Lack of Response to Intravenous Calcium in Severe Verapamil Poisoning

Crump, B J; Holt, David W.; Vale, J. A.

doi:10.1016/s0140-6736(82)90912-6

Cited by 90 publications

(26 citation statements)

References 8 publications

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“…He was ventilated, and haemofiltered because of acidosis and a rising serum creatinine (maximum 424 g1M). His cardiac output was 8.6 1 min -1 (reference range 4-8), pulmonary capillary wedge pressure 21 mm Hg (6)(7)(8)(9)(10)(11)(12), and systemic vascular resistance 456 dyn s-1 m-2 (800-1200). He required dopamine, noradrenaline, and adrenaline to maintain systolic pressure.…”

Section: Case Reportmentioning

confidence: 99%

“…In two patients the half-life was reportedly 8 and 13 h, but plasma concentrations were not shown in one case [6], and calculation of the half-life is not possible from the data given in another case [7].…”

Section: Pharmacokinetics Of Verapamil In Overdosementioning

confidence: 99%

“…Treatment regimens and outcomes in verapamil overdose have been inconsistent [6,7,[9][10][11][12][13][14][15][16][17]. There is no concentration-survival relation and serum concentrations do not predict outcome [11].…”

Section: Treatment Of Verapamil Overdosementioning

confidence: 99%

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Prolonged half‐life of verapamil in a case of overdose: implications for therapy.

Buckley

Aronson

1995

Brit J Clinical Pharma

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After an overdose of verapamil (2.4 g) in a 59‐year‐old man the apparent half‐life of verapamil was prolonged (15 h). The most likely mechanism is rate‐limiting absorption, although changes in clearance and volume of distribution may contribute. As the elimination half‐life of verapamil is increased in overdose, therapy may have to be continued for longer than expected. Moreover since the half‐life of absorption of verapamil in overdose may be prolonged, activated charcoal should be given in repeated doses, even if an ordinary‐release formulation has been taken.

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Section: Case Reportmentioning

confidence: 99%

Section: Pharmacokinetics Of Verapamil In Overdosementioning

confidence: 99%

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Prolonged half‐life of verapamil in a case of overdose: implications for therapy.

Buckley

Aronson

1995

Brit J Clinical Pharma

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“…The management of hypotension due to CCB toxicity remains a challenge. Calcium, glucagon, atropine, catecholamines, insulin/glucose, cardiac pacing, intra-aortic balloon counterpulsation, and extracorporeal membrane oxygenation have not been uniformly successful (1)(2)(3)(4)(5)(6)(7)(8). We report two patients with massive CCB overdose in whom addition of vasopressin restored the blood pressure (BP) and SVR, an effect not achieved by calcium, glucagon, insulin, and maximal standard vasopressor therapies.…”

Section: Introductionmentioning

confidence: 99%

The use of vasopressin in the setting of recalcitrant hypotension due to calcium channel blocker overdose

Kanagarajan

Marraffa

Bouchard

et al. 2007

Clinical Toxicology

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Treatment of hypotension caused by calcium channel blocker overdose (CCB) remains a challenge. We describe the successful use of vasopressin in two patients with massive CCB overdoses in whom hypotension was unresponsive to calcium, glucagon, insulin, and conventional vasopressor therapies. While various modes of treatments have been used to treat the hypotension of CCB overdose, this is the first report to our knowledge of the successful use of vasopressin in this clinical setting.

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“…Hemodynamic collapse with bradyarrhythmias and heart block have been reported with intentional overdoses as well as with usual therapeutic doses of verapamil. There are case reports of successful treatment ofthese effects with intravenous calcium (1)(2)(3)(4) and beta adrenergic agonists (5,6). There are also conflicting reports of failure of calcium administration (5,6) and sympathomimetic amines (4,5) to reverse the toxic effects of verapamil.…”

Section: Introductionmentioning

confidence: 99%

Treatment of verapamil toxicity in intact dogs.

Gay¹,

Algeo²,

Lee³

et al. 1986

J. Clin. Invest.

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The treatment of verapamil toxicity was examined in lightly sedated dogs. Verapamil, administered as a bolus (0.72 mg/kg) followed by a continuous infusion (0.11 mg/kg per min), decreased cardiac output (CO) from 3.1±0.1 to 1.7±0.1 liter/min (P < 0.001), heart rate (HR) from 85±4 to 57±3 beats/min (P < 0.001), left ventricular derivative of pressure with respect to time (LV dP/dt) from 2,085±828 to 783±78 mm Hg/s (P < 0.001), mean aortic pressure (AO) from 77±4 to 38±2 mm Hg (P < 0.001) and stroke volume from 39±3 to 28±2 ml/beat (P < 0.01). In verapamil-toxic animals isoproterenol increased HR, CO, LV dP/dt, and AO, calcium chloride increased LV dP/dt and AO; norepinephrine, epinephrine, and dopamine increased CO, AO, and LV dP/dt, atropine increased HR, CO, and AO. Phenylephrine (13-55 ,ug/kg per min) produced no changes except a small increase in AO while very high dose phenylephrine (300 Ag/kg per min) increased AO, CO, and LV dP/dt. 4-Aminopyridine (4-AP) increased HR, CO, LV dP/dt, and AO. When administered prior to verapamil, 4-AP prevented the development of verapamil toxicity as shown by the significantly higher AO (P < 0.001), CO (P < 0.01), and LV dP/dt (P < 0.01) when 4-AP followed by verapamil was compared to verapamil alone. In conclusion, there does not appear to be a single specific therapy for verapamil toxicity, however it can be partially corrected by presently available pharmacologic therapy and 4-AP.

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Lack of Response to Intravenous Calcium in Severe Verapamil Poisoning

Cited by 90 publications

References 8 publications

Prolonged half‐life of verapamil in a case of overdose: implications for therapy.

Prolonged half‐life of verapamil in a case of overdose: implications for therapy.

The use of vasopressin in the setting of recalcitrant hypotension due to calcium channel blocker overdose

Treatment of verapamil toxicity in intact dogs.

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