Sinus rhythm criteria
Sinus rhythm criteria
- Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children)
- Each QRS complex is preceded by a normal P wave
- Normal P wave axis: P waves upright in leads I and II, inverted in aVR
- The PR interval remains constant
- QRS complexes < 100 ms wide (unless co-existent interventricular conduction delay present)
AFib criteria
AFib criteria
- Irregularly irregular rhythm
- No P waves
- Absence of an isoelectric baseline
- Variable ventricular rate
- QRS complexes usually < 120ms, unless pre-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
- Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude > 0.5mm)
- Fibrillatory waves may mimic P waves leading to misdiagnosis
Atrial Flutter criteria
Atrial Flutter criteria
- Narrow complex tachycardia
- Regular atrial activity at ~300 bpm
- “Saw-tooth” pattern of inverted flutter waves in leads II, III, aVF
- Upright flutter waves in V1 that may resemble P waves
- Loss of the isoelectric baseline
- Ventricular rate depends on AV conduction ratio (see below)
Fixed AV conduction ratio (“AV block”)
Ventricular rate is a fraction of the atrial rate, e.g.
- 2:1 block = 150 bpm
- 3:1 block = 100 bpm
- 4:1 block = 75 bpm
Variable AV conduction ratio
The ventricular response is irregular and may mimic AF
On closer inspection, there may be a pattern of alternating 2:1, 3:1 and 4:1 conduction ratios.
Picture: Atrial flutter with a 3:1 block
LBBB criteria
LBBB criteria
- QRS duration > 120ms
- Dominant S wave in V1
- Broad monophasic R wave in lateral leads (I, aVL, V5-6)
- Absence of Q waves in lateral leads
- Prolonged R wave peak time > 60ms in leads V5-6
RBBB criteria
RBBB criteria
- QRS duration > 120ms
- RSR’ pattern in V1-3 (“M-shaped” QRS complex)
- Wide, slurred S wave in lateral leads (I, aVL, V5-6)
- Appropriate discordance refers to the fact that abnormal depolarisation should be followed by abnormal repolarisation, which appears discordant to the preceding QRS complex
- In RBBB, this manifests as ST depression and/or T-wave inversion in leads V1-3
Left anterior hemiblock (LAH)/
Left anterior fascicular block (LAFB) criteria
Left anterior hemiblock (LAH)/
Left anterior fascicular block (LAFB) criteria
- Left axis deviation (usually -45 to -90 degrees)
Left Axis Deviation (LAD): Leads II, III and aVF are NEGATIVE; Leads I and aVL are POSITIVE
- qR complexes in leads I, aVL
- rS complexes in leads II, III, aVF
- Prolonged R wave peak time in aVL > 45ms
Left ventricular hypertrophy (LVH) criteria
Left ventricular hypertrophy (LVH) criteria
- There are numerous voltage criteria for diagnosing LVH, summarised below
- The most commonly used are the Sokolov-Lyon criteria: S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm
- Voltage criteria must be accompanied by non-voltage criteria to be considered diagnostic of LVH
Voltage Criteria
Limb Leads
- R wave in lead I + S wave in lead III > 25 mm
- R wave in aVL > 11 mm
- R wave in aVF > 20 mm
- S wave in aVR > 14 mm
Precordial Leads
- R wave in V4, V5 or V6 > 26 mm
- R wave in V5 or V6 plus S wave in V1 > 35 mm
- Largest R wave plus largest S wave in precordial leads > 45 mm
Non Voltage Criteria
- Increased R wave peak time > 50 ms in leads V5 or V6
- ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
1st degree AV block criteria
1st degree AV block
PR interval > 200ms (five small squares)
- There is delay, without interruption, in conduction from atria to ventricles
- ‘Marked’ first degree heart block is present if PR interval > 300ms
AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)
AV Block: 2nd degree, Mobitz I (Wenckebach Phenomenon)
Definition:
Progressive prolongation of the PR interval culminating in a non-conducted P wave:
- PR interval is longest immediately before dropped beat
- PR interval is shortest immediately after dropped beat
Other Features:
- The P-P interval remains relatively constant
- The greatest increase in PR interval duration is typically between the first and second beats of the cycle
- The RR interval progressively shortens with each beat of the cycle
- The Wenckebach pattern tends to repeat in P:QRS groups with ratios of 3:2, 4:3 or 5:4
AV Block: 2nd degree, Mobitz II (Hay block)
AV Block: 2nd degree, Mobitz II (Hay block)
A form of 2nd degree AV block in which there is intermittent non-conducted P waves without progressive prolongation of the PR interval
Other features:
- The PR interval in the conducted beats remains constant
- The P waves ‘march through’ at a constant rate
- The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, triple for two dropped beats, etc)
AV block: 2nd degree, “fixed ratio” blocks
AV block: 2nd degree, “fixed ratio” blocks
Fixed Ratio AV blocks
- Second degree heart block with a fixed ratio of P waves: QRS complexes (e.g. 2:1, 3:1, 4:1).
- Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.
Picture of 2:1
AV block: 2nd degree, “high-grade” AV block
AV block: 2nd degree, “high-grade” AV block
High Grade AV block
Second degree heart block with a P:QRS ratio of 3:1 or higher, producing an extremely slow ventricular rate.
- Unlike 3rd degree heart block there is still some relationship between the P waves and the QRS complexes.
- High-grade AV block may result from either Mobitz I or Mobitz II AV block.
Anterior Myocardial Infarction
Anterior Myocardial Infarction
- ST segment elevation with subsequent Q wave formation in precordial leads (V1-6) +/- high lateral leads. These changes are often preceded by hyperacute T waves
- Reciprocal ST depression in inferior leads (mainly III and aVF)
Patterns of Anterior Infarction
The nomenclature of anterior infarction can be confusing, with multiple different terms used for the various infarction patterns. The following is a simplified approach to naming the different types of anterior MI.
The precordial leads can be classified as follows:
- Septal leads = V1-2
- Anterior leads = V3-4
- Lateral leads = V5-6
The different infarct patterns are named according to the leads with maximal ST elevation:
- Septal = V1-2
- Anterior = V2-5
- Anteroseptal = V1-4
- Anterolateral = V3-6, I + aVL
- Extensive anterior / anterolateral = V1-6, I + aVL
Picture is of Hyperacute Anteroseptal STEMI
Lateral STEMI
Lateral STEMI
How to recognise a lateral STEMI
- ST elevation in the lateral leads (I, aVL, V5-6).
- Reciprocal ST depression in the inferior leads (III and aVF).
- ST elevation primarily localised to leads I and aVL is referred to as a high lateral STEMI.
Patterns of lateral infarction
- Three broad categories of lateral infarction:
- Anterolateral STEMI due to LAD occlusion.
- Inferior-posterior-lateral STEMI due to LCx occlusion.
- Isolated lateral infarction due to occlusion of smaller branch arteries such as the D1, OM or ramus intermedius.
Picture is of High Lateral STEMI
Inferior STEMI
Inferior STEMI
- ST elevation in leads II, III, aVF
- Hyperacute T waves may precede these changes
- Reciprocal ST depression in aVL
- Progressive development of Q waves in II, III, aVF
Associated features, all of which confer a worse prognosis, include:
- Concomitant right ventricular infarction (40% of patients); these patients may develop severe hypotension in response to nitrates
- Significant bradycardia due to second or third-degree AV block (20%)
- Posterior infarction due to extension of infarct area
Don’t neglect aVL
- aVL is the only lead truly reciprocal to the inferior wall, as it is the only lead facing the superior part of the ventricle. It is thus a sensitive marker for inferior infarction
- In patient cohorts with inferior occlusion myocardial infarction (OMI), ST depression in aVL has been shown to be more prevalent than STE in inferior leads
- 91% of “subtle” inferior STEMIs that do not meet STEMI criteria but show occlusion on PCI demonstrate ST depression in aVL
Which Artery is the Culprit?
Inferior STEMI can result from occlusion of any of the three main coronary arteries:
- Dominant right coronary artery (RCA) in 80% of cases
- Dominant left circumflex artery (LCx) in 18%
- Occasionally, a “type III” or “wraparound” left anterior descending artery (LAD), producing the unusual pattern of concomitant inferior and anterior ST elevation.
While both RCA and LCx occlusion may cause infarction of the inferior wall, the precise area of infarction and thus ECG pattern in each case is slightly different:
- The RCA territory covers the medial part of the inferior wall, including the inferior septum. The injury current in RCA occlusion is directed inferiorly and rightward, producing ST elevation in lead III > lead II (as lead III is more rightward facing)
- The LCx territory covers the lateral part of the inferior wall and the left posterobasal area. The injury current in LCx occlusion is directed inferiorly and leftward, producing ST elevation in the lateral leads I and V5-6
These differences allow for electrocardiographic differentiation between RCA and LCx occlusion.
RCA occlusion is suggested by:
- ST elevation in lead III > lead II
- Presence of reciprocal ST depression in lead I
- Signs of right ventricular infarction: STE in V1 and V4R
Circumflex occlusion is suggested by:
- ST elevation in lead II = lead III
- Absence of reciprocal ST depression in lead I
- Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6
Posterior Myocardial Infarction
Posterior Myocardial Infarction
How to spot posterior infarction
As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.
Posterior MI is suggested by the following changes in V1-3:
- Horizontal ST depression
- Tall, broad R waves (>30ms)
- Upright T waves
- Dominant R wave (R/S ratio > 1) in V2
In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.
Explanation of the ECG changes in V1-3
The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:
- ST elevation becomes ST depression
- Q waves become R waves
- Terminal T-wave inversion becomes an upright T wave
The progressive development of pathological R waves in posterior infarction (the “Q wave equivalent”) mirrors the development of Q waves in anteroseptal STEMI.
NSTEMI criteria
NSTEMI criteria
Myocardial Ischaemia Background
Non-ST-elevation acute coronary syndrome (NSTEACS) encompasses two main entities:
- Non-ST-elevation myocardial infarction (NSTEMI).
- Unstable angina pectoris (UAP).
The differentiation between these two conditions is usually retrospective, based on the presence/absence of raised cardiac enzymes at 8-12 hours after the onset of chest pain.
Both produce the same spectrum of ECG changes and symptoms and are managed identically in the Emergency Department.
Patterns of Myocardial Ischaemia
Two main ECG patterns associated with NSTEACS:
- ST segment depression
- T wave flattening or inversion
While there are numerous conditions that may simulate myocardial ischaemia (e.g. left ventricular hypertrophy, digoxin effect), dynamic ST segment and T wave changes (i.e. different from baseline ECG or changing over time) are strongly suggestive of myocardial ischaemia.
Other ECG patterns of ischaemia
- Hyperacute (peaked) T waves or pseudonormalisation of previously inverted T waves (i.e. becoming upright) suggest hyperacute STEMI.
- Another, less well-known ECG feature of myocardial ischaemia is U-wave inversion.
