What are common symptoms following a heart attack?

Correct answer: B.

B: Ventricular depolarization is the electrical activation of the ventricles that triggers ventricular contraction. It occurs after the impulse travels from the sinoatrial . On an electrocardiogram (ECG), ventricular depolarization is represented by the QRS complex, labelled as B in the diagram.

D: artrial depolarization - Atrial depolarization initiates atrial contraction, driven by impulses from the SA node. This electrical activity spreads across atrial myocardium, generating the P wave on the ECG and enabling ventricular filling.

E: ventricular repolarization - Ventricular repolarization restores the ventricles to their resting state after contraction. Represented by the T wave, it prepares the heart for the next depolarization, ensuring rhythmic cardiac cycles and effective pumping.

A. SA node: The sinoatrial node is the primary pacemaker of the heart. It is richly innervated by both sympathetic and parasympathetic fibers, allowing autonomic modulation of heart rate. Its sympathetic and parasympathetic balance is critical for initiating and regulating cardiac rhythm rather than forceful contraction.

B. Atria: The atrial myocardium receives autonomic innervation from both sympathetic and parasympathetic fibers. Parasympathetic input via the vagus nerve predominates in controlling heart rate and atrial conduction, whereas sympathetic input modulates contractility modestly. Atrial innervation is less dominated by sympathetic fibers compared with the ventricles.

C. Ventricles: Ventricular myocardium is more richly innervated by sympathetic fibers than parasympathetic fibers. Sympathetic stimulation increases ventricular contractility (positive inotropy) and conduction velocity, which enhances stroke volume and cardiac output during stress or exercise. Parasympathetic influence on ventricles is minimal.

D. AV node: The atrioventricular node is innervated by both sympathetic and parasympathetic fibers. Parasympathetic input slows conduction through the AV node, prolonging the PR interval, while sympathetic stimulation increases conduction velocity. However, its innervation is not predominantly sympathetic compared with ventricular myocardium.