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Wide‐complex tachydysrhythmia can be due to VT or SVT with abnormal conduction. Until proven otherwise, assume any new wide‐complex tachydysrhythmia is due to VT. Hospital data suggest that about two thirds of patients with new wide‐complex tachydysrhythmias have VT. With a history of previous myocardial infarction, the frequency of VT increases to 90%. Although it is possible to assemble evidence to detect supraventricular rhythms from a detailed examination and 12‐lead ECG, these data are not easily obtained in the field. Thus, actions in managing wide‐complex tachydysrhythmia should either treat or cause no harm in VT.

All unstable patients with wide‐complex tachydysrhythmia should be cardioverted with 100 J, with escalating energy doses if needed. When stable or borderline, a few simple measures can help stratify patients. Observing this group is always an option, intervening only if conditions worsen.

If P waves precede each QRS complex during a stable wide‐complex tachydysrhythmia with a rate of 140/minute or less, a supraventricular source is likely, especially sinus or atrial tachycardia, although VT is a remote possibility. Treatment focuses on correcting any potential causes (e.g., pain, hypovolemia, or hypoxemia) and observation. Irregular QRS complexes suggest atrial fibrillation or multifocal atrial tachycardia. Neither requires field rhythm‐directed therapy in stable patients, although other actions (e.g., oxygen, bronchodilators) may be needed.

When no clear P‐QRS relationship exists, differentiating between SVT and VT is difficult during a wide‐complex tachydysrhythmia. These key features help decide a clinical course of action:

 A patient with new‐onset wide‐complex tachydysrhythmia and a history of previous myocardial infarction or VT very likely will have VT.

 VT will often not slow during vagal maneuvers. Therefore, slowing of a wide‐complex tachydysrhythmia during these efforts suggests SVT. However, the absence of change does not diagnose VT.

 Most VT does not respond to adenosine, whereas SVT usually slows or terminates. Conversely, lidocaine has little effect on most SVT and terminates 75% to 85% of VT.

 VT is usually regular and rarely seen at a rate of greater than 220/minute. Any chaotic wide‐complex tachydysrhythmia should be considered atrial fibrillation with abnormal conduction. When a chaotic wide‐complex tachydysrhythmia at a rate of greater than 220/minute occurs, atrial fibrillation from Wolff‐Parkinson‐White syndrome is present. This rhythm is prone to deterioration.

From these clinical observations, the following scheme can be used in approaching a stable or borderline (one minor sign or symptom of instability alone) patient with a wide‐complex tachydysrhythmia:

 All stable patients with regular wide‐complex tachydysrhythmia at a rate of 120 to 220/minute should attempt or receive vagal maneuvers. Those who slow but then elevate again should receive adenosine (6‐12 mg IV). If no slowing with vagal maneuvers occurs, one of three paths should be taken:

 Young (age <50 years) previously healthy patients with stable (or borderline) regular wide‐complex tachydysrhythmia that slows with vagal maneuvers should receive adenosine. If this fails, or nonresponse to vagal maneuvers exists or if the patient has had prior VT or prior MI, assume VT and give amiodarone (5 mg/kg IV over 5 minutes) or possibly lidocaine (1.0‐1.5 mg/kg IV up to 3 mg/kg). The American Heart Association has emphasized the role of amiodarone over lidocaine despite limited direct comparisons. If lidocaine converts the rhythm, repeat boluses at 5 to 10 minutes of 0.5 mg/kg should be given during transport to prevent recurrence. Continuous infusions after lidocaine loading are generally impractical in the field unless prolonged transport times are likely and infusion pumps are available.

 Because of the risk of deterioration, any patient with wide‐complex tachydysrhythmia at a rate of greater than 220/minute deserves countershock with 100 J, irrespective of symptoms.

 Patients with chaotic wide‐complex tachydysrhythmias usually have atrial fibrillation with altered conduction. If stable with a heart rate of less than 200/minute, close observation and expeditious transport will suffice. If the rate elevates to 220/minute or higher, immediate countershock with 100 J is indicated.