Emeritus Faculty, Acad Council, Anesthesiology, Perioperative and Pain Medicine
Medical Director of Intensive and Intermediate Intensive Care Units, Stanford University Hospital (1975 - 1997)
Director (President - 1997-1998), American Board of Anesthesiology (1986 - 1998)
Board of Directors (President and Chairman of Board - 2001-2004), Foundation for Anesthesia Education and Research (2000 - 2009)
Honors & Awards
Lifetime Achievement Award, American Society of Critical Care Anesthesiologists (2001)
Distinguished Alumni Achievment Award, University of Vermont School of Medicine (2004)
Arthur L. Bloomfield Award for Excellence in the Teaching of Clinical Medicine, Stanford University School of Medicine (1979, 1987, 2004)
Kaiser Award for Clinical Teaching, Stanford University School of Medicine (1991, 2004)
Jack R. Collins Memorial Award for Outstanding Leadership in Anesthesia Education, Dannemiller Society (1990)
Ellis N. Cohen Award for Outstanding Achievement in Anesthesiology, Stanford University Department of Anesthesia (1980)
Board Recertification, American Board of Anesthesiology, Anesthesia (1993)
Pituitary apoplexy after leuprolide injection for ovum donation
JOURNAL OF ADOLESCENT HEALTH
2003; 32 (1): 89-93
Patients with occult pituitary adenomas infrequently present with pituitary apoplexy. Precipitation of pituitary apoplexy by gonadotropin releasing hormone or gonadotropin releasing hormone agonists has been described. The pathophysiologic mechanism by which these agents induce apoplexy remains unclear. We describe a case of pituitary apoplexy in a young woman receiving leuprolide in preparation for ovum donation. Severe hyponatremia, cerebral vasospasm and infarction, and diabetes insipidus complicated this patient's prolonged hospital course. To our knowledge, pituitary apoplexy after gonadotropin releasing hormone agonist use for ovum donation has not been previously described. The use of leuprolide or other gonadotropin releasing hormone agonists for pituitary down-regulation in conjunction with ovarian stimulation can have serious consequences in women harboring unrecognized pituitary adenomas. Thorough endocrine screening should be performed prior to initiating therapy.
View details for Web of Science ID 000180206800014
View details for PubMedID 12507807
Pathophysiology and management of renal insufficiency in the perioperative and critically ill patient.
Anesthesiology clinics of North America
2000; 18 (4): 773-789
Acute renal failure remains a common, devastating complication of the postoperative period and in the critically ill patient. The most common cause is the progression of prerenal insufficiency to ATN. Despite improved understanding of the pathogenic mechanisms, including impaired hemodynamic autoregulation, medullary hypoxia, and proximal tubular obstruction and transtubular backleak, the treatment, to date, remains largely supportive. Avoidance by ensuring hemodynamic stability, with provision of adequate renal perfusion, provides the best means for minimizing the complications of this organ dysfunction.
View details for PubMedID 11094690
Intraoperative fluid management - What and how much?
1999; 115 (5): 106S-112S
An approach to intraoperative fluid management based on a monitored physiologic application of the Starling principles of cardiac function is recommended to individualize therapy to optimize hemodynamic function and tissue perfusion. The complexity of intraoperative fluid administration, beginning with preoperative cardiovascular function followed by innumerable intraoperative considerations, including anesthetic pharmacology, positive pressure ventilation, operative site, and surgical technique may lead to serious intraoperative and postoperative complications. Emphasis must be given to intraoperative fluid shifts resulting in hidden fluid loss and intravascular hypovolemia that must be replaced. Explanations for this fluid redistribution have included tissue trauma, endotoxemia, and proinflammatory cytokines with resultant increased capillary permeability.
View details for Web of Science ID 000080356600014
View details for PubMedID 10331342
PATIENTS REQUIRING SEDATION
CRITICAL CARE CLINICS
1995; 11 (4): 791-?
Recent advances in the pharmacology of sedative drugs have expanded their use in the intensive care unit. Indications and endpoints for sedation, however, often are defined poorly and are difficult to assess. Nevertheless, the complications of sedative drug administration are real. New indications for sedation have been proposed in recent years, including enforcing sleep/wake cycles, manipulating cellular metabolism, and preventing myocardial ischemia. The evidence supporting the efficacy of these new indications is not yet complete.
View details for Web of Science ID A1995TB57000002
View details for PubMedID 8535979
HEMODYNAMIC PROFILES OF PROSTAGLANDIN-E1, ISOPROTERENOL, PROSTACYCLIN, AND NIFEDIPINE IN EXPERIMENTAL PORCINE PULMONARY-HYPERTENSION
CRITICAL CARE MEDICINE
1991; 19 (1): 60-67
We compared the hemodynamic effects of four vasodilators in experimental embolic pulmonary hypertension in a randomized controlled trial, using nine pigs weighing 16 to 23 kg. After anesthesia induction and cannulation with arterial, central venous, and thermodilution output pulmonary artery catheters, animals were repetitively embolized with glass beads (60 to 160 mu) in order to establish pulmonary hypertension (pulmonary artery pressure [PAP] doubled from baseline). Prostaglandin E1 (PGE1), isoproterenol, prostacyclin (PGI2), and nifedipine were compared at doses producing equivalent reduction in systemic BP.Only PGE1 and PGI2 decreased both PAP and pulmonary vascular resistance (PVR). PGE1 decreased PAP from 39 +/- 1 to 33 +/- 1 mm Hg; prostacyclin decreased PAP from 38 +/- 1 to 31 +/- 1 mm Hg and produced the largest increase in cardiac output (Qt). Isoproterenol did not change PAP, markedly increased heart rate (162 +/- 8 to 216 +/- 11 beats/min), and resulted in significant arrhythmias. Nifedipine increased PVR from 1044 +/- 113 to 1125 +/- 100 dyne.sec.cm-5 and decreased Qt.Vasodilators demonstrate unique hemodynamic drug profiles. Isoproterenol infusion is characterized by tachycardia and arrhythmias. Both PGE1 and PGI2 effectively decrease PAP and PVR. Nifedipine depressed Qt significantly in this glass-bead embolization model of acute pulmonary hypertension.
View details for Web of Science ID A1991EU89500015
View details for PubMedID 1986891
VASODILATOR THERAPY IN MICROEMBOLIC PORCINE PULMONARY-HYPERTENSION
ANESTHESIA AND ANALGESIA
1990; 71 (1): 35-41
The hemodynamic effects of prostaglandin E1, sodium nitroprusside (SNP), nitroglycerin, and hydralazine were studied in a porcine model of elevated pulmonary vascular resistance (PVR) due to glass bead microembolization (60-150-microns diameter). Each animal received all four drugs. Each drug was titrated to produce a 30% reduction in mean systemic arterial pressure. Although all four drugs decreased PVR, distinct differences in the hemodynamic profiles of the four drugs were evident. Prostaglandin E1 produced the largest reduction in mean pulmonary artery pressure (from 41 +/- 1 to 32 +/- 9 mm Hg, mean +/- SEM) and PVR (25 +/- 3 to 18 +/- 2 mm Hg.L-1.min-1), and did not affect the ratio of PVR to systemic vascular resistance (PVR/SVR). Sodium nitroprusside and nitroglycerin produced moderate decreases in PVR (nitroglycerin 21 +/- 2 to 18 +/- 2 mm Hg.L-1.min-1, SNP 22 +/- 2 to 19 +/- 2 mm Hg.L-1.min-1) and in mean pulmonary artery pressure (nitroglycerin 39 +/- 1 to 35 +/- 1; SNP 40 +/- 1 to 36 +/- 2 mm Hg). Both drugs significantly increased the PVR/SVR ratio. Hydralazine was the only drug that significantly increased cardiac output (1.6 +/- 0.2 to 1.9 +/- 0.3 L/min). Hydralazine had no significant effect on mean pulmonary artery pressure, reduced PVR to the smallest extent (11%), and resulted in the largest increase in the PVR/SVR ratio (from 0.52 +/- 0.04 to 0.80 +/- 0.08). In this model of increased pulmonary vasculature resistance prostaglandin E1 caused an equivalent amount of pulmonary and systemic vasodilation, as expressed by the PVR/SVR ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1990DK76300006
View details for PubMedID 2114065
SHORT-ACTING BETA-ADRENERGIC-BLOCKADE AS INITIAL-DRUG THERAPY IN PHEOCHROMOCYTOMA
CRITICAL CARE MEDICINE
1990; 18 (6): 673-674
View details for Web of Science ID A1990DH23600022
View details for PubMedID 1971559
The appropriate use of inotropes in shock.
Canadian journal of anaesthesia = Journal canadien d'anesthésie
1990; 37 (4): Slxiv-Slxx
View details for PubMedID 2193721
HEMODYNAMIC PROFILES OF PROSTAGLANDIN-E1, ISOPROTERENOL, PROSTACYCLIN, AND NIFEDIPINE IN VASOCONSTRICTOR PULMONARY-HYPERTENSION IN SHEEP
ANESTHESIA AND ANALGESIA
1988; 67 (8): 722-729
Patients with pulmonary hypertension challenge the anesthesiologist with complex alterations of hemodynamic function. To study the effects of multiple therapeutic interventions, a stable model of pulmonary hypertension in sheep was developed using continuous infusion of the vasoconstrictor U46619, a thromboxane A2-mimetic. The pulmonary and systemic effects of four pulmonary vasodilators (prostaglandin E1, isoproterenol, prostacyclin, and nifedipine) were compared at doses producing equivalent reduction in systemic blood pressure. Although all four drugs decreased pulmonary artery pressure and resistance, distinct differences in drug hemodynamic profiles were found. Prostaglandin E1 and isoproterenol demonstrated the greatest pulmonary specificity, increased cardiac output significantly, and decreased pulmonary vascular resistance. Prostaglandin E1 produced the largest decrease in pulmonary artery pressure (from 31 +/- 1 to 22 +/- 2 mm Hg). Isoproterenol markedly increased heart rate (from 119 +/- 6 to 182 +/- 10 beats/min) and resulted in significant dysrhythmias that necessitated limiting infusion of this drug; isoproterenol did not affect stroke volume. Prostacyclin demonstrated intermediate pulmonary specificity and produced the largest increase in cardiac output (from 1.7 +/- 0.2 to 3.1 +/- 0.3 L/min). Nifedipine exhibited the least pulmonary specificity and was the least effective agent in decreasing pulmonary artery pressure. In this model different pulmonary vasodilators exerted different hemodynamic effects, suggesting that appropriate drug selection for treatment of pulmonary hypertension should depend on baseline heart rate and rhythm, pulmonary artery pressure, systemic artery pressure, arterial oxygenation, and cardiac output.
View details for Web of Science ID A1988P427600002
View details for PubMedID 3293483
VASODILATOR THERAPY IN VASOCONSTRICTOR-INDUCED PULMONARY-HYPERTENSION IN SHEEP
1988; 68 (4): 552-558
A stable preparation of pulmonary hypertension in sheep was developed using a continuous infusion of the vasoconstrictor U46619, a stable endoperoxide thromboxane A2-mimetic. Using this model, the pulmonary and systemic effects of nitroglycerin, sodium nitroprusside, hydralazine, and prostaglandin E1 were compared at doses producing equivalent reductions in systemic blood pressure. Although all four drugs decreased pulmonary artery pressure and resistance, different drug hemodynamic profiles were found. Prostaglandin E1 demonstrated the greatest pulmonary specificity and resulted in the largest decrease in pulmonary artery pressure (from 33 +/- 1 to 23 +/- 1 mmHg). Nitroglycerin and sodium nitroprusside demonstrated intermediate pulmonary specificity and did not affect cardiac output. Hydralazine demonstrated the least pulmonary specificity and resulted in a large decrease in systemic vascular resistance, with only a moderate decrease in pulmonary artery pressure and resistance. Rational selection of pulmonary vasodilators for clinical application will vary depending on baseline heart rate and rhythm, pulmonary artery pressure, systemic artery pressure, and cardiac output.
View details for Web of Science ID A1988M799800013
View details for PubMedID 3128144
EFFECTS OF SPINAL-ANESTHESIA ON RESPONSE TO MAIN PULMONARY ARTERIAL DISTENSION
JOURNAL OF APPLIED PHYSIOLOGY
1988; 64 (2): 742-747
Nonocclusive main pulmonary arterial distension produces peripheral pulmonary hypertension. The mechanism of this response is unknown. The effects of total spinal anesthesia on the response were studied in halothane-anesthetized dogs. Before total spinal anesthesia, main pulmonary arterial balloon inflation increased pulmonary arterial pressure and resistance without affecting systemic hemodynamic variables. Both right and left pulmonary arterial pressures were monitored to exclude unilateral obstruction with main pulmonary arterial balloon inflation. Total spinal anesthesia decreased cardiac output and systemic arterial pressures. After total spinal anesthesia, main pulmonary arterial distension still increased pulmonary arterial pressure and resistance. Right atrial pacing, discontinuation of halothane anesthesia, and norepinephrine infusion during total spinal anesthesia partially reversed the hemodynamic changes caused by total spinal anesthesia. The percent increase in pulmonary vascular resistance due to main pulmonary arterial distension was similar before total spinal anesthesia and during all experimental conditions during total spinal anesthesia. The pulmonary hypertensive response is therefore not dependent on central synaptic connections.
View details for Web of Science ID A1988M317200033
View details for PubMedID 3372430
PULMONARY EFFECTS OF CRYSTALLOID AND COLLOID RESUSCITATION FROM HEMORRHAGIC-SHOCK IN THE PRESENCE OF OLEIC ACID-INDUCED PULMONARY CAPILLARY INJURY IN THE DOG
1988; 68 (1): 12-20
The effects of resuscitation with crystalloid and colloid solutions in the presence of increased pulmonary capillary permeability were studied. Twenty-four hours after oleic acid administration, dogs were anesthetized and bled to produce hemorrhagic shock. One hour later, resuscitation was performed with saline, 5% albumin, or 6% hydroxyethyl starch solution to restore and then maintain cardiac output at pre-oleic acid values for 6 h. Dogs were recovered and, 24 h later, were reanesthetized for final measurements. Oleic acid administration resulted in increases in pulmonary artery pressure, pulmonary vascular resistance, and extravascular lung water (EVLW). Resuscitation from hemorrhagic shock restored pulmonary hemodynamics to pre-hemorrhage levels and did not affect EVLW, PaO2, shunt fraction, dead-space-to-tidal-volume ratio, or pulmonary compliance. There were no differences in these parameters related to the choice of resuscitation fluid. Saline resuscitation markedly reduced plasma oncotic pressure and the plasma oncotic-pulmonary artery occlusion pressure gradient. Values for these two variables were markedly lower with saline than with colloid resuscitation. The authors conclude that the pulmonary effects of crystalloid and colloid solutions are similar in the presence of moderate increases in pulmonary capillary permeability.
View details for Web of Science ID A1988L597700004
View details for PubMedID 3337363
Hematologic effects of cardiac and noncardiac surgery.
Journal of cardiothoracic anesthesia
1987; 1 (3): 205-209
The intraoperative and postoperative changes in number and type of WBCs in patients undergoing cardiac surgery were studied. These changes were then compared with those that occurred in patients undergoing four noncardiac surgical procedures (abdominal vascular reconstruction, thoracotomy, cholecystectomy, and carotid thromboendarterectomy). Both cardiac surgery and abdominal vascular surgery resulted in a marked increase in bands and decrease in lymphocytes. Thoracotomy and cholecystectomy resulted in similar but smaller changes. Carotid thromboendarterectomy did not produce hematologic changes. We conclude that the hematologic changes that occur with cardiac surgery are primarily a result of the stress and trauma of major surgery rather than a result of cardiopulmonary bypass itself.
View details for PubMedID 2979095
Pulmonary and systemic hemodynamic effects of central venous and left atrial sympathomimetic drug administration in the dog.
Journal of cardiothoracic anesthesia
1987; 1 (1): 29-35
Systemic vasopressor or inotropic therapy may exacerbate existing pulmonary hypertension; the optimal agent and route of administration in this situation are unknown. The systemic and pulmonary hemodynamic effects of four sympathomimetic agents (dopamine, epinephrine, norepinephrine, and phenylephrine) during central venous and left atrial administration were investigated in the anesthetized dog. All four drugs increased both systemic and pulmonary artery pressures. Dopamine and epinephrine increased cardiac output and reduced systemic vascular resistance. Phenylephrine decreased cardiac output and increased systemic vascular resistance and left atrial pressure. Norepinephrine did not significantly affect cardiac output, systemic vascular resistance, or left atrial pressure. None of the four drugs affected pulmonary vascular resistance. The ratio of systemic to pulmonary vascular resistance decreased with epinephrine and increased with phenylephrine. There were no hemodynamic differences related to the route of infusion for any of the four drugs. However, pulmonary arterial concentrations of the three drugs measured (dopamine, epinephrine, and norepinephrine) were markedly lower during left atrial compared to central venous drug administration; systemic drug concentrations were similar or increased during left atrial compared to central venous drug administration. It is concluded that the relative effects on the systemic and pulmonary circulations differ for the four drugs; rational choice of a vasopressor will depend upon the hemodynamic situation and the desired effect. Left atrial catecholamine administration is effective in decreasing pulmonary arterial drug concentrations and may decrease adverse pulmonary effects in clinical practice.
View details for PubMedID 2979068