An example is an elderly patient with an irregular narrow‐complex tachydysrhythmia at a rate of 130/minute, complaining of weakness. Although rapid atrial fibrillation may contribute to the symptoms, no field treatment is needed in the absence of other clear signs or symptoms of decompensation. Those with instability deserve immediate countershock with 50 to 100 J. If transport is prolonged and the patient has either borderline symptoms or a rate of 140 to 180/minute, metoprolol (5‐10 mg intravenously) or diltiazem (0.15‐0.25 mg/kg intravenously) will control the ventricular rate in 85% to 90% cases of rapid atrial fibrillation [10, 11].
One pitfall in the treatment of stable narrow‐complex tachydysrhythmia is very rapid rates. When the ventricular rate is greater than 220/minute, the risk of decompensation rises and the ability to detect irregularity is limited [2]. Therefore, all adults with a very fast regular narrow‐complex tachydysrhythmia (heart rate >220/minute) should be either cardioverted with 100 J or treated with adenosine plus prepared for cardioversion. If the rate rises greater than 250/minute, cardioversion is the best choice given the risk of deterioration. Irregular narrow‐complex tachydysrhythmia greater than 220/minute deserves countershock promptly as previously noted (50‐100 J).
Stable wide‐complex tachydysrhythmias
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.
Controversies
Rhythm strip versus monitor interpretation
Besides clearly abnormal rhythms (e.g., obvious VT or severe bradycardia), interpret ECG from a tracing and not from the monitor screen. Not printing strips is tempting, but misclassifications may result from a “screen look.” Prehospital strips are valuable in the emergency department evaluation, documenting conditions before and after field treatment, which helps unravel the causes in certain dysrhythmias. At least two leads should be sampled.
Synchronization and sedation during countershock
When possible, delivering a countershock synchronized with the intrinsic QRS complexes is preferred. Synchronization helps avoid depolarization during the vulnerable phases of repolarization, theoretically decreasing the risk of postcountershock VF. During most dysrhythmias, the defibrillator unit senses the underlying QRS pattern and delivers the shock at the appropriate time. When the rhythm is extremely fast or irregular or the QRS complexes are markedly abnormal (i.e., very wide or small), sensing is difficult. In these cases, an unsynchronized countershock is appropriate. Electrophysiological data do not support the notion that this will increase the likelihood of VF. If postcountershock VF occurs, repeat countershock is usually successful in restoring an organized rhythm.
The usual controversy surrounding field countershock is the awake unstable patient. Medical oversight must clearly communicate the need for this unpleasant but lifesaving intervention for appropriate patients. Sedation with a benzodiazepine before countershock may improve patient comfort. However, countershock should not be delayed for unstable patients while awaiting clinical sedation.
Pediatric dysrhythmias
Children under the age of 5 years can sustain a sinus tachycardia at much higher rates (up to 225/minute) in response to physiological stresses. Look for hypovolemia, hypercarbia, and hypoxemia in stable children with narrow‐complex tachydysrhythmia before drug therapy is used. A volume challenge with 10 to 20 mL/kg of Ringer’s solution or another
