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Initially, classify the rate as fast (>120/minute), slow (<60/minute), or normal/near normal (60‐120/minute) based on the frequency of QRS complexes over 6 seconds multiplied by 10. After estimating rate, look for sinus P waves in those patients with normal or fast rates. Sinus P waves always precede the QRS complexes and have a consistent appearance and relationship (i.e., distance) to the QRS complexes.

As a simple rule, all unstable patients with nonsinus fast rhythms (no discernible P waves and QRS rate >120/ min) deserve immediate synchronized countershock with 100 J, increasing quickly if unsuccessful. Lower energy levels may convert specific rhythms, such as supraventricular tachycardia (SVT) or atrial flutter, but little benefit is gained by attempting to make fine distinctions in unstable patients. Although changes in heart rate that fall into the normal range can cause symptoms, these are usually of little importance during field management.

In general, lower energy biphasic waveform shocks are equally or more effective than monophasic shocks [4, 5]. However, no outcome benefit to biphasic waveforms exists [6]. If possible, use the defibrillator manufacturer’s recommended energy levels for cardioversion and defibrillation, recognizing that 100 J is a good first dose if unstable.

Patients with slow dysrhythmias only require classification of their stability. All other details (e.g., P wave characteristics, Type I or II second‐degree block, junctional versus ventricular escape) add little value in prehospital management. Slow stable dysrhythmias need no intervention besides continued monitoring for deterioration. Slow unstable dysrhythmias require external pacing (preferred) or atropine (0.5‐1 mg IV in adults, repeated up to 2‐3 mg total). Transcutaneous pacing is best started as early as possible to maximize the potential for mechanical or clinical capture and restoration of perfusion [7, 8]. Also, do not delay pacing in unstable patients to administer atropine. Conversely, concerns of clinical deterioration after atropine are unwarranted when the correct dose is given to those with symptomatic bradycardia, though there may be no response. In adults, a vasopressor infusion and an IV fluid bolus should be administered if transcutaneous pacing (or atropine) has normalized the heart rate but hypotension persists.

Internal pacemakers should prevent bradycardias, but they may malfunction. When a patient has pacer spikes on the ECG and is still bradycardic, the pacemaker is not working properly, and the patient should be treated in the same fashion previously described with atropine or external pacing. The pacer pads should be kept 10 cm or more away from the internal pacemaker pouch. In‐depth evaluation of pacemaker function should be deferred to the emergency department (see Chapter 11).

Bradycardias resulting from beta‐blocker or calcium channel blocker overdoses may be refractory to atropine. In these cases, glucagon (1‐3 mg IV) may improve the heart rate. Again, drug administration should not delay transcutaneous pacing.