The effect of newer antiarrhythmic drugs on defibrillation threshold

Tacker, Willis A.; Niebauer, Mark; Babbs, Charles F.; Combs, W.; Hahn, B; Barker, Melissa; Seipel, J F; Bourland, J. D.; Geddes, L. A.

doi:10.1097/00003246-198003000-00018

Cited by 83 publications

(12 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our observed effects of D M following lidocaine and bretylium are in accordance with previous studies (6,7) in pentobarbital anesthetized non-CPR dogs. In the previous study (6), a 3 mg/kg intravenous dose of lidocaine was shown to significantly increase DFT, but the onset of such an effect (at 20-30 min) was much delayed in comparison to our study (7).…”

supporting

confidence: 93%

“…In the previous study (6), a 3 mg/kg intravenous dose of lidocaine was shown to significantly increase DFT, but the onset of such an effect (at 20-30 min) was much delayed in comparison to our study (7). This difference may be attributable to differences in the anesthesia as well as experimental condition.…”

contrasting

confidence: 88%

“…Theoretically, drugs which influence sodium and potassium conductance of the transmembrance potential of the cardiac muscle cell can alter the defibrillation threshold (8). Lidocaine is known to increase potassium conductance and therefore can be expected to increase the defibrillation threshold (7,8).…”

mentioning

confidence: 99%

See 2 more Smart Citations

The Effect of Lidocaine and Bretylium on the Defibrillation Threshold during Cardiac Arrest and Cardiopulmonary Resuscitation

Chow

Kluger

Lawrence

et al. 1986

Experimental Biology and Medicine

View full text Add to dashboard Cite

The effect of intravenous lidocaine, 2 mg/kg, and bretylium, 5 mg/kg, on defibrillation threshold (DFT) was investigated in a-chloralose anesthetized dogs undergoing conventional closed chest cardiopulmonary resuscitation (CPR) following induced ventricular fibrillation. Ventricular fibrillation was induced electrically and CPR was performed by a pneumatic device set to compress the chest 60 times and inflate the lung 12 times a minute. Defibrillation was achieved using underdamped sinusoidal current shocks from a special defibrillator which allowed determination of delivered energy. The DFT was defined as the peak current which defibrillated, but no more than 20% higher than a current which did not defibrillate. All DFTs were obtained within 5 min of CPR. The mean k SD current and energy thresholds required for defibrillation during lidocaine-CPR (seven dogs) were 17.0 k 8.9 A and 53.0 k 40.7 J as compared to 12.5 k 6.2 A and 34.3 k 30.7 J, respectively during control-CPR (P < 0.05). The mean f SD current and energy thresholds during bretylium-CPR were 1 1 .O f 3.4 A and 24.1 k 1.3 J as compared to 1 1.8 k 1.7 A and 29.4 f 9.6 J, respectively, during control-CPR (NS). These results show that lidocaine acutely elevated defibrillation threshold whereas bretylium did not produce such an effect. The effect on DFT along with other pharmacologic properties should be considered when lidocaine or bretylium is used in the setting of cardiac arrest and CPR. o

show abstract

supporting

confidence: 93%

contrasting

confidence: 88%

See 1 more Smart Citation

The Effect of Lidocaine and Bretylium on the Defibrillation Threshold during Cardiac Arrest and Cardiopulmonary Resuscitation

Chow

Kluger

Lawrence

et al. 1986

Experimental Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…153,[155][156][157][158][159][160] Bretylium also makes defibrillation easier by lowering the electrical defibrillation threshold (DFT) (electrical energy needed to defibrillate the heart) compared with lidocaine and other class 1 drugs, all of which increase the DFT. 248 Indeed, bretylium may be given to any pulseless patient because in patients with cardiac standstill or severe hypotensive bradycardia, bretylium will increase impulse formation and powerfully potentiate administered catecholamines if they are needed to support blood pressure, as shown by Shifrin et al 154 in their septic shock patients. This would decrease the damage to the myocardium caused by excessive catecholamine administration and damage by frequent countershocks, as shown by the studies of Menegazzi et al 249 The ACLS protocol recommendation for immediate electrical countershock as the first step in resuscitation has a number of serious disadvantages.…”

Section: Bretylium Is a Unique Antifibrillatory Drugmentioning

confidence: 99%

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

View full text Add to dashboard Cite

It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholestero...

show abstract

“…Such a low dose of quinidine, although unlikely to cause adverse effects, can apparently facilitate electrical cardioversion, presumably by inhibiting vagal tone and prolonging refractoriness. Although results of some experimental studies 31,32 indicate that quinidine increases the energy needed for cardioversion, these findings could not be reproduced in other studies. 33 It is recommended that human patients receive quinidine 24 to 48 hours prior to cardioversion to prevent early relapse of atrial fibrillation.…”

mentioning

confidence: 90%

Use of biphasic electrical cardioversion for treatment of idiopathic atrial fibrillation in two horses

Frye

Selders²,

Mama³

et al. 2002

javma

View full text Add to dashboard Cite

Rectilinear biphasic cardioversion was used in 2 horses with idiopathic sustained atrial fibrillation; 1 horse converted to sustained sinus rhythm. Variables that potentially affected outcome of the electrical cardioversion procedures in these horses included duration of arrhythmia, placement of cardioverter pads and paddles, serum electrolyte concentrations, and treatment with quinidine. Serum cardiac troponin I concentration, measured to determine whether the myocardium was damaged from the electrical shocks, was within the reference range in both horses after the procedure. Biphasic electrical cardioversion may provide an alternative to pharmacologic cardioversion with quinidine in horses. The rectilinear biphasic defibrillator-cardioverter uses a unique biphasic waveform to deliver constant current to the myocardium during cardioversion, regardless of transthoracic impedance. Biphasic cardioversion is safer and more effective than traditional monophasic cardioversion in humans and animals.

show abstract

The effect of newer antiarrhythmic drugs on defibrillation threshold

Cited by 83 publications

References 10 publications

The Effect of Lidocaine and Bretylium on the Defibrillation Threshold during Cardiac Arrest and Cardiopulmonary Resuscitation

The Effect of Lidocaine and Bretylium on the Defibrillation Threshold during Cardiac Arrest and Cardiopulmonary Resuscitation

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Use of biphasic electrical cardioversion for treatment of idiopathic atrial fibrillation in two horses

Contact Info

Product

Resources

About