Circulatory Failure after Anesthesia Induction in a Patient with Severe Primary Pulmonary Hypertension 

A 48-yr-old man with PPH was scheduled to undergo lung transplantation after a 3-yr history of progressive dyspnea with home oxygen therapy. Right-sided heart catheterization showed elevated pulmonary artery pressures (125/59 mmHg) with normal cardiac output (4.5 l/min) and mixed venous oxygen saturation (Smv^O2) of 74%. Pulmonary hypertension was unresponsive to inhaled nitric oxide, and treatment trials with calcium antagonists and prostacyclin failed to improve dyspnea and exercise tolerance. Twelve-lead electrocardiography (ECG) showed sinus tachycardia with right-axis deviation and right atrial and right ventricular hypertrophy. Lung volumes were within normal values, and resting arterial partial pressure of oxygen (Pa^O2) was 57 mmHg while breathing room air.

Before surgery, electrocardiography leads and a pulse oximeter probe were placed, and arterial and pulmonary artery catheters were inserted during local anesthesia for continuous monitoring of mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP) and central venous pressure. After a 3-min oxygenation period, arterial oxygen saturation (Sp^O2) and Smv^O2increased (Sp^O2from 91 to 95% and Smv^O2from 72 to 78%), with no change in systemic and pulmonary artery pressures (150/100 mmHg and 130/62 mmHg, respectively). General anesthesia was induced with incremental doses of fentanyl (250 μg) and midazolam (3.5 mg). Succinylcholine (75 mg) was given to facilitate airway intubation with a double-lumen tracheobronchial tube, and controlled mechanical ventilation was initiated using low tidal volumes (5–7 ml/kg). Anesthesia was maintained with 0.5–1% isoflurane in oxygen.

As shown in figure 1, anesthesia induction was associated with a marked decrease in MAP (from 125 to 85 mmHg). A large increase in MPAP (from 80 to 115 mmHg) occurred in response to tracheal intubation, with MPAP exceeding the level of MAP. Within 2 min after the start of positive-pressure ventilation, right ventricular failure developed, as indicated by high end-expiratory central venous pressure, a dramatic decrease in cardiac output (from 3.9 to 1.2 l/min) and by low Sp^O2(< 85%), Smv^O2(30%), and expired carbon dioxide values (< 2%). Hemodynamics and gas exchange improved transiently with the administration of epinephrine (two repeated doses of 50 μg followed by an infusion of 0.01 μg · kg⁻¹· min⁻¹). At that time, transesophageal echocardiography (TEE) showed marked dilatation of the right cardiac chambers, with massive tricuspid dilatation and underfilling of the left cardiac cavities caused by a leftward shift of the interatrial and interventricular septa (fig. 2A). Shortly after thoracotomy (10 min after the start of positive-pressure ventilation), hemodynamics dramatically deteriorated (MAP of 50 mmHg with sinus rhythm at 50 beats/min); therefore, heparin (300 IU/kg) was administered and cardiac arrest ensued; open-chest cardiac massage was initiated while the femoral vessels were cannulated. Immediately after the institution of partial cardiopulmonary bypass (3.5 l/min, pump flow), MAP increased, right-sided cardiac pressures (MPAP and central venous pressure) decreased, and arterial oxygenation recovered to normal values.

Bilateral sequential lung transplantation was uneventful and adequate gas exchange was easily achieved. Temporary inotropic support was necessary during weaning from cardiopulmonary bypass. At the end of surgery, transesophageal echocardiography showed marked improvement of cardiac function, with normalization of right ventricular size and interventricular septum position (fig. 2B).

Postoperatively, the patient slowly emerged from anesthesia. Pressure support ventilation was necessary for 10 days, and the patient was discharged, fully ambulant and self-caring, from the hospital 70 days after undergoing transplantation. At the 2-yr follow-up, the patient's lung function volumes and arterial gas exchange are within normal values (forced vital capacity of 85%, and forced expiratory volume in 1 s of 75% of predicted values and arterial P^O2of 95 mmHg breathing room air).

Despite several reports concerning the effects of epidural anesthesia in patients with severe PPH, 4–6there is a paucity of literature regarding the management of general anesthesia and lung ventilation. Myles et al.  7described a single case of near-fatal anesthesia induction for heart–lung transplantation that also necessitated direct cardiac compression and urgent cardiopulmonary bypass.

In the current case, anesthesia induction and positive-pressure ventilation precipitated the onset of circulatory failure. First, the anesthetic-induced suppression of sympathetic tone was associated with decreased cardiac output and a 35% decrease in MAP. Although catecholamines administered exogenously or released in response to tracheal intubation transiently restored MAP, there was a further increase in MPAP. Second, the institution of positive-pressure ventilation impeded systemic venous return and could increase right ventricular afterload by closing of small pulmonary arteries. 8Third, right ventricular dilatation with tricuspid regurgitation and leftward septal shift resulted from right-sided pressure overload. Subsequently, incomplete filling of the left ventricle with decreased diastolic compliance further impaired left ventricular function. 9A positive feedback mechanism involving interventricular coupling could be triggered, whereby the decreased left ventricular function (via  septal motion) tends to reduce right ventricular systolic function and vice versa.  10Taken together, ventricular interdependence–positive feedback mechanisms and the series connections between the pulmonary and systemic circulation are implicated in the development of circulatory failure during anesthesia induction and positive-pressure mechanical ventilation.

In many patients with long-lasting PPH, pulmonary vasodilators are ineffective because of irreversible hypertrophic and fibrotic changes within the pulmonary arteries. 11In the current case, preoperative tests involving inhaled nitric oxide, prostaglandins, calcium-channel blockers, or nitroglycerin failed to show beneficial effects; therefore, we did not consider the administration of these agents. Isoflurane was chosen in this patient because it was shown to lower pulmonary vascular resistance. 12Any factor that worsens pulmonary hypertension (hypoxia, acidosis, light anesthesia, nitrous oxide) or that may decrease ventricular function (hyperinflation, depressant anesthetics, hypothermia) should be avoided. A pulmonary artery catheter (with mixed venous oximetry) and transesophageal echocardiography are the best ways to track cardiac function and fluid management during lung transplantation.

A cautious approach consists of cannulation of the femoral vessels, either immediately after induction or when the patient is still breathing spontaneously, during local anesthesia and light sedation. Because cardiopulmonary bypass is always indicated in lung transplantation for PPH, 13and given the risk of circulatory collapse after anesthesia induction and mechanical ventilation, such a protocol has been adopted in our institution for all patients with PPH undergoing lung transplantation.