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Anesth Analg 2004;99:221-226
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000117285.12600.C1

CRITICAL CARE AND TRAUMA

Clinical Management of Cardiogenic Shock Associated with Prolonged Propofol Infusion

Kimberley E. Culp, MD, John G. Augoustides, MD, Andrew E. Ochroch, MD, and Bonnie L. Milas, MD

Department of Anesthesia (Cardiothoracic Section), Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania

Address correspondence and reprint requests to John G. Augoustides, MD, Assistant Professor of Anesthesia, Department of Anesthesia (Cardiothoracic Section), Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104–4283 USA. Address email to yiandoc{at}hotmail.com


   Abstract
Top
 Abstract
Introduction
 Case Report
 Discussion
 Conclusions
 References
 
This case report details the development of cardiogenic shock after craniotomy in a patient sedated with a propofol infusion. The patient survived with the assistance of extracorporeal membrane oxygenation. A literature review summarizes the syndrome of cardiogenic shock associated with prolonged propofol infusion. This is the first report of survival in this syndrome resulting from mechanical circulatory support.

IMPLICATIONS: This case report details survival of a patient who developed postoperative cardiogenic shock associated with a prolonged propofol infusion. The pivotal role of mechanical circulatory support is emphasized. The management of circulatory collapse in a patient sedated with propofol should include prompt discontinuation of propofol and early institution of mechanical circulatory support.


   Introduction
Top
 Abstract
 Introduction
Case Report
 Discussion
 Conclusions
 References
 
Propofol is one of the commonly accepted drugs administered as an infusion for the sedation of adult patients in the intensive care unit (ICU) (1–3). Propofol permits rapid awakening for frequent neurological examination (4). Despite this clinical advantage, a series of case reports have documented severe metabolic acidosis, cardiogenic shock, and death in pediatric ICU patients on prolonged propofol infusion (5–14). Although our patient presented in a similar fashion, he was managed early with mechanical circulatory support that allowed complete recovery. This highlights the unique life-saving application of extracorporeal circulation for cardiogenic shock associated with a prolonged propofol infusion.


   Case Report
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 Abstract
 Introduction
 Case Report
Discussion
 Conclusions
 References
 
A 13-yr-old, 40-kg male with mild asthma presented with an acute intraventricular hemorrhage secondary to an arteriovenous malformation (AVM). The subsequent hydrocephalus was managed with a ventriculoperitoneal shunt. He made a full neurologic recovery. Approximately 6 wk after the original insult, the patient presented to our institution for elective craniotomy and resection of the 6 cm left parietal AVM.

In the operating room (OR), ASA routine monitors were placed and anesthesia was induced with propofol (100 mg, Diprivan®; AstraZeneca, Wilmington, DE) and fentanyl (50 µg). The patient was in sinus rhythm with a normal QT interval. Neuromuscular blockade was obtained with titrated vecuronium; the train-of-four ratio (left ulnar nerve) was monitored throughout the entire case. After endotracheal intubation, a radial arterial line and large-bore peripheral venous access were placed. Initially, the patient was maintained on nitrous oxide (70%) and isoflurane (0.2%–0.5%), with titrated vecuronium to maintain the train-of-four ratio at 1/4. During the dissection of the AVM there was considerable bleeding and significant brain edema ensued. To facilitate brain relaxation, the head of the bed was further elevated, hyperventilation to a PCO2 of 30 mm Hg was maintained, nitrous oxide was discontinued, and propofol (Diprivan®; AstraZeneca) was infused at 50 µg · kg–1 · min–1. These intraoperative maneuvers facilitated further brain dissection, but severe intermittent bleeding continued. Hemostasis was achieved and further AVM resection was abandoned. The total operative time was 17 hours. Throughout the operation the mean arterial blood pressure (MAP) was 55–65 mm Hg. Intravascular volume resuscitation consisted of 6 L crystalloid, 13 U of packed red blood cells, 10 U of fresh-frozen plasma, and 12 U of platelets. Immediately after surgery, the patient underwent a computed tomographic scan of the brain; sedation was achieved with a propofol infusion at 140 µg · kg–1 · min–1.

The patient was admitted to the neurosurgical ICU with adequate vital signs and was placed on mechanical ventilation. The patient was in sinus rhythm with a normal QT interval; the MAP was 60 mm Hg. Although there was no parenchymal bleeding on the recent CAT scan of the brain, there was significant brain edema. An intracranial pressure (ICP) monitor (Camino Laboratories, San Diego, CA) was placed within 30 min of ICU admission. To maintain an ICP <20 mm Hg, ICU maneuvers included:

  • Elevation of the head of the patient’s bed;
  • Sedation with a propofol infusion titrated between 100–190 µg · kg–1 · min–1;
  • Mechanical ventilation, with goals of normoxia and hypocarbia (PCO2 of 30 mm Hg);
  • Maintenance of a normal MAP of 55–65 mm Hg.

As the ICP was adequately controlled with these interventions, concomitant steroid administration or cerebrospinal fluid drainage was not added. Daily computed tomographic scans of the brain documented no new parenchymal brain pathology. Neurological examinations were performed during weaning of the propofol infusion to the point of patient comfort and response to verbal command. At 66 h after surgery, a prolonged QT interval and T wave inversions were noted on telemetry. Laboratory values at this time showed no change in serum electrolytes, acid-base status, or cardiac enzymes. At 74 h after surgery, hemodynamically unstable polymorphic ventricular tachycardia developed (Fig. 1). The propofol infusion was discontinued. The ventricular tachycardia was managed with immediate cardioversion, IV magnesium and potassium supplementation, as well as infusions of lidocaine and amiodarone. Because of increasing pharmacologic circulatory support, an emergent transthoracic echocardiogram (TTE) was obtained. This revealed severe biventricular dysfunction, no pericardial effusion, and no significant valvular disease.



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  		Figure 1. Ventricular tachycardia as major initial arrhythmia that prompted cardioversion, aggressive antiarrhythmic therapy, and urgent echocardiography.

 
The patient continued to deteriorate because of persistent ventricular tachycardia refractory to cardioversion, lidocaine, and amiodarone. Cardiogenic shock ensued: it became refractory to infusions of epinephrine (8 µg/min) and norepinephrine (10 µg/min). Systolic blood pressures ranged from 60–80 mm Hg, ICP was 35 mm Hg, and central venous pressure was 38 mm Hg. Blood chemistry revealed severe metabolic acidosis with a bicarbonate level of 9 mmol/L despite aggressive bicarbonate replacement. The patient also became oliguric, and the peak creatinine was 3.0 mg/dL. The metabolic acidosis only began with the onset of biventricular dysfunction (inadequate tissue perfusion), and was subsequently aggravated by renal failure (inadequate acid clearance). There was biochemical evidence of rhabdomyolysis, as reflected by a creatine kinase in the thousands. The cardiac enzymes, including troponin and creatine kinase MB isoenzyme, were within normal limits. The chest film showed pulmonary edema.

Urgent cardiothoracic surgical consultation was obtained for consideration of mechanical circulatory support because of refractory cardiogenic shock. Despite the increased risk of intracranial bleeding from heparinization, it was decided that the best survival strategy was to proceed with mechanical circulatory support. Extracorporeal circulation with membrane oxygenation (ECMO) was instituted emergently at the bedside (Fig. 2).



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  		Figure 2. Bedside extracorporeal membrane oxygenation: note compactness.

 
ECMO was initiated via the left femoral vessels. Because of the narrow caliber of the femoral artery, arterial perfusion of the left lower extremity via a smaller cannula was added to avoid left lower extremity ischemia. ECMO flows were maintained at 3.7–4.5 L/min and the activated clotting time was maintained between 150–180 s with titrated heparin. Pharmacologic support of the circulation was discontinued. The patient remained oliguric, despite normalization of cardiac index. The renal failure was felt to be attributable to continuing rhabdomyolysis with myoglobinuria, as well as hemolysis from exposure to the ECMO circuit. The patient had a mild unconjugated hyperbilirubinemia (2–3 mg/dL), consistent with continuing hemolysis. The hemoglobin was maintained in the 9–10 g/dL range with transfusion of 1–2 U of packed red blood cells every 24 h. To prevent fluid overload, the patient was dialyzed by means of a dialysis filter connected into the ECMO circuit.

Twenty-four hours later, the patient continued to have biventricular failure by TTE and accelerated junctional tachycardia. Forty-eight hours later, the patient demonstrated marked improvement, with native cardiac ejection and normalization of cardiac rhythm (Fig. 3). TTE now demonstrated normal biventricular function, even when ECMO support was temporarily weaned. Sixty hours after its institution, ECMO was successfully discontinued in the OR. Normal biventricular function was confirmed by intraoperative transesophageal echocardiography. The left femoral artery was repaired, with no ischemia of the left lower extremity.



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  		Figure 3. Normalization of cardiac conduction: sinus rhythm, no ventricular ectopy, and normalization of QT.

 
The remaining hospital course was uneventful. The patient continued to improve neurologically. Mechanical ventilation was discontinued on postoperative day 19. He was discharged to a rehabilitation facility on postoperative day 28. The patient was in sinus rhythm with a normal QT interval. He made a full recovery and returned to school.


   Discussion
Top
 Abstract
 Introduction
 Case Report
 Discussion
Conclusions
 References
 
This is the first report of survival with mechanical circulatory support after cardiogenic shock associated with propofol infusion. Propofol (2,6-diisopropylphenol) is an IV sedative/hypnotic for the induction/maintenance of anesthesia and continuous sedation in the ICU. The formulations of propofol available in the United States are Diprivan® (AstraZeneca Pharmaceuticals) and propofol (Baxter Pharmaceutical Products, Inc., New Providence, NJ). The generic formulation of propofol incorporates sodium metabisulfite (0.25 mg/mL) as the preservative and has a lower pH (4.5–6.4) (15). Diprivan® uses the preservative disodium edentate (0.005%) with sodium hydroxide to adjust to a pH of 7–8.5 (16). The lower pH of the generic propofol has been linked to significant clinical metabolic acidosis in a patient on a prolonged infusion (17). Our institution uses Diprivan®; all references to propofol in this article imply the Diprivan® formulation.

The effect of propofol is dose-dependent: infusion rates are titrated to clinical effect (18) with a rapid onset and short duration (19). The Food and Drug Administration approved propofol for ICU sedation by 1993. In the neurosurgical ICU, sedation is important to facilitate mechanical ventilation as well as to avoid increases in MAP and ICP in response to stimuli (20). In a prospective, randomized, double-blind clinical trial, Kelly et al. (21) demonstrated that a propofol-based sedation and ICP control regimen is a safe and effective alternative to an opiate-based regimen in the head-injured patient. In addition to the benefit of rapid awakening for frequent neurological examination, propofol confers neuroprotective effects by decreasing cerebral metabolic rate, potentiating {gamma}-aminobuturate A inhibition, and inhibiting methyl-D-aspartate glutamate receptors and voltage-dependent calcium channels (22). The main risks of propofol infusion include respiratory depression (23), hypotension (24), bradycardia (25,26), arrhythmias (27), infection (28), hyperlipidemia (29), and pain on injection (30).

There is controversy in the literature regarding the safety of propofol for continuous sedation in the pediatric ICU population. Although many authors report no adverse effects (31–34), the drug manufacturer clearly states that propofol is not indicated for use in pediatric ICU sedation because the safety of this regimen has not been established (16).

In our review of the literature, we identified several case reports in which pediatric ICU patients on a prolonged propofol infusion experienced adverse effects (Table 1) (5–14). These cases have the following features in common: large dosage (mean, 140 µg · kg–1 · min–1), prolonged duration of infusion (mean, 68 hours), severe metabolic acidosis, significant arrhythmias, ventricular failure, and death.


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  		Table 1. Propofol-associated Cardiac Toxicity
 
Although there is no proven causative relationship, this phenomenon has been labeled the "propofol infusion syndrome" (13,37). The syndrome occurs in the susceptible pediatric patient who has received a propofol dose in excess of 67 µg · kg–1 · min–1 for at least 48 hours. The clinical features include acute refractory bradycardia with asystole and the presence of one or more of the following: lipemic plasma, clinically enlarged liver/or fatty liver at autopsy, metabolic acidosis with a base deficit >10, or muscle involvement with evidence of rhabdomyolysis or myoglobinuria (35).

Although the mechanism for this syndrome remains elusive, it is probably multifactorial. Several hypotheses regarding the adverse cardiac effects of the drug have been proposed. Propofol is associated with bradycardia (25,26). Propofol reduces sympathetic tone more than parasympathetic tone, thus resulting in bradycardia from an unopposed parasympathetic response (25). In rat models, Zhou et al. (36,37) have demonstrated that propofol is a cardiac depressant by the mechanisms of antagonism of ß-receptors and calcium channel binding with resulting decrease in myocardial contractility. Propofol also affects mitochondrial performance: it depresses mitochondrial oxidative phosphorylation and hence total energy production, as reflected by adenosine triphosphate metabolism (38). This interference with mitochondrial performance impairs oxygen and electron kinetics in the myocyte and hence depresses myocardial contractility (39). Furthermore, the ventricular arrhythmias in our patient may have been the result of high circulating levels of fatty acids as a consequence of impaired mitochondrial oxidation in the presence of large serum concentrations of propofol (13,40). Excess serum fatty acids have proarrhythmic effects that are responsible for ventricular arrhythmias (40). Thus, there is evidence linking propofol to ventricular dysfunction and ventricular arrhythmias on the basis of mitochondrial dysfunction.

Our 13-year-old patient meets the definition of propofol infusion syndrome with respect to dose, duration, myocardial failure, and metabolic acidosis. The majority of children in the published literature died from myocardial failure. The common feature of those that survived was early hemodialysis (6,9,12,13). This response to dialysis suggests a possible metabolic mechanism. Our child also survived and eventually made a full neurologic recovery. We attribute this outcome to early institution of mechanical circulatory support via the use of ECMO. This bedside mechanical circulatory support allowed immediate patient survival and further time to assess whether the myocardium would recover. The relatively short time for total myocardial recovery allowed prompt withdrawal of ECMO. If there had been delayed myocardial recovery, then prolonged ECMO or perhaps even a ventricular-assist device might have had to be considered.


   Conclusions
Top
 Abstract
 Introduction
 Case Report
 Discussion
 Conclusions
References
 
We conclude that despite the series of case reports, no causative relationship between prolonged propofol infusion and myocardial failure has been proven. However, the manufacturer does caution against propofol for pediatric ICU sedation (16). The cardiogenic shock in our patient was refractory to aggressive medical therapy. The prompt institution of ECMO was life-saving in this patient because it gave the heart time to recover.


   References
Top
 Abstract
 Introduction
 Case Report
 Discussion
 Conclusions
 References
 

  1. Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med 2002; 30: 119–41.[Web of Science][Medline]
  2. Young C, Knudsen N, Hilton A, et al. Sedation in the intensive care unit. Crit Care Med 2000; 28: 854–66.[Web of Science][Medline]
  3. Angelini G, Ketzler JT, Coursin DB. Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. Crit Care Clin 2001; 17: 863–80.[Web of Science][Medline]
  4. Izurieta R, Rabatin JT. Sedation during mechanical ventilation: a systematic review. Crit Care Med 2002; 30: 2644–8.[Web of Science][Medline]
  5. Parke TJ, Stevens JE, Rice ASC, et al. Metabolic acidosis and fatal myocardial failure after propofol infusion in children: five case reports. BMJ 1992; 305: 613–6.
  6. Barclay K, Williams AJ, Major E. Propofol infusion in children. BMJ 1992; 305: 953.[Free Full Text]
  7. Bray RJ. Fatal myocardial failure associated with a propofol infusion in a child. Anaesthesia 1995; 50: 94.
  8. Strickland RA, Murray MJ. Fatal metabolic acidosis in a pediatric patient receiving an infusion of propofol in the intensive care unit: is there a relationship? Crit Care Med 1995; 23: 405–9.[Web of Science][Medline]
  9. Van Straaten EA, Hendriks JJE, Ramsey G, et al. Rhabdomyolysis and pulmonary hypertension in a child, possibly due to long-term high-dose propofol infusion. Intensive Care Med 1996; 22: 997.
  10. Plotz FB, Waalkens HJ, Verkade HJ, et al. Fatal side effects of continuous propofol infusion in children may be related to malignant hyperthermia. Anaesth Intens Care 1996; 24: 724.[Medline]
  11. Hanna JP, Ramundo ML. Rhabdomyolysis and hypoxia associated with prolonged propofol infusion in children. Neurology 1998; 50: 301–3.[Abstract/Free Full Text]
  12. Cray SH, Robinson BH, Cox PN. Lactic acidemia and bradyarrhythmia in a child sedated with propofol. Crit Care Med 1998; 26: 2087–92.[Web of Science][Medline]
  13. Wolf A, Weir P, Segar P, et al. Impaired fatty acid oxidation in propofol infusion syndrome. Lancet 2001; 357: 606–7.[Web of Science][Medline]
  14. Cannon ML, Glazier SS, Bauman LA. Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion. J Neurosurg 2001; 95: 1053–6.[Web of Science][Medline]
  15. Propofol injectable emulsion [package insert]. New Providence, NJ: Baxter Pharmaceutical Products, Inc.
  16. DIPRIVAN® 1% (propofol) injectable emulsion [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals LP, 2001.
  17. Badr AE, Mychaskiw GII, Eichhorn JG. Metabolic acidosis associated with a new formulation of propofol. Anesthesiology 2001; 94: 536–8.[Web of Science][Medline]
  18. Smith I, White PF, Nathanson M, et al. Propofol, an update on its clinical use. Anesthesiology 1994; 81: 1005–43.[Web of Science][Medline]
  19. Hughes MA, Glass PSA, Jacobs JR. Context-sensitive half-time in multicompartment pharmacokinetic models for intravenous anesthetic drugs. Anesthesiology 1992; 76: 334–41.[Web of Science][Medline]
  20. Fulton B, Sorkin EM. Propofol: an overview of its pharmacology and a review of its clinical efficacy in intensive care sedation. Drugs 1995; 50: 636–57.[Web of Science][Medline]
  21. Kelly DF, Goodale DB, Williams J, et al. Propofol in the treatment of moderate and severe head injury: a randomized, prospective, double-blinded pilot trial. J Neurosurg 1999; 90: 1042–52.[Web of Science][Medline]
  22. Marik PE, Varon J, Trask T. Management of head trauma. Chest 2002; 122: 699–711.[Abstract/Free Full Text]
  23. Sternlo JEG, Sandin RH. Recurrent respiratory depression after total intravenous anaesthesia with propofol and alfentanil. Anaesthesia 1998; 53: 378–81.[Web of Science][Medline]
  24. Claeys MA, Gepts E, Camu F. Haemodynamic changes during anesthesia induced and maintained with propofol. Br J Anaesth 1988; 60: 3–9.[Abstract/Free Full Text]
  25. Deutschman CS, Harris AP, Fleisher LA. Changes in heart rate variability under propofol anesthesia: a possible explanation for propofol-induced bradycardia. Anesth Analg 1994; 79: 373–7.[Abstract/Free Full Text]
  26. Tramer MR, Moore RA, McQuay HJ. Propofol and bradycardia: causation, frequency, and severity. Br J Anaesth 1997; 78: 642–51.[Abstract/Free Full Text]
  27. Munoz R, Goldberg ME, Cantillo J, et al. Perioperative arrhythmias with a propofol-based anesthestic. J Clin Anesth 1991; 3: 149–52.[Medline]
  28. Bennett SN, McNeil MM, Bland LA, et al. Postoperative infections traced to contamination of an intravenous anesthetic, propofol. N Engl J Med 1995; 333: 147–54.[Abstract/Free Full Text]
  29. Eddleston JM, Shelly MP. The effect of serum lipid concentrations of a prolonged infusion of propofol-hypertriglyceridemia associated with propofol administration. Intensive Care Med 1991; 17: 424–6.[Web of Science][Medline]
  30. Tan CH, Onsiong MK. Pain on injection of propofol. Anaesthesia 1998; 53: 468–76.[Web of Science][Medline]
  31. Norreslet J, Wahlgreen C. Propofol infusion for sedation of children. Crit Care Med 1990; 18: 890–2.[Web of Science][Medline]
  32. Macrae D, James I. Propofol infusion in children. BMJ 1992; 305: 953–4.
  33. Reed MD, Blumer JL. Propofol bashing: the time to stop is now! Crit Care Med 1996; 24: 175–6.[Web of Science][Medline]
  34. Susla G. Propofol toxicity in critically ill pediatric patients: show us the proof. Crit Care Med 1998; 26: 1959–60.[Web of Science][Medline]
  35. Bray RJ. Propofol infusion syndrome in children. Paediatr Anaesth 1998; 8: 491–9.[Web of Science][Medline]
  36. Zhou W, Fontenot HJ, Wang SN, et al. Propofol induced alterations in myocardial beta-adrenoceptor binding and responsiveness. Anesth Analg 1999; 89: 604–8.[Abstract/Free Full Text]
  37. Zhou W, Fontenot HJ, Liu S, et al. Modulation of cardiac calcium channels by propofol. Anesthesiology 1997; 86: 670–6.[Web of Science][Medline]
  38. Branca D, Roberti MS, Vincenti E, et al. Uncoupling effect of the general anesthetic 2,6-diisopropylphenol in isolated rat liver mitochondria. Arch Biochem Biophys 1991; 290: 517–21.[Web of Science][Medline]
  39. Schenkman KA, Yan S. Propofol impairment of mitochondrial respiration in isolated perfused guinea pig hearts determined by reflectance spectroscopy. Crit Care Med 2000; 28: 172–7.[Web of Science][Medline]
  40. Jouven X, Charles MA, Desnos M, et al. Circulating nonesterified fatty acid level as a predictive risk factor for sudden death in the population. Circulation 2001; 104: 756–61.[Abstract/Free Full Text]
Accepted for publication January 2, 2004.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2004 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press