Clonidine bradycardia caused

The fact that the modes of action of clonidine and a-methylnoradrenaline are similar to the mode of action of the physiological transmitter noradrenaline indicates the importance of the role of the latter in the central control of blood pressure. It may be mentioned that 1-dopa too, the precursor of noradrenaline, penetrates the blood-brain barrier and causes hypotension and bradycardia after systemic administration, when do-... 

Caution [C, ] CrCl <30 Contra Component sensitivity, asthma, severe COPD, sinus bradycardia Disp Soln SE Irritation, bitter taste, superficial keratitis, ocular allergic Rxn EMS Drug is absorbed systemically OD May cause electrolyte disturbances (K), acidosis and bradycardia monitor ECG Doxazosin (Cardura, Cardura XL) [Antihypertensive/Alpha Blocker] Uses HTN symptomatic BPH Action < [-Adrenergic blocker relaxes bladder neck smooth muscle Dose HTN Initial 1 mg/d PO may be T to 16 mg/d PO BPH Initial 1 mg/d PO, may T to 8 mg/d XR 2-8mg qAM Caution [B, ] Use w/ PDE5 inhibitor (eg, sildenafil) can cause 1 BP Contra Component sensitivity Disp Tabs SE Dizziness, HA, drowsiness, sexual dysfxn, doses >4 mg T postural BP risk Interactions T Effects W/ nitrates, antihypertensives, EtOH i effects W/ NSAEDs, butcher s broom -t effects OF clonidine EMS Concurrent EtOH use can T drowsiness syncope may occur w/in 90 min of initial dose OD May cause profound hypotension place pt in supine position, give IV fluids, use pressors if needed... 

Toxicants may have three effects on pulse rate bradycardia (decreased rate), tachycardia (increased rate), and arrhythmia (irregular pulse). Alcohols may cause either bradycardia or tachycardia. Amphetamines, belladonna alkaloids, cocaine, and tricyclic antidepressants (see imi-primine hydrochloride in Figure 6.12) may cause either tachycardia or arrhythmia. Toxic doses of digitalis may result in bradycardia or arrhythmia. The pulse rate is decreased by toxic exposure to carbamates, organophosphates, local anesthetics, barbiturates, clonidine, muscaric mushroom toxins, and opiates. In addition to the substances mentioned above, those that cause arrhythmia are arsenic, caffeine, belladonna alkaloids, phenothizine, theophylline, and some kinds of solvents. 

Clonidine causes sinus bradycardia and atrioventricular block, as illustrated by two cases, one a 10-year-old boy (6) and the other a 71-year-old woman (7), who developed Wenckebach s phenomenon. Clonidine was also studied in seven patients subjected to electrophysiological studies after 5 weeks of therapy (8). It slowed the sinus rate and increased the atrial pacing rate, producing Wenckebach s phenomenon, indicating depressed function of the sinus and AV nodes. 

The most common side effect of clonidine is dose-dependent sedation that usually subsides after 2 to 3 weeks of therapy. Of concern are reports of bradycardia, rebound hypertension, heart block, and sudden death. Four children have died on the combination of methylphenidate and clonidine however, complicating factors make it impossible to link the drug combination directly with the cause of death. Of 10,060 children exposed to clonidine and assessed by a poison control center over a 7-year period, moderate (19%) to major (2%) toxic effects (bradycardia, hypotension, and respiratory depression) including one death were reported. Overdoses, concurrent clonidine and stimulant administration, as well as missed doses of clonidine aU add to the risk of adverse cardiovascular events. Similar adverse-effect concerns apply to treatment with guanfacine, although its U2a selectivity may result in less sedation and hypotension than clonidine. ... 

Overdosage with clonidine causes bradycardia, hypotension, CNS depression, respiratory depression, hypothermia, apnea, and hypoventilation. Atropine sulfate is able to reverse bradycardia, and epinephrine, dopamine, or tolazine are effective in combating hypotension. 

III. Clinical presentation. Manifestations of intoxication result from generalized sympathetic depression and include pupillary constriction, lethargy, coma, apnea, bradycardia, hypotension, and hypothermia. Paradoxic hypertension, caused by stimulation of peripheral alpha-1 receptors, may occur with clonidine, oxymetazoline, and tetrahydrozoline (and possibly guanabenz) and is usually transient. The onset of symptoms is usually within 30-60 minutes, although peak effects may occur more than 6-12 hours after ingestion. Full recovery is usual within 24 hours. In an unusual massive overdose, a 28-year-old man who accidentally ingested 100 mg of clonidine powder had a three-phase intoxication over 4 days initial hypertension, followed by hypotension, and then a withdrawal reaction with hypertension. 

Receptor interactions clonidine acts at postsyn-aptic alpha-2-adrenoreceptors in the CNS, mimicking the effects of norepinephrine to produce analgesia in animals and humans. Clonidine also stimulates release of the inhibitory neurotransmitters acetylcholine and norepinephrine in the dorsal horn. Stimulation of postsynaptic alpha-2-adrenoceptors in the brainstem and sympathetic preganglionic neurons in the spinal cord decreases sympathetic outflow, causing hypotension and bradycardia depending on the extent of spread. Alpha-2-adrenergic activity in the... 

Cardiovascular effect by virtue of its affinity for imidazoline receptors and alpha-2 receptors, tazani-dine causes bradycardia, a decrease in SBP and DBP of about 7-15% from the baseline. The effect is due to central sympatholytic activity similar to clonidine, albeit of lower magnitude. Change is dose-dependent and peaks at 90-120 minutes after oral intake [Ij. 

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