As a consequence, the LV is electrically activated throughout myocardial tissue. Although the term “block” suggests an abrupt interruption of conduction, there is a spectrum of conduction abnormalities varying from a proximal barrier to a more diffuse slowing of conduction. Secondly, a large number of heart failure patients have ventricular conduction disturbances, predominantly left bundle branch block (LBBB). As the atrial booster effect also contributes to timely closure of the atrioventricular valves, a prolonged AV delay can also lead to premature inversion of the atrioventricular pressure gradient resulting in diastolic mitral regurgitation. In case of a shortened or prolonged AV conduction, this preload enhancement is diminished or even lost. This booster function generates an increase in LV end-diastolic pressure at a relatively low mean venous pressure, thus protecting the pulmonary system from edema. The atrial contraction enhances ventricular preload by optimizing sarcomere length of ventricular myocytes prior to contraction which in turn increases LV stroke volume. First, in a subset of patients, there is a disturbance in coordination of atrial and ventricular activation with suboptimal timing of atrial contraction ( AV dyssynchrony). Pathophysiological electrical activation and mechanical contractionĪpart from decreased myocardial contractility, there are several other causes for decreased cardiac output in heart failure. Shortening of ventricular systole also enables longer ventricular filling time. Sympathetic stimulation at increasing heart rate shortens AV delay and ventricular systole, thus preventing atrial systole to occur against a closed mitral valve during exercise. Regulation and feedback is provided by pressure sensors in the venous and arterial vascular system. Autonomic and neurohormonal regulatory mechanisms ensure adequate cardiac output under varying physiological conditions. The latter is not only influenced by neurohormones, but also dependent on heart rate ( staircase phenomenon or Bowditch effect) and afterload ( Anrep effect). Ĭardiac output is dependent on preload ( Frank– Starling relation), afterload and myocardial contractility. Ventricular activation proceeds from subendocardially located breakthroughs of the bundle branches to the epicardium in a centrifugally and tangentially direction. Rapid conduction of the electrical impulse through the His bundle, bundle branches and the Purkinje system activates the whole left ventricle (LV) within 60–80 ms. Slowing of conducting through the AV node delays the onset of ventricular activation with approximately 80 ms to allow optimal atrial contribution to ventricular preload. The cardiac action potential originates in the sinus node and reaches the atrioventricular node (AV node) within 100 milliseconds (ms). Physiological electrical activation and mechanical contractionĪ coordinate contraction sequence of the heart chambers is facilitated by rapid activation via the specialized conduction system.
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