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PEDIATRIC ANESTHESIOLOGY

Ketamine Does Not Increase Pulmonary Vascular Resistance in Children with Pulmonary Hypertension Undergoing Sevoflurane Anesthesia and Spontaneous Ventilation

Glyn D. Williams, FFA(SA)^*, Bridget M. Philip, MD^*, Larry F. Chu, MD, MS^*, M. Gail Boltz, MD^*, Komal Kamra, MD^*, Heidi Terwey, PA, Gregory B. Hammer, MD^*, Stanton B. Perry, MD, Jeffrey A. Feinstein, MD, MPH, and Chandra Ramamoorthy, MD^*

From the *Department of Anesthesia, Stanford School of Medicine, and Department of Pediatrics, Division of Pediatric Cardiology, Stanford School of Medicine, Stanford University, Stanford, California.

Address correspondence to Glyn D. Williams, MB, Department of Anesthesia, Stanford University School of Medicine, 300 Pasteur Dr., H3587, Stanford, CA 94305-5640. Address e-mail to jumbo{at}stanford.edu).

Abstract

BACKGROUND: The use of ketamine in children with increased pulmonary vascular resistance is controversial. In this prospective, open label study, we evaluated the hemodynamic responses to ketamine in children with pulmonary hypertension (mean pulmonary artery pressure >25 mm Hg).

METHODS: Children aged 3 mo to 18 yr with pulmonary hypertension, who were scheduled for cardiac catheterization with general anesthesia, were studied. Patients were anesthetized with sevoflurane (1 minimum alveolar anesthetic concentration [MAC]) in air while breathing spontaneously via a facemask. After baseline catheterization measurements, sevoflurane was reduced (0.5 MAC) and ketamine (2 mg/kg IV over 5 min) was administered, followed by a ketamine infusion (10 µg · kg^–1 · min^–1). Catheterization measurements were repeated at 5, 10, and 15 min after completion of ketamine load. Data at various time points were compared (ANOVA, P < 0.05).

RESULTS: Fifteen patients (age 147, 108 mo; median, interquartile range) were studied. Diagnoses included idiopathic pulmonary arterial hypertension (5), congenital heart disease (9), and diaphragmatic hernia (1). At baseline, median (interquartile range) baseline pulmonary vascular resistance index was 11.3 (8.2) Wood units; 33% of patients had suprasystemic mean pulmonary artery pressures. Heart rate (99, 94 bpm; P = 0.016) and Pao₂ (95, 104 mm Hg; P = 007) changed after ketamine administration (baseline, 15 min after ketamine; P value). There were no significant differences in mean systemic arterial blood pressure, mean pulmonary artery pressure, systemic or pulmonary vascular resistance index, cardiac index, arterial pH, or Paco₂.

CONCLUSIONS: In the presence of sevoflurane, ketamine did not increase pulmonary vascular resistance in spontaneously breathing children with severe pulmonary hypertension.