How long is qrs complex

The third measurement is to check for regularity. This can be done by measuring the "p-p interval" or the "R-R interval".

To measure the P-P interval, place the edge of a piece of paper along the line of the rhythm and mark the centre of 2 consecutive P waves. Compare this measurement with the next 2 P waves.

When the duration is between 0. A QRS duration of greater than 0. The QRS duration will lengthen when electrical activity takes a long time to travel throughout the ventricular myocardium. You also have the option to opt-out of these cookies. But opting out of some of these cookies may have an effect on your browsing experience. Necessary Necessary. Necessary cookies are absolutely essential for the website to function properly.

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Uncategorized uncategorized. Undefined cookies are those that are being analyzed and have not been classified into a category as yet. Because an accessory pathway inserts directly into ventricular myocardium, the resulting QRS complex during antidromic AVRT is generated by muscle-to-muscle spread propagating away from the ventricular insertion site, rather than via His-Purkinje spread, and therefore meets all the QRS complex morphology criteria for VT.

However, such patients are usually young, do not have associated structural heart disease, and most importantly, show manifest preexcitation WPW pattern during sinus rhythm. Carotid massage and adenosine will terminate this WCT by causing transmission block in the retrograde limb the AV node. Bundle branch reentry BBR is a special type of VT wherein the VT circuit is comprised of the right and left bundles and the myocardium of the interventricular septum. In its commonest form, the impulse travels down the RBB, across the interventricular septum, and then up one of the fascicles of the left bundle branch.

However, such patients have severe, dilated cardiomyopathy, and preexisting BBB or intraventricular conduction delays wide QRS in sinus rhythm. Furthermore, there will often be evidence of VA dissociation, with the ventricular rate being faster than the atrial rate, pointing to the correct diagnosis of VT. Electrolyte disorders such as severe hyperkalemia and drug toxicity such as poisoning with antiarrhythmic drugs can widen the QRS complex.

Toxicity with flecainide, a class Ic antiarrhythmic drug with potent sodium channel blocking capabilities, is a well-known cause of bizarrely wide QRS complexes and low amplitude P waves. Once again, the clinical scenario in which such a patient is encountered such as history of antiarrhythmic drug use , along with other ECG findings such as tall peaked T waves in hyperkalemia will help make the correct diagnosis. Pacing results in a wide QRS complex since the wave front of depolarization starts in the myocardium at the ventricular lead location, and then propagates by muscle-to-muscle spread.

Any cause of rapid ventricular pacing will result in result in a WCT. Known history of pacemaker implantation and comparison to prior ECGs usually provide the correct diagnosis. Figure 1. WCT tachycardia obtained from a year-old man with a history of remote anteroseptal myocardial infarction and reduced ejection fraction. At first observation, there appears to be clear evidence for VA dissociation, with the atrial rate being slower than the ventricular rate. For complete dissociation, this would require that the VT rate would fortuitously have to be at an exact multiple of the sinus rate.

Figure 2. A year-old woman with end-stage renal disease presented with dizziness and altered mental status. She has missed her last two hemodialysis appointments. An ECG from a year-old woman with end-stage renal disease who presented with dizziness and altered mental status. She had missed her last two hemodialysis appointments. The ECG in Figure 2 was obtained upon presentation. Her serum potassium was 7.

As expected, the P waves are of low amplitude in hyperkalemia. Figure 3. A year-old woman with prior inferior wall MI presented with an episode of syncope resulting in lead laceration, followed by spontaneous recovery by persistent light-headedness. Her initial ECG is shown. Initial ECG from a year-old woman with prior inferior wall MI who presented with an episode of syncope resulting in head laceration, followed by spontaneous recovery by persistent light-headedness.

Figure 4: A year-old woman with palpitations for many years and idiopathic globally dilated cardiomyopathy was admitted for incessant wide complex tachycardia.

The ECG in Figure 4 is representative.