Cardiac arrhythmia during propofol sedation

Douglas, R J W; Cadogan, Mike D

doi:10.1111/j.1742-6723.2008.01126.x

Cited by 19 publications

(25 citation statements)

References 16 publications

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“…[1][2][3] However, the mechanism implicated in these arrhythmic events is still unclear. We observed the development of TDP during the infusion of propofol in the presence of severe hypoalbuminemia, and discuss a putative link between TDP and low serum albumin.…”

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confidence: 99%

QT Interval Prolongation and Torsade de Pointes Induced by Propofol and Hypoalbuminemia

et al. 2010

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SummaryWe report the case of a 70-year-old man presenting with the development of torsade de pointes (TDP) during infusion of propofol in the setting of severe hypoalbuminemia. TDP developed 15 hours after the beginning of a standard infusion of propofol, following the development of a prominent U wave and prolongation of the QTc interval. While the serum concentrations of electrolytes were within normal ranges, serum albumin as low as 1.4 mg/dL was observed. TDP disappeared during the infusion of isoproterenol, and QTc normalized after the discontinuation of propofol. We hypothesize that hypoalbuminemia increased the free fraction of propofol, causing marked QTc prolongation and TDP. (Int Heart J 2010; 51: 365-366) Key words: Torsade de pointes, Long QT syndrome A few cases of propofol-induced QT prolongation complicated by torsade de pointes (TDP) have been reported. 1-3) However, the mechanism implicated in these arrhythmic events is still unclear. We observed the development of TDP during the infusion of propofol in the presence of severe hypoalbuminemia, and discuss a putative link between TDP and low serum albumin. Case ReportA 70-year-old man was admitted to our hospital with a diagnosis of infective endocarditis. He had a history of paroxysmal atrial fibrillation and was permanently paced for sick sinus syndrome. On admission, his body height was 166 cm and weight 70 kg. Cefazoline, 8 g daily, was administered intravenously. The patient developed large, bilateral pleural effusions and, on the 14 th day after his admission to the hospital, he was intubated and artificially ventilated. A 95-mg bolus of propofol was given intravenously for the induction of sedation, followed by a 0.98-mg/kg/hour continuous infusion to allow continuous ventilation. Following the development of a prominent U wave and prolongation of the QTc interval to 712 ms ( Figure 1B ; after the administration of propofol, the QTc interval lengthened from 398 to 712 ms (B); after discontinuation of propofol, the QTc interval shortened to 461 ms (C).

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QT Interval Prolongation and Torsade de Pointes Induced by Propofol and Hypoalbuminemia

et al. 2010

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“…Bununla birlikte uzun QT'li olgularda öncelikli beklenen aritmi torsades de pointes (kıvrılan noktalar) olup, ventriküler fibrilasyonun sonradan geliştiği olgular literatürde bildirilmektedir. 8 Propofolle birlikte indüksiyonda kullanılan fentanil ve roküronyumun normal dozlarda QT mesafesini uzatıcı etkileri gösterilememiştir. 9 Bununla birlikte fentanilin propofol sedasyonu altında entübe edilen hastalarda QT uzamasını azalttığı bildirilmektedir.…”

Section: Discussionunclassified

Cardiogenic Shock and Lung Injury as a Complication of Defibrillation

Kıhtır¹,

Yeşilbaş²,

Şevketoğlu³

et al. 2017

cayd

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Olgu hem literatürdeki ilk çocuk olgu olması hem de transpulmoner termodilüsyon sonuçlarının kalp işlevleriyle birlikte akciğer hasarıyla ilgili de bilgi verebildiğini bildirmek amacıyla sunulmuştur.Anahtar Kelimeler: Akciğer ödemi, defibrilatör, akciğer hasarı, termodilüsyon Local burns, embolism, and arrhythmia are the most common side effects observed after electrical shock treatments. However, systolic function may be rarely affected and pulmonary edema may develop. The cases of pulmonary edema after electrical shock treatments have been reported since 1960s and the proposed mechanism is the inadequacy of the left atrium cuff and ventricle. It was learned that a 7-year-old-girl without any known disease except vesicoureteral reflux had a ventricular fibrillation during general anesthesia induction and defibrillation at 2 joule/kg was attempted. It was also learned that the procedure was delayed and the patient was diagnosed with a long QT (QTc: 0.47 ms) and had respiratory distress and circulatory disturbances after four hours. Pulmonary edema and heart failure was determined, and due to hipoxemia (SpO 2 <88%) not getting any better with non-invasive ventilation, the patient was intubated and followed with mechanical ventilation. A thermodilution catheter was inserted into the femoral artery and a low cardiac index (CI): 1.58 L/min/m 2 , elevated extravascular lung water index (EVLWI): 18 mL/kg and high pulmonary vascular permeability index (PVPI): 7.6 were determined. The patient was treated by mechanical ventilation and vasoactive/inotropic management and discharged at the fifth day of hospitalization without any sequela. Having high EVLWI with high PVPI suggest that the pulmonary edema mechanism may also be caused by alveolocapillary membrane damage, which is not accompanied by heart failure alone. This case is presented to show that it is the first child in the literature and that the results of transpulmonary thermodilution can also give information about lung function as well as cardiac function.

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“…Prior to this analysis, only case reports have described the potential ADE of QTc 2 prolongation among patients receiving propofol for sedation in the ICU, making our study the largest assessment of propofol's effect on the QTc interval in the ICU at the time of writing [Sakabe et al 2002;Irie et al 2010;Douglas and Cadogan, 2008]. While the use of QTc-prolonging medications was measured during the infusion time period, specific factors including doses, dosing intervals or durations of use may have also been associated with outcomes.…”

Section: Discussionmentioning

confidence: 99%

“…Conversely, a 78-year-old woman developed torsade de pointes after receiving two bolus doses of propofol for sedation for cast placement of a spiral fracture of the distal tibia. An ECG was not obtained during cast placement, though baseline QTc and post event QTc were both within normal range (415 and 405 ms, respectively) [Douglas and Cadogan, 2008]. Finally, a 70-year-old man with multiple acute medical issues and an albumin of 1.4 g/dl was given propofol for mechanical ventilation.…”

Section: Discussionmentioning

confidence: 99%

“…Case reports have suggested propofol induces QTc prolongation in acutely ill patients with risk factors, such as acute cardiovascular disease, hypoalbuminemia or trauma [Sakabe et al 2002;Irie et al 2010;Douglas and Cadogan, 2008]. Additionally, propofol has been associated with fatal ventricular dysrhythmias secondary to propofol infusion syndrome [Fong et al 2008], a rare but potentially fatal adverse reaction to propofol infusions.…”

Section: Introductionmentioning

confidence: 99%

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Propofol-associated QTc prolongation

Scalese

Herring

Rathbun

et al. 2016

Therapeutic Advances in Drug Safety

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Objectives: Propofol is a preferred agent for sedation in patients in the intensive care unit (ICU) due, in part, to its established safety profile. Despite this, recent case reports have suggested a potential for prolongation of the corrected QT interval (QTc) in ICU patients receiving propofol, though limited empirical work has been conducted to evaluate this association. As such, the purpose of this study was to assess the relationship between propofol infusion and QTc prolongation in a historical cohort of ICU patients. Methods: A single-center, historical, observational, pre-post cohort analysis of medical records from admitted patients ⩾18 years old with cardiovascular disease was conducted, involving cases who received propofol infusion for ⩾3 hours with sequential electrocardiogram monitoring from 2006 to 2012. A multivariable, generalized linear model regression was employed to assess the primary outcome of on-propofol QTc interval (QTc 2 ), controlling for various demographic and clinical factors. Results: A total of 96 patients met inclusion criteria, averaging 56.1 ± 14.1 years of age and 86.1 ± 25.0 kg, with 37.5% being female. A mean prolongation in QTc interval of 30.4 ± 55.5 ms (p < 0.001) was observed during the propofol infusion, with 43.8% of cases exhibiting an on-infusion QTc 2 of ⩾ 500 ms. Regression analyses suggested that prolongation in on-propofol QTc was independently associated with baseline QTc interval and amiodarone use, while weight as inversely associated with QTc 2 (p < 0.05). Conclusion:This historical cohort analysis of adult ICU patients receiving propofol suggests that on-infusion QTc prolongation was associated with increasing baseline QTc interval and with amiodarone use. Further research is needed to evaluate the clinical significance and cause-and-effect relationship between potential QTc changes and propofol use in the ICU.

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Cardiac arrhythmia during propofol sedation

Cited by 19 publications

References 16 publications

QT Interval Prolongation and Torsade de Pointes Induced by Propofol and Hypoalbuminemia

QT Interval Prolongation and Torsade de Pointes Induced by Propofol and Hypoalbuminemia

Cardiogenic Shock and Lung Injury as a Complication of Defibrillation

Propofol-associated QTc prolongation

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