Pacemaker induced ventricular fibrillation in coronary care units
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《英国医生杂志》
1 Cardiac Department, Poole Hospital NHS Trust, Poole BH15 2JB
Correspondence to: A A McLeod heartdoc@tcp.co.uk
Introduction
Case 1
A 64 year old man was admitted to the coronary care unit with acute inferior myocardial infarction. He was noted to be hypotensive and have a nodal rhythm with no atrial activity at 30 beats/min. There was no response to atropine. A temporary pacing electrode was inserted and connected to an external ventricular demand pacemaker. During the following two days, at least 15 episodes of ventricular fibrillation and many sustained episodes of ventricular tachycardia occurred. Review of the electrocardiograms showed occasional failure of pacing and sensing and of pacing impulses delivered into the ST segment and the T wave of spontaneous beats causing ventricular fibrillation (fig 1). The pacemaker was turned off. A bradycardia with first degree atrioventricular block was noted, but the episodes of ventricular fibrillation stopped immediately and did not recur.
Fig 1 Case 1. Top: Apparently satisfactory pacing (first QRS complex) is followed by fusion beats, but failure to sense becomes apparent when the pacemaker spike (narrow artefact) discharges into the ST segment. The first captured premature complex leads to ventricular tachycardia, which later degenerates into ventricular fibrillation. Further pacing spikes can be seen during the ventricular tachycardia. Bottom: Another ventricular fibrillation episode. The first paced beat is premature. The pacemaker has not sensed the first QRS complex. After two further beats, with the pacemaker discharging harmlessly during the QRS complex, another discharge in the vulnerable recovery phase of repolarisation leads to repetitive activity and ventricular fibrillation
Case 2
A 73 year old man was admitted with breathlessness and lethargy. He had experienced pain typical of myocardial infarction two days previously. He was taking an angiotensin converting enzyme inhibitor, a calcium antagonist, and a blocker for hypertension. His pulse was 32 beats/min, and an electrocardiogram showed complete heart block with left bundle branch block. His blood pressure was 70/30 mm Hg even after intravenous fluid administration. A temporary pacing electrode was inserted and ventricular demand pacing started. Troponin T was 4.58 μg/l (normal < 0.03 μg/l); creatine kinase was 1025 units/l (normal < 190 units/l). There was evidence of undiagnosed diabetes and renal impairment (glucose 20.8 mmol/l; urea 16.5 mmol/l; creatinine 311 μmol/l; HbA1C 0.092%). An echocardiogram showed inferior wall akinesis, moderate mitral regurgitation, and raised right ventricular systolic pressure.
He was treated with insulin, and blockade was stopped. Aspirin and simvastatin were also given.
His condition improved, but four days after admission he suddenly developed ventricular fibrillation. Defibrillation was achieved with a 360 J shock, after two shocks at 200 J were ineffective. Episodes of ventricular tachycardia also occurred. He was given an intravenous loading dose of amiodarone followed by a continuous infusion.
Three days later ventricular fibrillation recurred. Defibrillation with a single 200 J shock was successful. A magnesium infusion was started. Two further episodes occurred that night, each requiring defibrillation. Plans were made for referral to a tertiary cardiac centre for consideration of angiography, electrophysiological study, and a possible cardioverter or defibrillator implant.
Two days later he developed a temperature of 37.7°C. Intravenous benzylpenicillin and flucloxacillin were given. The following day the temporary pacing electrode was removed. The underlying rhythm was atrial fibrillation with a satisfactory ventricular response rate.
On day 10 a consultant cardiologist reviewed the monitor tracings of all the available episodes of ventricular fibrillation. All episodes seemed to be triggered by inadvertent pacing during the repolarisation phase of a non-sensed ventricular extrasystole. This was particularly noticeable when the extrasystole developed after a long escape cycle (fig 2). The ventricular stimulation threshold of the pacemaker was 1.0 V on day 1 and 0.6 V on day 2 but had risen to 1.8 V on day 4 and 2.1 V thereafter. blockers were subsequently reintroduced without further conduction problems, and warfarin treatment was started. Prolonged cardiac monitoring, including ambulatory monitoring, showed no recurrence of ventricular arrhythmias.
Fig 2 Case 2: The underlying cardiac rhythm is atrial fibrillation with a broad complex idioventricular rhythm at 55 beats/min. A ventricular extrasystolic escape beat is followed by pacemaker discharge (sharp biphasic spike artefact) with immediate ventricular fibrillation
Discussion
Wood M, Ellenbogen KA. Temporary cardiac pacing. In: Ellenbogen KA, ed. Cardiac pacing. 2nd ed. Oxford: Blackwell Sciences, 1996.
Mooss AN, Ross WB, Esterbrooks DJ, Nair C, Mohiuddin S, Sketch MH. Ventricular fibrillation complicating pacemaker insertion in acute myocardial infarction. Cath Cardiovasc Diag 1982;8: 253-9.
Mittal SR, Mahar MS, Gokhroo RK. Transvenous pacing in the presence of acute right ventricular infarction. Int J Cardiol 1992;34: 100-1.
Tavel ME, Fisch C. Repetitive ventricular arrhythmia resulting from artificial internal pacemaker. Circulation 1964;30: 493-500.
Chardack WM, Ishikawa H, Fochler FJ, Souther S, Gage AA. Pacing and ventricular fibrillation. Ann N Y Acad Sci 1969;167: 919-33.
Preston TA. Anodal stimulation as a cause of pacemaker-induced ventricular fibrillation. Am Heart J 1973;86: 366-72.
Sallam IA. Induced ventricular tachycardia and fibrillation by a fixed rate pacemaker. The fibrillation threshold in humans. Case report. J Cardiovasc Surg 1973;14: 443-5.
Seipel L, Bub E, Loogen F. Ventricular fibrillation induced by a unipolar implanted pacemaker (cathodal stimulation). Am Heart J 1976;92: 810-1.
Oupadia P, Ramaswamy K. Images in clinical medicine. "R-on-T" phenomenon. N Engl J Med 1998;338: 1812.
Preisman S, Cheng DCH. Life-threatening ventricular dysrhythmia with inadvertent asynchronous temporary pacing after cardiac surgery. Anesthesiol 1999;91: 880-3.
Langendorf R, Pick A, Winternitz M. Mechanisms of intermittent ventricular bigeminy. I. Appearance of ectopic beats dependent upon the length of the ventricular cycle, the "rule of bigeminy." Circulation 1955;11: 422-30.
Palmer DG. Interruption of T waves by premature QRS complexes and the relationship of this phenomenon to ventricular fibrillation. Am Heart J 1962;63: 367-73.
Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease. A textbook of cardiovascular medicine. 5th ed. London: Saunders, 2001.
Darp? B. Spectrum of drugs prolonging QT interval and the incidence of torsades de pointes. Eur Heart J 2001;3(suppl K): K70-80.(Andrew A McLeod, consulta)
Correspondence to: A A McLeod heartdoc@tcp.co.uk
Introduction
Case 1
A 64 year old man was admitted to the coronary care unit with acute inferior myocardial infarction. He was noted to be hypotensive and have a nodal rhythm with no atrial activity at 30 beats/min. There was no response to atropine. A temporary pacing electrode was inserted and connected to an external ventricular demand pacemaker. During the following two days, at least 15 episodes of ventricular fibrillation and many sustained episodes of ventricular tachycardia occurred. Review of the electrocardiograms showed occasional failure of pacing and sensing and of pacing impulses delivered into the ST segment and the T wave of spontaneous beats causing ventricular fibrillation (fig 1). The pacemaker was turned off. A bradycardia with first degree atrioventricular block was noted, but the episodes of ventricular fibrillation stopped immediately and did not recur.
Fig 1 Case 1. Top: Apparently satisfactory pacing (first QRS complex) is followed by fusion beats, but failure to sense becomes apparent when the pacemaker spike (narrow artefact) discharges into the ST segment. The first captured premature complex leads to ventricular tachycardia, which later degenerates into ventricular fibrillation. Further pacing spikes can be seen during the ventricular tachycardia. Bottom: Another ventricular fibrillation episode. The first paced beat is premature. The pacemaker has not sensed the first QRS complex. After two further beats, with the pacemaker discharging harmlessly during the QRS complex, another discharge in the vulnerable recovery phase of repolarisation leads to repetitive activity and ventricular fibrillation
Case 2
A 73 year old man was admitted with breathlessness and lethargy. He had experienced pain typical of myocardial infarction two days previously. He was taking an angiotensin converting enzyme inhibitor, a calcium antagonist, and a blocker for hypertension. His pulse was 32 beats/min, and an electrocardiogram showed complete heart block with left bundle branch block. His blood pressure was 70/30 mm Hg even after intravenous fluid administration. A temporary pacing electrode was inserted and ventricular demand pacing started. Troponin T was 4.58 μg/l (normal < 0.03 μg/l); creatine kinase was 1025 units/l (normal < 190 units/l). There was evidence of undiagnosed diabetes and renal impairment (glucose 20.8 mmol/l; urea 16.5 mmol/l; creatinine 311 μmol/l; HbA1C 0.092%). An echocardiogram showed inferior wall akinesis, moderate mitral regurgitation, and raised right ventricular systolic pressure.
He was treated with insulin, and blockade was stopped. Aspirin and simvastatin were also given.
His condition improved, but four days after admission he suddenly developed ventricular fibrillation. Defibrillation was achieved with a 360 J shock, after two shocks at 200 J were ineffective. Episodes of ventricular tachycardia also occurred. He was given an intravenous loading dose of amiodarone followed by a continuous infusion.
Three days later ventricular fibrillation recurred. Defibrillation with a single 200 J shock was successful. A magnesium infusion was started. Two further episodes occurred that night, each requiring defibrillation. Plans were made for referral to a tertiary cardiac centre for consideration of angiography, electrophysiological study, and a possible cardioverter or defibrillator implant.
Two days later he developed a temperature of 37.7°C. Intravenous benzylpenicillin and flucloxacillin were given. The following day the temporary pacing electrode was removed. The underlying rhythm was atrial fibrillation with a satisfactory ventricular response rate.
On day 10 a consultant cardiologist reviewed the monitor tracings of all the available episodes of ventricular fibrillation. All episodes seemed to be triggered by inadvertent pacing during the repolarisation phase of a non-sensed ventricular extrasystole. This was particularly noticeable when the extrasystole developed after a long escape cycle (fig 2). The ventricular stimulation threshold of the pacemaker was 1.0 V on day 1 and 0.6 V on day 2 but had risen to 1.8 V on day 4 and 2.1 V thereafter. blockers were subsequently reintroduced without further conduction problems, and warfarin treatment was started. Prolonged cardiac monitoring, including ambulatory monitoring, showed no recurrence of ventricular arrhythmias.
Fig 2 Case 2: The underlying cardiac rhythm is atrial fibrillation with a broad complex idioventricular rhythm at 55 beats/min. A ventricular extrasystolic escape beat is followed by pacemaker discharge (sharp biphasic spike artefact) with immediate ventricular fibrillation
Discussion
Wood M, Ellenbogen KA. Temporary cardiac pacing. In: Ellenbogen KA, ed. Cardiac pacing. 2nd ed. Oxford: Blackwell Sciences, 1996.
Mooss AN, Ross WB, Esterbrooks DJ, Nair C, Mohiuddin S, Sketch MH. Ventricular fibrillation complicating pacemaker insertion in acute myocardial infarction. Cath Cardiovasc Diag 1982;8: 253-9.
Mittal SR, Mahar MS, Gokhroo RK. Transvenous pacing in the presence of acute right ventricular infarction. Int J Cardiol 1992;34: 100-1.
Tavel ME, Fisch C. Repetitive ventricular arrhythmia resulting from artificial internal pacemaker. Circulation 1964;30: 493-500.
Chardack WM, Ishikawa H, Fochler FJ, Souther S, Gage AA. Pacing and ventricular fibrillation. Ann N Y Acad Sci 1969;167: 919-33.
Preston TA. Anodal stimulation as a cause of pacemaker-induced ventricular fibrillation. Am Heart J 1973;86: 366-72.
Sallam IA. Induced ventricular tachycardia and fibrillation by a fixed rate pacemaker. The fibrillation threshold in humans. Case report. J Cardiovasc Surg 1973;14: 443-5.
Seipel L, Bub E, Loogen F. Ventricular fibrillation induced by a unipolar implanted pacemaker (cathodal stimulation). Am Heart J 1976;92: 810-1.
Oupadia P, Ramaswamy K. Images in clinical medicine. "R-on-T" phenomenon. N Engl J Med 1998;338: 1812.
Preisman S, Cheng DCH. Life-threatening ventricular dysrhythmia with inadvertent asynchronous temporary pacing after cardiac surgery. Anesthesiol 1999;91: 880-3.
Langendorf R, Pick A, Winternitz M. Mechanisms of intermittent ventricular bigeminy. I. Appearance of ectopic beats dependent upon the length of the ventricular cycle, the "rule of bigeminy." Circulation 1955;11: 422-30.
Palmer DG. Interruption of T waves by premature QRS complexes and the relationship of this phenomenon to ventricular fibrillation. Am Heart J 1962;63: 367-73.
Zipes DP. Specific arrhythmias: diagnosis and treatment. In: Braunwald E, ed. Heart disease. A textbook of cardiovascular medicine. 5th ed. London: Saunders, 2001.
Darp? B. Spectrum of drugs prolonging QT interval and the incidence of torsades de pointes. Eur Heart J 2001;3(suppl K): K70-80.(Andrew A McLeod, consulta)