What do qrs waves represent

The information contained within a single lead electrocardiogram can be extensive. Learning how to interpret the subtle differences in characteristic changes that can arise is a specialized skill that can take years to learn.

Fortunately, basic ECG interpretation can be rather straightforward, as long as you know the basics. An electrocardiogram is a tracing of the electrical activity that is taking place within the heart. Under normal circumstances, an electrical impulse will travel from the sinoatrial node, spread across the atrium, to the atrioventricular node and through the ventricular septum of the heart.

This electrical impulse causes the four chambers of the heart to contract and relax in a coordinated fashion. Studying these electrical impulses allows us to understand how the heart is functioning. The P wave represents the depolarization of the left and right atrium and also corresponds to atrial contraction. Strictly speaking, the atria contract a split second after the P wave begins.

U-wave inversion is rare but when seen, it is a strong indicator of pathology, particularly for ischemic heart disease and hypertension. The QT duration represents the total time for de- and repolarization. It is measured from the beginning of the QRS-complex to the end of the T-wave.

Prolonged QT duration predisposes to life-threatening ventricular arrhythmias and therefore QT duration must always be assessed. Prolonged QT duration may either be congenital genetic mutations, so-called long QT syndrome or acquired medications, electrolyte disorders. QT duration is inversely related to heart rate; QT duration increases at low heart rate and vice versa. The formula follows all variables in seconds :. QTc duration is calculated automatically in all modern ECG machines.

The result is based on the lead with the longest QTc duration typically leads V2—V3. Causes of prolonged QTc duration: antiarrhythmics procainamide, disopyramide, amiodarone, sotalol , psychiatric medications tricyclic antidepressants, SSRI, lithium etc ; antibiotics macrolides, kinolones, atovaquone, klorokine, amantadine, foscarnet, atazanavir ; hypokalemia, hypocalcemia, hypomagnesemia; cerebrovascular insult bleeding ; myocardial ischemia; cardiomyopathy; bradycardia; hypothyroidism; hypothermia.

A complete list of drugs causing QT prolongation can be found here. It is very rare but may cause malignant arrhythmias. The QT interval varies somewhat in the different leads. The difference between the shortest and the longest QT interval is the QT dispersion. Increased QT dispersion is associated with increased morbidity and mortality.

This is presumably explained by a higher incidence of malignant ventricular arrhythmias. It has been suggested that the high risk of ventricular arrhythmias is due to the vulnerability caused by marked local differences in the repolarization. Although often ignored, assessment of the electrical axis is an integral part of ECG interpretation.

The electrical axis reflects the average direction of ventricular depolarization during ventricular contraction. The direction of the depolarization and thus the electrical axis is generally alongside the hearts longitudinal axis to the left and downwards.

Figure 38 shows the coordinate system where the green area displays the range of normal heart axis. The axis is calculated to the nearest degree by the ECG machine. The following rules apply:. Normal in newborns. Right ventricular hypertrophy. Acute cor pulmonale pulmonary embolism. Chronic cor pulmonale COPD, pulmonary hypertension, pulmonary valve stenosis. Lateral ventricular infarction. Situs inversus. Left bundle branch block. Left ventricular hypertrophy. Inferior infarction. Most likely due to misplaced limb electrodes.

If the rhythm is tachycardia with wide QRS complexes, then ventricular tachycardia is the most likely cause.

A systematic approach to ECG interpretation. Introduction to ECG interpretation. Cardiac electrophysiology: action potentials, automaticity, electrical vectors. Cabrera format of the lead ECG.

Video lecture on ECG interpretation. Mechanisms of cardiac arrhythmias. Introduction to coronary artery disease ischemic heart disease. No products in the cart. Sign in Sign up. Search for:. Introduction to ECG Interpretation.

Clinical electrocardiography and ECG interpretation. Arrhythmias and arrhythmology. Mechanisms of cardiac arrhythmias: from automaticity to re-entry reentry.

Conduction Defects. Overview of atrioventricular AV blocks. Atrial and ventricular enlargement: hypertrophy and dilatation on ECG. Exercise stress test treadmill test, exercise ECG : Introduction.

Section 1, Chapter 5. In Progress. Overview of the normal electrocardiogram ECG. The QRS complex. The J point and the ST segment. The T-wave. The U-wave.

QT duration and QTc duration. The P-wave. P-wave checklist. PR interval and PR segment. PR interval checklist. The QRS complex ventricular complex. Naming of the waves in the QRS complex:. Net direction of the QRS complex. Electrical vectors that engender the QRS complex. Implications and causes of wide broad QRS complex. Amplitude of the QRS complex. R-wave amplitude. R-wave peak time. R-wave progression.

The Q-wave. Normal variants of Q-waves. Abnormal pathological Q-waves. Primary and secondary ST-T changes. ST segment depression.

Primary ST depressions. Secondary ST depression. ST segment elevation. Positive T-waves. Secondary T-wave inversion. Flat T-waves. Biphasic diphasic T-waves. The T-waves in children and adolescents. T-wave progression. T-wave checklist. QT dispersion. The electrical axis of the heart heart axis. Next chapter. Related chapters. Section Progress. ECG example 1. Normal sinus rhythm. ECG example 2.

R-waves have low amplitude, suggesting low voltage see below. ECG example 3. ECG example 4. ECG example 5. Sinus rhythm. Discrete ST-segment depressions in leads V5-V6. Some QRS complexes do not have all three deflections.

But irrespective of the number of waves present, they are all QRS complexes:. NB: The first wave of the last complex is a negative deflection. Therefore, it qualifies to be called a Q wave. Since all QRS complexes have an R wave, there must be one in this example as well, although it may be so small that it is not visible.

A negative deflection following an R wave is an S wave. Hence this single negative deflection deserves to be called a QS wave. QRS duration is the width of that complex from beginning to end, irrespective of the number of deflections present. Thus, normal conduction of an electrical impulse through the atrioventricular, or AV, node, then to the ventricles via the His-Purkinje system, is fast and results in a normal QRS duration.

When electrical activity does not conduct through the His-Purkinje system, but instead travels from myocyte to myocyte, a longer time is necessary, and the QRS duration is widened. A widened QRS duration occurs in the setting of a right bundle branch block, left bundle branch block, non-specific intraventricular conduction delay and during ventricular arrhythmias such as ventricular tachycardia — all of which are discussed in detail inside their respective sections in ECG Reviews and Criteria.