Effects of Lidocaine and Verapamil on Defibrillation in Humans

Jones, Douglas L.; Klein, G. J.; Guiraudon, G; Yee, Raymond; Brown, Jason C. L.; Sharma, Aakriti

doi:10.1097/00132586-199208000-00064

Cited by 5 publications

(7 citation statements)

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“…Class IV drugs increase the DFT. This has been shown in human studies for verapamil [46,47]. The DFT was increased in the rabbit heart with diltiazem [48].…”

Section: Mixed Sotalol [56] Decreasesupporting

confidence: 59%

“…This in turn implies that there are less wavefronts for the defibrillation shock to extinguish. This is also demonstrated by the reduction in the frequency content and increase in signal coherence of VF by K + blocking agents [44,46]. In addition, the shock-induced extension of the refractory period is important for defibrillation.…”

Section: Mixed Sotalol [56] Decreasementioning

confidence: 95%

“…However, there are dramatic case reports of mexilitene raising the DFT [32,33]. II Atenelol [35], metoprolol [35], carvedilol [36] Minimal Case report of a patient whose DFT was doubled with carvedilol [38] III Ibutilide [39,40], dofetilide [38], azimilide [41][42][43] Decrease IV Diltiazem [47], verapamil [46,129] Increase…”

Section: Anti-arrhythmicsmentioning

confidence: 99%

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Achieving low defibrillation thresholds at implant: pharmacological influences, RV coil polarity and position, SVC coil usage and positioning, pulse width settings, and the azygous vein

Kroll

Schwab

2010

Fundamemntal Clinical Pharma

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Approximately 30% of implantable cardioverter defibrillator (ICD) patients still die of sudden death. A major cause of these sudden deaths is the failure to defibrillate because of failure to achieve a low defibrillation threshold (DFT). Anti‐arrhythmic drugs can have a profound positive or negative effect on the DFT. Unfortunately, present clinical practice continues to feature many procedures and tactics that have minimal to negative DFT benefit. In addition, many demonstrated helpful tactics are not understood or followed. This review covers the optimal RV (right ventricular) coil position and polarity, superior vena cava (SVC) coil positioning and usage, pulse width settings, and azygous vein coil implants. Specifically, the RV coil should be set to an anodal polarity and never ‘reversed’. The optimal RV coil position appears to be along the mid‐septum. The SVC coil should be kept out of the right atrium and placed in the innominate vein junction. The SVC coil should be always on for high impedance patients. For low impedance patients, the SVC coil should be set on or off depending on which setting gives the lowest DFT. Pulse widths should be set to correspond to optimally charging and discharging a cardiac membrane time constant of between 3.5 and 4.5 ms. For the highest DFT patients, a separate coil should be placed in the azygous vein and connected to the ICD ‘SVC’ port. Anachronistic approaches such as the use of polarity reversal, apical RV coil tip forcing, and subcutaneous arrays are also discussed.

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“…Class IV drugs increase the DFT. This has been shown in human studies for verapamil [46,47]. The DFT was increased in the rabbit heart with diltiazem [48].…”

Section: Mixed Sotalol [56] Decreasesupporting

confidence: 59%

Section: Mixed Sotalol [56] Decreasementioning

confidence: 95%

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Achieving low defibrillation thresholds at implant: pharmacological influences, RV coil polarity and position, SVC coil usage and positioning, pulse width settings, and the azygous vein

Kroll

Schwab

2010

Fundamemntal Clinical Pharma

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“…Verapamil increases DFTs. 175,176 It is prescribed to improve diastolic function in patients with hypertrophic cardiomyopathy and severe hypertrophy, who may independently be at risk for high DFTs. 128…”

Section: Cardiac Drugsmentioning

confidence: 99%

The Dilemma of ICD Implant Testing

Swerdlow

Russo

DeGroot

2007

Pacing Clinical Electrophis

130

112

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Ventricular fibrillation (VF) has been induced at implantable cardioverter defibrillator (ICD) implant to ensure reliable sensing, detection, and defibrillation. Despite its risks, the value was self-evident for early ICDs: failure of defibrillation was common, recipients had a high risk of ventricular tachycardia (VT) or VF, and the only therapy for rapid VT or VF was a shock. Today, failure of defibrillation is rare, the risk of VT/VF is lower in some recipients, antitachycardia pacing is applied for fast VT, and vulnerability testing permits assessment of defibrillation efficacy without inducing VF in most patients. This review reappraises ICD implant testing. At implant, defibrillation success is influenced by both predictable and unpredictable factors, including those related to the patient, ICD system, drugs, and complications. For left pectoral implants of high-output ICDs, the probability of passing a 10 J safety margin is approximately 95%, the probability that a maximum output shock will defibrillate is approximately 99%, and the incidence of system revision based on testing is < or = 5%. Bayes' Theorem predicts that implant testing identifies < or = 50% of patients at high risk for unsuccessful defibrillation. Most patients who fail implant criteria have false negative tests and may undergo unnecessary revision of their ICD systems. The first-shock success rate for spontaneous VT/VF ranges from 83% to 93%, lower than that for induced VF. Thus, shocks for spontaneous VT/VF fail for reasons that are not evaluated at implant. Whether system revision based on implant testing improves this success rate is unknown. The risks of implant testing include those related to VF and those related to shocks alone. The former may be due to circulatory arrest alone or the combination of circulatory arrest and shocks. Vulnerability testing reduces risks related to VF, but not those related to shocks. Mortality from implant testing probably is 0.1-0.2%. Overall, VF should be induced to assess sensing in approximately 5% of ICD recipients. Defibrillation or vulnerability testing is indicated in 20-40% of recipients who can be identified as having a higher-than-usual probability of an inadequate defibrillation safety margin based on patient-specific factors. However, implant testing is too risky in approximately 5% of recipients and may not be worth the risks in 10-30%. In 25-50% of ICD recipients, testing cannot be identified as either critical or contraindicated.

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“…Limited studies of intravenous calcium channel blockers [23] and some drugs with predominant Vaughan-Williams class I activity, such as quinidine, mexiletine and flecainide, may increase DFT (TaBle 2). Flecainide has been shown to increase the defibrillation energy requirements in animal models [24].…”

Section: Beadle Williams and Limmentioning

confidence: 99%

Drug-implantable cardioverter–defibrillator interactions

Beadle

Williams

Lim

2010

Expert Review of Cardiovascular Therapy

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Antiarrhythmic drugs are commonly used synergistically with implantable cardioverter defibrillators in the management of ventricular and supraventricular arrhythmias. However, these drugs may directly or indirectly interact with device function. In addition, expanding indications for implantable cardioverter defibrillators, particularly in patients with multiple comorbidities, further increases the potential for drug-device interactions. These potential drug-device interactions are summarized in this article.

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Effects of Lidocaine and Verapamil on Defibrillation in Humans

Cited by 5 publications

References 0 publications

Achieving low defibrillation thresholds at implant: pharmacological influences, RV coil polarity and position, SVC coil usage and positioning, pulse width settings, and the azygous vein

Achieving low defibrillation thresholds at implant: pharmacological influences, RV coil polarity and position, SVC coil usage and positioning, pulse width settings, and the azygous vein

The Dilemma of ICD Implant Testing

Drug-implantable cardioverter–defibrillator interactions

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