Features to consider on Analysis of QRS

Width of the complexes: Narrow versus broad

Voltage (height) of the complexes

Spot diagnoses: Specific morphology patterns that are important to recognise.

QRS Width

Normal QRS width is 70-100 ms (a duration of 110 ms is sometimes observed in healthy subjects)

The QRS width is useful in determining the origin of each QRS complex (e.g. sinus, atrial, junctional or ventricular):

Narrow complexes (QRS < 100 ms) are supraventricular in origin

Broad complexes (QRS > 100 ms) may be either:

Ventricular in origin,
or
Due to aberrant conduction of supraventricular complexes (e.g. due to bundle branch block, hyperkalaemia or sodium-channel blockade)

Narrow Complexes

Narrow (supraventricular) complexes arise from three main places:

Sino-atrial node (= normal P wave)

Atria (= abnormal P wave / flutter wave / fibrillatory wave)

AV node / junction (= either no P wave or an abnormal P wave with a PR interval < 120 ms)

Causes of ST Elevation

Click the Relevant section

Acute myocardial infarction

Coronary vasospasm (Printzmetal’s angina)

Pericarditis

Benign early repolarization

Left bundle branch block

Left ventricular hypertrophy

Ventricular aneurysm

Brugada syndrome

Ventricular paced rhythm

Raised intracranial pressure

Morphology of the Elevated ST segment

Myocardial Infarction

Acute STEMI may produce ST elevation with
either concave, convex or obliquely straight morphology

Morphology of the Elevated ST segment

Concave ST elevation with PR elongation

LV
 aneurysm

Brugada

Morphology of the Elevated ST segment

Causes ST segment elevation and Q-wave formation in contiguous leads, either:


Anteroseptal (V1-V4) - Left anterior Descending Artery

Lateral (I + aVL, V5-6) - Left circumflex Artery

Inferior (II, III, aVF) - Right Coronary Artery

Anterolateral (V4-6, I, aVL) - Left Anterior descending or Left Circumflex 

Posterior (Tall R waves V1-2) - Also Right Coronary

Reciprocal ST depression

During a MI there is usually reciprocal ST depression
in the electrically opposite leads 

For example, STE in the high lateral leads I + aVL typically produces reciprocal
ST depression in lead III (see example below)

Coronary Vasospasm 
(Prinzmetal’s Angina)

This causes a pattern of ST elevation that is very similar to
acute STEMI — i.e. localised ST elevation with reciprocal 
ST depression occurring during episodes of chest pain

However, unlike acute STEMI the ECG changes are transient, 
reversible with vasodilators and not usually associated with myocardial necrosis

It may be impossible to differentiate these two conditions 
based on the ECG  alone

Reciprocal ST depression

During a MI there is usually reciprocal ST depression
in the electrically opposite leads 

For example, STE in the high lateral leads I + aVL typically produces reciprocal
ST depression in lead III (see example below)

Posterior Myocardial Infarction

Acute posterior STEMI causes ST
depression in the anterior leads V1-3, along with dominant R waves (“Q-wave
equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9