title: ECG changes following cardioversion and defibrillation.
abstract: BACKGROUND
  changes of the QRS amplitude following defibrillation or cardioversion have never been reported in humans.
  
  
  METHODS
  prospective analysis of patients externally cardioverted or defibrillated for ventricular and supraventricular tachyarrhythmias. Patients with coronary artery disease (CAD) and acute coronary syndrome (ACS) formed group A and patients without CAD but with external cardioversion/defibrillation formed group B. Patients in the control group (group C) experienced a shock by an Internal Cardioverter Defibrillator (ICD). All patients underwent the same study protocol: serial ECG's were recorded and sums (Sigma) of the QRS amplitude created separately for the precordial and peripheral leads. Sigma were then compared with baseline values and changes indicated as percentage (%).
  
  
  RESULTS
  We included a total of 45 patients in our study: 21 patients (47%) in group A, 11 patients (24%) in group B and 13 patients (29%) in group C. Median age was 66 years in group A, 55 in group B and 52 in group C. In group A mean change of the R amplitude was -35% in precordial and -16% in the peripheral leads. In group B mean change of the R amplitude was -16% in the precordial and -2% in the peripheral leads. The QRS amplitude changed -23% in the precordial leads in group A and -14% in group B. 13 patients with external defibrillation or cardioversion of group A + B and all patients of the control group (n = 13) showed no voltage changes. The most pronounced R and QRS attenuation was seen in patients with acute coronary syndrome, CAD and those in whom manual chest compressions had been necessary. Changes appeared after a mean period of 23 hours and returned to normal after a mean of 62 hours.
  
  
  CONCLUSIONS
  we report the phenomenon of reversible voltage loss after external defibrillation or cardioversion. A possible explanation for this phenomenon might be tissue oedema in the chest area after electrical and traumatic injury. An alternative reason might be myocardial stunning. The exact pathophysiological mechanism leading to reversible voltage attenuation remains unclear and needs further exploration in studies with a larger sample of patients.
authors.affiliation: Department of Cardiology, Kantonsspital Luzern, Luzern, Switzerland.
authors.forename: Florim
authors.initials: F
authors.lastname: Cuculi
authors.forename: Richard
authors.initials: R
authors.lastname: Kobza
authors.forename: Paul
authors.initials: P
authors.lastname: Erne
mesh_terms: D000368:Aged; D017147:Defibrillators, Implantable; D004554:Electric Countershock / Q000295:instrumentation*; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D013318:Stroke Volume / Q000502:physiology; D013617:Tachycardia, Supraventricular / Q000503:physiopathology* / Q000628:therapy; D017180:Tachycardia, Ventricular / Q000503:physiopathology* / Q000628:therapy; D016896:Treatment Outcome