How long should the QRS complex be?
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Fred F. Ferri MD, FACP, in Ferri's Clinical Advisor 2022, 2022
FIG. 175. Algorithm for diagnosis of wide-QRS tachycardia. AP, Accessory pathway;AT, atrial tachycardia;AV, atrioventricular;AVRT, AV reentrant tachycardia;BBB, bundle branch block;LBBB, left bundle branch block;RBBB,
right bundle branch block;SVT, supraventricular tachycardia;VT, ventricular tachycardia. TABLE 64. Stepwise Criteria Favoring Ventricular Tachycardia Patients with Wide-Complex Tachycardias Using Different Algorithms
ACC, American College of Cardiology;AHA, American Heart Association;AV, atrioventricular;aVR, augmented vector right;ESC, European Society of Cardiology;LBBB, left bundle branch block;RBBB, right bundle branch block;VT, ventricular tachycardia. ‖Vereckei A et al: New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia.Heart Rhythm 5:89, 2008. ∗Blomström-Lundqvist C et al: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias).Circulation 108:1871, 2003.†Kindwall KE et al: Electrocardiographic criteria for ventricular tachycardia in wide complex left bundle branch block morphology tachycardias.Am J Cardiol 61:1279, 1988.‡Wellens HJ et al: The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex.Am J Med 64:27, 1978.§Brugada P et al: A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex.Circulation 83:1649, 1991.From Bloomstrom-Lundqvist C et al: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines [Writing Committee to Develop Guidelines for the Management of Patients with Supraventricular Arrhythmias],Circulation 108:1871, 2003; Mann DL et al:Braunwald’s heart disease, ed 10, Philadelphia, 2015, Elsevier. How to Make Basic ECG MeasurementsAry L. Goldberger MD, FACC, ... Alexei Shvilkin MD, PhD, in Goldberger's Clinical Electrocardiography (Ninth Edition), 2018 QRS ComplexThe QRS complex represents the spread of a stimulus through the ventricles. However, not every QRS complex contains a Q wave, an R wave, and an S wave—hence the possibility of confusion. The slightly awkward (and arbitrary) nomenclature becomes understandable if you remember three basic naming rules for the components of the QRS complex in any lead (Fig. 3.4): 1.When the initial deflection of the QRS complex is negative (below the baseline), it is called a Q wave. 2.The first positive deflection in the QRS complex is called an R wave. 3.A negative deflection following the R wave is called an S wave. Thus the following QRS complex contains a Q wave, an R wave, and an S wave: In contrast, the following complex does not contain three waves: If, as shown earlier, the entire QRS complex is positive, it is simply called an R wave. However, if the entire complex is negative, it is termed a QS wave (not just a Q wave as you might expect). Occasionally the QRS complex contains more than two or three deflections. In such cases the extra waves are called R′ (R prime) waves if they are positive and S′ (S prime) waves if they are negative. Fig. 3.4 shows the major possible QRS complexes and the nomenclature of the respective waves. Notice that capital letters (QRS) are used to designate waves of relatively large amplitude and small letters (qrs) label relatively small waves. (However, no exact thresholds have been developed to say when an s wave qualifies as an S wave, for example.) The QRS naming system does seem confusing at first. But it allows you to describe any QRS complex and evoke in the mind of the trained listener an exact mental picture of the complex named. For example, in describing an ECG you might say that lead V1 showed an rS complex (“small r, capital S”): or a QS (“capital Q, capital S”): Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323401692000032 ElectrocardiographyDouglas P. Zipes MD, in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 2019 QRS ChangesWith actual infarction, depolarization (QRS) changes often accompany repolarization (ST-T) abnormalities (Fig. 12.32). Necrosis of sufficient myocardial tissue can lead to decreased R wave amplitude or Q waves in the anterior, lateral, or inferior leads as a result of loss of electromotive forces in the infarcted area. Local conduction delays caused by acute ischemia also can contribute to Q wave pathogenesis in selected cases. Abnormal Q waves were once considered markers of transmural myocardial infarction, whereas subendocardial (nontransmural) infarcts were thought not to produce Q waves. However, careful experimental and correlative studies based on necropsy and imaging findings have convincingly indicated that transmural infarcts can occur without Q waves and that subendocardial or other nontransmural infarcts can be associated with Q waves.2,42,46 Accordingly, evolving or chronic infarcts are more appropriately designated by ECG as “Q wave” or “non–Q wave,” rather than as “transmural” or “nontransmural.” The QRS findings may also be somewhat different with posterior or lateral infarction (Fig. 12.33). Loss of depolarization forces in these regions can reciprocally increase R wave amplitude in lead V1 and sometimes V2, rarely without causing diagnostic Q waves in any of the conventional leads. The differential diagnosis for major causes of prominent right precordial R waves is presented inTable 12.9. In certain patients, fragmentation of the QRS complex, even without Q waves, may be a marker of myocardial scarring from ischemic or nonischemic causes.51 Approach to Wide QRS Complex TachycardiasZiad F. Issa MD, ... Douglas P. Zipes MD, in Clinical Arrhythmology and Electrophysiology: A Companion to Braunwald's Heart Disease (Second Edition), 2012 Clinical HistoryAgeWCT in a patient older than 35 years is likely to be VT (positive predictive value of up to 85%). SVT is more likely in the younger patient (positive predictive value of 70%). SymptomsSome patients with tachycardia can have few or no symptoms (e.g., palpitations, lightheadedness, diaphoresis), whereas others can have severe manifestations, including chest pain, dyspnea, syncope, seizures, and cardiac arrest. The severity of symptoms during a WCT is not useful in determining the tachycardia mechanism because symptoms are primarily related to the fast heart rate, associated heart disease, and the presence and extent of LV dysfunction, rather than to the mechanism of the tachycardia. It is important to recognize that VT does not necessarily result in hemodynamic compromise or collapse. Misdiagnosis of VT as SVT on the basis of hemodynamic stability is a common error that can lead to inappropriate and potentially dangerous therapy.2 Duration of the ArrhythmiaSVT is more likely if the tachycardia has recurred over a period of more than 3 years. The first occurrence of a WCT after myocardial infarction (MI) strongly implies VT. Presence of Underlying Heart DiseaseThe presence of structural heart disease, especially coronary heart disease and a previous MI, strongly suggests VT as the cause of WCT. In one report, over 98% of patients with a previous MI had VT as the cause of WCT, whereas only 7% of those with SVT had had an MI. It should be realized, however, that VT can occur in patients with no apparent heart disease, and SVT can occur in those with structural heart disease.2 Pacemaker or Implantable Cardioverter-Defibrillator ImplantationA history of pacemaker or implantable cardioverter-defibrillator (ICD) implantation should raise the possibility of a device-associated tachycardia. Ventricular pacing can be associated with a small and almost imperceptible stimulus artifact on the ECG. The presence of an ICD is also of importance because such a device should identify and treat a sustained tachyarrhythmia, depending on device programming, and because the presence of an ICD implies that the patient is known to have an increased risk of ventricular tachyarrhythmias. MedicationsMany different medications have proarrhythmic effects. The most common drug-induced tachyarrhythmia is torsades de pointes. Frequently implicated agents include antiarrhythmic drugs such as sotalol and quinidine, and certain antimicrobial drugs such as erythromycin. Diuretics are a common cause of hypokalemia and hypomagnesemia, which can predispose to ventricular tachyarrhythmias, particularly torsades de pointes in patients taking antiarrhythmic drugs. Furthermore, class I antiarrhythmic drugs, especially class IC agents, slow conduction and have a property of use dependency, a progressive decrease in impulse conduction velocity at faster heart rates. As a result, these drugs can cause rate-related aberration and a wide QRS complex during any tachyarrhythmia. Digoxin can cause almost any cardiac arrhythmia, especially with increasing plasma digoxin concentrations above 2.0 ng/mL (2.6 mmol/L). Digoxin-induced arrhythmias are more frequent at any given plasma concentration if hypokalemia is also present. The most common digoxin-induced arrhythmias include monomorphic VT (often with a relatively narrow QRS complex), bidirectional VT (a regular alternation of two wide QRS morphologies, each with a different axis), and nonparoxysmal junctional tachycardia.2 Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B978145571274800021X Diagnosis of Cardiac ArrhythmiasDouglas P. Zipes MD, in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 2019 QRS and QT Dispersion and T Wave AbnormalitiesHeterogeneity in refractoriness and conduction velocity is a hallmark of reentrant arrhythmias. One index of the heterogeneity of ventricular conduction is derived from the QRS complex duration on surface ECG leads, while heterogeneity of ventricular refractoriness can be found in differences in the length of the QT interval. Dispersion indices usually measure the maximum difference (shortest to longest) in the intervals of interest, which may be adjusted for heart rate and the number of leads sampled (e.g., when the T wave is flat in some leads for QT dispersion). Abnormally high QRS and QT dispersion have been correlated with risk for overall mortality and arrhythmic death in patients with various disorders, although the results are not consistent. Different techniques exist for determining dispersion (including automated algorithms), and the results of one study are often difficult to compare with those of another; in addition, the tests are sensitive to a variety of factors, including age, time of day, season of year, and even body position. More recently, T wave morphology and assessment of the interval from T wave peak to end in lead V5 have been correlated with increased sudden death risk.10 Overall, assessments of these indices have not gained popularity as useful clinical tools. Other details of the QRS complex, such as fragmentation of the conducted complex11 (multiple notches in the QRS;seeFig. 35.4) and the simple width of PVCs,12 have been associated with increased cardiovascular risk. Biomedical SignalsAbdulhamit Subasi, in Practical Guide for Biomedical Signals Analysis Using Machine Learning Techniques, 2019 2.3.4 The ECG WaveformThe QRS complex is an electrical ventricular system and is the most well-known waveform showing electrical activity inside the heart. It is the basis for automatic recognition of heart rate and also as an access point for classification schemes and ECG data-compression algorithms (Kohler, Hennig, & Orglmeister, 2002). The QRS complex morphology describes the mechanical action of the heart, offering a view into how each chamber functions. The waves of depolarization extending all the way through the heart via each cardiac cycle produce electrical impulses. These impulses travel via a variety of body fluids, that is, blood, up to the body’s surface where they can be recorded using surface electrodes. These signals are then sent to an ECG. The main characteristics of the QRS wave that describe significant data related to cardiac health are as follows (Begg et al., 2007): (a)P wave (b)QRS complex (c)T wave (d)QRS intervals P Wave: The original P wave is due to electrical action coming from atrial contraction (systole). In cardiovascular diseases (CVDs), the P wave can turn out to be unclear and shown as irregular. An inverted P wave resulting from positive to negative altered voltage symbolizes that polarization of the atria is irregular (Julian et al., 2005). This indicates that the source of the pacemaker signal is not in the SA node but could arrive from somewhere else, for example, the atrium or the AV node. If the P wave has a seemingly broadened or notched characteristic, this shows a stoppage in the depolarization of the left atrium, which could indicate trouble in the conduction system. Right atrial growth (P pulmonale) can direct high P waves, usually growing more than 3 mm on the ECG trace (Begg et al., 2007). QRS Complex: The QRS complex is the ventricular contraction (systole) consisting of the Q wave, which is the first negative deviation, followed by the R wave, a positive (upward) deviation. Any negative deflection following immediately after the R portion is termed the S wave. Models of abnormal QRS complexes could reveal a couple of R waves present or cases where the R part is not present. This wave’s analysis is dependent on the ECG electrode/lead recording. Unusually large Q waves could indicate MI, opposite to a healthy Q wave, which is not normally higher than 2 mm in amplitude or 0.03 s in width. The QRS complex is generally not larger than 0.1 s and on average is of 0.06 to 0.08 s duration (Begg et al., 2007). T Wave: Subsequent to ventricular contraction, the ventricles relax (diastole) producing the T wave. Contrasted with the earlier two wave segments, the T wave is a repolarization wave, usually lasting for 0.25–0.35 s subsequent to ventricular depolarization. In this phase, the lower heart chambers are relaxing electrically and getting ready for their subsequent muscle contraction. Atria repolarization is also present, but the signal amplitude is generally covered by the larger QRS complex because of ventricular contraction and is consequently hard to notice. The T wave goes in the same direction as the QRS component because repolarization happens from epicardium to endocardium, in a direction reverse to depolarization, which continues from endocardium to epicardium. T waves are generally not higher than 5 mm in the typical leads. Unusually high T waves may indicate MI, whereas smoothened T waves can be sign of myxedema or hypokalemia (Begg et al., 2007). QRS Segment Intervals: Besides the wave shapes, the time intervals are essential in the assessment of cardiac health. Among the start of the P wave and the start of the QRS complex is the PQ interval; because the Q wave is frequently not present, this interval is also called the PR interval and stays for the time among the start of atrial contraction and the start of ventricular contraction (normally about 0.16 s). In cases where heart disease is present, particularly with scarred or reddened heart tissue, a longer PR interval may be noticed as more time is necessary for the depolarization wave to extend through the atrial myocardium and the AV node. Reduced PR intervals could represent that the impulse is coming in the junction tissue or could be because the Wolff-Parkinson-White syndrome (Begg et al., 2007; Julian et al., 2005). The ST segment is an additional interval significant for recognition of many CVDs. As a rule, it comes as a leveled straight line among the QRS complex and the T wave. An eminent or dejected ST segment (relying on the ECG lead being noticed) is an indication of MI because the heart muscle is injured or does not collect enough blood, resulting in a disorder in ventricular repolarization. Pericarditis can be discovered by noticing ST segments concaving upward over a many cardiac cycles. In digitalis therapy, it has been found that ST segments are depressed with a tender drooping, whereas the T wave stays unchanged or flattened (Begg et al., 2007). The QT interval lasts roughly 0.35 s and gives relevant data concerning the state of ventricular contractions. Its duration decreases as the heart rate goes up, and typically the QT interval does not last more than half the time between the earlier RR interval for rates among 60 and 90 beats per min. From time to time, this is hard to compute because it cannot be instantly noticed. But extended QT intervals can point to the danger of ventricular tachycardia (VT) or the occurrence of certain drugs, for example, antidepressants (Begg et al., 2007). Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780128174449000027 ECG Differential DiagnosesAry L. Goldberger MD, FACC, in Clinical Electrocardiography: A Simplified Approach (Seventh Edition), 2006 Wide QRS Complex I.Intrinsic intraventricular delay (IVCD)* A.Left bundle branch block and variants B.Right bundle branch block and variants C.Other (nonspecific) patterns of IVCD II.Extrinsic (“toxic”) intraventricular delay A.Hyperkalemia B.Drugs: class I antiarrhythmic drugs and other sodium-channel blocking agents (e.g., tricyclic antidepressants and phenothiazines) III.Ventricular beats: premature, escape, or paced VI.Ventricular preexcitation: Wolff-Parkinson-White pattern and variants Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B0323040381500251 Wide-Complex TachycardiaChristopher Pickett MD, Peter Zimetbaum MD, in Decision Making in Medicine (Third Edition), 2010 Wide QRS complex tachycardia (WCT), defined as heart rate (HR) >100 beats per minute (bpm) with a QRS duration >120 ms, is a common arrhythmia with potentially life-threatening consequences, making rapid and accurate diagnosis with initiation of appropriate therapy essential. A.After recognition of this arrhythmia, the clinician must immediately evaluate the patient for hemodynamic stability. If the patient is unstable, then Advanced Cardiac Life Support (ACLS) protocol should be initiated with direct current (DC) cardioversion of the patient. If the rhythm is sustained but tolerated or if it is not sustained, then the clinician should perform an evaluation with the goal of differentiation between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrant conduction. Prognosis and therapy of these two conditions differ considerably. B.The clinical history can be helpful in suggesting a diagnosis. Presence of prior myocardial infarction (MI) and structural heart disease is the strongest clinical predictor of VT. Patients with ischemic cardiomyopathy and WCT will have VT <98% of the time. Advanced age and presence of congestive heart failure (CHF) also favor VT. Younger patients or adults with a history of recurrent tachycardia since a young age or for >3 years are more likely to have SVT with aberrancy. Symptoms during tachycardia may be far ranging, from malaise to syncope. It is a common misconception that WCT is less likely to be VT if it is hemodynamically stable. Many VTs are hemodynamically tolerated and dismissing this diagnosis can lead to inappropriate triage and therapy, with subsequent cardiovascular collapse. After assessment of vital signs, the physical examination should be directed toward noting evidence of atrioventricular (AV) dissociation, which is frequently seen in VT but rarely in SVT. Beat-to-beat change in blood pressure, variability in S1, and cannon A waves are all signs of AV dissociation. Carotid massage that terminates the arrhythmia indicates that the AV node was involved in the tachycardia circuit and that the mechanism is an SVT. C.A 12-lead electrocardiogram (ECG) offers a great deal more information than a rhythm strip and should be obtained promptly. A prior ECG can also offer helpful clues. If there is evidence of ventricular pre-excitation or previous bundle branch block with similar morphology to the WCT, then it suggests SVT with aberrancy. If there are Q waves or other evidence of prior MI, the case for VT is supported. D.Initial evaluation of the ECG should begin with the search for P waves and their relationship to the QRS. Dissociation of the P from the QRS or other evidence of AV dissociation, such as fusion or capture beats, is diagnostic of VT. It should be noted that the rate of the WCT does not reliably differentiate VT from SVT and that, although irregularity suggests atrial fibrillation, it can also be seen at the onset and termination of VT. E.If the initial assessment fails to yield a diagnosis, more detailed analysis is necessary. This is done by identifying the WCT as right bundle branch block (RBBB)-type (V1 positive) or left bundle branch block (LBBB)-type (V1 negative) and applying specific morphologic criteria. F.In RBBB-type WCT, a ventricular origin is suggested by QRS complex duration >140 ms, left axis deviation, a single (R) or biphasic (QR or RS) R wave in lead V1, or a triphasic R wave in lead V1 with the initial R wave taller than the secondary R wave, R:S ratio of <1 in V6, positive concordance. G.In LBBB-type WCT, a ventricular origin is suggested by QRS complex >160 ms, a broad (>40 ms) R in V1, notching of the QRS and/or delayed downstroke with R to S interval >100 ms in V1, right axis deviation, a Q wave in V6, negative concordance. Unless there is definitive evidence that the WCT is SVT, one should never use adenosine or verapamil because it may lead to rapid hemodynamic collapse. Procainamide is the preferred agent for pharmacologic control of WCT. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323041072500235 Bradycardias and TachycardiasAry L. Goldberger MD, FACC, in Clinical Electrocardiography: A Simplified Approach (Seventh Edition), 2006
Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B0323040381500214 Cardiac ArrhythmiasMyung K. Park MD, FAAP, FACC, in Pediatric Cardiology for Practitioners (Fifth Edition), 2008 Description.The QRS complex appears prematurely. The P wave may be upright in lead II when the ectopic focus is high in the atrium. The P wave is inverted when the ectopic focus is low in the atrium (so-called coronary sinus rhythm). The compensatory pause is incomplete; that is, the length of two cycles, including one premature beat, is less than the length of two normal cycles (see Fig. 24-2). An occasional premature atrial contraction (PAC) is not followed by a QRS complex (i.e., a nonconducted PAC; see Fig. 24-2). A nonconducted PAC is differentiated from a second-degree AV block by the prematurity of the nonconducted P wave (P' in Fig. 24-2). The P' wave occurs earlier than the anticipated normal P wave, and the resulting P-P' interval is shorter than the normal P-P interval for that individual. In second-degree AV block, the P wave that is not followed by the QRS complex occurs at the anticipated time, maintaining a regular P-P interval. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323046367500344 How long is a normal QRS complex?The normal duration (interval) of the QRS complex is between 0.08 and 0.10 seconds — that is, 80 and 100 milliseconds. When the duration is between 0.10 and 0.12 seconds, it is intermediate or slightly prolonged. A QRS duration of greater than 0.12 seconds is considered abnormal.
How tall should the QRS complex be?The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or. The amplitudes of all the QRS complexes in the precordial leads are < 10 mm.
What does a long QRS complex mean?A “wide QRS complex” refers to a QRS complex duration ≥120 ms. Widening of the QRS complex is related to slower spread of ventricular depolarization, either due to disease of the His-Purkinje network and/or reliance on slower, muscle-to-muscle spread of depolarization.
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