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There exist four stages of pericarditis:
Stage 1 – diffuse concave ST elevation and PR depression in all leads (reciprocal ST depression and PR elevation in aVR)
Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks)
Stage 3 – flattened T waves become inverted (3 to several weeks)
Stage 4 – ECG returns to normal or persistence of T-wave inversions (several weeks onwards).
Spodick’s sign is downsloping TP segment seen as an early ECG manifestation in ~80% of patients with pericarditis, best visualised in leads II and the lateral precordial leads.
Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.
How can you differentiate between Pericarditis and STEMI: 1) STE in pericarditis are concave; in AMI - convex or horizontal, 2) STE in pericarditis - diffuse; in AMI - localised, 3) Pericarditis - PR depression; AMI - Q waves, 4) Pericarditis - inversion of T waves appear after normalising of ST segment; AMI - T wave inversion appears with STE ECG manifestation.
ECG findings of Mobitz I type AV block include:
1) progressive prolongation of PR interval - shortest PR interval after dropped beat - longest PR interval before dropped beat
2) constant P-P interval and changing R-R intervals with the cycle ending with a P wave not followed by a QRS complex
3) the classic Wenckebach pattern occurs usually with ratios of 3:2, 4:3, or 5:4
ECG manifestation of Right ventricular hypertrophy include:
1) right axis deviation (greater than 110°)
2) dominant R in V1 (R> 7mm, R/S ratio is > 1)
3) dominant S in V5/V6 (S > 7 mm, R/S ratio < 1).
Secondary changes are:
1) P pulmonale (> 2.5mm) due to right atrium enlargement
2) right ventricular strain pattern in V1-V3/V4, sometimes II, III, aVF - ST depression/ T wave inversion
3) SI, S II, S III pattern - dominant S waves in leads I, II, III
4) complete or incomplete RBBB.
Other possible causes of an R/S ratio of > 1 in in lead V1 are:
1) Posterior wall MI (also causes ST depression in V1-V3, but T waves symmetrically inverted and the patient would be presenting with chest pain)
2) Right bundle branch block
3) Wolff-Parkinson-White Type A
4) Lead misplacement (if V1 is placed too high)
5) Isolated posterior wall hypertrophy (occurs in Duchenne's muscular dystrophy)
What is the key for diagnosis?
1) flattening of T waves
2) U waves best seen in V1-V2
3) ST depressions I, V5-V6
ECG manifestations of hypokalemia include:
1) flattening of T waves
2) T wave inversion
3) U wave development - best seen in precordial leads (V2-V3)
4) tall P waves and prolonged PR interval
5) ST segment depression
6) pseudo prolonged QT interval, because of T wave and U wave fusion (actually the QU interval with an absent T wave)
7) SVT or VT
*Hypokalemia is often associated with hypomagnesaemia, which increases the risk of malignant ventricular arrhythmias.
What is the key for diagnosis?
1) slow atrial fibrillation
2) typical ST depressions seen in lateral leads.
ECG changes related to digoxin toxicity include:
1) Therapeutic effects:
a) ST segment depression resembling “reverse tick”, “scoop appearance”, “Salvador Dali sign”
b) flattened, inverted, or biphasic T wave
c) shortened QT interval
d) mild PR interval prolongation (due to increased vagal tone)
e) increased U wave amplitude
2) Toxic effects:
The classic digoxin toxic dysrhythmia combines: a)supraventricular arrhythmia (increased automaticity), b)slow ventricular rate (decreased AV conduction). Arrhythmias that typically occur:
a) bradycardia due to AV block or significant decrease in heart rate
b) atrial tachycardia with a 2:1 conduction, bidirectional ventricular tachycardia and atrial fibrillation with a slow ventricular response
c) digoxin intoxication can also cause ventricular tachycardia or ventricular fibrillation resulting in death.
ECG manifestation of posterior STEMI include (Posterior myocardium is not directly visualised by 12-lead ECG, given the placement of anteroseptal leads V1-V3, they are indirectly examining the posterior wall too):
1) Horizontal ST depressions V1-V3
2) Dominant R wave (R/S ratio > 1) in V2-V3
3) Large/upright broad R waves (>30ms), 4) Upright T waves V1-V3.
Posterior leads: Posterior MI is confirmed by the presence of ST elevation in the posterior leads (V7-9). The degree of ST elevation seen in V7-9 is typically modest – only 0.5 mm of ST elevation is required to make the diagnosis of posterior MI!
ECG manifestation of Tako-Tsubo cardiomyopathy include:
1) ST elevations
2) T wave inversions
3) No reciprocal ST depressions
4) Absence of Q waves
5) QT interval prolongation.
How to differentiate between STEMI ?
1) ST elevations in TTC are most commonly in precordial leads
2) ST elevations in TTC are usually not present in V1, in contrast ST elevations are usually present in aVR!
ECG characteristics of Acute idioventricular rhythm include:
1) regular or irregular ventricular rhythm with a rate of 60-110/min
2) > 3 consecutive wide (>120 ms) QRS complexes
3) capture beats and fusion beats may be present
What is the key for diagnosis for this slow-fast AVNRT?
1) regular narrow complex tachycardia, ventricular rate 138 bpm
2) pseudo S waves in the inferior leads II, III, aVF
3) discrete P waves following QRS complexes in lead V1 - pseudo R wave
ECG features of AVNRT are:
1) Since this arrhythmia is usually initiated by a premature atrial complex, there is an initial ectopic atrial P wave and prolonged PR interval
2) Regular narrow complex tachycardia (unless there is aberrant conduction)
3) Ventricular rate is generally between 120 - 220 bpm
4) ST segment depression – represents abnormalities in the repolarization
5) T wave inversions following termination – in the anterior or inferior leads, immediately upon termination or may develop within the first six hours, and can persist for hours to days
P waves in relation to QRS complexes:
1) Typical slow-fast AVNRT: a) The P wave is either hidden or is seen just emerging from the terminal part of the QRS complex > short RP interval, b) Pseudo-S wave in leads II, III, and AVF, c) Pseudo-R' in lead V1
2) Fast-slow AVNRT: a) atria are activated via the slow pathway and the P wave occurs late after the QRS complex, b) P wave often appears shortly before the next QRS resembling a long RP pattern of atrial tachycardia
What is the key for diagnosis?
1) Regular, broad complex tachycardia, ventricular rate at 165 bpm
2) retrograde P waves following QRS complexes best seen in lead V2
3) left posterolateral accessory pathway origin
Based on direction of reentry circuit AVRT is divided into 2 groups:
A) Orthodromic AVRT (>90% of AVRT, re-entrant impulse goes from the atria to the ventricles through the AV node - normal ventricular activation- and then retrogradely activates atria through accessory pathway
ECG signs include: 1) narrow complex tachycardia, 2) ventricular rate 150-250 bpm, 3) inverted P wave following a QRS complex - retrograde activation of the atrium, 4) short RP interval that is usually less than half of RR interval (< ½ RR)
B) Antidromic AVRT (<10% of AVRT, ventricles are activated through an accessory pathway - atria are retrogradely activated over the AV node, or over another accessory pathway - some patients might have multiple accessory pathways),
ECG signs include: 1) wide QRS complex tachycardia, 2) ventricular rate 150-250 bpm, 3) Inverted P waves are often hidden in ST-T segment and therefore the RP interval is usually difficult to assess
1) Early ECG changes of hyperkalemia (5.5-6.5mmol/l):
a) Tall, peaked T waves with a narrow base, best seen in precordial leads
b) Shortened QT interval.
2) ECG changes if blood potassium is 6.5-8.0 mmol/l:
a) Peaked T waves
b) Prolonged PR interval
c) Decreased or disappearing P wave
d) Widening of the QRS
e) ST elevations that can mimic STEMI / ST depressions.
3) At a serum potassium level higher than 8.0 mmol/l, the ECG shows the following:
a) Absence of P waves
b) Progressive QRS widening
c) Intraventricular/fascicular/bundle
d) branch blocks
e) asystoly
f) ventricular fibrillation
Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with: a) renal failure, b) on haemodialysis or c) taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements
ECG changes in pulmonary embolism are related to:
1) dilatation of the right heart
2) right ventricular ischemia
3) increased stimulation of the sympathetic system
Main ECG findings in PE are:
1) T wave inversion in the precordial leads V1-V4 (best correlated to the severity of the PE)
2) sinus tachycardia
3) complete or incomplete RBBB
4) T wave inversion in anterior leads
5) dominant R wave in V1 (sign of acute right ventricular dilatation)
6) P pulmonale (peaked P wave in lead II > 2.5 mm)
7) right axis deviation
8) non-specific ST segment and T wave changes, including ST elevation and depression
9) S I, Q III, T III (sign of acute cor pulmonale - deep S in I, Q and negative T in lead III).
What is the key for diagnosis?
1) Wide complex tachycardia with LBBB morphology
2) inferior axis (positive QRS in inferior leads)
Apart from typical features of a VT, the following ECG features are used to localise RVOT VT/PVCs:
1) LBBB morphology
2) Inferior axis
3) Anterior sites in the RVOT show a dominant Q-wave or a qR complex in lead I and a QS complex in aVL. Pacing at the posterior sites produces a dominant R-wave in lead I, QS or R-wave in aVL and an early precordial transition (R/S = 1 by V3)
4) Precordial transition in V3 or later and shorter R wave duration in V1 and V2 (distinguishes RVOT origin from LVOT)
ECG manifestations of Wellens syndrome include:
1) Characteristic T-wave changes (symmetric and deeply inverted T waves or biphasic T waves in leads V2 and V3)
2) Absence of precordial Q waves
3) isoelectric or minimal (< 1mm) ST elevation
4) normal precordial R wave progression.
There are two patterns of T-wave abnormality in Wellens syndrome:
a) Type A – Biphasic, with initial positivity and terminal negativity
b) Type B – Deeply and symmetrically inverted. T wave changes can evolve over time from Type A to Type B pattern!
Hypercalcemia manifests on ECG as :
1) short QT interval
2) ST segment may be completely absent and replaced by inverted small T-wave directly after R-wave
3) Osborn wave (usually a feature of hypothermia) - a positive deflection at the J point (negative in aVR and V1), most prominent in the precordial leads
4) J-point elevation mimicking ST segment elevation is a common observation
5) Ventricular irritability and VF arrest may occur in extreme hypercalcemia
Infefolateral STEMI manifests on ECG as:
1) ST segment elevations in the leads II, III, aVF, V5-6 (+-I, aVL)
2) Reciprocal changes in anterior leads- ST depressions
ECG features of early repolarization are:
1) An elevated take-off of the ST segment at the J point of the QRS complex, varying from 1 to 4 mm relatively to isoelectric line
2) Notch (J wave) or slur of QRS terminal portion
3) Upward concavity of ST segment
4) Positive concordant T waves
Type 1 is associated with ER in the lateral precordial leads. This form is common among healthy male athletes and is thought to be largely benign
Type 2 is associated with ER in the inferior or inferolateral leads and is associated with a moderate level of risk
Type 3 is associated with ER globally in the inferior, lateral, and right precordial leads, and appears to be associated with the highest relative risk, though the absolute risk of sudden death remains small
Type 4, or Brugada syndrome, is marked by J-wave/point elevation in the right precordial leads
What is the key for diagnosis?: 1) Typical Coved type ST segment elevations in V1-V2.
ECG signs of Brugada syndrome are:
1) Some form of a pseudo-right bundle branch block
2) persistent ST segment elevations in leads V1 to V2.
Brugada syndrome: patients with typical ECG features who have experienced sudden cardiac death or a sustained ventricular tachyarrhythmia, or who have one or more of the other associated clinical criteria (syncope, seizures, and nocturnal agonal respiration due to polymorphic ventricular tachycardia or VF).
Type 1 (“coved type”): This alteration is the only diagnostic pattern for BrS. It is characterized by an ST-segment elevation ≥2 mm in ≥1 right precordial lead (V1 to V3), followed by an rʹ-wave and a concave or straight ST segment. The descending ST segment crosses the isoelectric line and is followed by a negative and symmetric T-wave.
Type 2 (“saddle-back type”): This ECG anomaly is only suggestive of BrS. It is characterized by an ST-segment elevation ≥0.5 mm (generally ≥2 mm in V2) in ≥1 right precordial lead (V1 to V3), followed by a convex ST. The rʹ-wave may or may not overlap the J point, but it has a slow downward slope. The ST segment is followed by a positive T-wave in V2 and is of variable morphology in V1.
The Long QT Syndrome (LQTS) is characterized on the ECG by prolongation of the heart rate corrected QT interval (QTc).
Overall, the average QTc in healthy persons during infancy is 400±20 milliseconds and increases slightly after puberty to 420±20 milliseconds.
Clinical diagnosis is made when:
1) Corrected QT (QTc) ≥480 ms or a LQT score >3
2) In the presence of unexplained syncope, a QTc ≥460 ms is sufficient to make a diagnosis
3) Irrespective of the QT duration if pathogenic LQT syndrome is confirmed
ECG signs of AV block - Mobitz type II are:
1) The PR interval in the conducted beats is constant
2) Block of one or more P waves that fail to conduct to the ventricles
3) The P waves ‘march through’ at a constant rate
4) In Mobitz type II the block is generally located below the AV junction in the His bundle (intra-His block) or lower in the His-Purkinje system (infra-His block). Because of this, the QRS complexes are typically wide or demonstrate bundle branch block morphology.
Mobitz type I and Mobitz type II second degree AV blocks cannot be differentiated from the ECG when a 2:1 AV block is present. In this situation, every other P wave is non-conducted and there is no opportunity to observe for the constant PR interval that is characteristic of Mobitz type II second degree AV block.
VF is characterised by:
1) the presence of irregular ventricular activity varying in appearance and amplitude described as undulating baseline
2) P waves, QRS complexes and T waves are not present
3) Eventually electrical activity of the heart ceases as VF degenerates to asystole
1) VF can be classified as coarse VF and fine VF based on the amplitude of the QRS complex. The amplitude of the QRS complex decreases over time and patients who present with fine VF therefore have worse prognosis
2) VF can be distinguished from ventricular flutter - typical ECG findings of ventricular flutter are regular large oscillations with a sine wave appearance at a rate of 150-300/min.
Lateral STEMI manifests on ECG as:
1) ST elevations in the lateral leads (I, aVL, V5-6)
2) Reciprocal ST depressions in the inferior leads (III and aVF)
ST elevations primarily localised to leads I and aVL is referred to as a high lateral STEMI (usually caused by occlusion of the first diagonal branch of LAD)
Inferolateral STEMI - ST elevations involving lateral (I, aVL, V5, V6) and inferior leads (II, III, aVF) - usually seen with occlusion of the proximal LCx artery
Anterolateral STEMI - ST elevations involving lateral (I, aVL, V5, V6) and anterior leads (V1, V2, V3) - usually highly indicative of proximal LAD occlusion
What is the key for diagnosis?
1) RBBB
2) right axis deviation (dominant negative deflection in leads I and aVL)
3) R wave > 7mm in V1
4) ST depressions in V1-V3
5) P pulmonale
A) ECG findings suggestive of right ventricular hypertrophy in pulmonary hypertension includes: 1) Right axis deviation, 2) R/S ratio > 1 in V1, 3) R wave > 7mm in V1, 4) rSR' complex in V1 with R' > 10mm and 5) qR complex in V1.
B) Right ventricular strain pattern includes (more sensitive than signs of RVH on ECG): 1) ST segment and T wave inversion in V1-V3 and occasionally in inferior leads (II, III, AVF), 2) Right bundle branch block.
C) ECG findings suggestive of right atrial enlargement: 1) P pulmonale (P wave amplitude >2.5mm in inferior leads - II, III, AVF or >1.5mm in V1/V2), 2) P wave axis shifted rightward >70°, 3) Prolongation of the QRS complex and QTc suggest severe disease, and 4) Supraventricular arrhythmias may occur in advanced disease, in particular atrial flutter, but also atrial fibrillation.
Main ECG sign of hypocalcemia is prolongation of the QT interval (increased risk of Torsade de Pointes).
Clinical presentation of acute hypocalcemia includes: tetany, seizures, papilledema.
Chronic hypocalcemia manifests as: ectodermal and dental changes, cataracts, basal ganglia calcification, extrapyramidal disorders.
Chvostek’s sign (normal in 10% of people).
Trousseau’s sign - very specific for hypocalcemia.
With reversal of the LA and RA electrodes, Einthoven’s triangle flips 180 degrees horizontally around an axis formed by lead aVF:
1) Lead I becomes inverted
2) Leads II and III switch places
3) Leads aVL and aVR switch places
4) Lead aVF remains unchanged
Trigeminy – every second sinus beat is followed by atrial premature complex.
1) abnormal P wave is followed by a QRS complex
2) premature P wave usually has a different configuration based on its origin (inverted P waves arise in the lower parts of atria close to AV node)
3) P wave may be hidden in the preceding T wave – peaked appearance of T wave
4) QRS complex can be identical to completely aberrant, but it is typically narrow
5) most SVES reset the sinus node (the pause following SVES is non-compensatory = the interval from the previous sinus P wave to the sinus P wave following APB is shorter than 2x sinus cycle length (< 2x P-P) - this can differentiate them from ventricular premature beats))
APB may initiate a re-entrant atrial tachyarrhythmia such as atrial flutter (activation around tricuspid annulus, AV nodal reentrant tachycardia (AVNRT) or the disorganized rhythm of atrial fibrillation
The U wave is a small (0.5 mm) deflection immediately following the T wave
ECG signs of U wave are:
1) U wave is concordant with the T wave (has the same polarity as a T wave)
2) Amplitude is approx. 0.5 - 2mm
3) Best visible in V2-V3
4) most commonly present in bradycardia
Sinus tachycardia is characterized by:
1) one P wave for every QRS complex
2) The PR interval is shorter than during normal sinus - increased sympathetic tone also speeds AV nodal conduction
3) he QRS complex is usually normal (if there is no fixed or transient intraventricular conduction disturbance)
P wave morphology:
a) Upright in leads I, II and usually aVF
b) Inverted in aVR
c) Upright, biphasic or inverted in III and aVL
d) The right to left activation results in P waves that are upright or biphasic in V1 and V2, and upright in V3 through V6
This distinction of sinus tachycardia from atrial tachycardias is generally based on the clinical presentation and the onset and termination of the tachycardia.
Unlike sinus tachycardia, atrial tachycardias typically have abrupt onset and termination.
ECG findings in this patient should be - RBBB pattern with right axis deviation:
1) Right bundle branch block (RBBB)
a) QRS duration > 120ms
b) RsR’ pattern in leads V1 to V2 – M shaped, “rabbit-ear” pattern
c) Deep, broad S wave in leads I, aVL and V5 to V6
d) ST segment depression and/or T wave inversion in leads V1–V3 - altered sequence of repolarization
2) Right axis deviation
a) QRS is POSITIVE (dominant R wave) in Lead II, Lead III and aVF
b) QRS is NEGATIVE (dominant S wave) in Lead I
What is the key for diagnosis of this posterior fascicular ventricular tachycardia that terminated after verapamil administration?
1) narrow QRS (116ms)
2) RBBB morphology + left axis deviation
ECG characteristics of fascicular ventricular tachycardia are:
1) Monomorphic VT with typical features of VT such as AV dissociation, possible presence of fusion beats and other ECG signs
2) VT with a relatively narrow QRS complex that usually doesn’t exceed 140-150 ms and RS of 60-80 ms
3) Typically having RBBB morphology
4) Immediately after tachycardia termination, T wave inversion may be present
5) Because of its narrow QRS complex morphology it can be mistaken for SVT conducted with aberrancy
Pacemaker syndrome is a phenomenon associated with suboptimal atrioventricular (AV) synchrony that leads to loss of atrial “kick”.
Pacemaker syndrome can occur in any implantable device, but is most commonly seen in the setting of a single chamber device with ventricular sensing and pacing lead.
Since there is no atrial sensing lead to guide the ventricle, the ventricle contracts at the programmed rate regardless of the timing of atrial contraction.
This leads to loss of AV synchrony which leads to a loss in stroke volume and cardiac output.
It can also occur in patients with dual chamber pacemaker, who develop atrial capture loss (no p waves present after atrial spike on ECG). In this case, pacemaker ventricular stimulation became dissociated from atrial depolarization, leading to AV dyssynchrony and symptoms of Pacemaker syndrome.
Junctional rhythm is characterized by:
1) regular rhythm with a rate corresponding to the type of junctional rhythm
2) no visible P waves or retrograde P waves
3) relatively narrow QRS complexes of normal morphology
What is the key for diagnosis?
1) see clear AV dissociation (e.g. lead I)
2) see fusion beat (e.g. lead I)
Characteristics of ventricular tachycardia include:
1) heart rate is >100/min
2) wide QRS complexes with LBBB or RBBB morphology are present, as well as atypical morphology can be present
3) tachycardias with very wide complexes are usually of ventricular origin
4) AV dissociation (atrial activation, usually from the sinus node, is independent from ventricular activation, which is originating from the AV junction, His-Purkinje system, or ventricles)
5) capture beats (the sinoatrial node transiently 'captures' the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration)
6) fusion beats (supraventricular and a ventricular impulse coincide to produce a hybrid complex)
7) morphologic criteria which are considered in algorithms for VT diagnosis such as Brugada or Vereckei criteria
What is the key for diagnosis? 1) Typical sawtooth pattern in inferior leads.
ECG findings in typical atrial flutter are:
1) Narrow complex tachycardia with an atrial rate of 250-350 beats/min
2) Typical sawtooth pattern = flutter waves best seen in the inferior leads II, III, aVF
3) Absence of isoelectric baseline
4) In rates >150 bpm it can be difficult to identify flutter waves = to slow ventricular response, use vagal maneuvers or medication to slow AV node conduction (adenosine, verapamil).
Ventricular Trigeminy = PVC occurs as every third beat includes:
1) the QRS complex occurs earlier than expected = premature
2) the QRS complex is abnormal in shape and duration usually exceeds 120ms (exceptions apply as the duration depends on origin of the PVC, examples of a narrow complex PVCs are fascicular to inter ventricular septal origin
3) the morphology of the PVC (LBBB, RBBB) can be used to determine the origin of the PVC
A PVC is followed by: a) a compensatory pause = the next QRS occurs at two times the preceding R-R interval
b) a noncompensatory pause = the atria are retrogradely activated and the sinus node is reset, the next QRS occurs after an interval other than two times the preceding R-R interval
c) no pause - an interpolated PVC is followed by a sinus beat with a slightly prolonged PR interval but without a pause
d) a ventricular echo - the impulse initially propagates retrogradely but reverses its direction and returns to activate the ventricles after a delay
Cabrera's sign is defined as a prominent notching of at least 0.04 sec in the ascending limb of the S wave in any of leads V3-V4.
Although specificity is high, sensitivity for myocardial infarction is only 27% overall, 47% for anteroseptal MI.
What is the key to diagnosis?
1) epsilon wave in V1 (V2-V3)
2) T wave inversions in V1-V4.
What are the characteristics of arrhythmogenic cardiomyopathy on ECG?
1) Inverted T waves in right precordial leads (V1, V2, and V3) in absence of RBBB
2) Epsilon wave (reproducible low-amplitude signals between end of QRS complex to onset of the T wave) in the right precordial leads (V1 to V3)
3) Localised QRS widening in V1-3 (> 110ms)
4) Prolonged S wave upstroke of 55ms in V1-3
5) Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours
6) Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)
Key to the diagnosis: negative P wave best visible in lead III
ECG characteristics of coronary sinus rhythm include:
1) negative P waves in leads II, III and aVF
2) narrow QRS complexes
3) normal PR interval
4) slightly slower rate than in sinus rhythm
ECG features of left anterior fascicular block include:
1) rS complexes in the inferior leads II, III, aVF
2)Left axis deviation between −45 and −120 degrees
3) QRS complex duration normal or slightly prolonged (80-110ms)
4) qR complexes with R wave slurring in leads I and aVL
Left axis deviation QRS is POSITIVE (dominant R wave) in Lead I, QRS is NEGATIVE (dominant S wave) in leads II, III and aVF
ECG features of AV block 2:1 are:
1) every other P wave is not followed by a QRS complex and
2) QRS complexes may be narrow or wide depending on the site of the AV block
What is the key for diagnosis?
1) positive flutter waves in V1 – suggesting left atrium re-entrant circuit
ECG signs of Atypical atrial flutter are:
1) P waves are absent
2) F waves are regular, but there may be an isoelectric appearance between F waves
3) No clear F wave morphology - atrial scar can alter conduction velocity and direction
A) Right atrial flutters: 1) negative F wave in V1
B) Left atrial flutters: 1) variable morphology, 2) positive or isoelectric F waves in V1, 3) often positive F waves in the inferior leads II, III, aVF C) Lower loop re-entry (around the inferior vena cava): 1) negative F waves in the inferior leads
D) Upper loop re-entry (right atrium): 1)positive F waves in the inferior leads and negative, flat, or barely positive F waves in lead I
What are the keys for the diagnosis for FBI (fast broad irregular) - atrial fibrillation conducted to ventricles through accessory pathway?:
1) irregular wide complex tachycardia
2) ventricular rate >200 bpm
3) QRS complexes usually have variable morphology – APs bypassing the AV node can produce wide and bizarre looking complexes
4) axis remains stable
What are the keys for the diagnosis?
1) regular narrow complex tachycardia, ventricular rate 150 bpm
2) inverted P waves following QRS complexes – short RP interval > AVRT
Wolff-Parkinson-White (WPW) syndrome has a typical pattern during sinus rhythm:
1) the PR interval is short <120ms – rapid conduction through the accessory pathway that bypasses the AV node
2) delta wave - the initial part of ventricular activation is slowed, and the upstroke of the QRS complex is slurred, because of slow muscle-fiber-to-muscle-fiber conduction
3) wide QRS complex >120ms - the QRS complex represents a fusion beat - the initial part results from slow ventricular activation via the accessory pathway, while the terminal portion of ventricular activation is via the normal conduction system
4) ST-T segment is usually directed oppositely to delta waves
5) The more rapid the conduction along the accessory pathway, the greater the amount of myocardium depolarized via the accessory pathway, resulting in a more prominent or wider delta wave, and increasing prolongation of the QRS complex
6) The QRS duration is equal to or greater than 0.12 seconds because of preexcitation (the delta wave), Right-sided pre-excitation can be mistaken for LBBB; left sided pre-excitation can be mistaken for RBBB
7)Tachyarrhythmias associated with WPW syndrome are AVRT (Atrioventricular reentrant tachycardia) and FBI (Fast Broad Irregular tachycardia)
ECG characteristics of R on T phenomenon are:
1) Premature ventricular complex occurin during a T wave of the preceding beat
2) can be followed by an onset of ventricular arrhythmia like in this case
ECG findings in atrial fibrillation are:
1) Irregular R-R intervals – no repetitive pattern
2) Absence of distinct repeating P waves
3) Irregular atrial activation
4) There may be an evidence of an old myocardial infarction, left atrial and ventricular hypertrophy, pericardial disease, cardiomyopathy and ventricular preexcitation.
ECG features of Third–degree atrioventricular (AV) block are:
1) The atrial (P wave) rate is faster than the ventricular (QRS complex) rate
2) P waves bear no relationship to the ventricular QRS complexes
3) If block occurs in the AV node - QRS complexes are usually narrow due to a subsidiary pacemaker arising in the bundle of His
4) If block occurs below the AV node - QRS complexes are usually broad due to a subsidiary pacemaker arising in the left or right bundle branches
5) Any atrial rhythm can coexist with third-degree AV block - the P waves may be abnormal or even absent
The Modified Sgarbossa Criteria (proof of myocardial infarction in patients with LBBB or with paced rhythm):
1) ≥1 mm of concordant ST elevation in any lead
2) ≥ 1 mm of concordant ST depression in ≥ 1 lead V1-V3
3) ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave
ECG features of Q wave myocardial infarction are:
Simple ´´cooking book´´ for pathologic q waves in clinical practice:
1) > 40 ms (1 mm) wide
2) > 2 mm deep
3) > 25% of depth of QRS complex'
4) Q waves in leads V1-3
Pathologic Q waves are defined by:
1) any Q waves in leads V2-V3 ≥ 0.02 seconds or QS complex in leads V2-V3
2) Q-wave ≥ 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4–V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4–V6; II, III, and aVF)
3) in two contiguous leads, Q wave ≥ 0.03 sec and ≥ 0.1mV deep, or QS complex in leads I, II, aVL, aVF, or V4-V6.
Normal Q waves:
1) small Q waves may appear in most leads and do not represent any abnormality
2) deeper Q waves (>0.2 mV) may be seen in leads III and aVR as a normal variant
3) under normal circumstances, Q waves are not seen in the leads V1-V3
ECG findings suggestive of right atrial enlargement are:
1) P pulmonale: P wave amplitude >2.5mm in inferior leads (II, III, AVF) or >1.5mm in V1/V2
2) P wave axis shifted rightward >70°
ECG manifestation of subarachnoid hemorrhage include:
1) ST-segment elevations or depressions that can mimic acute myocardial infarction
2) widespread giant T wave inversions (“cerebral T waves”)
3) large U waves
4) prolonged QT interval
5) rhythm disturbances
ECG manifestation of De Winter Pattern:
1) upsloping ST depression at J-point > 1 mm in precordial leads
2) tall, prominent, symmetrical T waves in precordial leads
3) absence of ST elevation in the precordial leads
4) slight ST segment elevation (0.5mm-1mm) in aVR.
De Winter T wave pattern initially reported in 2008 by De Winter et al. is an equivalent to anterior STEMI due to proximal LAD occlusion. It presents without obvious ST segment elevation.
ECG characteristics of catecholaminergic polymorphic ventricular tachycardia are:
1) patients typically have a normal resting ECG
2) during exercise stress test atrial arrhythmias and/or bidirectional or polymorphic VT can occur and be used to establish the diagnosis
3) bidirectional VT is a rare form of VT in which the axis changes in the frontal plane beat to beat, it can occur in CPVT, digitalis toxicity or herbal aconite poisoning
ECG characteristics of First-degree atrioventricular (AV) block include:
1) PR interval longer than 200 ms
2) 1:1 conduction – every P wave is followed by QRS complex
3) normal morphology and duration of QRS complex (unless there is another aberrancy in conduction)
ECG manifestation of hypothermia include:
1) shivering artefact
2) bradyarrhythmia
3) prolonged PR, QRS and QT intervals
4) Osborn waves (J waves) - a positive deflection at the J point (negative in aVR and V1), most prominent in inferior and precordial leads; the height is roughly proportional to the degree of hypothermia, 5) ectopic activity -> atrial fibrillation
If temperature below 30°C: ventricular fibrillation If temperature below 28°C: cardiac arrest due to VT, VF or asystole
ECG manifestation of STEMI inferolateral is:
1) ST elevations in the leads II, III, aVF, V5-6 (+-I, aVL) are indicating an extensive infarction of inferior and lateral walls
2)Reciprocal changes in anterior leads
ECG features of anterior STEMI are:
1) ST elevations in V1(V2)-V4
2) Reciprocal ST depressions in the inferior leads (II, III and aVF)
ECG features of LBBB are:
1) QRS duration > 120ms, slurring in the mid-portion of the QRS
2) QS or rS pattern in V1 – usually deep and abnormal waves
3) Single broad R wave in leads I, aVL and V5,V6
4) aVR – a QS pattern with a positive T wave
5) ST and T wave abnormalities - T wave inversions and ST segment depression, in the opposite direction from the QRS complex
6) Absent Q wave in lead V6 – septum depolarizes from right to left
7) Leftward QRS axis
ECG signs of RBBB are:
1) QRS duration > 120ms
2) RsR’ pattern in leads V1 to V2 – M shaped, “rabbit-ear” pattern
3) Deep, broad S wave in leads I, aVL and V5 to V6
4) ST segment depression and/or T wave inversion in leads V1 – V3 - altered sequence of repolarization
5) RBBB does not lead to axis deviation
ECG features of Biventricular pacing are:
1) large Q wave or QS complex in lead I
2) leads V5-V6 also frequently demonstrate a QS complex
3) tall R wave in lead V1
* A QS complex in leads V5-V6 and a tall R wave in lead V1 are strongly suggestive of a biventricular pacemaker, an initial Q wave or a QS complex in lead I is more definitive for left or biventricular pacing.
ECG features of Right ventricular pacing are:
1) Pacing spike precedes the QRS complex
2) Right ventricular pacing lead placement results in a QRS morphology similar to LBBB
3) ST segments and T waves should be discordant with the QRS complex (i.e. the major terminal portion of the QRS complex is located on the opposite side of the baseline from the ST segment and T wave)
ECG presentation of dilated left atrium may include:
1) broad, bifid P wave in lead II (P mitrale) = bifid P wave with > 40 ms between the two peaks, total P wave duration > 110 ms
ECG manifestation of NSTEMI include:
A) ST segment depressions: ST depression can be either upsloping, downsloping, or horizontal:
1) Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia
2) ST depression ≥ 1 mm is more specific and conveys a worse prognosis
3) ST depression ≥ 2 mm in ≥ 3 leads is associated with a high probability of NSTEMI and predicts significant mortality (6x higher risk of death)
4) Upsloping ST depression is non-specific for myocardial ischaemia
5) Presence of widespread ST depressions plus ST elevation in aVR > 1 mm is suggestive of left main coronary artery occlusion
B) T wave inversions: T wave inversion must fulfill these criteria:
1) be present in ≥ 2 contiguous leads that have dominant R waves (R/S ratio > 1)
2) be dynamic, 3) be at least 1 mm deep T wave inversion is not a very specific sign if present in leads III, aVR and V1
Other reported ecg abnormalities include a tall and broad R wave, disappearance of the S wave, a taller T wave, and negative U waves
You can’t localise NSTEMI and NAP based on ECG!
ECG characteristics of left ventricular outflow tract tachycardia include:
1) LVOT VT is suggested by LBBB morphology with inferior axis with small R-waves in V1 and early precordial transition (R/S = 1 by V2 or V3) or RBBB morphology with inferior axis and presence of S-wave in V6
2) inferior axis (positive deflections in leads II, III and aVF).
Aortic sinus cusp origin is sometimes difficult to differentiate from RVOT VT because both are so close to each other. Coronary cusp origin has to be thought when we fail an ablation in the RVOT, ECG shows a LBBB inferior axis morphology with taller monophasic R-waves in inferior leads and an early precordial R-wave transition by V2-V3.
ECG manifestation of Left ventricular aneurysm include:
1) Persistent ST elevations (most commonly in precordial leads) seen post an acute MI with with well-formed Q- or QS waves
2) T waves have a relatively small amplitude in comparison to the QRS complex (unlike the hyperacute T-waves of acute STEMI)
It is very important to distinguish between LVA and acute STEMI: - absence of reciprocal ST depressions, well-formed Q waves, no dynamic ST segment changes
Atrial Triplet = three consecutive Premature atrial complexes.
ECG features of Triplet (Premature atrial contraction) are:
1) abnormal P wave followed by a QRS complex
2) premature P wave usually has a different configuration based on its origin
3) inverted P waves arise in the lower parts of atria close to AV node
4) P wave may be hidden in the preceding T wave – peaked appearance of T wave
5) QRS complex can be identical to completely aberrant, but it is typically narrow
6) most SVES reset the sinus node – the pause following SVES is non-compensatory = the interval from the previous sinus P wave to the sinus P wave following APB is shorter than 2x sinus cycle length (< 2x P-P) – this can differentiate them from ventricular premature beats
7) SVES can be stopped in an AV node resulting in an abnormal P wave not followed by a QRS complex with a non-compensatory pause. This is also the commonest reason for sudden stops in ECG
8) SVES that comes too early may encounter refractoriness in one of the bundle branches or fascicles resulting in aberrant ventricular conduction and a different morphology of the QRS complex. Usually with a RBBB morphology – the right bundle branch has a longer refractory period
9) APB may initiate a re-entrant atrial tachyarrhythmia such as atrial flutter (activation around tricuspid annulus, AV nodal reentrant tachycardia (AVNRT) or the disorganized rhythm of atrial fibrillation
Triplet = three consecutive Premature ventricular complexes.
ECG features of Triplet (Premature ventricular contraction) are:
1) the QRS complex occurs earlier than expected = premature
2) the QRS complex is abnormal in shape and duration usually exceeds 120ms (exceptions apply as the duration depends on origin of the PVC, examples of a narrow complex PVCs are fascicular to inter ventricular septal origin
3) the morphology of the PVC (LBBB, RBBB) can be used to determine the origin of the PVC.A PVC is followed by: a) a compensatory pause = the next QRS occurs at two times the preceding R-R interval, b) a noncompensatory pause = the atria are retrogradely activated and the sinus node is reset, the next QRS occurs after an interval other than two times the preceding R-R interval, c) no pause - an interpolated PVC is followed by a sinus beat with a slightly prolonged PR interval but without a pause, d) a ventricular echo - the impulse initially propagates retrogradely but reverses its direction and returns to activate the ventricles after a delay
What is the key for diagnosis?
1) P waves are hidden within T waves and QRS complexes, respectivelly = atrial tachycardia 2:1.
ECG findings in atrial tachycardia are:
1) Regular atrial rate typically 130 – 240 beats/min
2) P wave present before QRS complex = RP interval is longer than the PR interval
3) P waves must be seen and should have isoelectric baseline between them
4) P waves have different morphology and axis than sinus rhythm P waves at higher rates (P waves may be embedded in T wave or are completely obscured)
5) QRS is usually narrow Finding the site of origin (P wave morphology): a) positive P wave in lead V1 – probable left atrial focus, b) positive or biphasic P wave in lead aVL – probable right atrial focus.
Bigeminy = Premature ventricular complex that occurs as every other beat
Typical ECG of Bigeminy (Premature ventricular contraction) include:
1) the QRS complex occurs earlier than expected = premature
2) the QRS complex is abnormal in shape and duration usually exceeds 120ms (exceptions apply as the duration depends on origin of the PVC, examples of a narrow complex PVCs are fascicular to inter ventricular septal origin
3) the morphology of the PVC (LBBB, RBBB) can be used to determine the origin of the PVC.A PVC is followed by: a) a compensatory pause = the next QRS occurs at two times the preceding R-R interval, b) a noncompensatory pause = the atria are retrogradely activated and the sinus node is reset, the next QRS occurs after an interval other than two times the preceding R-R interval, c) no pause - an interpolated PVC is followed by a sinus beat with a slightly prolonged PR interval but without a pause, d) a ventricular echo - the impulse initially propagates retrogradely but reverses its direction and returns to activate the ventricles after a delay
Ventricular Couplet = two consecutive Premature ventricular complexes.
Typical ECG of Couplet (Premature ventricular contraction) include:
1) the QRS complex occurs earlier than expected = premature
2) the QRS complex is abnormal in shape and duration usually exceeds 120ms (exceptions apply as the duration depends on origin of the PVC, examples of a narrow complex PVCs are fascicular to inter ventricular septal origin
3)the morphology of the PVC (LBBB, RBBB) can be used to determine the origin of the PVC
A PVC is followed by:
1) a compensatory pause = the next QRS occurs at two times the preceding R-R interval
2) a noncompensatory pause = the atria are retrogradely activated and the sinus node is reset, the next QRS occurs after an interval other than two times the preceding R-R interval
3) no pause - an interpolated PVC is followed by a sinus beat with a slightly prolonged PR interval but without a pause
4) a ventricular echo - the impulse initially propagates retrogradely but reverses its direction and returns to activate the ventricles after a delay
Based on direction of reentry circuit Atrioventricular reentrant tachycardia (AVRT) is divided into 2 groups:
1) Orthodromic AVRT: >90% of AVRT, re-entrant impulse goes from the atria to the ventricles through the AV node (normal ventricular activation) and then retrogradely activates atria through accessory pathway
ECG findings:
1) narrow complex tachycardia
2) ventricular rate 150-250 bpm
3) inverted P wave following a QRS complex - retrograde activation of the atrium
4) short RP interval that is usually less than half of RR interval (< ½ RR)
2) Antidromic AVRT: <10% of AVRT, Ventricles are activated through an accessory pathway - atria are retrogradely activated over the AV node (or over another accessory pathway - some patients might have multiple accessory pathways)
ECG findings:
1) wide QRS complex tachycardia
2) ventricular rate 150-250 bpm
3) Inverted P waves are often hidden in ST-T segment and therefore the RP interval is usually difficult to assess
ECG features of Left posterior fascicular block (LPFB) are:
1) Right axis deviation ≥+90 degrees
2) RS or rS pattern in I and aVL
3) qR pattern in II, III, aVF
4) QRS duration < 120 ms
ECG manifestation of left ventricular hypertrophy include:
A) Sokolow-Lyon index (specificity > 85%, sensitivity 20%):
1) R wave in V5/V6 + S wave in V1/V2 > 35 mm
2) R wave in aVL > 11 mm
B) Cornell voltage criteria:
1) men: S wave in V3 + R wave in aVL > 28 mm
2) women: S wave in V3 + R wave in aVL > 20 mm
C) Modified Cornell criteria:
1) R wave in aVL > 12 mm
D) Other voltage criteria: 1) R wave in I + S wave in III > 25 mm, 2) R wave in aVF > 20 mm, 3) S wave in aVR > 14 mm
E) Non-voltage criteria: 1) increased R wave peak time > 50 ms in leads V5 or V6, 2) ST depression and T wave inversion in the left-sided leads
ECG signs of Premature Atrial Contraction include:
1) abnormal P wave followed by a QRS complex
2) premature P wave usually has a different configuration based on its origin
3) inverted P waves arise in the lower parts of atria close to AV node
4) P wave may be hidden in the preceding T wave – peaked appearance of T wave
5) QRS complex can be identical to completely aberrant, but it is typically narrow
6) most SVES reset the sinus node – the pause following SVES is non-compensatory = the interval from the previous sinus P wave to the sinus P wave following APB is shorter than 2x sinus cycle length (< 2x P-P) – this can differentiate them from ventricular premature beats
7) SVES can be stopped in an AV node resulting in an abnormal P wave not followed by a QRS complex with a non-compensatory pause. This is also the commonest reason for sudden stops in ECG
8) SVES that comes too early may encounter refractoriness in one of the bundle branches or fascicles resulting in aberrant ventricular conduction and a different morphology of the QRS complex. Usually with a RBBB morphology – the right bundle branch has a longer refractory period
9) APB may initiate a re-entrant atrial tachyarrhythmia such as atrial flutter (activation around tricuspid annulus, AV nodal reentrant tachycardia (AVNRT) or the disorganized rhythm of atrial fibrillation
The ECG manifesation of Premature Ventricular Contraction include:
1) the QRS complex occurs earlier than expected = premature
2) the QRS complex is abnormal in shape and duration usually exceeds 120ms (exceptions apply as the duration depends on origin of the PVC, examples of a narrow complex PVCs are fascicular to inter ventricular septal origin
3) the morphology of the PVC (LBBB, RBBB) can be used to determine the origin of the PVCA PVC is followed by: a) a compensatory pause = the next QRS occurs at two times the preceding R-R interval, b) a noncompensatory pause = the atria are retrogradely activated and the sinus node is reset, the next QRS occurs after an interval other than two times the preceding R-R interval, c) no pause - an interpolated PVC is followed by a sinus beat with a slightly prolonged PR interval but without a pause, d) a ventricular echo - the impulse initially propagates retrogradely but reverses its direction and returns to activate the ventricles after a delay
ECG findings of Inferior STEMI are:
1) ST elevations in leads II, III and aVF
2) Reciprocal ST depression in the lateral and/or high lateral leads (I, aVL, V5 and V6)
3) Hyperacute T waves may precede these changes
Torsade de Pointes is characterized by:
1) morphology in which the QRS complexes “twist” around the isoelectric line (cycling of the QRS axis through 180 degrees every 5 to 20 beats)
2) TdP occurs in the setting of acquired or congenital QT interval prolongation and typically has a rate between 160 and 250 beats per minute
Drug-related TdP ia caused by early afterdepolarizations and triggered activity resulting from prolonged repolarization
ECG features of pseudo-pacemaker syndrome include:
1) Extremely prolonged PR interval (300-400 ms).
In some cases, loss of AV synchrony because of a marked prolongation of the PR interval may cause important haemodynamic alterations, with subsequent decrease in cardiac output and symptoms of heart failure, mimicking a pacemaker syndrome, so-called ‘pseudo-pacemaker syndrome’.
ECG characteristics of ventricular flutter include:
1) It is usually not possible to distinguish the P wave, QRS complex, ST segment and T wave
2) It has a rapid frequency at approximately 200-300/min
3) It usually has a sinusoidal pattern
Unipolar atrial pacing is characterized by large pacing spikes followed by p waves.
ECG features of Short QT syndrome include:
1) Short QT interval
2) Peaked T waves (most commonly seen in precordial leads)
3) Episodes of VF and AFib
Short QT syndrome is diagnosed in the presence of a QTc ≤340 ms.
SQTS should be considered in the presence of a QTc ≤360 ms and one or more of the following:
a) A confirmed pathogenic station
b) A family history of SQTS
c) A family history of sudden death at age 40 years
d) Survival from a VT/VF episode in the absence of heart disease
Suspicion on Pacemaker mediated tachycardia should be raised in all paced tachycardias that run at the upper tracking rate limit of the device (usually 130/min).
Pacemaker mediated tachycardia (PMT), also known as endless-loop tachycardia, generally refers to all tachyarrhythmias in which the pacing device plays a major role.
Classically PMT usually denotes a form of reentrant tachycardia that is encountered in patients with dual-chamber pacemakers in which:
1) pacemaker forms the antegrade limb'
2) AV node (or an accessory pathway) forms the retrograde limb of the reentrant circuit
On this ECG:
1) runs of non sustained VT from RVOT with interposed sinus beats
2) LBBB morphology
3) inferior axis (positive QRS complex in II, III and aVF)
4) precordial transition in V4
The following ECG features are used to localise RVOT VT/PVCs:
1) LBBB morphology
2) Inferior axis
3) Anterior sites in the RVOT show a dominant Q-wave or a qR complex in lead I and a QS complex in aVL. Pacing at the posterior sites produces a dominant R-wave in lead I, QS or R-wave in aVL and an early precordial transition (R/S = 1 by V3)
4) Precordial transition in V3 or later and shorter R wave duration in V1 and V2 (distinguishes RVOT origin from LVOT).
If multiple morphologies are present, scar related VT as in arrhythmogenic cardiomyopathy should be suspected
ECG findings of left main coronary artery occlusion are:
1) Widespread horizontal ST depressions, most prominent in leads I, II and V4-6'
2) ST elevation in aVR ≥ 1mm, 3) ST elevation in aVR ≥ V1
The Delta wave is a slurred upstroke in the QRS complex (see anterolateral leads).
It relates to pre-excitation of the ventricles, and therefore often causes an associated shortening of the PR interval.
It is most commonly associated with pre-excitation syndromes such as WPW.
ECG manifestation of delta wave include:
1) PR interval is shorter around 120ms
2) The initial part of ventricular activation is slowed = wide QRS complex >120ms (the QRS complex represents a fusion beat - the initial part results from slow ventricular activation via the accessory pathway, while the terminal portion of ventricular activation is via the normal conduction system)
3) ST segment and T wave abnormalities - reflecting abnormal ventricular repolarization
Key for diagnosis: 1) negative concordance in all precordial leads, 2) positive R wave in aVR (Vereckei criteria), 3) superior axis (negative concordance in inferior leads) = VT originates in post-infarction apical aneurysm.
ECG characteristics of VT:
ECG after cardioversion (scar on the anterior wall):
What is the key for diagnosis?
1) low QRS voltage
2) sinus tachycardia
ECG manifestations of cardiac tamponade include:
1) sinus tachycardia
2) low QRS voltage
3) electrical alternans (alternation of QRS complex amplitude or axis between beats)
4) PR segment depression
