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For patients who present in an emergency setting with symptomatic bradycardias, usually drugs like atropine or sympathomimetic drugs (epinephrine or dopamine) can be used to increase the heart rate to an adequate level until the underlying cause of the bradycardia can be isolated and then, possibly, a permanent pacemaker can be placed.
Sinus bradycardia due to a hypersensitive vagus nerve; Organophosphate based nerve agent poisoning, such as VX, sarin, tabun, and soman (atropine is favoured in conjunction with an oxime, usually pralidoxime) [6] [7]
For symptomatic bradycardia, the usual dosage is 0.5 to 1 mg IV push; this may be repeated every 3 to 5 minutes, up to a total dose of 3 mg (maximum 0.04 mg/kg). [23] Atropine is also useful in treating second-degree heart block Mobitz type 1 (Wenckebach block), and also third-degree heart block with a high Purkinje or AV-nodal escape rhythm.
Bradycardia can also result from the inhibition of the flow of action potentials through the atrioventricular (AV) node. While this can be normal in young patients due to excessive vagus nerve tone, symptomatic bradycardia due to AV node dysfunction in older people is commonly due to structural heart disease, myocardial ischemia, or age-related ...
Acetylcholine hyperpolarizes the sinoatrial node; this is overcome by MRAs, and thus they increase the heart rate. If atropine is given by intramuscular or subcutaneous injection, it causes initial bradycardia. This is because when administered intramuscularly or subcutaneously atropine acts on presynaptic M1 receptors (autoreceptors).
The primary endogenous agonists of the sympathetic nervous system are the catecholamines (i.e., epinephrine [adrenaline], norepinephrine [noradrenaline], and dopamine), which function as both neurotransmitters and hormones. Sympathomimetic drugs are used to treat cardiac arrest and low blood pressure, or even delay premature labor, among other ...
In the 1850s, atropine was used as antispasmodic in asthma treatment and as morphine antidote for its mydriatic effect. [4] Bezold and Bloebaum showed that atropine blocked the effects of vagal stimulation on the heart in 1867. Subsequently in 1872, Heidenhain found its ability to prevent salivary secretion. [6]
The mainstay of drug therapy for PEA is epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit. [3]