The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations

Brady, William J.; Swart, Gary L.; DeBehnke, Daniel J.; Ma, O.John; Aufderheide, Tom P.

doi:10.1016/s0300-9572(99)00032-5

Cited by 79 publications

(22 citation statements)

References 25 publications

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“…Clinical trials in adults [363][364][365][366][367] showed that IV atropine improved heart rate, symptoms, and signs associated with bradycardia. Atropine sulfate reverses cholinergic-mediated decreases in heart rate and should be considered a temporizing measure while awaiting a transcutaneous or transvenous pacemaker for patients with symptomatic sinus bradycardia, conduction block at the level of the AV node, or sinus arrest.…”

Section: Therapy (Figure 3 Box 5)mentioning

confidence: 99%

Part 8: Adult Advanced Cardiovascular Life Support

Neumar¹,

Otto²,

Link³

et al. 2010

Circulation

1,348

872

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Section: Therapy (Figure 3 Box 5)mentioning

confidence: 99%

Part 8: Adult Advanced Cardiovascular Life Support

Neumar¹,

Otto²,

Link³

et al. 2010

Circulation

1,348

872

View full text Add to dashboard Cite

“…2 Although several clinical studies have shown that administration of atropine improves heart rate, signs and symptoms in both in-hospital and out-of-hospital adults with acute symptomatic bradycardia, atropine is not indicated in bradycardia from high degree (second degree with Mobitz or third degree) atrioventricular block. 22 Atropine exerts its antibradycardic effects at the atrioventricular node and is unlikely to be effective if this block is at or below the Bundle of His. In such instances atropine can rarely accelerate sinus rate and atrioventricular node conduction.…”

Section: Discussionmentioning

confidence: 99%

Atropine Sulfate for Patients With Out-of-Hospital Cardiac Arrest due to Asystole and Pulseless Electrical Activity

Nagao

Yagi

Sakamoto

et al. 2011

Circ J

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Background:The 2005 guidelines for cardiopulmonary resuscitation (CPR) have recommended that administration of atropine can be considered for non-shockable rhythm, but there are insufficient data in humans. Methods and Results:The effects of atropine were assessed in 7,448 adults with non-shockable rhythm from the SOS-KANTO study. The primary endpoint was a 30-day favorable neurological outcome after cardiac arrest. In the 6,419 adults with asystole, the epinephrine with atropine group (n=1,378) had a significantly higher return of spontaneous circulation (ROSC) rate than the epinephrine alone group (n=5,048) with an adjusted odds ratio of 1.6 (95% confidence interval (CI) 1.4-1.7, P<0.0001), but the 2 groups had similar 30-day favorable neurological outcome with an adjusted odds ratio of 0.6 (95%CI 0.2-1.7; P=0.37). In the 1,029 adults with pulseless electrical activity (PEA), the 2 groups had similar rates of ROSC and 30-day favorable neurological outcome, and the epinephrine with atropine group had a significantly lower 30-day survival rate than the epinephrine alone group with an adjusted odds ratio of 0.4 (95%CI 0.2-0.9, P=0.016).Conclusions: Administration of atropine had no long-term neurological benefit in adults with out-of-hospital cardiac arrest due to non-shockable rhythm. Atropine is not useful for adults with PEA. (Circ J 2011; 75: 580 -588)

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“…One randomized clinical trial (LOE 1), 407 2 retrospective cohort studies (LOE 4), 408,409 and 2 additional observational studies (LOE 4) 410,411 documented that IV atropine improved heart rate and symptoms and signs associated with bradycardia. An initial dose of 0.5 to 1 mg, repeated as needed to a total of 1.5 to 3 mg, was effective in both in-hospital and out-of-hospital treatment of symptomatic bradycardia.…”

Section: Consensus On Sciencementioning

confidence: 99%