Normal Electrocardiography (ECG) Intervals 

Updated: May 18, 2020
  • Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Buck Christensen  more...
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Normal Electrocardiography Intervals

Electrocardiography (ECG) is one of the most vital and readily used screening tool in clinical medicine. It is inexpensive and easily obtained in both the inpatient and outpatient setting. The ECG is used to diagnose numerous cardiac conditions, including prior infarction and active cardiac ischemia, as well as conduction abnormalities such as atrial fibrillation and life-threatening tachycardias. The information provided by ECGs is also used in determining which type of implantable cardiac defibrillator should be used for the management of advanced heart failure. Numerous noncardiac conditions, including electrolyte abnormalities and medication side effects, are also detectable on ECG owing to their distinct effect on conduction patterns. [1]

A well-planned approach to 12-lead ECG interpretation will prevent the interpreter from missing crucial information. Key aspects in the interpretation of the 12-lead ECG include the heart rate, the heart rhythm (both atrial and ventricular), the electrical axis (both the P-wave axis and the QRS axis), and knowledge of the normal intervals. Next, determine the relationship of P waves to QRS complexes. Finally, analyze the QRS morphology and ST and T-wave segments.

ECG paper commonly moves at 25 mm/second; thus, each small box (1 mm) is equivalent to 0.04 seconds (40 milliseconds), and each large box (5 mm) is equivalent to 0.2 seconds (200 milliseconds). At the beginning of an ECG, make note of the standardization square, normally 10 mm high by 5 mm wide. This will alert you to the correct paper speed and standard amplification of P, QRS, and T-wave complexes.

Normal ECG values for waves and intervals are as follows:

  • RR interval: 0.6-1.2 seconds
  • P wave: 80 milliseconds
  • PR interval: 120-200 milliseconds
  • PR segment: 50-120 milliseconds
  • QRS complex: 80-100 milliseconds
  • ST segment: 80-120 milliseconds
  • T wave: 160 milliseconds
  • QT interval: 420 milliseconds or less if heart rate is 60 beats per minute (bpm)

Basic Physiology of the Cardiac Conduction System

Physiologically, ECG tracing represents the conduction pathway through the heart. The normal conduction pathway originates in the sinoatrial (SA) node, which initiates sinus impulses, and a wave of depolarization spreads out over the right and left atria, forming the P wave. At the level of the atrioventricular (AV) node, the beat is conducted to the ventricles over the His bundle to the right and left bundle branches and the Purkinje system. The resulting atrial repolarization and early ventricular depolarization result in the QRS complex. Ventricular depolarization and subsequent repolarization lead to the completion of the cycle, forming the T-wave. The periods between each wave and complex are made up of intervals and segments. The PR, QT, and RR intervals represent the duration of conduction through the AV node, the duration of ventricular depolarization to repolarization, and the duration between each cardiac cycle, respectively. The PR and ST segments represent the isoelectric interval between depolarization and repolarization of the atria and ventricles.

Anatomy Corresponding to the Cardiac Conduction System

The right coronary artery (RCA) typically supplies blood to the SA node, right atrium, right ventricle, and right bundle branch; it may also supply the left posterior fascicle. When the posterior descending artery (PDA) arises from the RCA (“right dominance”), it usually supplies blood to the AV node. The left main coronary artery is typically 1-2 cm in length and gives rise to the left anterior descending coronary artery (LAD) and the left circumflex artery (LCx). The LAD typically gives off perpendicular branches (septal perforators) that supply the AV node and the left anterior and posterior fascicles. The posterior fascicle also receives blood from the RCA and thus has a dual blood supply. Other branches, called diagonal branches, supply areas of the left ventricle. The LCx supplies blood to the back of the heart, and its branches are called obtuse marginals (OM). A PDA that arises from the LCx are is described as “left dominance.” This explains why patients with proximal RCA infarcts often present with complete heart block or sinus arrest.

Cardiac Action Potential

At the molecular level, the complex phenomenon surrounding depolarization and repolarization of the cardiac action potential results from the movement of ions—mainly sodium, calcium, and potassium—across the cell membrane. [2]

The cardiac action potential cycle comprises five phases. The rapid upstroke of the ventricular myocyte action potential in phase 0 is caused by the rapid influx of sodium ions into the cell, generating a depolarizing (positive) current. When net intracellular charge reaches a well-defined threshold, cellular depolarization occurs. During the next 4 phases, the cardiac cell enters repolarization, which is the electrical reset allowing for the next beat.

Phase 1 results from inactivation of the inward sodium current and activation of a short-lived outward current. Phase 2 represents the plateau phase and consists of inward, depolarizing calcium currents and outward, repolarizing potassium currents. As the calcium currents decay, the potassium currents increase, ending the plateau phase. Phase 3 includes more rapid repolarizing currents and is generated by a family of potassium channels. The two main currents are described by their kinetics (slow and fast), and these channels are the targets for many class-III antiarrhythmic drugs. Phase 4 represents the resting state or electric diastole.

Cardiac arrhythmias are believed to result from abnormalities of impulse formation, impulse propagation, or repolarization. Tachycardias that result from impulse formation are termed automatic. Tachycardias that result from impulse propagation are considered reentrant. Tachycardias generated from abnormal repolarization result from genetic defects in ion channels (so-called channelopathies) and can be lethal. In addition, catecholamines, ischemia, cellular ion concentrations (potassium), and cardioactive medicines all influence the development of cardiac arrhythmias.