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Nidine-Induced Bradycardia Nee L If Reports ) nidine-Induced Bradycardia nee L. Golusinski, Jr, MD, and B. Wayne Blount, MD, MPH , Georgia ne is an alpha-adrenergic agent that is used in atic or asymptomatic. This report proposes mechanisms itment of hypertension. Bradycardia has been de- for clonidine-induced bradycardia, describes persons at as a common effect of clonidine poisoning, but risk for this effect, and outlines treatments and preven­ dv been described as a side effect at commonly tive measures. ltd dosages. Bradyarrhythmias, as a side effect, Key words. Clonidine, bradycardia, hypertension. ,ve several manifestations and may be symptom­ (JFam Pract 1995; 41:399-401) intis an alpha-adrenergic agonist with sympatho- 100) and naproxen (Naprosyn) as needed. The 0.3 mg [tivity1-9 used in the treatment of hyperten- clonidine patch had been increased from a 0.2 mg 5,8,10-12 Clonidine has also been used to treat mi- clonidine patch 5 days before com ing to our office. His , menopausal complaints, narcotic withdrawal blood pressure at the first visit was 178/92 and his pulse ms,5 spasticity after spinal cord injury,9 and atten- was 62 beats per minute. H e was advised to discontinue :Scit hyperactivity disorder.6 Bradycardia is a side the enalapril and clonidine patch and was started on ena- Inly rarely described when clonidine is used at pre- lapril-hydrochlorothiazide (Vaseretic 10-25) twice daily. 1 dosages. Tw o days later, he returned to the office for a blood (e present a case report o f clonidine-induced brady- pressure check. His blood pressure was 170/96 and pulse jin the treatment of hypertension, followed by a was 84 beats per minute. The 0.2 mg clonidine patch was of the mechanisms, risk factors, treatment, and restarted. tion of this drug-induced side effect. Two weeks later, he returned with a blood pressure of 130/84 and pulse of 46 beats per minute. He had stopped taking the amlodipine because of concern regard­ i Report ing a blood pressure of 104/68 measured at home, but had continued taking his other medications. He had no ient was a 49-year-old man with a history of hy- symptoms of chest pain, shortness of breath, dizziness, or on. Four months before coming to our office, he orthostasis. He was instructed to monitor his pulse rate a hemorrhagic stroke with a left hemiparesis. He and to call should he develop symptoms. history of renal insufficiency or cardiac disease. One week later, he returned with a blood pressure of K presented to our office for follow-up of his 148/78 and a pulse of 50 beats per minute. An electro­ nsion, his medications included amlodipine (Nor- cardiogram (ECG) showed sinus bradycardia with bor­ 1 mg daily; enalapril maleate (Vasotec) 2 0 mg derline first-degree atrioventricular block and voltage cri­ illy; clonidine patch (Catapres-TTS-3) delivering teria for left ventricular hypertrophy. He complained of per day, applied weekly; paroxetine (Paxil) 20 mg fatigue, especially during physical therapy, but had no nd propoxyphene-acetaminophen (Darvocet-N orthostasis, dizziness, or other cardiovascular symptoms. The clonidine patch was discontinued and oral doxazosin imistd, July 3, 1995. mesylate (Cardura) 1-mg by mouth once a day, was added ypartment o f Family and Preventive Medicine, Emory University School o f to his regimen. Atlanta, Georgia. Requests fo r reprints should be addressed to Lawrence L. Six days later, he returned with blood pressure of ffMD, Department o f Family and Preventive Medicine, Emory Univer- MMedicine, 490 Peachtree St, NE, Suite 472-C, Atlanta, GA 30308. 160/90 and pulse of 64 beats per minute. He still had Appleton & Lange ISSN 0094-3509 urnal of Family Practice, Vol. 41, No. 4(Oct), 1995 399 Clonidine-Induced Bradycardia Golusinski and Bloun; symptoms of fatigue. His doxazosin was increased to 2 The exact mechanism responsible for this clonidine mg by mouth once a day. Subsequently, he elected to associated bradycardia is not well understood. The most have his hypertension managed by another physician. He plausible mechanisms are: (a) reduced sympathetic tone was contacted by telephone 1 month later and reported from central mediators,15 (b) increased vagal activity that his medications included lisinopril-hydrochlorothia- (c) stimulation of presynaptic alpha-2 receptors in the zide (Zestoretic 20-25) daily and doxazosin 8 mg at heart which have a blocking effect on heart rate,15 (J, bedtime. His blood pressure was 120/65 and pulse con­ decreased automaticity o f the bundles o f His,1-3-9 and (ej sistently greater than 60 beats per minute. He had no atrioventricular nodal block.1-7-11 It is probable that the complaints of fatigue. mechanisms vary from patient to patient. Patients at higher risk for clonidine-induced brady­ cardia seem to be those with an already-diseased conduc­ Discussion tion system, renal failure, high doses of clonidine, con­ comitant therapy with medications known to cause Clonidine enjoys wide clinical use, mainly as an antihyper­ bradycardia or heart block, (eg, b e t a blockers, verapamil tensive agent. It is an alpha-2 receptor agonist which acts hydrochloride, diltiazem, digoxin, reserpine, guanethi- centrally on postsynaptic alpha-adrenergic receptors in dine sulfate, and other antiarrhythmics), and a history of the medulla oblongata.1-2'412 This central effect results in bradycardia or advanced heart block while on these med­ decreased sympathetic outflow and enhanced vagal tone, ications. M-7-8-11-19 Our patient had none o f these risk fac­ lowering blood pressure and heart rate.1”3-7-10-13-15 This tors; however, his renal function was not checked, and may cause side effects of drowsiness, lethargy, dry records were not available to examine for previous con­ mouth,4-10 and parotidynia.13 Clonidine may also act duction abnormalities. peripherally within the heart to inhibit norepinephrine When treating a patient with clonidine-induced bra­ release,7-14-15 contributing to further reductions in dycardia, one should obtain an EGG to ascertain the type heart rate. Intentional overdoses and accidental poison­ and severity of the bradycardia. Clonidine should be re­ ings have resulted in depressed consciousness and duced in dosage or discontinued altogether. For severe, respirations, hypotension, miosis, seizures, hypotonia, symptomatic bradycardia, atropine can be used.2-4-6-16-19 hypothermia, hypertension, arrhythmias, and brady­ Because atropine’s half-life is shorter than that of cardia.^2-4-6,n,i2,i6,i7 pn contrast to the widely reported clonidine, repeated doses may be necessary'. For refractory bradycardiac results of clonidine poisoning, there have symptomatic cases, isoproterenol, epinephrine, dopa­ been only a few reports of symptomatic bradycardia as a mine, and pacing can be considered.4-12 side effect of antihypertensive therapy (<0.3% inci­ It is prudent to weigh these risk factors when consid­ dence),1-3-7^9-11-18_2H and none have been in the family ering initiating or increasing clonidine therapy,8 or when practice literature. using other centrally acting alpha-2 receptor agonists, The bradycardias reported have included sinus bra­ such as guanabenz and guanfacine, which may cause the dycardia, sinus arrest, nodal and junctional rhythms, sick same effect.21-22 This should include taking a thorough sinus syndrome, and all degrees of atrioventricular cardiac and medication history and possibly obtaining block.1-3-7-8-11-18“2H Our patient showed only sinus brady­ renal function tests and an EGG if the history indicates cardia and first-degree atrioventricular block. Some pa­ potential problems.9 W hen following a patient on tients were asymptomatic, whereas others experienced clonidine, the patient’s pulse rate and blood pressure symptoms of syncope,3-7-19 weakness and dizziness,3-19 should be checked.9 Clonidine should be used with cau­ fatigue with ambulation,20 and palpitations.3 Our pa­ tion in a patient with known sinus node dysfunction,19 tient’s fatigue during physical therapy resolved after and patients with renal impairment should be considered clonidine was discontinued. All patients reported in the for reduced dosages. literature developed the bradycardia after either starting clonidine or increasing its dosage. There was no consis­ tent dosage, however, above which bradycardia oc­ Acknowledgment curred.19 There were no reported deaths secondary to the We are grateful for the assistance o f Cindy Meier in the preparation of bradycardia, and most patients recovered normal cardiac this manuscript. activity after clonidine was discontinued or decreased in dosage. However, a few patients were unable to convert to normal sinus rhythm.8 Atropine was used successfully References in several patients to treat severely symptomatic bradycar­ 1. Kibler, LE , Gazes PC. Effect of clonidine on atrioventricular con­ dia.6-8-16-19 duction. JAMA 1977; 238:1930-2. 400 The Journal of Family Practice, Vol. 41, No. 4(Oct), 199o Clonidihc-1nduccd Bradycardia Golusinski and Blount ? Anderson RJ, Hart GR, Grumpier CP, Lerman MJ. Clonidine o v e r­ 13. van Zwieten PA. Antihypertensive action of clonidine (Catapresan). dose: report o f six cases and review o f the literature. Ann Emerg Contr Nephrol 1977; 8:200-12. Med1981; 1 0 :1 0 7 -1 2 . 14. De Jonge A, Timmermans PB, van Zwieten PA. Quantitative as­ I 2 Thormann J, Neuss H , Schlepper M, Mitrovic V. Effects of pects of alpha adrenergic effects induced by clonidine-like imidazo- I donidine on sinus node function in man. Chest 1981; 80:201-6. lidines. II. Central and peripheral bradycardia activities. J Pharma­ 4 Artman M, Boerth RC. Clonidine poisoning. Am J Dis Child 1983; col Exp Therapeut 1982;222:712-9. ' ' 137:171-4. 15. Van Zwieten PA, Thoolen MJ, Timmermans PB.
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