Skip to main content

The QRS - Things you Don't know!!!

 

Qrs
So the QRS !!!!! 

A few have posed me this question about the true value of QRS , its morphological presentations ,especially the clues in it , for the identification of the various types of abnormalities especially the tachycardias based on these QRS features . 


But To understand the abnormalities , one must be able to understand the normalities & especially the slight aberrations associated with the other wise normalities ! 


The QRS is usually a very well-defined electrical signal on surface ecg and is indicative of underlying ventricular depolarisation phase( since a large mass of muscle is activated almost synchronously hence the larger deflections & this time interval coincides with repolriazation of atrium, hence the latter repolriazation is masked in the QRS complex) .


The QRS usually lasts about 100 msec or even less (on average May be of 60 msec to 80 msec duration) ! Generally a duration longer than 120 msec is considered longer!

The even more longer values may be suggestive of some underlying pathologies such as a conduction block, like in one of the Bundle branches (BB) 


Before focusing on the abnormalities , the normality has to be known first ! 

So The usual surface 12 lead ECG will mostly show the 3 consecutive peaks in QRSs!! These are the following ! 

a .negative Q peak, 

b.positive R peak, 

c. a negative S peak. 


So One of the most confusing aspects of the surface ecg especially for the beginners / student or jnr drs is the exact nomenclature of the qrs complex , 



As described above, the QRS complex represents the spread of a stimulus through the ventricles. However, surprisingly not every QRS complex will contain , a Q or R and an S wave—hence the confusion. 


This bothersome but unavoidable nomenclature can become understandable if you understood the following several basic features of the QRS complex and the reasoning behind ! 


a. So When the initial/first deflection of the QRS complex is negative recorded (meaning going below the baseline), it is then referred to as q wave !!!

b. And so the first ever positive deflection recorded in the QRS complex is called an R wave ! 

c. The negative deflection or recording at the end the R wave is called an S wave . 

d. Now If , the entire QRS complex is recorded positive or comprises of only the positive deflection it will simply be called an R wave! 

e. Now If the entire complex is negatively recorded , it is termed a QS complex (not just a Q wave, as might be expected !!!!! 


f. Occasionally, the QRS complex comprises of more than two or three deflections. In such cases, the extra wave/component or if their is a second R wave , it is referred to as R prime or “R’ “ if it is positively recorded !! and S′ (S prime) if it’s a negatively recorded complex ! 


G. capital letters (QRS) are used to designate waves of relatively large amplitude and small letters (qrs) label relatively small waves.


h. This above description of QRS nomenclature May be lot of confusing at first, especially to the jnr dr / learners however it needed to be known especially if it has to be describe to an expert like an electrophysiologist especially if ecg to see !! to help him making up his mind to the exact picture of the complex named & hence the underlying activity/ circuitry inside the heart ! 


So for the jnr drs . How to describe and especially standardise these features in exact words ! 

And remember the best lead to look for these changes will be chest lead V1 or at the best V2 , as they record right on top of the heart ! 

So like in describing an ECG one can say that chest lead V1 shows an rS complex (which will automatically suggest that small r, capital S” is being recorded ) 

One can also use the term like QS ( automatically will lead the learned to the presence of a “capital Q, & capital S”)


So rSR it is ! 

And remember whenever there is some depolarisation abnormality/ abnormalities one should expect some repolriazation changes , in this case the resultant S- T appearance.

So now , as an example Some Common ECG abnormalities , especially affecting the pattern of the QRS !! 


So some of These may include the following ! 


1. A qR complex in V1 

So this can be because of either severe underlying right ventricular hypertrophy . 

Or Enlarged right atrium 

Or even Extreme rotation of heart ! However one must admit that echocardiograms have superseded in making these diagnosis ! 


2. Unusually large “Q” waves 

Which could otherwise indicate MI, versus a normal Q wave, ( remember the normal less higher than 2 mm in amplitude or 30msec in width) .         


       3. WPW & QRS pattern,     

(This is basically a competition between 2 currents flow , one going down the normal AVN and the other trying to go down the Accessory pathway !)

So if both flowing together /or alternatively , Resultantly QRS in WPW, therefore, will be a kind of fusion complex !!

While if the Abnormal activation of the ventricles is all via the AP this lead to QRS shape change ( hence the difficulty in QRS component naming ) and May mimick the following 

a. BBB, 

b. hypertrophy or 

c. infarction, as well as to 

d. secondary ST-T changes simulating Ischemia . 


4. In some cases, the usual QRS pattern May be slightly prolonged and notched, and sometimes especially in the the chest leads (v3/4), most probably as a result of an Intra ventricular conduction defect !!.


Comments

Popular posts from this blog

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB)

Brugada ECG vs Incomplete Right Bundle Branch Block (iRBBB) Why this differentiation matters Brugada pattern is a malignant channelopathy associated with sudden cardiac death, while incomplete RBBB is usually a benign conduction variant. Mislabeling Brugada as iRBBB can be fatal; overcalling iRBBB as Brugada can lead to unnecessary anxiety and ICD implantation. --- 1. Basic Definitions Brugada ECG Pattern Primary repolarization abnormality Genetic sodium-channel disorder Characteristic ST-segment elevation in V1–V3 Risk of ventricular fibrillation and sudden death Incomplete RBBB (iRBBB) Depolarization abnormality Delay in right ventricular conduction Common in healthy individuals Usually asymptomatic and benign --- 2. ECG Morphology: Side-by-Side Comparison QRS Duration Brugada: QRS usually <120 ms iRBBB: QRS <120 ms, but with RBBB morphology --- V1–V2 Pattern (Key Differentiator) Brugada Pseudo-RBBB appearance ST elevation ≥2 mm ST segment is coved or saddleback Terminal QRS bl...

Acute Treatment of Hyperkalemia

Acute Treatment of Hyperkalemia – A Practical, Bedside-Oriented Guide Hyperkalemia is a potentially life-threatening electrolyte abnormality that demands prompt recognition and decisive management. The danger lies not only in the absolute potassium value but in its effects on cardiac conduction, which can rapidly progress to fatal arrhythmias. Acute treatment focuses on three parallel goals: stabilizing the cardiac membrane, shifting potassium into cells, and removing excess potassium from the body. Understanding this stepwise approach helps clinicians act quickly and rationally in emergency settings. Why Hyperkalemia Is Dangerous Potassium plays a key role in maintaining the resting membrane potential of cardiac myocytes. Elevated serum potassium reduces the transmembrane gradient, leading to slowed conduction, ECG changes, ventricular arrhythmias, and asystole. Importantly, ECG changes do not always correlate with potassium levels, so treatment decisions should be based on clinical c...

π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š

 π˜Όπ™£π™©π™žπ™˜π™€π™–π™œπ™ͺπ™‘π™–π™©π™žπ™€π™£ π˜Όπ™›π™©π™šπ™§ π™Žπ™©π™§π™€π™ π™š in  Patient with AF and acute IS/TIA European Heart Association Guideline recommends: • 1 days after TIA • 3 days after mild stroke • 6 days after moderate stroke • 12 days after severe stroke Early anticoagulation can decrease a risk of recurrent stroke and embolic events but may increase a risk of secondary hemorrhagic transformation of brain infarcts.  The 1-3-6-12-day rule is a known consensus with graded increase in delay of anticoagulation between 1 and 12 days after onset of ischemic stroke or transient ischemic attack(TIA), according to neurological severity based on European expert opinions. However, this rule might be somewhat later than currently used in a real-world practical setting.