Key result
Intravenous clonidine significantly prolonged the sinus cycle by 71 ms (p<0.01), corrected sinus node recovery time by 81 ms (p<0.05), and functional refractory period of the AV node by 16 ms.
Why the study?
Does intravenous clonidine alter electrophysiologic properties and blood pressure in volunteers with normal baseline electrophysiologic data?
Does intravenous clonidine alter electrophysiologic properties and blood pressure in volunteers with normal baseline electrophysiologic data?
Mean Difference: 71
p-value: p=<0.01
Intravenous clonidine exerts electrophysiologic depressant effects similar to beta-blockers, suggesting caution when used in patients with baseline bradycardia or conduction delays.
Clonidine was associated with sinus and AV nodal depression in normal volunteers; leaves open net effects in patients with baseline conduction disease.
A few cases of sinus node dysfunction (SND) and AV block (AVB) were described with clonidine therapy. The aim of this study is to evaluate the electrophysiologic properties of clonidine in volunteers with normal electrophysiologic data. Twenty-eight subjects were investigated by endocavitary techniques. The following parameters were measured before and 20 min after intravenous administration of clonidine: systolic and diastolic blood pressure (BP); sinus cycle (SC); PA, AH, and HV intervals; effective (ERP) and functional (FRP) refractory period of right atria (RA); AV node (AVN); His Purkinje system (HP); right ventricle (RV); corrected sinus node recovery time (SNRT); and sinoatrial conduction time (SACT). Blood pressure was reduced from 149/89 to 115/74 mm Hg. Sinus cycle was prolonged by 71 ms (p less than 0.01), corrected SNRT by 81 ms (p less than 0.05), and FRP of AVN by 16 ms (p less than 0.05). SND was more marked when initial SC was longer. Atrioventricular node depression was more marked when the PR interval was longer and when subject was older. Electrophysiologic effects of clonidine are similar to those of beta-blockers. The tensional effects are more marked than electrophysiologic effects. Clonidine in the high risk subject (age, bradycardia, long PR) may be cautiously dosed. Drug association with digitalis antiarrhythmic drugs, beta-blockers, and calcium antagonists may be avoided.
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Clémenty et al. (1986) studied Normal electrophysiologic data (n=28). Clonidine vs. Baseline (before administration) was evaluated on Sinus cycle (71 ms prolongation, p=<0.01). Intravenous clonidine significantly prolonged the sinus cycle by 71 ms (p<0.01), corrected sinus node recovery time by 81 ms (p<0.05), and functional refractory period of the AV node by 16 ms.
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