Correspondence  |   September 2000
Extreme Pulmonary Hypertension and Anesthesia Induction
Author Notes
  • Staff Anesthesiologist
  • Staff Anesthesiologist; Department of Anesthesiology; University Hospital of Geneva; Geneva, Switzerland;
Article Information
Correspondence   |   September 2000
Extreme Pulmonary Hypertension and Anesthesia Induction
Anesthesiology 9 2000, Vol.93, 903-904. doi:
Anesthesiology 9 2000, Vol.93, 903-904. doi:
In Reply:—
We thank Dalibon et al.  for drawing the attention of clinicians to the delicate anesthetic and surgical treatment of patients with severe pulmonary hypertension. Indeed, some patients with end-stage pulmonary hypertension experience such extreme respiratory distress that they are unable to sustain the supine position. In this situation, the patient should be prepared and draped during light sedation, and the surgeon should be ready to cannulate the femoral vessels immediately after anesthesia induction and tracheal intubation. A short-term increase in pulmonary artery pressure may cause transient right-to-left shunting through a patent foramen ovale, which may cause platypnea, hypoxemia, and intolerance to the upright position. 1 Right-to-left atrial shunting may be diminished by a semi–left lateral position, allowing free access to the femoral vessels. Transesophageal echocardiography should be performed to rule out this mechanism and document right ventricular function. In the majority of severe PT cases, circulatory depression induced by anesthetics and positive-pressure ventilation can be managed temporarily with use of slow titration of intravenous β- and α-adrenergic medications (epinephrine, norepinephrine) or type III phosphodiesterase inhibitors, which allow time for the initiation of cardiopulmonary bypass. 2 In a different context, if PT is (partly) secondary to left ventricular failure or mitral insufficiency, initiation of positive-pressure ventilation partially alleviates right ventricular function by reducing afterload.
Al Khouzaie T, Busser JR: A rare cause of dyspnea and arterial hypoxemia. Chest 1997; 112: 1681–2Al Khouzaie, T Busser, JR
Schermuly RT, Ghofrani HA, Enke B, Weissmann N, Grimminger F, Seeger W, Schudt C, Walmrath D: Low-dose systemic phosphodiesterase inhibitors to amplify pulmonary vasodilatory response to inhaled prostacyclin in experimental pulmonary hypertension. Am J Respir Crit Care Med 1999; 160: 1500–6Schermuly, RT Ghofrani, HA Enke, B Weissmann, N Grimminger, F Seeger, W Schudt, C Walmrath, D