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Curriculum · Cardiovascular and Hypertension

ECG interpretation (general)

What it is

ECG interpretation is the reading of the 12 lead ECG, and the cardiology course lists it first among its general topics. A rhythm strip carries its lead and its paper speed in its label, as in lead II at a paper speed of 50 mm/s and lead II at a paper speed of 25 mm/s. The 12 leads are I, II, III, aVR, aVL, aVF and V1 to V6, with lead II usually run as the rhythm strip below them. Reading it has an order: look first for any ST elevation, then at the corresponding leads, then at the reciprocal leads for depression, then for a Q wave, which marks a past infarction, and usually compare with a past ECG.

How it is diagnosed

In acute coronary syndrome the electrocardiogram is the first step, and it sorts the patient in one move.

Two more rows sit beside those. Stable angina has no ST elevation and negative cardiac biomarkers, with symptoms on exertion lasting under 15 min; unstable angina has no ST elevation and negative biomarkers but symptoms at rest. Localizing infarcts on the 12 lead ECG goes lead by lead: I, aVL, V5 and V6 are lateral and belong to the circumflex; II, III and aVF are inferior and belong to the right coronary artery; V1 and V2 are anterior and septal and belong to the left anterior descending; V4 is anterior and belongs to the left anterior descending. Read by wall instead of by lead: the anterior wall is V2 to V4, LAD diagonal branch; the septal wall V1 and V2, LAD septal branch; the lateral wall aVL, I, V5 and V6, left coronary artery circumflex branch; the inferior wall II, III and aVF, right coronary artery posterior descending branch; the posterior wall V1 to V4, circumflex or right coronary artery posterior descending branch. Posterior MI is the mirror of an anterior one: where the anterior infarct gives ST elevation, a pathologic Q wave and T wave inversion, the posterior gives ST depression, a pathologic R wave and an upright T wave. So ST depression in V1, V2 and V3 means a possible posterior MI, and the answer is to do a posterior ECG and not to activate the cath lab until ST elevation is seen on it. ST elevation in V1 and V2 is septal infarction. Right ventricular infarction is found the same way: all inferior STEMI cases should have a right sided ECG, and ST elevation in V4 on that ECG indicates right side infarction. Its clinical triad is hypotension, an elevated jugular venous pressure and clear lung fields. The rhythms are read by their own ECG features:

  1. Atrial fibrillation: an irregularly irregular rhythm, no P waves, absence of an isoelectric baseline, a variable ventricular rate.
  2. Supraventricular tachycardia: a regular tachycardia around 140-280 bpm, QRS complexes usually narrow, under 120 ms, and no visible P waves.
  3. Ventricular tachycardia: a rapid heart rate over 100 bpm and broad QRS complexes over 120 ms.
  4. Ventricular fibrillation: chaotic irregular deflections of varying amplitude, no identifiable P waves, QRS complexes or T waves, and a rate of 150 to 500 per minute.

Wolff-Parkinson-White gives a delta wave at the onset of the QRS with a short PR interval under 120 ms. The blocks run in order. First degree: a PR interval over 200 ms, five small squares. Second degree Mobitz I: a dropped beat, the P wave alone, with the PR interval longest immediately before the dropped beat and shortest immediately after it. Second degree Mobitz II: a dropped beat with the PR interval constant. Complete heart block: a dropped beat, the PR interval not fixed, and the RR interval constant. In hyperkalaemia the earliest changes are peaked, narrow T waves and widening of the QRS complex; if plasma levels continue to rise the PR interval is prolonged, followed by disappearance of the P waves, and the progression runs from normal to a tented T wave, then a reduced P wave with a widened QRS, then a sine wave pattern before cardiac arrest. In hypokalemia an increase in the amplitude of the U waves, which occur at the end of the T wave, is characteristic, alongside a slightly prolonged PR interval, a slightly peaked P wave, ST depression and a shallow T wave. Pulmonary embolism gives S1Q3T3: S waves in lead I, Q waves in lead III and inverted T waves in lead III. Reciprocal change is the same damage seen from the other side: myocardium damage shown by ST elevation is reflected as ST depression on the anatomically opposite side. The inferior leads are reciprocal to the high lateral leads, especially I and aVL, and to the anterior leads. The anterior leads are reciprocal to the posterior leads, and depression in the septal leads means elevation in the posterior leads. Either way, the reciprocal leads help confirm the elevation. Set out as a table of localisation: anterior MI is V1-V6 with no reciprocal depression and the LAD; septal MI is V1-V4 with disappearance of the septum Q in V5 and V6, no reciprocal change, and the LAD septal branches; lateral MI is I, aVL, V5 and V6 with reciprocal change in II, III and aVF, and the LCX or MO; inferior MI is II, III and aVF with reciprocal change in I and aVL, and the RCA in 80% or the RCX in 20%; posterior MI is V7, V8 and V9, seen as a high R in V1-V3 with ST depression in V1-V3 greater than 2 mm, and the RCX; right ventricle MI is V1 and V4R with reciprocal change in I and aVL, and the RCA; atrial MI is PTa in I, V5 and V6 with PTa reciprocal in I, II or III, and the RCA. The Q wave is read by size: compared with the small Q waves generated during normal depolarization, a pathologic Q wave is more prominent, with a width of 1 mm or more, one small box, and a depth over 25% of the height of the QRS complex. A long QT interval is read from the corrected value. A heart rate of 62/min with a PR interval of 160 ms, a QRS duration of 90 ms, a QT interval of 410 ms and a corrected QT of 500 ms is a prolonged corrected QT interval, and it can follow a collapse that required defibrillation. Cor pulmonale shows on the ECG as a peaked P wave in leads II, III and aVF. The infarct has a time course on the tracing. The earliest ECG finding is the hyperacute T wave, which may appear minutes after the interruption of blood flow; it is short-lived and evolves to progressive elevation of the ST segments. Q waves represent established myocardial necrosis and usually develop within 8 to 12 hours after a ST-elevation MI, though they may be noted as early as 1 to 2 hours after the onset of complete coronary occlusion. Pericarditis is the tracing most often confused with it, and the difference matters because thrombolytic therapy is contraindicated in pericarditis, where it may precipitate hemorrhagic tamponade. The earliest changes are in the first few hours to days of illness: diffuse ST-segment elevation in leads I, II, III, aVL, aVF and V2 to V6, with concurrent PR-segment depression in most patients. The ST elevations in early pericarditis are concave upward rather than convex upward, subsequent tracings do not evolve through a typical MI pattern, and Q waves do not appear. Pulmonary embolism has its own set, and they are not always there. The classic findings of right-heart strain and acute cor pulmonale are tall, peaked P waves in lead II, right-axis deviation, right bundle-branch block, an S1Q3T3 pattern, or atrial fibrillation - but only 20% of patients with proven PE have any of these classic ECG abnormalities, and the S1Q3T3 pattern is nonspecific and insensitive in the absence of clinical suspicion for PE. Hyperkalemia writes itself on the ECG in order: as potassium levels rise, peaked T waves are the first characteristic manifestation, and further rises bring progressive changes including loss of P waves. The QT interval is measured from the beginning of the QRS complex to the end of the T wave, and represents the duration of activation and recovery of the ventricular myocardium; HR corrected QTc values above 440 msec are considered abnormal. Long QT syndrome is a congenital disorder of QT prolongation with a propensity to ventricular tachydysrhythmias, which may lead to syncope, cardiac arrest or sudden death in otherwise healthy individuals. It is recognized as the Romano-Ward syndrome, familial with autosomal dominant inheritance, QT prolongation and ventricular tachydysrhythmias, or the Jervell and Lang-Nielsen syndrome, familial with autosomal recessive inheritance, congenital deafness, QT prolongation and ventricular arrhythmias. Second-degree AV block type II, Mobitz type II, presents with a prolonged PR interval, PR greater than 0.2 seconds, and random dropped beats, that is a P wave without a QRS complex; the PR intervals are always the same duration. The block is below the level of the AV node, generally the His-Purkinje system, it reflects serious cardiac pathology and may be seen with an anterior wall MI. Mobitz type I, the Wenckebach phenomenon, shows progressive prolongation of the PR interval with each beat until AV conduction is lost, causing a dropped beat. First-degree AV block presents with a prolonged PR interval without loss of AV conduction, and it is asymptomatic. Third-degree AV block, also called complete heart block, is absent conduction through the AV node with dissociation of atrial and ventricular rhythms and independent P waves and QRS complexes; Mobitz type II often progresses to it, and the immediate step is a transcutaneous pacemaker for ventricular pacing as a temporizing measure, with an implantable ventricular pacemaker for definitive management. Atrial flutter is different again: a tachydysrhythmia with rapid atrial beat and variable AV block, with a sawtooth appearance of the flutter waves.