Diastolic cardiac arrest induction

Diastolic cardiac arrest induction refers to the pharmacological process used mostly during cardiac surgery to stop the heart in a relaxed diastolic state ("diastolic arrest"), reducing metabolic demand and oxygen consumption. This is achieved by targeting the excitation-contraction coupling in cardiac myocytes, most commonly by using cardioplegic solutions containing potassium (and often magnesium), which alter the resting membrane potential to inactivate sodium channels and induce arrest without sustained contraction. Beta-blockers such as esmolol can also induce diastolic arrest by strong negative inotropy and suppression of action potentials at high concentrations[1][3][4][5]. This process is not a molecular target but a clinical and physiological endpoint; the true molecular targets are the ion channels involved in myocardial excitation. The target entry "Diastolic cardiac arrest induction" is *incorrect*: it describes a surgical/physiological approach, not a single molecule, protein, receptor, or gene. For structured data, list the relevant individual molecular targets (e.g., sodium channel, L-type calcium channel, potassium channel) or the specific induced state, not the induction process itself[1][3][5].

Other names

Cardioplegic arrest (diastolic)Diastolic arrestDiastolic cardiac standstill

Inhibition of action potential via elevated extracellular potassium (depolarized arrest); Inhibition of sodium and calcium entry; Blockade of adrenergic stimulation (e.g., by beta-blockers)