Electrophysiologic changes induced by external transthoracic countershock

Anderson, Gary J.; Reiser, Joseph

doi:10.1016/s0022-0736(83)80023-5

Cited by 7 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Over the next 24 h, glycogen depletion occurs with progressive mitochondrial damage, disruption of myofibrils, and dilation of sarcoplasmic reticulum and ttubules [8]. Functional cardiac abnormalities after shocks have also been described including regional contractile abnormalities after epicardial shocks, atrioventricular block, ectopy, supraventricular and ventricular tachycardia, pulseless electrical activity, and refractory ventricular fibrillation [8][9][10][11]. Profound but potentially reversible myocardial failure after resuscitation from cardiac arrest has been described by Tang et al [12] and Gazmuri et al [13].…”

Section: Defibrillation Injurymentioning

confidence: 99%

The nitric oxide synthase inhibitor NG-nitro-l-arginine decreases defibrillation-induced free radical generation

et al. 2004

View full text Add to dashboard Cite

show abstract

Section: Defibrillation Injurymentioning

confidence: 99%

The nitric oxide synthase inhibitor NG-nitro-l-arginine decreases defibrillation-induced free radical generation

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Multiple forms of conduction disturbance and bradyarrhythmias, as well as tachyarrhythmias, can evolve following electrical cardioversion 1-3. Rhythm abnormalities have been attributed to the depolarising action of the shock on the myocardium,4 5 but they may also be due to neurohumoral influences 6-8. Sympathetic activity is an important modulator of the electrophysiological properties and contractile function of the heart.…”

mentioning

confidence: 99%

Differential effects of defibrillation on systemic and cardiac sympathetic activity

Bode

Wiegand

Raasch

et al. 1998

Heart

View full text Add to dashboard Cite

Objective-To assess the eVect of defibrillation shocks on cardiac and circulating catecholamines. Design-Prospective examination of myocardial catecholamine balance during dc shock by simultaneous determination of arterial and coronary sinus plasma concentrations. Internal countershocks (10-34 J) were applied in 30 patients after initiation of ventricular fibrillation for a routine implantable cardioverter defibrillator test. Another 10 patients were externally cardioverted (50-360 J) for atrial fibrillation. Main outcome measures-Transcardiac noradrenaline, adrenaline, and lactate gradients immediately after the shock. Results-After internal shock, arterial noradrenaline increased from a mean (SD) of 263 (128) pg/ml at baseline to 370 (148) pg/ml (p = 0.001), while coronary sinus noradrenaline fell from 448 (292) to 363 (216) pg/ml (p = 0.01), reflecting a shift from cardiac net release to net uptake. After external shock delivery, there was a similar increase in arterial noradrenaline, from 260 (112) to 459 (200) pg/ml (p = 0.03), while coronary sinus noradrenaline remained unchanged. Systemic adrenaline increased 11-fold after external shock (p = 0.01), outlasting the threefold rise following internal shock (p = 0.001). In both groups, a negative transmyocardial adrenaline gradient at baseline decreased further, indicating enhanced myocardial uptake. Cardiac lactate production occurred after ventricular fibrillation and internal shock, but not after external cardioversion, so the neurohumoral changes resulted from the defibrillation process and not from alterations in oxidative metabolism. Conclusions-A dc shock induces marked systemic sympathoadrenal and sympathoneuronal activation, but attenuates cardiac sympathetic activity. This might promote the transient myocardial depression observed after electrical discharge to the heart. (Heart 1998;79:560-567)

show abstract

Defibrillatoren

Baubin

Breiteneder

2010

Notfall Rettungsmed

View full text Add to dashboard Cite

Electrophysiologic changes induced by external transthoracic countershock

Cited by 7 publications

References 21 publications

The nitric oxide synthase inhibitor NG-nitro-l-arginine decreases defibrillation-induced free radical generation

The nitric oxide synthase inhibitor NG-nitro-l-arginine decreases defibrillation-induced free radical generation

Differential effects of defibrillation on systemic and cardiac sympathetic activity

Defibrillatoren

Contact Info

Product

Resources

About