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Published on: July 3, 2013
Calcium channel blockers do not enhance increases in plasma potassium after succinylcholine in humans
G A Rooke1, P R Freund, J Tomlin
1Department of Anesthesiology, University of Washington School of Medicine, Seattle.
Insights
Chronic calcium channel blocker therapy does not increase the risk of hyperkalemia after succinylcholine administration. This study found no significant difference in plasma potassium levels between patients on these medications and those who were not.
Area of Science:
- Anesthesiology
- Clinical Pharmacology
- Cardiovascular Medicine
Background:
- Calcium channel blockers (CCBs) are widely used for cardiovascular conditions.
- Succinylcholine administration can cause a transient rise in plasma potassium.
- Potential for CCB therapy to exacerbate succinylcholine-induced hyperkalemia is a clinical concern.
Purpose of the Study:
- To investigate whether chronic calcium channel blocker therapy alters the plasma potassium response to succinylcholine.
- To assess the risk of hyperkalemia in patients on CCBs undergoing procedures requiring succinylcholine.
Main Methods:
- Prospective clinical study conducted at university and Veterans Affairs hospitals.
- 36 male patients (ASA III-IV) were divided into two groups: 21 on chronic CCBs and 15 not on CCBs.
- Anesthesia induced with opioids and hypnotics, followed by succinylcholine (1-1.5 mg/kg) for intubation without neuromuscular blocker pretreatment.
Main Results:
- Plasma potassium levels were monitored for 15 minutes post-succinylcholine administration.
- A modest average peak increase of 0.5 mEq/L in plasma potassium was observed.
- No significant difference in plasma potassium rise was detected between patients receiving CCBs and those who were not.
Conclusions:
- Chronic calcium channel blocker therapy does not appear to increase the risk of hyperkalemia following succinylcholine administration.
- Patients on CCBs can be safely administered succinylcholine without an exaggerated potassium response.
- Findings suggest current CCB use does not necessitate modification of succinylcholine protocols regarding hyperkalemia risk.
Study Objective:
To determine whether chronic calcium channel blocker therapy exaggerates the rise in plasma potassium concentration ([K+]) after succinylcholine administration.
Design:
Prospective clinical study.
Setting:
University and Veterans Affairs hospitals.
Patients:
36 ASA physical status III and IV male patients: 21 patients taking chronic calcium channel blockers and 15 patients not receiving calcium channel blockers, all of whom were scheduled for inpatient surgical procedures with general anesthesia.
Interventions:
In all patients, anesthesia was induced with high-dose opioids plus a sedative-hypnotic, and intubation was facilitated with 1 to 1.5 mg/kg succinylcholine without nondepolarizing neuromuscular blocker pretreatment.
Measurements And Main Results:
Plasma [K+] was measured prior to induction and 1, 3, 5, 8, 11, and 15 minutes after succinylcholine was administered. A modest average peak rise of 0.5 mEq/L in plasma [K+] was observed, but there were no differences between patients who were or were not receiving calcium channel blockers.
Conclusions:
Patients receiving chronic calcium channel blocker therapy are at no greater risk of hyperkalemia after succinylcholine than those not taking such medications.
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