QRS duration shows how long ventricular depolarization takes on the ECG. In a healthy heart, this happens quickly, so the QRS complex is narrow. The normal upper limit is about 120 milliseconds (0.12 seconds), with many sources citing 60–100 ms as typical. Therefore, a QRS duration shorter than 120 ms is considered normal. When the QRS duration exceeds 120 ms, it signals delayed intraventricular conduction, such as a bundle branch block or other conduction abnormalities. Values like 150–170 ms or over 200 ms clearly indicate abnormal conduction. A value of 40–60 ms is shorter than typical for adults and is not regarded as the normal range in standard ECG interpretation.

Paroxysmal atrial fibrillation describes episodes that start and stop on their own, terminating within seven days (often within 24–48 hours). This duration pattern is what sets paroxysmal AF apart from persistent AF, which lasts longer than seven days and typically requires intervention to terminate. Long-standing persistent AF refers to continuous AF lasting more than 12 months, and nonvalvular AF simply describes AF not caused by a valvular issue, not its episode length. In this case, the spontaneous termination within seven days points to paroxysmal atrial fibrillation.

Pharmacological induction of arrhythmias relies on a drug that increases sympathetic stimulation to make abnormal electrical circuits more likely to fire. Isoproterenol, a beta-adrenergic agonist, does exactly that by raising heart rate and conduction and shortening refractory periods in atrial and AV nodal tissue. This makes it easier to provoke tachyarrhythmias in a controlled electrophysiology study, which is why it’s used for induction. Adenosine, by contrast, blocks AV conduction and often terminates AV nodal–dependent tachycardias rather than inducing them. Digoxin tends to slow conduction and can be proarrhythmic mainly in toxicity, not used to provoke inducible arrhythmias. Epinephrine can increase sympathetic activity but is less specific and not the standard induction agent in EP protocols.

In automatic tachycardia, the driving factor is increased automaticity of the pacemaker tissue, which comes from the diastolic depolarization phase. This is phase 4 of the cardiac action potential. When the slope of phase 4 is elevated, the membrane potential climbs to the threshold more quickly, causing impulses to fire sooner and at a faster rate. The other phases represent rapid depolarization (phase 0), the plateau (phase 2), and repolarization (phase 3) in working myocardium and are not the source of automatic firing. So the elevated phase is phase 4.