inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen. Attach a monitorto the patient, evaluate blood pressure, and establish IVaccess. If possible, obtain a 12-lead ECG to better define therhythm. While initiating treatment, evaluate the patient’sclinical status and identify potentially reversible causes.The provider must identify signs and symptoms of poorperfusion and determine if those signs are likely to be causedby the bradycardia (Figure 3,
). If the signs andsymptoms are not due to bradycardia, the provider shouldreassess the underlying cause of the patient’s symptoms.Remember that signs and symptoms of bradycardia may bemild; asymptomatic or minimally symptomatic patients donot necessarily require treatment (Figure 3,
) unlessthere is suspicion that the rhythm is likely to progress tosymptoms or become life-threatening (eg, Mobitz type IIsecond-degree AV block in the setting of acute myocardialinfarction [AMI]). If the bradycardia is suspected to be thecause of acute altered mental status, ischemic chest discom-fort, acute heart failure, hypotension, or other signs of shock,the patient should receive immediate treatment.Atrioventricular (AV) blocks are classified as first-, second-,and third-degree. Blocks may be caused by medications orelectrolyte disturbances, as well as structural problems resultingfromAMIorothermyocardialdiseases.Afirst-degreeAVblock is defined by a prolonged PR interval (
0.20 second) and isgenerally benign. Second-degree AV block is divided intoMobitz types I and II. In Mobitz type I block, the block is at theAV node; the block is often transient and asymptomatic. InMobitz type II block, the block is usually below the AV nodewithin the His-Purkinje system; this block is often symptomatic,with the potential to progress to complete (third-degree) AVblock. Third-degree AV block may occur at the AV node,bundle of His, or bundle branches. When third-degree AV block is present, no impulses pass between the atria and ventricles.Third-degree AV block can be permanent or transient, depend-ing on the underlying cause.
Therapy (Figure 3, Box 5)
Atropine remains the first-line drug for acute symptomaticbradycardia (Class IIa, LOE B). Clinical trials in adults
showed that IV atropine improved heart rate, symptoms, andsigns associated with bradycardia. Atropine sulfate reversescholinergic-mediated decreases in heart rate and should beconsidered a temporizing measure while awaiting a transcu-taneous or transvenous pacemaker for patients with symp-tomatic sinus bradycardia, conduction block at the level of theAV node, or sinus arrest.
The recommended atropine dose for bradycardia is 0.5 mgIV every 3 to 5 minutes to a maximum total dose of 3 mg.Doses of atropine sulfate of
0.5 mg may paradoxicallyresult in further slowing of the heart rate.
Atropine admin-istration should not delay implementation of external pacingfor patients with poor perfusion.Use atropine cautiously in the presence of acute coronaryischemia or MI; increased heart rate may worsen ischemia orincrease infarction size. Atropine will likely be ineffective in
Neumar et al Part 8: Adult Advanced Cardiovascular Life Support