ECG Flashcards
List of Conduction Abnormalities
Left Bundle Branch Block (LBBB)Right Bundle Branch Block (RBBB)Left Anterior Fascicular BlockLeft Posterior Fascicular BlockBifascicular BlockTrifascicular BlockFirst Degree AV BlockSecond Degree AV Block Type I (Wenkebach)Second Degree AV Block Type II (Mobitz type II)2:1 AV BlockThird Degree AV Block
Left Bundle Branch Block
QRS > 120 msecAbsence of Q waves in leads I, V5, and V6Monomorphic R wave in I, V5, and V6ST and T wave displacement opposite major QRS deflection.
Simple LBBB diagnosis
QRS > 120 msec with a downward deflected QRS on V1.
Simple RBBB diagnosis
QRS >120 msec with an upward deflected QRS on V1
Incomplete LBBB
QRS between 100-199 msec with other positive LBBB criteria.
Rate dependent LBBB
Caused by myocardial ischemia or refractoriness of LBBB at faster heart rates. Difficult to distinguish from ventricular tachycardia, both have wide QRS complex.
Brugada Criteria
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Sgarbossa Criteria
Use to diagnose acute myocardial infarction with LBBB present. Need 3 points, criteria 3 is in debate so either 1 or 2 suffice to diagnose acute myocardial infarction with LBBB. 1) ST elevation > 1 mm and concordant with QRS complex. (5 points)2) ST depression > 1 mm in leads V1, V2, or V3. (3 points)3) ST elevation > 5 mm discordant with QRS. (2 points)
Right Bundle Branch Block
QRS > 120 msecrSR’ bunny ear pattern in anterior precordial leads (V1-V3)Slurred S waves in leads I, aVL, and frequently V5 and V6.
Additional ECG abnormalities often seen with RBBB
TWI and ST depressions in V1-V3. This makes is hard to see myocardial ischemia in anterior precordial leads, MI are easy to see unlike LBBB.
Ashman beat
A variation of RBBB, a premature atrial contraction or supraventricular beat that happens during right bundle refractory period.
Left Anterior Fascicular Block
Left axis deviation of at least -45 degrees.The presence of a qR complex in lead I and rS complex on lead III.Usually a rS complex in lead II and III (sometimes aVF as well).
Quick diagnosis of LAFB
Determine left axis deviation. Then look for upward QRS in lead I and downward in lead aVF and lead II. An rS complex in lead III.
Old inferior wall MI and LAFB
Old inferior MI can not be diagnosed in setting of LAFB due to the inferior Q waves present from the LAFB.
Left Posterior Fascicular Block
Right axis deviation of 90 to 180 degrees. The presence of a qR complex in lead III and rS complex in lead I.ABSENCE of right atrial enlargement and/or RVH.
Bifascicular Block
RBBB + LAFB/LPFB. Indicate significant conduction disease and are at higher risk of higher degree blocks. Usually leading to symptomatic bradycardia requiring pacemaker implantation.
Lev’s disease
Also known as Lenegre-Lev syndrome or senile degeneration of the conduction system. Presents as an acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. Most commonly seen in the elderly. Associated with Stokes-Adams attacks, involving temporary LOC 2/2 marked bradycardia.
Trifascicular Block
RBBB + LAFB/LPFB + First degree AV block. A trifascicular block is a precursor to complete heart block. Does not need immediate treatment, but up to 50% will progress and need permanent pacemaker.
First Degree AV Block
PR > 200. Due to slow conduction through AV node. Delaying the time it takes for SA node impulse to reach the ventricles, thus the increase in the PR interval. No treatment, but should avoid AV nodal blockers.
Second Degree AV Block Type I
Also called Wenckebach or Mobitz Type I AV block. Increasing delay in AV nodal conduction until failure of a P wave conduction through AV node.
Second Degree AV Block Type II
Also known as Mobitz Type II AV block. AV node becomes completely refractory to conduction on intermittent bases. Equal PR intervals with predictable drop in QRS in a 2:1 or 3:1 pattern. This indicates significant conduction disease of His-Purkinje system, it is irreversible. Due to increased risk of progression to complete third degree block, patients receive permanent pacemakers.
2:1 AV Block
A form of second degree AV nodal block with every other P wave conducting through AV node and reaching ventricles. Can be hard to determine if from second degree type I or II.
Ways to distinguish 2:1 AV nodal Block
Remember type I is a nodal issue, type II is infranodal, the problem is with His-Purkinje system. Carotid sinus massage or Adenosine (slow AV node conduction). Gives more time for AV node to recover and can unmask PR prolongations. Atropine, enhances AV nodal conduction and could eliminate second degree type I AV nodal block (this is the type due to AV nodal delay). Exercise would work via the same mechanism.
Third Degree AV Block
A complete heart block. No action potentials are conducting through AV node. Results in complete disassociation of P and QRS complexes, with atria and ventricle contracting at their intrinsic rhythms. P waves at a rate of 60-100 with QRS complexes at a rate of 30-40.
High Grade AV nodal Block
A type of 3rd degree heart block with occasional P wave conduction through AV node and generate an associated QRS.
Anterior Wall STEMI
Lack of blood supply to Anterior Wall, supplied by the left anterior descending artery (LAD). On ECG ST elevation at the J point in at least 2 contiguous lead of > 2 mm (0.2 mV) i men or 1.5 mm (0.15 mV) in women n V2-V3 and/or >1 mm in chest leads.
Extensive anterior MI
Site of lesion is proximal to LAD or in left main coronary artery. The MI will extend from the anterior wall to the septal and lateral regions.
ECG findings in old anterior wall MI
There is a lost of anterior forces. On ECG Q waves in leads V1 and V2 with poor R wave progression.
Poor R wave progression
Normally R:S ration increases with R wave predominance in the left side precordial leads (V4-V6).
Causes of poor R wave progression
1) Old anterior wall MI2) lead misplacement (frequently in obese women)3) LBBB or LAFB4) LVH5) Dextrocardia7) Tension pneumothorax with mediastinal shift8) Congenital Heart Disease
Persistent ST elevation in V1 and V2
Consider ventricular aneurysm, a known complication of myocardial infraction.
Inferior Wall STEMI
Due to infarction of tissue supplied by the right coronary artery (RCA). Can be associated with a posterior wall MI. ECG findings include ST segment elevation in the inferior leads (II, II, aVF) with reciprocal ST depressions in lateral or high lateral leads (I, aVL, V5, and V6).
Posterior Wall MI
Usually supplied by the posterior descending artery (a branch of the RCA in 80% of people). ECG findings include:1) ST depressions in septal and anterior precordial leads (V1-V4). These leads are seeing the MI backwards.2) Ratio R:S wave in V1 or V2 > 1.3) ST elevation in posterior leads of posterior ECG (V7-V9)4) ST elevations consistent with inferior wall MI.
Sinus Tachycardia
Indicated on ECG with normal upright P wave in leads II with NSR and atrial rate of 100 with ventricular rate of 100. A dissociation between the two rates indicates an AV dissociation.
Differential diagnosis for sinus tachycardia
1) Exercise2) Anemia3) Dehydration or shock4) Fevers/sepsis/infection5) Hypoxia6) Chronic pulmonary disease7) Hyperthyroidism8) Pheochromocytoma9) Medications/stimulants10) Decompensated congestive heart failure11) Pulmonary embolus
Sinus Bradycardia
Normal upright P wave in lead II, NSR, at a rate of less than 60 bpm.
Causes of sinus bradycardia
1) AV blockers 2) Heightened vagal tone (eg well trained athletes)3) Sick sinus syndrome4) Hypothyroidism5) Hypothermia6) OSA7) Hypoglycemia
Sinus Arrhythmia
Refers to changing sinus node rate with respiratory cycle. Common in young healthy individuals and has no clinical significance. The heart rate increases with inspiration, due to Bainbridge Reflex and decreases with expiration. On ECG a PP interval variation of at least 0.12 secs (120 msec).
Bainbridge Reflex
Heart rate increase in response to increased atrial pressure. A compensatory mechanism since increased right atrial pressures frequently result from elevated left heart pressures from decreased cardiac output. The Bainbridge reflex acts in opposition of the carotid reflex.
Carotid baroreceptor reflex
Increase in heart rate with decreased tension on baroreceptors in hypotension or hypovolemia.
Premature Atrial Contractions
Due to a focus in atrium generating an action potential before the next scheduled SA node action potential. PAC have four characteristics.1) Premature.2) Ectopic, thus P wave morphology will be different from normal.3) Narrow complex, PACs come from atrium and will travel through AV node leading to normal conduction and spread through ventricles. Note that PVC are wide complex. 4) Compensatory pause after PAC, the atrial action potential sends the SA node into a refractory period.
Atrial Fibrillation
Due rapid firing AP within the pulmonary veins or atrium in a chaotic manner. Results in a very fast atrial rate (400-600 bpm). On ECG, no P waves, instead coarse fibrillatory waves from the fast and low amplitude atrial AP firing. The irregular entry of atrial AP through AV node leads to the “irregularly irregular” pattern, with ventricular rate between 100-200.
Irregular irregular rhythms
1) Atrial fibrillation2) Atrial flutter with variable conduction3) Multifocal Atrial Tachycardia.
Atrial Flutter
Due to “reentrant circuit” causing a repeated loop of electrical activity depolarizing the atrium at a rate of about 250-350 bpm. Produces characteristic “sawtooth” pattern of P waves. Usually everyother P waves gets through producing a ventricular rate of about 150 bpm with regular RR intervals if there is no variable conduction. A narrow complex tachycardia at a ventricular rate of exactly 150 bpm is often atrial flutter.
Counterclockwise flutter
Negative flutter waves in II, III, aVF
Clockwise flutter
Positive flutter waves in II, III, aVF
Multifocal Atrial Tachycardia
A tachycardic version of a wandering atrial pacemaker, with atrial rate > 100 bpm. MAT is due to multiple ectopic areas within atrium generating consecutive action potentials. On ECG, at least 3 P wave morphologies with NSR with ventricular rate > 100 bpm. Usually occurs in setting of severe lung disease and with exacerbation of severe lung disease.
AV Nodal Re-entrant Tachycardia (AVNRT)
Most common form of paroxysmal supraventricular tachycardia in adults. AVNRT is due to re-entrant circuit in AV node itself. On ECG:1) Narrow complex tachycardia2) A P wave that occurs after the QRS complex (a short RP interval)3) This tachycardia will quickly terminate with AV blocking maneuvers (carotid massage or adenosine).
AV Re-entrant Tachycardia (AVRT)
Due to re-entrant circuit outside of AV node that connects atrium to ventricles. The pathway is called an “accessory pathway” or a “bypass tract.” A presence of a congenital abnormal accessory pathway is seen in WPW. On ECG1) A narrow complex tachycardia2) Variable findings depending on the direction of circuit and location of accessory conduction.
