwide. Recognizing symptoms during the preoperative evaluation and understanding how to formulate the safest anesthetic plan is crucial for anesthesiologists because of the high morbidity and mortality rates.

Enhancing Healthcare Team Outcomes

Pulmonary hypertension is a complex, high-risk condition that significantly increases perioperative morbidity and mortality. Management requires a comprehensive understanding of pulmonary vascular pathophysiology, right ventricular function, and the impact of anesthetic and surgical stressors. Optimal care begins with a detailed preoperative evaluation, including history, physical examination, echocardiography, right heart catheterization, and functional assessment, alongside review of pulmonary hypertension-targeted medications such as prostanoids, endothelin receptor antagonists, PDE-5 inhibitors, inhaled nitric oxide, and inhaled treprostinil. In selected patients, interventional procedures such as pulmonary endarterectomy or balloon pulmonary angioplasty can further improve hemodynamics and functional status. Intraoperative management emphasizes meticulous hemodynamic monitoring, lung-protective ventilation, avoidance of abrupt changes in preload or systemic vascular resistance, and maintenance of pulmonary hypertension therapy. Complications—including right ventricular failure, arrhythmias, and hypotension—require rapid, targeted interventions with vasopressors, inotropes, or inhaled vasodilators.

Effective care depends on interprofessional collaboration. Anesthesiologists, surgeons, cardiologists, pulmonologists, critical care specialists, and nursing staff must communicate in real-time, coordinate monitoring and pharmacological interventions, and develop contingency plans for the perioperative period. Pharmacists and respiratory therapists ensure appropriate dosing and delivery of pulmonary hypertension-targeted therapies. This collaborative, team-based approach flattens traditional hierarchies, enhances decision-making, reduces complications, and ultimately improves patient outcomes by ensuring safe, individualized care for high-risk patients with pulmonary hypertension.