Bradydysrhythmias can be caused by two mechanisms: depression of sinus nodal activity or conduction system blocks. In both situations, subsidiary pacemakers take over and pace the heart; and provided the pacemaker is located above the bifurcation of the bundle of His, the rate is generally adequate to maintain cardiac output.
The need for emergent treatment of bradycardias is guided by two considerations: (1) evidence of hypoperfusion and (2) the potential to degenerate into a more profound bradycardia or ventricular asystole. In general, emergent treatment is not required, unless (1) the heart rate is below 50 and there is clinical evidence of hypoperfusion or (2) the bradycardia is due to structural disease of the infranodal conducting system (either transient or permanent) that has a risk of progressing to complete AV block. The first group of patients requires immediate treatment during assessment of the etiology of the bradycardia and consideration of whether internal pacing will be required. The second group of patients does not always require immediate treatment but should be monitored closely, with therapy readily available, while arrangements are made for further evaluation and possible internal cardiac pacing.
Three methods are currently available for emergent treatment of bradycardias: atropine, isoproterenol, and transcutaneous cardiac pacing.
Atropine should be the initial agent, at doses of 0.5 mg IV every 5 min until the desired response is achieved or a total vagolytic dose (about 0.05 mg/kg in humans) is given. Usually, if no response is seen by a dose of 2.0 mg, further doses are not effective. The vast majority of bradycardias due to problems of either the sinus or AV node respond to atropine. Even some patients with infranodal blocks may respond, so atropine deserves consideration in most bradycardias when emergent treatment is desired. Atropine can increase rate and myocardial oxygen consumption; therefore it has no place in an otherwise stable patient with bradycardia.
Isoproterenol can be used when atropine is ineffective, generally as a result of disease of the infranodal conducting system. Isoproterenol is given as a constant infusion, starting at a rate of around 0.5 pg/min and increasing as required to maintain a heart rate of 60. Isoproterenol increases myocardial oxygen demand, stimulates ventricular ectopy, and produces peripheral vasodilation, making it a less attractive agent than atropine. The reported response to isoproterenol is less than that observed with atropine, although isoproterenol is usually used only in patients who fail while receiving atropine. It is difficult to say how effective isoproterenol would be if used initially, and we do not suggest that.
External cardiac pacing represents a reemergence of an old concept with new electronics that make the technique more sensitive and likely to capture rhythm. This should be available in every emergency facility. The emergency physician must become familiar with the technique of applying the transcutaneous pacemaker so that it will sense and pace appropriately.
Internal pacing is the definitive treatment for progressive or persistent bradycardias. Emergent internal pacing is possible with the use of balloon-tipped flotation catheters, although, without fluoroscopic guidance, it is often technically difficult to achieve stable placement in a patient with low cardiac output.
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