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Case Reports  |   July 2002
Propofol Induced Marked Prolongation of QT Interval in a Patient with Acute Myocardial Infarction
Author Affiliations & Notes
  • Masao Sakabe, M.D.
    *
  • Akira Fujiki, M.D.
  • Hiroshi Inoue, M.D.
  • *Fellow, †Assistant Professor, ‡Professor.
  • Received from the Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.
Article Information
Case Reports
Case Reports   |   July 2002
Propofol Induced Marked Prolongation of QT Interval in a Patient with Acute Myocardial Infarction
Anesthesiology 7 2002, Vol.97, 265-266. doi:
Anesthesiology 7 2002, Vol.97, 265-266. doi:
PROPOFOL is a widely used anesthetic drug and does not prolong corrected QT interval as much as other anesthetic agents, including midazolam. 1 Propofol is also used for induction and maintenance of general anesthesia, even in patients with either congenital or acquired long QT syndrome. 2 However, we experienced marked prolongation of the QT interval during anesthesia with propofol to allow mechanical ventilation in a patient with acute myocardial infarction.
Case Report
A 71-yr-old woman was admitted to our hospital because of acute anterior myocardial infarction. On admission, her pulse rate was 129 beats/min, and her blood pressure was 204/120 mmHg. An electrocardiogram showed QS pattern and ST elevation in V1–V3 and normal QRS duration (80 ms). QT interval corrected by heart rate (QTc) according to Bazett's formula 3 was 440 ms (fig. 1A). Serum potassium was 3.2 mEq/l, calcium was 8.9 mg/dl, and magnesium was 2.0 mg/dl. Blood gas analysis revealed pH 6.96, Pao275.9 mmHg, Paco2106.2 mmHg, base excess −11.3, and HCO323.4 mEq/l. The patient was intubated for ventilatory support. Propofol was given intravenously for induction (100 mg or 1.7 mg/kg) and maintenance (1.7 mg · kg−1· h−1) of sedation to allow mechanical ventilation. Four hours later, the QT interval was markedly prolonged as compared with the baseline value, and the QTc interval was prolonged to 690 ms (fig. 1B). QRS duration was not affected. At that time, serum concentrations of electrolytes still remained within the physiologic range; potassium was 3.9 mEq/l, calcium was 8.9 mg/dl, and magnesium was 2.0 mg/dl. Drugs concomitantly used were heparin (8,000 U/day), nitroglycerin (0.15 mg/h), dopamine (2.0 μg · kg−1· min−1), and piperacillin (4 g/day). Fortunately, lethal ventricular tachyarrhythmias, such as torsade de pointes, were not induced. The QTc interval was shortened to 490 ms after withdrawal of propofol (fig. 1C). Serum potassium was 3.9 mEq/l and calcium was 9.8 mg/dl, but magnesium was not measured at this point. Administration of propofol was repeated for challenge, and the QTc interval was prolonged again (fig. 1D). The QRS duration was 100 ms, and serum concentrations of electrolytes remained unchanged (potassium was 3.9 mEq/l and calcium was 10.0 mg/dl). Instead of propofol, midazolam (0.15 mg · kg−1· h−1) was given without prolongation of the QT interval. The patient has been free from any arrhythmic events for 1 yr after discharge. QT prolongation has not been documented at each visit of our outpatient clinic.
Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A  ) and after the administration of propofol (B  ). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C  ) and was reproduced with readministration (D  ) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C  ), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A 
	) and after the administration of propofol (B 
	). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C 
	) and was reproduced with readministration (D 
	) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C 
	), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A  ) and after the administration of propofol (B  ). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C  ) and was reproduced with readministration (D  ) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C  ), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
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Discussion
Many causes are known to induce prolongation of QT interval: antiarrhythmic drugs, psychotropic drugs, changes in electrolyte concentrations, lesions of the central nervous system, and changes in sympathetic tone. 4 Several investigators described unexpected, life-threatening ventricular tachyarrhythmias, sudden cardiac arrest, and death during general anesthesia in patients suffering from undiagnosed long QT syndrome. 5 The effect of anesthetic agents on QT interval has been studied. McConachie et al  . 3 reported that propofol prolonged the QT interval significantly, but the prolongation was small as compared with thiopentone. During induction of anesthesia with propofol, the QTc interval remained below the upper limit (440 ms) of the normal range in patients with normal QT intervals. In contrast, methohexital and midazolam did prolong the QT interval to exceed the upper limit. 2 Other investigators reported both propofol and midazolam did not change the QTc interval significantly. 6 Furthermore, sevoflurane prolonged the QTc interval significantly, and that was fully reversible when propofol was substituted for sevoflurane. 7,8 
The mechanism of QT prolongation during anesthesia might be due to a reduction in sympathoadrenergic activity with a concomitant increase in vagal tone. Sympathetic nerve activity was inhibited and sensitivity of baroreflex was decreased during anesthesia with propofol. 9 
Propofol inhibits L-type calcium channel directly and shortens the duration of action potential in isolated cardiac myocytes. 10 This effect is significantly greater than that on K+currents. 11 Both thiopentone and midazolam also have similar effects on inward Ca2+current. 11 The mean open time of single sodium channels was significantly reduced with propofol. 12 Taken together, the effects of propofol on the QT interval are quite complicated.
In the present case, the mechanism for QT prolongation remains unclear. There were no apparent causes for QT prolongation except the administration of propofol. QT prolongation disappeared after withdrawal of propofol and was reproduced with challenge test with propofol. In patients with coronary artery disease, prolongation of the QT interval could be associated with polymorphic ventricular tachycardia, known as torsade de pointes, and sudden death. 13 This was, however, not supported by other investigators. 14,15 Although ventricular tachyarrhythmias were not induced in our patient, propofol should be given cautiously in patients with acute myocardial infarction.
The authors thank Akira Masuda, M.D. (Associate Professor, Department of Anesthesiology, Toyama Medical and Pharmaceutical University, Toyama, Japan), for critical review of the manuscript.
References
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Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A  ) and after the administration of propofol (B  ). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C  ) and was reproduced with readministration (D  ) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C  ), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A 
	) and after the administration of propofol (B 
	). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C 
	) and was reproduced with readministration (D 
	) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C 
	), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
Fig. 1. Effects of propofol on QT interval. Electrocardiogram on admission (A  ) and after the administration of propofol (B  ). QTc interval was prolonged from 440 to 690 ms. QTc prolongation disappeared after withdrawal (C  ) and was reproduced with readministration (D  ) of propofol. Although R-R interval was also shortened after withdrawal of propofol (C  ), QTc was shortened disproportionately with shortening of R-R interval. All electrocardiograms were recorded at a standard gain (1 mV/10 mm) and paper speed (25 mm/s). On admission, echocardiography showed the presence of pericardial effusion (550 ml). The R-wave amplitude increased in accordance with reduction of the pericardial effusion.
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