C A S E R E P O R T

Transient Acute Decompensated Heart Failure Following Propofoland Fentanyl Administration in a Healthy 19-Year-Old Patient

A 19-year-old woman was admittedto the Harbor-UCLA gynecology

service for elective resection of a com-plex ovarian cyst. The patient had a his-tory of gastroschisis repair as a newborn.According to the patient’s family, shetolerated the procedure well withoutcomplications. Medical history wasotherwise unremarkable, with no knowndrug allergies. There was no family his-tory of coronary artery disease, suddencardiac death, or complications fromgeneral anesthesia. The patient admit-ted smoking 3 cigarettes per day anddenied alcohol or recent drug use.

Findings of a preoperative evaluation(including physical examination, basicchemistry panel, complete blood cellcount, and urinalysis) were within nor-mal limits, with an overall AmericanSociety of Anesthesiologists class I phys-ical status. Preoperative vital signs werenormal: blood pressure, 113 ⁄65 mm Hg;heart rate, 77 beats per minute; andrespiratory rate, 18 breaths per minute.and the patient then weighed 70 kg.She was taken to the operating room forlaparotomy and received fentanyl100 lg IV and midazolam 2 mg IV. Atotal propofol dose of 150 mg IV wasused for induction, and sevoflurane2.5% was administered for general anes-thesia. The patient was paralyzed withsuccinylcholine 60 mg�1 and was sub-sequently intubated without complica-tions. However, 10 minutes afterinduction and while the surgery teamwas preparing the patient for incision,her heart rate and blood pressure rapidlydecreased to 47 beats per minute and55 ⁄25 mm Hg, respectively. The brady-cardia and hypotension did not respondto atropine, glycopyrrolate, andephedrine, but they improved with1 mg of epinephrine. Oxygen saturation

remained 100%. Pink frothy sputum wasnoted in the endotracheal tube. Thepatient remained afebrile throughoutthe resuscitation.

The surgery was postponed whileefforts were undertaken to stabilize thepatient and determine the cause of thebradycardia and hypotension. Portablechest radiography demonstrated a nor-mal heart size and bilateral hazy opaci-ties consistent with pulmonary edema.An electrocardiogram revealed normalsinus rhythm without evidence of ische-mia. Transthoracic echocardiographydemonstrated normal left ventricular(LV) size with a severely reduced LVejection fraction of 20% to 25%, ante-rior wall akinesis, and moderate globalhypokinesis of the left ventricle. Thepatient remained intubated and wastransferred to the cardiac intensive careunit for further evaluation. On physicalexamination, the patient had bilateralrales consistent with pulmonary edema;cardiac auscultation revealed no mur-murs, gallops, or rubs; and the jugularvenous pressure was not elevated.Results of laboratory studies performedapproximately 7 hours after the hypo-tensive episode were notable for an ele-vated troponin level of 3.9. Findings of abasic chemistry panel, complete blood

cell count, and coagulation profile werewithin normal limits. Intravenous furo-semide was administered for treatmentof the pulmonary edema. Sedation wasdiscontinued, and the patient wasweaned from mechanical ventilationand extubated. The patient remainedhemodynamically stable overnight.Serial electrocardiography revealed sinusrhythm with T-wave flattening, pro-gressing to inversion in the anterolateralleads. Subsequent laboratory studieswere performed to examine for causes ofheart failure—thyroid-stimulating hor-mone level was within normal limitsand results of a rapid human immunode-ficiency virus test, urine toxicologypanel, and Coxsackie viral panel wereall negative. Repeat transthoracic echo-cardiography performed 25 hours afterinitial echocardiography revealed nor-mal ventricular size and function withan LV ejection fraction of 55% to 60%and no wall motion abnormalities. Thepatient remained asymptomatic and he-modynamically stable with an improvedmean arterial pressure (MAP) of 62 mmHg. She was discharged the followingday. Given the rapid improvement inhemodynamics after the initial event,the transient decrease in cardiac func-tion and subsequent non-ST elevation

Sheryl L. Chow, PharmD;1,2 Daniel Houseman, MD;2 Theresa Phung, PharmD;3

William J. French, MD2,4

From the College of Pharmacy, Western University of Health Sciences, Pomona,CA;1 the Harbor-UCLA Medical Center, Torrance, CA;2 the Fountain ValleyRegional Hospital, Fountain Valley, CA;3 and the Division of Cardiology, UCLASchool of Medicine, Los Angeles, CA4

Address for correspondence:Sheryl L. Chow, PharmD, 309 East Second Street, Pomona, CA 91766E-mail: schow@westernu.eduManuscript received April 22, 2009; revised July 29, 2009;accepted September 1, 2009

doi: 10.1111/j.1751-7133.2009.00125.x

anesthesia-induced acute decompensated heart failure march • april 201080

myocardial infarction were attributed toone of, or a combination of, the medica-tions received during anesthesia induc-tion.

DiscussionGeneral anesthesia is largely used duringmost surgical procedures, but given theunpredictable adverse effects that canoccur, careful observation and monitor-ing are required. Agents such as pro-pofol and fentanyl have knownvasodilatory effects and LV depressionin patients with and without preexistingheart failure. Several reports havedemonstrated significant systolic anddiastolic blood pressure reductions asso-ciated with propofol that were relatedto decreases in systemic vascular resis-tance. In the absence of heart failure,systolic and diastolic arterial pressureswere observed to be reduced as much as30% and 25%, respectively,1 whereasother studies demonstrated a less signifi-cant impact on MAP2–4 at standarddoses of propofol. Inhaled anestheticssuch as sevoflurane have produced onlymild reductions in MAP when usedconcurrently with propofol.5 However,fentanyl in combination with propofolhas been associated with even greaterreductions in MAP compared withpropofol alone.4 The pronounced hypo-tensive effects of the fentanyl ⁄propofolcombination may lead to significanthypoperfusion and pose an even greater

risk to patients with underlying cardiacconditions such as ischemic heart dis-ease. The published reports of theseagents are not limited to hemodynamicsbut also demonstrate direct myocardialdepressive action on cardiac function.Even without preexisting heart failure,the effects of these agents on ejectionfraction in patients with normal LVfunction have been reported to bemildly reduced.3,6

The mechanisms by which the pro-pofol ⁄ fentanyl combination producescardiac depression are multifactorial.Propofol produces vasodilation throughinduction of nitric oxide, blockingcalcium channels, and protein kinaseactivation. Furthermore, cardiovasculardepression has also been associated withpropofol mainly through reduced baro-receptor response to blood pressureresulting in alterations in peripheralresistance, inotropy, and heart rate.2

The combination of propofol and fenta-nyl for anesthesia may produce an exag-gerated effect on cardiovascular functionand hemodynamics and even more so inpatients with limited cardiac reserve. Inaddition to attenuating the autonomicsympathetic response, fentanyl producesan additional negative chronotropiceffect and suppression of reflex tachy-cardia during concomitant propofoladministration.4 The overall impact ofthe propofol ⁄ fentanyl combination mayhave detrimental hemodynamic and

cardiac manifestations even in younghealthy patients.

We believe the profound and signifi-cant impact of propofol and fentanylat standard doses on myocardial depres-sion in an otherwise healthy youngwoman is an unusual case that iscurrently unreported in the literature.Furthermore, the progression to decom-pensated heart failure with cardiogenicshock and subsequent myocardial dam-age underscores the severity of thisadverse event. A cause and effect rela-tionship between propofol and fentanylanesthesia and significant cardiovasculardepression is likely given the rapidchange in clinical symptoms and hemo-dynamics only 10 minutes after induc-tion coupled with a rapid improvementin MAP (77% increase) and ejectionfraction (LV ejection fraction increasedby 150%) within 24 hours of the initialadverse event. Reproducibility, how-ever, cannot be established becauseof ethical considerations surroundingpatient care.

The cardiovascular depressive effectsof individual agents on patients under-going general anesthesia have been wellestablished. When these agents are usedin combination, such as with propofoland fentanyl, additional precautionsshould be taken in all patients, includingthose with normal LV function.

REFERENCES

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volunteers after 8-h exposure, including kineticsof degradation products. Anesthesiology.1997;87(3):517–526.

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