QRS duration

The electrophysiological effects of amiodarone may be a composite of several properties. In addition to prolonging action potential duration and refractory period in ad tissues of the heart, the compound is an effective sodium channel blocker (49), calcium channel blocker (50), and a weak noncompetitive -adrenoceptor blocking agent (51). Amiodarone slows the sinus rate, markedly prolongs the QT interval, and slightly prolongs the QRS duration (1,2). 

Several intervals and durations are routinely measured on the ECG. The PR interval represents the time of conduction of impulses from the atria to the ventricles through the AV node the normal PR interval in adults is 0.12 to 0.2 seconds. The QRS duration represents the time required for ventricular depolarization, which is normally 0.08 to 0.12 seconds in adults. The QT interval represents the time required for ventricular repolarization. The QT interval varies with heart rate—the faster the heart rate, the shorter the QT interval, and vice versa. Therefore, the QT interval is corrected for heart rate using Bazett s equation3, which is ... 

Conscious studies using devices for measurement of blood pressure and six chest lead ECG measurements (V2, V4, V6, V10, rV2 and rV4). ECG interval analysis is performed on the V2 lead (RR, PR, QT, QTc intervals, QRS duration). QT dispersion can also be measured. Locomotor activity can be monitored and behavior captured on video using CCTV. 

CRT is now recommended for patients with LVEF less than or equal to 35%, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal medical therapy and who have cardiac dyssynchrony, which is currently defined as a QRS duration greater than 0.12 ms, unless contraindicated. To date, over 4,000 patients have been studied in randomized clinical trials of CRT. A recent evaluation of complications from those studies suggest a risk of implant mortality of 0.4%, failure to implant a functioning LV lead in 10%, lead malfunction or dislodgement in 8.5%, and pacemaker infection in 1.4% [123]. 

The MADIT-CRT trial is enrolling patients who have an indication for an ICD, a low ejection fraction (LVEF < 40%), Class I or II heart failure, and a prolonged QRS duration to either an ICD alone or a CRT-D device. The primary endpoint of this study is all-cause mortality. 

Shamim W, Yousufuddin M, Cicoria M, Gibson DG, Coats AJ, Henein MY. Incremental changes in QRS duration in serial ECGs over time identify high risk elderly patients with heart failure. Heart 2002 88 47-51. 

Molhoek SG, Van Erven L, Bootsma M, Steendijk P, Van Der Wall EE, Schalij MJ. QRS duration and shortening to predict clinical response to cardiac resynchronization therapy in patients with end-stage heart failure. Pacing Clin. Electrophysiol. 2004 27 308-13. 

Shenkman HJ, Pampati V, Khandelwal AK, et al. Congestive heart failure and QRS duration establishing prognosis study. Chest 2002 122 528-34. 

Flecainide increases the PR, QRS, and to a lesser extent, QTc intervals. The rate of ventricular repolarization is not affected, and the QT interval prolongation is caused by the increase in the QRS duration. 

Administration of sotalol is associated with dose- and concentration-dependent slowing of the heart rate and prolongation of the PR interval. The QRS duration is not affected with plasma concentrations within the therapeutic range. The corrected QT interval is prolonged as a result of the increase in the ERP of ventricular myocardium. 

Ibutilide increases the ERP of ventricular myocytes and Purkinje fibers but has no clinically significant effect on QRS duration. 

The most profound effect of adenosine is the induction of an A-V block within 10 to 20 seconds of administration. Mild sinus slowing may be observed initially followed by sinus tachycardia. There is no effect on the QRS duration or QT interval. Rarely, an adenosine bolus injection is accompanied by atrial fibrillation or ventricular tachyarrhythmias. 

Overdose may increase QRS duration, prolong QT interval, cause conduction disturbances, reduce myocardial contractility, and cause hypotension. 

Tricyclic antidepressants have effects on heart rate (HR), blood pressure (BP), and three distinct measures of the electrocardiogram (EKG). The EKG parameters affected are (1) the PR interval, which represents depolarization of the aorta (2) the QRS duration, which represents intraventricular conduction time and (3) the QTc, which represents the depolarization and subsequent repolarization of the ventricles, corrected for cardiac rate. 

It is difficult to estimate the risk of seizures in children with toxic levels of TCAs. In adults, studies have been done that show a correlation between a QRS complex length 100 msec and an increased risk of seizures. Increased risk of seizures was not related to other monitored parameters, including plasma blood level, and patients with QRS duration within normal limits (<100 msec) had no incidence of seizures or arrhythmias (Boehnert and Lovejoy, 1985). It is unclear... 

Boehnert, M.T. and Lovejoy, F.H. (1985) Value of the QRS duration versus the serum drug level in predicting seizures and ventricular arrhythmias after and acute overdose of tricyclic antidepressants. N Engl Med 313 474 79. 

TCAs may adversely affect left ventricular function (LVF). This phenomenon was addressed using the systolic time interval (STI), a measurement partly dependent on the QRS duration. However, TCAs prolong QRS, and hence the STI method can overestimate the effect of TCAs on LVF because of their prolongation of the QRS interval. 

Although the literature indicates that seizures and arrhythmias are associated with TCA plasma levels greater than 1,000 ng/mL, the QRS duration might be a better early predictor than plasma levels in overdose cases. For example, in a series of 49 TCA overdoses, seizures occurred only in cases with a QRS duration above 0.10 second, and ventricular arrhythmia was seen with a QRS greater than 0.16 second (430). Thus, for acute overdose, the ECG may provide a reliable and quick measure of risk with TCA drugs however, how well a QRS of less than 0.10 second predicts ultimate safety or how long after ingestion the ECG must be followed, is uncertain (431). 

Schematic representation of the heart and normal cardiac electrical activity (intracellular recordings from areas indicated and ECG). Sinoatrial (SA) node, atrioventricular (AV) node, and Purkinje cells display pacemaker activity (phase 4 depolarization). The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. Thus, the PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated (ie, the intraventricular conduction time). The QT interval reflects the duration of the ventricular action potential.

By blocking sodium channels, procainamide slows the upstroke of the action potential, slows conduction, and prolongs the QRS duration of the ECG. The drug also prolongs the action potential duration by nonspecific blockade of potassium channels. The drug may be somewhat less effective than quinidine (see below) in suppressing abnormal ectopic pacemaker activity but more effective in blocking sodium channels in depolarized cells. 

A 38-year-old woman with a psychosis who took 4020 mg of ziprasidone had borderline intraventricular conduction delay (QRS duration 111 ms) the QTC interval was 445 ms (17). She oscillated between being drowsy and calm, and alert and agitated her blood pressure fell from 129/81 to 99/34 mmHg 4 hours later. She also had diarrhea and urinary retention. 

The association between methadone treatment and QTC interval prolongation, QRS widening, and bradycardia has been explored prospectively in 160 patients with at least a 1-year history of opioid misuse (19). The QTC interval increased significantly from baseline at 6 months (n = 149) and 12 months (n = 108). The QRS duration and heart rate did not change. There were no cases of torsade de pointes, cardiac dysrhythmias, syncope, or sudden death. There was a positive correlation between methadone concentration and the QTC interval. 

Quinidine has direct and indirect, or antimuscarinic, effects on cardiac tissue. Quinidine decreases myocardial excitability, conduction velocity, and contractility. As quinidine concentrations increase, conduction velocity progressively decreases. This is evident in an increase in PR interval, an increase in QRS duration, and an increase in QT interval. The effective refractory period is prolonged by quinidine. The anticholinergic effect on the heart is a decrease in vagal tone. In overdose, sinus node automaticity may be depressed. It is the a-adrenergic blocking properties of quinidine that cause vasodilatation and hypotension. 

Figure 4.53 Arrhythmogenic right ventricular dysplasia (ARVD). Note the image of atypical right bundle branch block, negative T wave in the V1-V4 leads, and premature ventricular complexes of the right ventricle. QRS duration...

Recently, it has been reported (Wong et al., 2005, 2006a, b) that patients with RBBB or LBBB have different prognoses, depending on the ST-segment morphology and QRS duration (p. 248). 

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