Pacing may improve cardiac output independently of effects on heart rate. Lone ventricular pacing dissociates the atrioventricular contraction sequence, in which atria contract against closed atrioventricular valves (pacemaker syndrome), reducing output by more than 20 per cent. Atrioventricular sequential pacing maintains the late diastolic atrial 'kick' and improves early diastolic inflow (the atrioventricular valves are open when the atria are full). Thus ventricular preload and cardiac output increase without a rise in venous pressures, particularly where ventricular filling is obstructed (e.g. mitral stenosis) or compliance is reduced. Such ventricular 'stiffness' may complicate myocardial hypertrophy, ischemia, fibrosis, or infiltration. Maintained atrioventricular synchrony may have advantages even in sinus bradycardia, as well as in dysrhythmias complicated by a lack of atrial contraction or a lack of co-ordination between atrial and ventricular contractions (e.g. complete heart block). Atrial activity can be sensed and the ventricle paced in response ('physiological pacing' or 'tracking'), or the chambers can be sequentially paced. The interval between atrial and ventricular activation is usually set at 150 to 200 ms.
Atrioventricular sequential pacing may improve ventricular performance in right ventricular infarction. A short atrioventricular delay may benefit the patient with poor left ventricular compliance, hypertrophic cardiomyopathy, severe dilated cardiomyopathy, or if an interatrial conduction time delay is causing late left atrial activation and contraction against a closed mitral valve.
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