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  • Title: Cardiac dysrhythmias in the acute setting: recognition and treatment or anyone can treat cardiac dysrhythmias.
    Author: Harken AH, Honigman B, Van Way CW.
    Journal: J Emerg Med; 1987; 5(2):129-34. PubMed ID: 3295015.
    Abstract:
    The two primary goals in dysrhythmia therapy are: to control the ventricular rate (between 70 and 100 beats per minute) and to maintain sinus rhythm. Maintenance of sinus rhythm is definitely secondary. If a patient is hemodynamically unstable, but has a ventricular rate between 60 and 100 beats per minute, the trouble is almost certainly not due to the cardiac rhythm. Normal conduction velocity is fast. An impulse is transmitted by healthy Purkinje fibers at 2 to 3 meters per second. This means that the entire ventricle, when activated by the Purkinje system, is activated in 80 milliseconds. When a superventricular impulse is transmitted to the ventricles via the A-V node, the ventricle should be activated (depolarized) in less than 80 milliseconds. Conversely, if an impulse is generated at an ectopic ventricular site, it does not access the high velocity Purkinje system as rapidly. A ventricular origin beat (PVC) thus, takes longer to activate the entire ventricle. The QRS is, therefore, longer (or wider). A wide QRS signifies aberrant ventricular conduction. When a dysrhythmia originates above the A-V node, the therapy is pharmacologic A-V nodal blockade (verapamil). When a dysrhythmia originates below the A-V node, therapy is pharmacologic (Lidocaine) or electrical (cardioversion). If uncertain or a patient is unstable, cardioversion is always acceptable. Thus; with an unstable patient, proceed immediately to cardioversion; with a narrow complex tachycardia (superventricular) proceed to verapamil; and with a wide complex (ventricular) tachycardia give Lidocaine and proceed to cardioversion.
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