Cor Pulmonale

Stage the right ventricle preoperatively - On exam, look for distended neck veins, tricuspid regurgitation, an S3 gallop, hepatomegaly, ascites, and peripheral edema. On paper, get an ECG, echocardiogram, chest radiograph, hemoglobin and hematocrit, and a metabolic panel for renal and hepatic function; add an arterial blood gas and pulmonary function testing when the pulmonary disease status is unclear.

Postpone the decompensated patient - Dyspnea at rest, syncope, or hypoxemia on the day of surgery is a reason to reschedule a non-emergent case. Right heart catheterization is worth considering when the disease is known to be severe or the RV findings are new.

Induction - Preoxygenate with 100% oxygen. Etomidate is the induction agent of choice because it minimally affects contractility and SVR. Add a benzodiazepine and/or opioid to blunt the sympathetic response; laryngoscopy at a light plane produces intense sympathetic stimulation and worsens pulmonary hypertension. Avoid spinal anesthesia — the onset is too rapid and the sympatholysis too profound.

Ventilator settings are a pulmonary vasodilator - Tidal volumes around 6 mL/kg, peak airway pressures under 30, PEEP 5 to 10 cm H2O, and ventilate to a CO2 of 30 to 35 mmHg. Raise FiO2 rather than PEEP to fix oxygenation; climbing PEEP compromises preload and drops systemic pressure. Avoid one-lung ventilation where possible — hypoxic pulmonary vasoconstriction in the non-ventilated lung acutely worsens pulmonary hypertension.

Monitoring - An arterial line for beat-to-beat pressure and serial gases; central venous and pulmonary artery pressures to target vasopressors, vasodilators, and fluid. TEE sizes the RV in the mid-esophageal four-chamber view: a volume-overloaded RV pushes the septum left in diastole and makes the LV look like a D, while a pressure-overloaded RV shifts it in systole.

Treat acute RV failure in order - Correct hypercapnia, hypoxia, and acidemia first, since all three raise RV afterload. If that does not turn it around, add a pulmonary vasodilator — inhaled nitric oxide or iloprost. Then support contractility with an inotrope; norepinephrine is commonly used. Give volume only when the patient is genuinely underfilled from blood or insensible loss.

Systemic hypotension is not tolerated - Treat it aggressively with vasopressin or phenylephrine. Persistent systemic hypotension from RV failure is the most dangerous intraoperative complication these patients have.

Supplemental oxygen is therapy, not comfort - Oxygen relieves hypoxemic pulmonary vasoconstriction, which improves cardiac output, reduces sympathetic vasoconstriction, and improves renal perfusion. Keep it on through transport and into PACU.

Pain control is hemodynamic management - Uncontrolled pain can trigger a pulmonary hypertensive exacerbation. Peripheral nerve blocks and epidurals are useful for perioperative analgesia.

SVT is the arrhythmia that decompensates them - Supraventricular tachycardias are the most common and can trigger right heart decompensation. Aim to restore sinus rhythm with cardioversion or amiodarone before settling for rate control with a beta-blocker or calcium channel blocker.

Know the procedure's specific insult - Laparoscopic insufflation raises abdominal pressure enough to impede lung compliance and venous return and can precipitate a respiratory acidosis needing more minute ventilation or bicarbonate. Cemented orthopedic cases can produce profound hypotension and carry fat and cement embolism risk.

Cor pulmonale is a change in right ventricular structure — hypertrophy, dilation, or both — and function caused by a primary respiratory disorder that produces pulmonary hypertension. Right heart failure secondary to left heart disease or congenital heart disease does not count. COPD is the most common chronic cause; massive pulmonary embolism is the most common cause of acute cor pulmonale.

The mechanism is chronic hypoxemia. Sustained hypoxic vasoconstriction plus reduced endothelial nitric oxide production drives smooth muscle proliferation in the small pulmonary arteries, pulmonary vascular resistance climbs, pulmonary artery pressure rises, and right ventricular work increases until the RV enlarges. Severity tracks with hypoxemia, hypercapnia, and airflow obstruction. That is what makes it an anesthesia problem: the RV normally pumps against about a tenth of systemic resistance, and nearly every lever you touch in the OR — oxygenation, CO2, pH, airway pressure — moves pulmonary vascular resistance.