defibrillator to the pacing mode with a rate of -80 bpm

and gradually increase the voltage until a normal ventricular rate is captured. Most patients will require IV analgesia

and sedation while pacing. When transcutaneous pacing

DYSRHYTHMIAS

fails, the placement of a temporary transvenous pacer

will be necessary. Obtain emergent cardiology consulta ­

tion in all Mobitz type II and third-degree patients, as

most will require intensive care/critical care unit admis ­

sion and definitive pacemaker placement.

Treat both junctional bradycardia and idioventricular

rhythms analogous to other bradyrhythmias if symptomatic. Accelerated idioventricular rhythms (rates >40 bpm)

often accompany myocardial infarction and reperfusion

and are typically well tolerated by the patient. Avoid treatment with typical antidysrhythmics and aggressively search

for the inciting event.

� Tachydysrhythmias

Tachydysrhythmias vary widely with regard to etiology,

severity, and treatment. Proper identification is essential to

ensure appropriate intervention. Rapidly determine patient

stability, as unstable patients require immediate electrical

cardioversion or defibrillation. For cardioversion, ensure

that the defibrillator is set to the SYNC mode before delivering the shock to avoid precipitating VF. Defibrillate

patients in pulseless VT and VF in the unsynchronized

(default) mode.

Treat AF and atrial flutter similarly by controlling the

ventricular response and evaluating for the source of the

tachycardia. Useful agents for slowing AV nodal conduction include beta-blockers, nondihydropyridine calcium

channel blockers (ie, diltiazem) and digoxin. Diltiazem is

an excellent first-line agent in the emergency department

(ED) and can be given as an initial bolus of 0.25 mg/kg

bolus followed by an infusion of 5-15 mg/hr. Carefully

monitor for signs of hypotension and administer a sec ­

ond bolus (0.35 mg/kg) in 15 minutes as necessary for

adequate rate control. Additional agents used to treat AF

with a rapid ventricular rate include procainamide and

amiodarone.

Treat SVT with vagal maneuvers and adenosine. Vagal

maneuvers such as carotid massage, ice-water immersion

of the face, and patient-induced Valsalva are sometimes

successful. If unsuccessful, administer escalating doses of

IV adenosine in doses of 6 mg, and then 12 mg. Administer

the medication rapidly, followed by a saline flush, as adenosine is quickly cleared from the circulation.

Clinically, VT can present as a stable perfusing rhythm,

a hemodynamically unstable patient, or a patient in cardiac

arrest. Treat such patients with antiarrhythmic agents

( eg, arniodarone, procainamide), synchronized cardioversion, or defibrillation, respectively.

Treatment of torsade de pointes should focus on

removing the inciting agent and narrowing the QT interval. IV magnesium sulfate (2 g slow IV push) is the firstline agent for treatment.

VF is never a stable rhythm. The rhythm tracing will

demonstrate no discernible P waves or QRS complexes. This

rhythm requires immediate defibrillation as it very quickly

deteriorates.

DISPOSITION

� Admission

Admit all patients with dysrhythmia accompanied by signs

of end-organ hypoperfusion or cardiac ischemia to an intensive care setting. Patients at risk for recurrent dysrhythmia or

in need of medication titration should be admitted to a

monitored setting.

� Discharge

Patients with known AVNRT who are successfully treated

in the ED or patients with AF/atrial flutter and adequate

rate control can be safely discharged provided they r emain

asymptomatic and have access to appropriate follow up.

SUGGESTED READING

Knight J Sarko J. Ventricular dysrhythmias. In: Peacock WF,