On the mechanisms underlying cardiac standstill: factors determining success or failure of escape pacemakers in the heart.

The mechanisms underlying cardiac standstill in health and disease are considered. Ventricular standstill results from failure of impulse formation or transmission in the ventricles. In the healthy heart, idioventricular automaticity is not brought into play and instead is suppressed by the sinus node by virtue of its faster rate (overdrive suppression). However, should the sinus node activity be suppressed or atrioventricular (AV) conduction blocked, overdrive suppression no longer persists. For this reason, the ventricular pacemakers activate the ventricles at a slow rate and under the regulatory activity of the sympathetic system. In the diseased heart, the idioventricular pacemakers or the regulatory mechanism can be altered structurally or functionally. This can be the result of the disease, compensatory mechanisms or therapeutic interventions. Disease may affect the idioventricular pacemakers directly or indirectly through anoxia, a change in ionic environment or an alteration of sympathetic innervation. Compensatory mechanisms may affect reflex actions, blood supply or heart rate. Drug administration may alter autonomic balance, block the action of neuromediators on their receptors or modify diastolic depolarization or its ability to attain the threshold. Because of these different direct and indirect actions, a sudden cessation of sinus node activity or sudden AV block may result in the diseased heart in a prolonged and even fatal cardiac standstill, especially if the tolerance to ischemia of other organs (notably the brain) is decreased.