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Flashcards in ECG criteria Deck (67):
1

LBBB criteria


 The ECG criteria for a left bundle branch block (LBBB) include:

1. QRS duration of > 120 milliseconds.

2. Absence of Q wave in leads I, V5, and V6.

3. Monomorphic R wave in I, V5, and V6.

4. ST and T wave displacement opposite to the major deflection of the QRS complex

If the QRS duration is [100-119] ms with criteria 2, 3, and 4 of the above, an incomplete LBBB is present.

A simple way to diagnose a  left bundle branch in an ECG with a widened QRS complex (> 120 ms) would be to look at lead V1. If the QRS complex is widened and downwardly deflected in lead V1, a LBBB is present.

If the QRS complex is widened and upward deflected in lead V1, then a RBBB is present.

2


rate dependant LBBB

A rate dependent left bundle branch block can occur at times of fast heart rates. This may be caused by myocardial ischemia or refractoriness of the left bundle at faster heart rates. A rate dependent left bundle branch block, when occurring at heart rates greater than 100 beats per minute, can at times be difficult to distinguish from ventricular tachycardia since both cause a wide complex QRS complex. The Brugada Criteria for diagnosing ventricular tachycardia is helpful to make this distinction.

3

Sgarbossa criteria

The Sgarbossa criteria is used in the diagnosis of an acute MI when a LBBB is present.

Traditionally it has been taught that MI is not able to be diagnosed via ECG in the presence of  (LBBB), however Sgarbossa et al in 1996 described some ECG changes seen in those with LBBB and concomitant MI and devised a point scoring system.


1) ST elevation > 1 mm and in the same direction (concordant) with the QRS complex. 5 points

2) ST depression > 1 mm in leads V1, V2, or V3. 3 points

3) ST elevation > 5 mm and in the opposite direction (discordant) with the QRS. 2 points

4

RBBB criteria

 The ECG criteria for a right bundle branch block include:

  1.     QRS duration of > 120 ms
  2.     rsR' "bunny ear" pattern in precordial leads
  3.     Slurred S waves in leads I, aVL and frequently V5 and V6.
     

T wave inversions and ST segment depression is normal in leads V1 - V3 in the presence of a RBBB, thus technically myocardial ischemia can not be easily determined in these leads. However, unlike in the presence of a LBBB, myocardial ischemia and infarction can easily be detected on ECG when a RBBB is present.

5

LAFB

 A left anterior fascicular block (LAFB, a.k.a. left anterior hemiblock or LAHB) occurs when the anterior fascicle of the left bundle branch is no longer able to conduct action potentials.

The criteria to diagnose a LAFB is as follows:

  1. Left axis deviation of at least -45 degrees
  2.     The presence of a qR complex in lead I and a rS complex in lead III.
  3.     Usually a rS complex in lead II and aVF as well (not always).

 Note: An old inferior wall myocardial infarction is not able to be diagnosed in the setting of a left anterior fascicular block due to the inferior Q waves present from the LAFB.

A left anterior fascicular block can also occur in the setting of a bifascicular or trifascicular block

6

LPFB

 A left posterior fascicular block (LPFB) also known as a left posterior hemiblock (LPHB) occurs when the posterior fascicle of the left bundle branch is no longer able to conduct action potentials. This is much less common than a LAFB since the posterior fascicle is much more sparsely distributed, so a large amount of myocardial tissue must be damaged to block the posterior fascicle.

The criteria to diagnose a LPFB is as follows:

1. Right axis deviation of 90 to 180 degrees
2. The presence of a qR complex in lead III and a rS complex in lead I.
3. Absence of right atrial enlargement and/or right ventricular hypertrophy

7


Bifasicular block

A bifascicular block is defined by the combination of RBBB and a LAFB or LPFB. When these occur in combination, significant conduction disease is usually present and there is a risk for higher degrees of AV block in the future causing symptomatic bradycardia and requiring pacemaker implantation

8

Trifascicular block

 trifascicular block is the combination of a RBBB, LAFB or LPFB block and a first degree AV block (prolonged PR interval).

The term “trifascicular block” is a misnomer term since the AV node itself is not a fascicle.

A trifascicular block is a precursor to complete heart block. While a trifascicular block itself does not require any treatment, high doses of AV blocking agents likely should be avoided.

Some series report a 50% lifetime need for a permanent pacemaker in the setting of a trifascicular block

9

1st degree AV block

A first degree AV node block occurs when conduction through the AV node is slowed, thus delaying the time it takes for the action potential to travel from the SA node, through the AV node, and to the ventricles.

 

It can be due to anatomical or functional impairment in the conduction system and can produce a
clinical condition similar to that of the pacemaker syndrome when the PR interval is greater than 0.3
seconds.

It is a relatively common condition with a prevalence of approximately 7%. [3] It is also commonly found
in highly trained athletes with supranormal cardiovagal tone.

10

2nd degree AV block Type 1

In second degree AV nodal block (a.k.a. Wenckebach block or Mobitz Type I AV block), varying failure of conduction through the AV node occurs such that some P waves may not be followed by a QRS complex. Unlike 1st degree AV nodal block, a 1:1 P wave to QRS complex ratio is not maintained. Second degree type I AV block is specifically characterized by increasing delay of AV nodal conduction until a P wave fails to conduct through the AV node. This is seen as progressive PR interval prolongation with each beat until a P wave is not conducted. There is an irregular R-R interval as well. Sometimes when the block is consistent, the QRS complexes are said to demonstrate "group beating".

11

2nd degree type 2 AV block

In second degree type II AV nodal block (a.k.a. Mobitz Type II AV block), the AV node becomes completely refractory to conduction on an intermittent basis. For example, three consecutive P waves may be followed by a QRS complex giving the ECG a normal appearance, then the fourth P wave may suddenly NOT be followed by a QRS complex since it does not conduct through the AV node to the ventricles.

 

The PR interval may be normal or prolonged, however it is constant in length unlike second degree AV block Mobitz Type I (Wenckebach) in which the PR interval progressively lengthens until a P wave is not conducted. A second degree type II AV block indicates significant conduction disease in this His-Purkinje system and is irreversible (not subject to autonomic tone or AV blocking medications). This is a very important distinguishing factor compared to second degree type I AV block. Because of this, a pemament pacemaker is indicated in every patient with second degree type II AV block.

12

2:1 AV block

2:1 AV block is a form of second degree AV nodal block and occurs when every other P wave is not conducted through the AV node to get to the ventricles and thus every other P wave is NOT followed by a QRS complex.

 2:1 AV block can possibly be from either second degree type I AV nodal block (Wenckebach) or second degree type II AV nodal block. This distinction is crucial since the former is usually benign while the later requires implantation of a permanent pacemaker.

A general rule to remember is that if the PR interval of the conducted beat is prolonged AND the QRS complex is narrow, then it is most likely second degree type I AV nodal block (Wenckebach).

Alternatively, if the PR interval is normal and the QRS duration is prolonged, then it is most likely second degree type II AV block and a pacemaker is probably warranted.

Remember that second degree type I AV nodal block is an issue in the AV node itself which is subject to sympathetic and parasympathetic tone while second degree type II AV block is "infranodal" conduction disease of the His-Purkinje system, therefore altering AV nodal conduction would have no effect.

In order to distinguish between the two potential rhythms when an ECG reveals 2:1 AV nodal block, a couple different maneuvers can be employed:

  •     Carotid sinus massage or adenosine: This slows the sinus rate allowing the AV node more time to recover, thus reducing the block from 2:1 to 3:2 and unmasking any progressing prolonging PR intervals that would indicate second degree type I AV nodal block.
  •     Atropine administration: This enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)
  •     Exercise ECG testing (enhances AV nodal conduction and could eliminate second degree type I AV nodal block since it is due to slowed AV nodal conduction)

13

3rd degree AV block

ccurs when NO action potentials conduct through the AV node. This results in the P waves (atrial depolarizations) being completely unrelated to the QRS complexes (ventricular depolarizations). So the P waves occur at one rate and the QRS complexes at another. This is termed “AV dissociation”.

 

High grade AV nodal block" (a type of 3rd degree heart block) occurs when there is AV dissociation similar to complete heart block, but occasional P waves DO conduct through the AV node to produce a QRS complex.

Complete heart block is usually symptomatic from the slow ventricular rates. These symptoms include fatigue, dyspnea, dizziness and syncope. Since intrinsic conduction disease of the His-Purkinje system is the cause of 3rd degree AV block (not autonomic tone or AV blocking medications), the rhythm is usually irreversible and a permanent pacemaker is indicated

14

Acute Anterior STEMI

 An anterior wall myocardial infarction (AWMI or anterior STEMI) occurs when anterior myocardial tissue usually supplied by the left anterior descending coronary artery (LAD) suffers injury due to lack of blood supply. When an AWMI extends to the septal and lateral regions as well, the culprit lesion is usually more proximal in the LAD or even in the left main coronary artery. This large anterior myocardial infarction is termed an "extensive anterior".

The ECG findings of an acute anterior wall myocardial infarction include:

1. ST segment elevation in the anterior leads (V3 and V4) and sometimes in septal and lateral leads depending on the extent of the myocardial infarction. This ST elevation is concave downward and frequently overwhelms the T wave. This is called "tombstoning" due to the similarity to the shape of a tombstone.

2. Reciprocal ST segment depression in the inferior leads (II, III and aVF).

15

Inferior STEMI

 An inferior wall myocardial infarction (IWMI, inferior MI or inferior STEMI) occurs when inferior myocardial tissue supplied by the right coronary artery (RCA), is injured due to thrombosis of that vessel. When an inferior myocardial infarction extends to posterior regions as well, an associated posterior wall myocardial infarction may occur. The ECG findings of an acute inferior myocardial infarction include:

  1.     ST segment elevation in the inferior leads (II, III, and aVF).
  2.     Reciprocal ST segment depression in the lateral and/or high lateral leads (I, aVL, V5 and V6).
     


Note: If the reciprocal ST depressions are not present, consider alternative causes of ST segment elevation such as pericarditis.

16

Pericarditis

signs of different stages

Stage I (acute phase): Diffuse concave upward ST segment elevation in most leads, PR depression in most leads (may be subtle), and sometimes notching at the end of the QRS complex.

Stage II: ST segment elevation and PR depression have resolved. T waves may be normal or flattened.

Stage III: T waves are inverted and the ECG is otherwise normal.

Stage IV: The T waves return to the upright position thus the ECG is back to normal.

Note: The ECG changes of pericarditis must be distinguished from those of early repolarization. The ST elevation seen in early repolarization is very similar; diffuse and concave upward. However three things may help to distinguish pericarditis from early repolarization:

  1.     The ratio of the T wave amplitude to the ST elevation should be > 4 if early repolarization is present. In other words, the T wave in early repolarization is usually 4 times the amplitude of the ST elevation. Another way to describe this would be that the ST elevation is less than 25% of the T wave amplitude in early repolarization.
  2.     The ST elevation in early repolarization resolves when the person exercises.
  3.     Early repolarization, unlike pericarditis, is a benign ECG finding that should not be associated with any symptoms.

17

Pericardial effusion

diagnosis

 Pericardial effusions are best diagnosed by echocardiography which is validated to estimate the size, location and determine if hemodynamic compromise is present causing cardiac tamponade. Right ventricular diastolic collapse would indicate cardiac tamponade.

The chest x-ray shows a markedly enlarged cardiac silhouette termed "water-bottle heart".Chest x-ray will show a “globular heart” with significant heart enlargement

 Computed tomography (CT) can detect the presence of a pericardial effusion, however is not accurate to estimate size.

The 12-lead ECG may show low voltage, pericarditis if present or electrical alternans

 A large pericardial effusion can muffle the heart sounds making them soft or even inaudible. A pericardial friction rub from pericarditis may be present.

Ewart’s sign is dullness to percussion at the left lung base due to compressive atelectasis from a large pericardial effusion.

Auenbrugger’s sign is an epigastric bulge due to a large pericardial effusion extending subxiphoid. Compression of this bulge may cause hemodynamic compromise and cardiac tamponade.

Physical exam findings of cardiac tamponade include sinus tachycardia, elevated jugular venous pressure with inspiration, pulsus paradoxus, and rarely Kussmaul’s sign.

18


Old anterior STEMI


Loss of anterior forces:

Q waves present in V1&V2

no identifiable R waves in V1 &/ V2

Poor R wave progression

19


OLD Inferior STEMI

Q wave in III wider than 1 mm

Q wave in aVF wider than 0.5mm

20


Poor R wave progression

 Poor R wave progression refers to the absence of the normal increase in size of the R wave in the precordial leads as you progress from lead V1 to V6.

In lead V1, the R wave should be small. The R wave becomes larger throughout the precordial leads to the point where the R wave is larger than the S wave in lead V4. The S wave then becomes quite small in lead V6.

 Note that an old anterior myocardial infarction can cause poor R wave progression. In this setting, there is no R wave in the anterior precordial leads and instead Q waves are present (see Anterior Myocardial Infarction).

The causes of poor R wave progression or PRWP are as follows:

1. Old anterior myocardial infarction
2. Lead misplacement (frequently in obese women)
3. Left bundle branch block or left anterior fascicular block
4. Left ventricular hypertrophy
5. WPW syndrome
6. Dextrocardia
7. Tension  pneumothorax with mediastinal shift
8. Congenital heart disease

21

VT

 The Brugada criteria/algorithm is below:
1. Do you see concordance present in the precordial leads (leads V1-V6)?

Also sometime explained as the absence of an RS complex, concordance is diagnostic of VT. A simple way to think of this would be to ask the question, are all of the QRS complexes completely upright or completely downward in the precordial leads? If the answer is yes, then VT is the diagnosis.

 2. Is the R to S interval > 100 ms in any one precordial lead?

If present, then VT is the diagnosis. Simply use calipers to measure the distance between the R wave to S wave in each precordial lead and see if it exceeds 100 ms

 3. Do you see atrioventricular (AV) dissociation?

If present, the diagnosis is ventricular tachycardia.

AV dissociation occurs when P wave (represents atrial depolarization) are seen at different rates than the QRS complex. This is present in only a small percentage of ventricular tachycardia ECG tracings, however is diagnostic of VT. Frequently, this is difficult to see due to the fast rate of the QRS complex. Below is an ECG strip of a ptient with ventricular tachycardia. See the P-P inteval when in sinus rhythm then march out the P waves within the wide QRS complex to find the AV dissociation that is present confirming the diagnosis of ventricular tachycardia:

 4. Examine the morphology of the QRS complex to see if it meets the below specific criteria for VT as below.

VT is frequently either in a RBBB (upright in V1) or a  LBBB(downward in V1).

If upward in lead V1 (RBBB pattern), then VT is present in the following situations:

  •     A monophasic R or biphasic qR complex in V1.
  •     If an RSR’ pattern (“bunny-ear”) is present in V1 with the R peak being higher in amplitude than the R’ peak, the VT is present (see image below).
  •     A rS complex in lead V6 favors VT

If downward in lead V1 (LBBB pattern), then VT is present in the following situations:

  •     The presence of any Q or QS wave in lead V6 favors VT
  •     A wide R wave in lead V1 or V2 of 40 ms or more favors VT (see below image)
  •     Slurred or notched downstroke of the S wave in V1 or V2 favors VT
  •     Duration of onset of QRS complex to peak of QS or S wave > 60 ms favors VT
     

22

Pulmonary embolism

The most common ECG finding in the setting of a pulmonary embolism is sinus tachycardia, however the "S1Q3T3" pattern of acute cor pulmonale is classic. This is termed the McGinn-White sign.

A large S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III indicates acute right heart strain. This pattern only occurs in about 10% of people with pulmonary embolisms and is similar to the ECG findings in a left posterior fascicular block (LPFB).

23

Mobitz type 1 an 2

mechanism differences

  • Mobitz II is usually due to failure of conduction at the level of the  His-Purkinje system (i.e. belowthe AV node).
  • While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs,reversible ischaemia), Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).
  • Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd degree AV block is produced by intermittent failure of the remaining fascicle (“bilateral bundle-branch block”).
  • In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.
  • In the remaining 25% of cases, the conduction block is located within the His Bundle itself causing narrow QRS
  • There may be no pattern to the conduction blockade, or alternatively there may be a fixed
    relationship between the P waves and QRS complexes, e.g. 2:1 block, 3:1 block.

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Causes of MOBITZ 2

  • Anterior MI (due to septal infarction with necrosis of the bundle branches).
  • Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease).
  • Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
  • Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).
  • Autoimmune (SLE, systemic sclerosis).
  • Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).
  • Hyperkalaemia.
  • Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

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Benign early repolarisation

  • Widespread concave ST elevation, most prominent in the mid- to left precordial leads (V2-5).
  • Notching or slurring at the J-point.
  • Prominent, slightly asymmetrical T-waves that are concordant with the QRS complexes
  • The degree of ST elevation is modest in comparison to the T-wave amplitude (less than 25% of the T wave height in V6)
  • ST elevation is usually < 2mm in the precordial leads and < 0.5mm in the limb leads, although precordial STE may be up to 5mm in some instances.
  • No reciprocal ST depression to suggest STEMI (except in aVR).
  • ST changes are relatively stable over time (no progression on serial ECG tracings).

26


ST segment and T wave morphology in BER

  • There is elevation of the J point
  • The T wave is peaked and slightly asymmetrical
  • The ST segment and the ascending limb of the T wave form an upward concavity
  • The descending limb of the T wave is straighter and slightly steeper than the ascending limb

One characteristic f eature of BER is the presence of
a notched or irregular J point: the so-called “fish
hook” pattern. This is of ten best seen in lead V4.

27


BER or pericarditis?

  • The vertical height of the ST segment elevation (from the end of the PR segment to the J point) is measured and compared to the amplitude of the T wave in V6.
  • A ratio of > 0.25 suggests pericarditis
  • A ratio of < 0.25 suggests BER

 

Features suggesting BER

  1. ST elevation limited to the precordial leads
  2. Absence of PR depression
  3. Prominent T waves
  4. ST segment / T wave ratio < 0.25
  5. Characteristic “fish-hook” appearance in V4
  6. ECG changes relatively stable over time

 

Features suggesting pericarditis:

  1. Generalised ST elevation
  2. Presence of PR depression
  3. Normal T wave amplitude
  4. ST segment / T wave ratio > 0.25
  5. Absence of “fish hook” appearance in V4
  6. ECG changes evolve over time

 

28


ATRIAL FLUTTER

Atrial flutter is a type of supraventricular tachycardia caused by a macro-re-entry circuit in
the right atrium.

The re-entry circuit results in an atrial rate of 200-400 bpm (typically 300 bpm).
Ventricular rate is determined by the AV conduction ratio

 

TYPE 1 (common)

Involves the inferior vena cava – tricuspid isthmus in the reentry circuit. Can be further classified based on the direction of the circuit:


Anticlockwise Reentry

  • Commonest form of typical atrial flutter: 90% cases
  • Positive flutter waves in V1
  • Negative flutter waves in leads II,III, aVF

 

Clockwise Reentry (Reversed Typical Atrial Flutter)

  • Wide negative flutter waves in V1
  • Positive flutter waves in leads II, III, aVF

 

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Atrial fibrillation

 

Classification

  • First episode – initial detection of AF regardless of symptoms or duration
  • Recurrent AF – More than 2 episodes of AF
  • Paroxysmal AF – Self terminating episode < 7 days
  • Persistent AF – Not self terminating, duration > 7 days
  • Long-standing persistent AF – > 1 year
  • Permanent (Accepted) AF – Duration > 1 yr in which rhythm control interventions are not
  • pursued or are unsuccessful

30


ESCAPE RHYTHMS

SA node (60-100 bpm)
Atria (< 60 bpm)
AV node (40-60 bpm)
Ventricles (20-40 bpm)

 

JUNCTIONAL ESCAPE RHYTHM:

  • A junctional rhythm with a rate of 40-60 bpm.
  • QRS complexes are typically narrow (<120 ms).
  • No relationship between the QRS complexes and any preceding atrial activity (e.g. Pwaves,  flutter waves, fibrillatory waves).
  • Junctional bradycardia = junctional rhythm at a rate of < 40 bpm.
  • Junctional escape rhythm = junctional rhythm at a rate of 40-60 bpm.
  • Accelerated junctional rhythm = junctional rhythm at 60-100 bpm.
  • Junctional tachycardia = junctional rhythm at > 100 bpm.

31

LAFB mechanism description and criteria

In left anterior fascicular block (aka left anterior hemiblock), impulses are conducted to the left ventricle via the left posterior fascicle, which inserts into the infero-septal wall of the left ventricle along its endocardial surface.

On reaching the left ventricle, the initial electrical vector is therefore directed downwards and rightwards (as excitation spreads outwards from endocardium to epicardium),

producing small R waves in the inferior leads (II, III, aVF) and small Q waves in the leftsided leads (I, aVL).

The major wave of depolarisation then spreads in an upwards and leftwards direction, producing large positive voltages (tall R waves) in the left-sided leads and large negative voltages (deep S waves) in the inferior leads.

This process takes about 20 milliseconds longer than simultaneous conduction via both fascicles, resulting in a slight widening of the QRS.

The impulse reaches the left-sided leads later than normal, resulting in a increased R wave peak time (the time from onset of the QRS to the peak of the R wave) in aVL.

 

Diagnostic Criteria for LAFB

  1. Left axis deviation (usually between -45 and -90 degrees)
  2. Small Q waves with tall R waves (= ‘qR complexes’) in leads I and aVL
  3. Small R waves with deep S waves (= ‘rS complexes’) in leads II, III, aVF
  4. QRS duration normal or slightly prolonged (80-110 ms)
  5. Prolonged R wave peak time in aVL > 45 ms
  6. Increased QRS voltage in the limb leads

 

32

LPFB diagnostic criteria and tips

Diagnostic Criteria for LPFB

  • Right axis deviation (> +90 degrees)
  • Small R waves with deep S waves (= ‘rScomplexes’) in leads I and aVL
  • Small Q waves with tall R waves (= ‘qR complexes’) in leads II, III and aVF
  • QRS duration normal or slightly prolonged (80-110ms)
  • Prolonged R wave peak time in aVF
  • Increased QRS voltage in the limb leads
  • No evidence of right ventricular hypertrophy
  • No evidence of any other cause for right axis deviation

 

  • LPFB is much less common thanLAFB, as the broad bundle offibres that comprise the leftposterior fascicle are relativelyresistant to damage when compared with the slim single tractthat makes up the left anterior fascicle.
  • It is extremely rare to see LPFB inisolation. It usually occurs along with RBBB in the context of a bifascicular block.
  • Do not be tempted to diagnose LPFB until you have ruled out more significant causes of right axis deviation: i.e. acute PE, tricyclic overdose, lateral MI, right ventricular hypertrophy.

33

Poor R Wave Progression

Definition

R wave height ≤ 3 mm in V3.

 

Causes:

  • Prior anteroseptal MI
  • Left ventricular hypertrophy
  • Inaccurate lead placement (e.g. transposition of V1 and V3)
  • Dilated cardiomyopathy
  • May be a normal variant

34


Intrinsicoid deflections/ R wave peak time

The time from the onset of the earliest Q or R wave to the peak of the R wave in the lateral leads (aVL, V5-6).


Represents the time taken for excitation to spread from the endocardial to the epicardial surface of the left ventricle.


R-wave peak time is said to be prolonged if > 45ms.

 

Causes of Prolonged RWPT:


Left anterior fascicular block
Left ventricular hypertrophy
Left bundle branch block

35


LMCA occlusion (left main coronary artery)

CLassical pattern:

  • Widespread horizontal ST depression, most prominent in leads I, II and V4-6
  • ST elevation in aVR ≥ 1mm
  • ST elevation in aVR ≥ V1

Mechanism of STE in aVR

  • Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.
  • Lead aVR also directly records electrical activity from the right upper portion of the heart,
  • including the right ventricular outflow tract and the basal portion of the interventricular septum; infarction in this area could theoretically produce ST elevation in aVR.


ST elevation is aVR is thought to result f rom two possible mechanisms:

  • Diffuse subendocardial ischaemia (producing reciprocal change in aVR)
  • Transmural ischaemia / infarction of the basal interventricular septum (e.g. due to a proximal occlusion within the left coronary system)

 

NB. The basal septum is supplied by the first septal perforator artery (a very proximal branch of the LAD), so ischaemia/infarction of the basal septum would imply involvement of the proximal LAD or LMCA.

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RBBB background, criteria

In RBBB, activation of the right ventricle is delayed as depolarisation has to spread across the septum from the left ventricle.
The left ventricle is activated normally, meaning that the early part of the QRS complex is unchanged.
The delayed right ventricular activation produces a secondary R wave (R’) in the right precordial leads (V1-3) and a wide, slurred S wave in the lateral leads.
Delayed activation of the right ventricle also gives rise to secondary repolarization abnormalities, with ST depression and T wave inversion in the right precordial leads.
In isolated RBBB the cardiac axis is unchanged, as left ventricular activation proceeds normally via the left bundle branch

 

Diagnostic Criteria

  • Typical RSR' pattern ('M'-shaped QRS) in V1
  • Wide, slurred S wave in the lateral leads (I, aVL, V5-6)
  • Broad QRS > 120 ms


Associated Features
ST depression and T wave inversion in the right precordial leads (V1-3)

37


LBBB background and diagnostic criteria

Normally the septum is activated from left to right, producing small Q waves in the lateral leads.
In LBBB, the normal direction of septal depolarisation is reversed (becomes right to left), as the impulse spreads first to the RV via the right bundle branch and then to the LV via the septum.
This sequence of activation extends the QRS duration to > 120 ms and eliminates the normal septal Q waves in the lateral leads.
The overall direction of depolarisation (from right to left) produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3), and usually leads to left axis deviation.
As the ventricles are activated sequentially (right, then left) rather than simultaneously, this produces a broad or notched (‘M’-shaped) R wave in the lateral leads.

 

Diagnostic criteria:

  • QRS duration of 120 ms
  • Dominant S wave in V1
  • Broad monophasic R wave in lateral leads (I, aVL, V5-V6)
  • Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL)
  • Prolonged R wave peak time > 60ms in left precordial leads (V5-6)

 

Associated Features

  • Appropriate discordance: the ST segments and T waves always go in the opposite direction to the main vector of the QRS complex
  • Poor R wave progression in the chest leads
  • Left axis deviation

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STE in aVR

        Lead aVR is electrically opposite to the left-sided leads I, II, aVL and V4-6; therefore ST depression in these leads will produce reciprocal ST elevation in aVR.


        Lead aVR also directly records electrical activity from the right upper portion of the heart, including the right ventricular outflow tract and the basal portion of the interventricular septum; infarction in this area could theoretically produce ST elevation in aVR.

39

Right ventricular infarction

        Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
        Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
        Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

 

In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:

  •         ST elevation in V1 — the only standard ECG lead that looks directly at the right ventricle.
  •         ST elevation in lead III > lead II — because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.

40

The SA node receives blood from

the SA node a.  - a branch of RCA in 60%, of the LCX in 20-30% .

41

blood to AVN is via

AV nodal a. - from RCA in 90%, remainder from LCX.

42

Left main coronary artery occlusion ECG features

widespread ST depression with ST elevation in aVR ≥ V1

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Wellens’ syndrome:

ECG and significance


deep precordial T wave inversions or biphasic T waves in V2-3,
 


indicating  SUBacute critical proximal LAD stenosis (a of imminent anterior infarction). There are two patterns:


 


Type A Wellens’ T-waves are deeply and symmetrically inverted




 




Type B Wellens’ T-waves are biphasic, with the initial deflection positive and the terminal deflection negative




 

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De Winter’s T Waves#

ECG and significance


anterior STEMI equivalent that presents without obvious ST elevation.require ACUTE cath-lab




Key diagnostic features include ST depression and peaked T waves in the precordial leads.
 

The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-recognised by clinicians

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old anterior stemi on ecg

Loss of anterior forces

Q eaves in V1, V2

no identifiable R waves in V1 +/-V2

PRWP

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ecg patter of LMCA occlusion


Widespread horizontal ST depression,  


most prominent in leads I, II and V4-6

 




ST elevation in aVR ≥ 1mm

 






ST elevation in aVR ≥ V1
 

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STE in aVR DDx


Proximal left anterior descending artery (LAD) 


occlusion

Severe triple-vessel disease (3VD)
 

LMCA occlusion

 

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ecg changes in posterior MI

these changes in V1-3:


  • Horizontal ST depression

     



  • Tall, broad R waves (>30ms) 





  • Upright T waves

     







  • Dominant R wave (R/S ratio > 1) in V2
     

  • Inferior MIs account for 40-50% of all MIs
     

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acute inferior stemi in ecg


  • ST elevation in leads II, III and aVF

     



  • Progressive development of Q waves in II, III and aVF

     





  • Reciprocal ST depression in aVL (± lead I)
     

50

old inferior stemi in ecg

  • Q wave in III wider than 1 mm
  • Q wave in aVF wider than 0.5mm

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complications of inferior STEMI

Up to 40% with an inferior STEMI have a concomitant RV INFARCTION.


Up to 20% with inferior STEMI will develop significant bradycardia due to second- or third-degree AV block. 




Inferior STEMI may also be associated with posterior infarction.
 

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In patients presenting with inferior STEMI, RIGHT VENTRICULAR INFARCTION is suggested by the presence of:


  • ST elevation in V1 - the only standard ECG lead that looks directly at the right ventricle.
     
  • ST elevation in lead III > lead II  - because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle

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which artery is the culprit in inferior stemi?

Inferior STEMI can result from occlusion of all three coronary arteries:


~80% of inferior STEMIs are due to the dominant right coronary artery (RCA).

 




In18% →dominant left circumflex artery (LCx).

 






Rarely, type III/wraparound left anterior descending artery (LAD) → concomitant inferior and anterior ST elevation.
 

54

how to differentiate RCA from LCX occlusion in inferior stemi?


RCA covers the medial part of the inferior wall, including the inferior septum


  • The injury current is directed inferiorly and rightward → ST elevation in lead III > lead II

     








  • Presence of reciprocal ST depression in lead I

     










  • Signs of RV infarction: STE in V1 and V4R
     

 

 


LCx covers the lateral part of the inferior wall and the left posterobasal area.
 


  • The injury current is directed inferiorly and leftward → ST elevation in the lateral leads I and V5-6.

     



  • ST elevation in lead II = lead III

     





  • Absence of reciprocal ST depression in lead I

     







  • Signs of lateral infarction: ST elevation in I and aVL or V5-6
     

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sgarbossa criteria


With LBBB or ventricular paced rhythm, infarct diagnosis based on the ECG is difficult.

ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”), which can mask or mimic acute MI.
 

The three criteria used to diagnose MI with LBBB are:


  1. Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

     



  2. Concordant ST depression > 1 mm in V1-V3 (score 3)

     





  3. Excessively discordant ST elevation > 5 mm in leads with a negative QRS complex (score 2). 

 






 

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HOCM on ecg


  1. LV hypertrophy 

  2. .

    Asymmetrical septal hypertrophy produces deep, narrow (“dagger-like”) Q waves in the lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads. These may mimic prior myocardial infarction, although the Q-wave morphology is different: infarction Q waves are typically >40 ms duration while septal Q waves in HCM are <40 ms. 



  3. Lateral Q waves are more common than inferior Q waves in HCM.

     





  4. LV diastolic dysfunction may → compensatory LA hypertrophy,→ signs of LA enlargement (“P mitrale”) on the ECG.

     







  5. Association between HCM and WPW syndrome. A 









  6. AF and SVTs are common. Ventricular dysrhythmias (e.g. VT) also occur 

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PRWP caused by

- R wave height ≤ 3 mm in V3.

Causes:


  1. Prior anteroseptal MI

     



  2. Left ventricular hypertrophy 





  3. Inaccurate lead placement (e.g. transposition of V1 and V3)

     







  4. Dilatedcardiomyopathy

     









  5. WPW

     











  6. Dextrocardia

     













  7. Congenital heart disease 















  8. May be a normal variant
     

58

LV aneurysm presentation and ecg

 


  1. Persistent ST elevation following an acute MI.

     



  2. ST elevation seen > 2 weeks following an acute MI 





  3. Most commonly seen in the precordial leads.

     







  4. May exhibit concave or convex morphology.

     









  5. Usually associated with well-formed Q- or QS waves.

     











  6. T-waves have a relatively small amplitude compared to the QRS complex (unlike the hyperacute T-waves of STEMI)
     

59

Brugada ecg

It is due to a mutation in the cardiac sodium channel gene. This is often referred to as a sodium channelopathy. Over 60 different mutations have been described so far and at least 50% are spontaneous mutations, but familial clustering and autosomal dominant inheritance has been demonstrated. ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by multiple factors

Type 1 (Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) is the only ECG abnormality that is potentially diagnostic

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Pulomary embolism ecg


  1. Sinus tachycardia - the most common abnormality; seen in 44%

     



  2. Complete or incomplete RBBB - in 18%.

     





  3. RV strain pattern -  T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III, aVF). 
  4. RAD
  5. S1Q3T3

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CAUSES OF MOBITZ 2


  1. Anterior MI (due to septal infarction with necrosis of the bundle branches).

     



  2. I


    diopathic


    fibrosis of the conducting system (Lenegre’s or Lev’s disease).

     





  3. Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)

     







  4. Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).

     









  5. Autoimmune (SLE, systemic sclerosis).

     











  6. Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).

     













  7. Hyperkalaemia.

     















  8. Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.
     

62

DEXTROCARDIA ecg


  • RAD 



  • Positive QRS  (with upright P and T waves) in aVR 





  • Lead I: inversion of all complexes, aka ‘global negativity’ (inverted P wave, negative QRS, inverted T wave)

     







  • Absent R-wave progression in the chest leads (dominant S waves throughout)
     

63

TCA/Na+ channel blocker overdose ecg


  • Interventricular conduction delay – QRS > 100 ms in lead II

     



  • Right axis deviation of the terminal QRS:

    • Terminal R wave > 3 mm in aVR 



    • R/S ratio > 0.7 in aVR
       

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digoxin effect ecg


  1. Downsloping ST depression with a characteristic “sagging” appearance.

     



  2. Flattened, inverted, or biphasic T waves.

     





  3. S




    hortened QT interval.

     







  4. Mild PR interval prolongation of up to 240 ms (due to increased vagal tone) 









  5. Prominent U waves.

     











  6. Peaking of the terminal portion of the T waves.

     













  7. J point depression (usually in leads with tall R waves).
     

65

digoxin toxicity clinical

 


GIT: Nausea, vomiting, anorexia, diarrhoea

 




Visual: Blurred vision, yellow/green discolouration, haloes

 






CVS: Palpitations, syncope, dyspnoea

 








C













NS: Confusion, dizziness, delirium, fatigue
 

66

digoxin toxicity ecg

 

A multitude of dysrhythmias, due to ↑ automaticity (↑intracellular Ca) and ↓ AV conduction (↑ vagal effects at the AVN)

Clasically, a SVT (due to ↑ automaticity) with a slow ventricular response (due to ↓ AV conduction), e.g.  ’atrial tachycardia with block’.

Other arrhythmias associated with digoxin toxicity are:
Frequent PVCs (the most common abnormality), including ventricular bigeminy and trigeminy

Sinus bradycardia or slow AF

Any type of AV block (1st degree, 2nd degree & 3rd degree)

Regularised AF = AF with complete heart block and a junctional or ventricular escaperhythm

Ventricular tachycardia, including polymorphic and bidirectional VT


 

67