Digitalis exerts its effect primarily on:
Myocardial depolarization
Digitalis (digoxin) acts primarily on the myocardium: by inhibiting the Na+/K+-ATPase it raises intracellular sodium and, through the Na+/Ca2+ exchanger, intracellular calcium. The result is enhanced excitation–contraction coupling and altered depolarisation of myocardial cells.
'Endocardial contraction' and 'endocardial systole' are not standard physiological terms, and digitalis is not primarily a repolarisation-only drug — its ECG footprint also involves depolarisation changes.
Hence, Myocardial depolarization.
During ECG monitoring, which drug is most likely to cause bradycardia?
During high-dose vasopressor therapy, which ECG change most reliably indicates supply–demand ischemia due to increased afterload?
Which type of stress test involves the use of medication instead of physical exercise?
Which ECG change most reliably indicates quinidine toxicity?
What is the most appropriate initial management for a patient presenting with symptomatic bradyarrhythmia?
What ECG change might be seen after administration of calcium channel blockers?
During ECG recording, which change most strongly suggests a therapeutic digitalis effect rather than myocardial ischemia?
During ECG monitoring, which drug is most likely to cause bradycardia?
During high-dose vasopressor therapy, which ECG change most reliably indicates supply–demand ischemia due to increased afterload?
Which type of stress test involves the use of medication instead of physical exercise?
Which ECG change most reliably indicates quinidine toxicity?
What is the most appropriate initial management for a patient presenting with symptomatic bradyarrhythmia?