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Transthoracic DC Shock May Represent a Serious Hazard in Pacemaker Dependent Patients
Author(s) -
ALTAMURA GIULIANO,
BIANCONI LEOPOLDO,
BIANCO FRANCESCO,
TOSCANO SALVATORE,
AMMIRATI FABRIZIO,
PANDOZI CLAUDIO,
CASTRO ANTONIO,
CARDINALE MARIO,
MENNUNI MAURO,
SANTINI MASSIMO
Publication year - 1995
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1995.tb02503.x
Subject(s) - medicine , defibrillation threshold , cardiology , shock (circulatory) , defibrillation , artificial cardiac pacemaker , cardioversion , anesthesia , atrial fibrillation
External defibrillation is widely used for the termination of various atrial and ventricular tachyarrhythmias, including pacemaker patients. Our study was intended to evaluate the effects of DC shocks in 36 patients with unipolar pacemakers implanted in the right pectoral region (25 DDD, 10 VVI, 3 AAI). The shocks were delivered with paddles on the anterior surface of the thorax, as far as possible away from the pacemaker. The pacing output was programmed at 0.5 msec and 5 V (25 patients), 4 V (1 patient), and 2.5 V (10 patients). Transient loss of capture occurred in 18 patients (50%). These patients, compared with those without capture failure, received higher peak and cumulative shock energies, respectively, 216 ± 99 versus 123 ± 50 joules (P < 0.002) and 352 ± 62 versus 147 ± 98 joules (P < 0.004) and had a lower pacemaker pulse amplitude (4.0 ± 1.2 vs 4.6 ± 1.0 V, P = 0.11). Failure to capture lasted from 5 seconds to 30 minutes (mean 157 sec). In 15 patients the ventricular stimulation threshold was measured before and serially after cardioversion. A six‐fold threshold increase was observed 3 minutes after the shock (P < 0.004) with gradual recovery to nearly baseline values at 24 hours. Transient sensing failure occurred in 7 of the 17 patients in whom it could be evaluated (41%). Furthermore, three cases of shock induced pacemaker malfunctions were observed requiring replacement of the stimulator in two patients. In conclusion, the incidence of loss of capture in pacemaker patients subjected to electrical cardioversion/defibrillation is high. The phenomenon is due to an abrupt rise in stimulation threshold, caused by the electrical shock, and may represent a serious hazard in pacemaker dependent patients. The risk of pacing failure could be reduced by utilizing low shock energies when possible, and by programming the pacemaker at its maximal output before cardioversion.