The key to managing pulmonary hypertension is lowering pulmonary vascular resistance (PVR) while maintaining preload and SVR.

Anesthetic Approach – Either very minimal sedation or full GETA. Recommendation are to avoid anything in between! For most cases, GETA with an art-line is recommended. The art-line will be helpful for BP monitoring and ABG’s – which should be taken regularly for longer cases. If doing a propofol MAC, use minimal dose and be sure to support the airway and ventilation to keep O2 high and pCO2 normal. Peripheral nerve block or a gradually-dosed epidural can be a good choice (even with GETA) to optimize post-op pain control and reduce the need for additional drugs. Subarachnoid block is generally avoided for the rapid drop in preload/BP.

Drugs to treat hypotension – Vasopressin may have pulmonary vasodilatory effects in addition to a systemic vasoconstrictive effect. This is why this drug is recommended as the primary vasopressor. Phenylephrine is generally avoided as it has been shown to increase PVR. Norepinephrine, in spite of being a potent alpha-1 agonist, has inotropic properties owing to b1 effects and appears to improve coupling between RV function and afterload. Dobutamine can significantly improve the right ventricular function and the arterio-ventricular coupling.

Inductions – Inductions should be gentle/gradual to avoid rapid drop in BP.

Ventilation – Keep FiO2 100% and pCO2 30-35%. Avoid high tidal volumes. Keep tidal volumes between 6-8 ml/kg of ideal body weight.

Strictly avoided – hypoxia, hypercapnia, hypothermia, hypotension, hypoventilation, hypercarbia, acidosis, atelectasis and inadequate anesthesia/analgesia (high pain levels) will all exacerbate pulmonary hypertension and should be avoided.

Drugs to Avoid – Avoid Nitrous oxide, morphine, atracurium. Some texts suggest avoiding ketamine, while others argue that it has excellent benefits for patients with PH.

New Risks – the literature emphasizes that otherwise harmless perioperative events such as transient hypotension, small bubbles in the IV, application of positive end-expiratory pressure (PEEP), trendelenburg position, pneumoperitoneum, and single-lung ventilation could have serious consequences.

Treatment – Anesthetics will lower PVR, especially volatile agents (with exception to N2O and ketamine). Mechanical ventilation with modest hyperventilation and increased FiO2 will also lower PVR. Inhalational pulmonary vasodilators (eg, nitric oxide or epoprostenol) should be considered for refractory increases in PVR.

Avoid Isoflurane – Isoflurane is known to increase total RV afterload in patients without PH. It is unclear whether or not the same occurs with patients diagnosed with PH.

Testing – Those with confirmed moderate to severe pulmonary hypertension are recommended to undergo right-sided heart catheterization prior to a moderate to severe surgical procedure. Left heart catheterization is also recommended in patients with coexisting left heart failure as this disease can lead to a false representation of pulmonary hypertension.

Further Testing – Patients with PH undergoing right-sided heart catheterization will also undergo nitric oxide testing. If the patient is responsive to nitric oxide (85-90% will NOT be), calcium channel blockers and preoperative inhalers etc. will likely improve the patient’s condition.

Suspected pulmonary hypertension warrants further investigation (eg. 6 minute walk to assess exercise capacity)

High-risk procedures – Intraoperatively, several factors can exaccerbate pulmonary hypertension. These include procedures that present a high possibility of pulmonary embolism (air, fat, or cement), anything that increases venous and/or airway pressures (eg. laparoscopy, Trendelenburg position), hypoxic pulmonary vasoconstriction (HPV), reduced pulmonary vascular volume, systemic inflammatory response, and emergency procedures.

Definition – a mean arterial pulmonary arterial pressure (mPAP) of greater than 25.

Classifications – mild (25-40 mmHg), moderate (41-55 mmHg), and severe (greater than 55 mmHg)

Etiology – Generally caused by a disruption in arterial and/or venous circulation. A hallmark of PH is increased right ventricular (RV) afterload, which leads to RV dilation and eventual RV failure. The most common cause of RV failure is LV failure. Suspect anyone with a poor LVEF to have PH.

Symptoms – Mild symptoms include fatigue and transient dyspnea. As the disease progresses in severity, angina pectoris and syncope will be seen with exercise. Patients may also exhibit a parasternal lift, S3 gallop, jugular venous distention.

Prognosis – patients with any of the following have a poor prognosis: coexisting scleroderma, reduced distance on a 6-minute walk test, central venous pressure above 20 mmHg, cardiac index below 2L/min/m2, and elevated brain natriuretic peptide.