ECG criteria Flashcards
LBBB criteria
The ECG criteria for a left bundle branch block (LBBB) include:
- QRS duration of > 120 milliseconds.
- Absence of Q wave in leads I, V5, and V6.
- Monomorphic R wave in I, V5, and V6.
- 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._
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.
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
RBBB criteria
The ECG criteria for a right bundle branch block include:
- QRS duration of > 120 ms
- rsR’ “bunny ear” pattern in precordial leads
- 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.
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:
- Left axis deviation of at least -45 degrees
- The presence of a qR complex in lead I and a rS complex in lead III.
- 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
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:
- Right axis deviation of 90 to 180 degrees
- The presence of a qR complex in lead III and a rS complex in lead I.
- Absence of right atrial enlargement and/or right ventricular hypertrophy
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
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
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.
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”.
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.
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)
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
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:
- 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.
- Reciprocal ST segment depression in the inferior leads (II, III and aVF).
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:
- ST segment elevation in the inferior leads (II, III, and aVF).
- 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.
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:
- 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.
- The ST elevation in early repolarization resolves when the person exercises.
- Early repolarization, unlike pericarditis, is a benign ECG finding that should not be associated with any symptoms.
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.
Old anterior STEMI
Loss of anterior forces:
Q waves present in V1&V2
no identifiable R waves in V1 &/ V2
Poor R wave progression
OLD Inferior STEMI
Q wave in III wider than 1 mm
Q wave in aVF wider than 0.5mm
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:
- Old anterior myocardial infarction
- Lead misplacement (frequently in obese women)
- Left bundle branch block or left anterior fascicular block
- Left ventricular hypertrophy
- WPW syndrome
- Dextrocardia
- Tension pneumothorax with mediastinal shift
- Congenital heart disease
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
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).
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.
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.
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).
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.
