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Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri
Address correspondence and reprint requests to Charles Hogue, MD, Campus Box 8054, 660 S. Euclid Avenue, St Louis, MO 63110–1093. Address email to hoguec{at}wustl.edu
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Abstract |
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IMPLICATIONS: Primary pulmonary hypertension (PPH) is a progressively fatal disease that is associated with cardiovascular collapse and death with general anesthesia. We present a patient with PPH who underwent skin grafting under spinal anesthesia while receiving a continuous IV epoprostenol infusion. IV vasopressin was used to avoid systemic hypotension associated with spinal anesthesia.
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Case Report |
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The physical examination demonstrated "moon facies" and flushed skin, with small lung volumes and generalized rhonchi. Laboratory assessments included arterial blood gases (3 L/min O2) pHa 7.40, PaCO2 41 mm Hg, PaO2 63 mm Hg, and HCO2 25 mmol/L, prothrombin time 14.5 s (normal range 13–15 s), international normalized ratio 1.17, activated partial thrombin time 27.5 s (normal range 18–45 s), and normal platelet count. A 20-gauge catheter was inserted in the right radial artery and right internal jugular venous cannulation was performed with a 3-lumen catheter. Vasopressin was then started at 1.2 U/h through the central venous catheter. The patient was placed in the sitting position and spinal anesthesia induced with 10 mg of 0.75% bupivacaine with 8.25% dextrose using a 27-gauge spinal needle at the L4-5 interspace. At the end of the spinal injection the patient was moved to a supine position. This resulted in a bilateral sensory level of T8-9. The patient was given 1.5 mg of midazolam IV in increments of 0.5 mg. IV epoprostenol and nasal oxygen were continued without change in dosage. She remained conscious throughout the procedure and did not require supplemental analgesia.
Before the procedure, arterial blood pressure was 125/56 mm Hg, heart rate 96 bpm, central venous pressure (CVP) 11 mm Hg, and O2 saturation 94%. After spinal anesthesia and during the procedure, systolic and diastolic arterial blood pressure ranged from 112–142 mm Hg and 56–84 mm Hg, respectively, whereas heart rate ranged from 82–96 bpm, and CVP from 9–17 mm Hg. Oxygen saturation remained >91%. Afterwards she was admitted to the postanesthesia care unit for 90 min, where the vasopressin infusion was incrementally decreased and then stopped. She was discharged from the hospital the next morning without evidence of neurologic deficit.
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The potential risks associated with regional versus general anesthesia were carefully considered for this patient. Regional anesthesia has been used successfully for cesarean delivery in patients with PPH, and it may allow for limiting central respiratory depressant drugs given with general anesthesia that might postoperatively lead to hypercarbia and increased pulmonary vascular pressures (7). The adverse platelet aggregation effects of epoprostenol and the potential of spinal hematoma with central neuroaxial block were a concern in this case. The alternative of peripheral nerve block was difficult given the surgeon’s wish to expose both groins for possible skin harvesting.
An additional concern with spinal anesthesia was hypotension due to sympathetic nervous system blockade. In patients with severe pulmonary hypertension, a reduction in systemic blood pressure and coronary perfusion pressure can precipitate acute cardiovascular decompensation resulting in cardiac arrest (8). IV administration of catecholamines to treat hypotension during spinal anesthesia could potentially increase pulmonary vascular resistance precipitating acute cor pulmonale. Because of the latter concern, we chose to infuse vasopressin preemptively to limit hypotension.
Vasopressin is secreted from the posterior pituitary in response to reduced plasma volume and/or increased serum osmolality and is involved in the regulation of water balance. It is also released, along with other stress hormones, during general and regional anesthesia (9). Plasma levels may be inappropriately low in patients with prolonged cardiopulmonary bypass or sepsis (10,11). Vasopressin increases systemic vascular resistance by binding to V1 receptors but, experimentally, it leads to pulmonary vasodilatation, most likely as a result of stimulation of endothelial nitric oxide release (12,13). Additionally, by affecting resistance vessels to a much larger degree than capacitance vessels, vasopressin decreases venous capacitance less than sympathetic agonists. Decreased venous capacitance could lead to increased cardiac output and pulmonary arterial pressures (14). In patients experiencing catecholamine-resistant hypotension, vasopressin infusion in the range of 0.07 to 0.1 U/min caused a significant increase in systemic vascular resistance and mean arterial blood pressure with decreased pulmonary arterial pressures (15).
In this case IV infusion of vasopressin was associated with hemodynamic stability during spinal anesthesia without evidence of worsening right ventricular failure for a patient with severe PPH. No neurologic sequelae from the spinal anesthetic were observed despite concerns regarding platelet inhibition secondary to epoprostenol infusion for her underlying condition.
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This article has been cited by other articles:
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  L. C. Price, P. Forrest, V. Sodhi, D. L. Adamson, C. Nelson-Piercy, M. Lucey, and L. S. Howard Use of vasopressin after Caesarean section in idiopathic pulmonary arterial hypertension Br. J. Anaesth., October 1, 2007; 99(4): 552 - 555. [Abstract] [Full Text] [PDF]
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 K. Subramaniam and J.-P. Yared Management of Pulmonary Hypertension in the Operating Room Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2007; 11(2): 119 - 136. [Abstract] [PDF]
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