ECG ABNORMALITIES

Anterior Wall MI
An anterior wall myocardial infarction (AWMI) occurs when anterior myocardial tissue usually supplied by the left anterior descending artery (LAD) dies 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 MI is termed an "extensive anterior". The ECG findings of an acute AWMI 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 MI. This ST elevation is concave downward and frequently overwhelms the T wave producing a "tombstoning" type appearance. 2) Reciprocal ST segment depression in the inferior leads (II, III and aVF). The ECG findings of an old AWMI includes: 1) Loss of anterior forces leaving Q waves in leads V1 and V2. This is sometimes termed "poor R wave progression" or PRWP. Note: To dinstinctly say that an old anterior wall MI is present on the ECG, there must be no identifiable R wave in lead V1 and usually V2 as well. If there is an R wave in V1or V2, the term PRWP can be used, but not an old anterior wall MI. 2) On rare occasions, persistant ST elevation may be seen in V1 and/or V2indicating a ventricular aneurysm (see the ventricular aneurysm section)

Inferior Myocardial Infarction

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

Posterior Myocardial Infarction

The ECG findings of a posterior wall MI are different than the typical ST elevation seen in other MIs. A posterior wall myocardial infarction occurs when posterior myocardial tissue, usually supplied by the posterior descending artery (a branch of the right coronary artery in 80% of people), dies due to thrombosus in that vessel. This frequently occurs along with an inferior wall

MI. The ECG findings of an acute posterior wall MI include: 1) ST segment depression (not elevation) in the septal and anterior precodial leads (V1 to V4). This occurs since these EKG leads will see the MI backwards (since the leads are placed anteriorly, but the MI is posterior). 2) The ratio of the R wave to the S wave in leads V1 or V2 is > 1. 3) ST elevation in the posterior leads of a posterior EKG (leads V7 to V9). Suspicion for a posterior MI must remain high, especially if inferior ST elevation is also present. 4) ST elevation in the inferior leads (II, III, and aVF) may be seen if an inferior MI is also present.

Myocardial Ischemia
Myocardial ischemia (not infarction) has two distinct ECG findings: 1) ST segment depression (not elevation) 2) Symmetric T wave inversions The lead in which these findings are seen will help to determine the area of myocardial ischemia.

First Degree AV Nodal Block

A first degree AV node block occurs when condcution 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. A first degree AV block is indicated on the EKG by a prolonged PR interval. Recall that the P wave indicates atrial depolarization (initiated by firing of the SA node). The atrial deplarization eventually spreads to the AV node where there is a slight delay before the electicle impulse is conducted to the ventricles. If the AV nodal conduction (dromotropy) is decreased, it will take longer for the impulse to reach the ventricles, so there will be a greater distance between the P wave and the QRS complex (remember the QRS complex indicates ventricular depolarization). Thus the PR interval will be prolonged. The PR interval is normally 0.12-0.20 seconds. A PR interval consistently longer than 0.20 seconds (greater than 5 small boxes) indicates a 1st degree AV block. Note: there is a 1:1 ratio between P waves and QRS complexes, unlike 2nd and 3rd degree AV nodal block. In general, a 1st degree AV block is a benign finding that does not require any treatment, however it may be an indicator of higher degree AV block in the future.

Second degree AV block type I

In 2nd degree AV nodal block (a.k.a. Wenkebach 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.

Specifically,. 2nd degree AV block type I is characterized by progressingly increasing delay of AV nodal conduction until a P wave fails to conduct through the AV node. Thus, the PR interval becomes progressively longer from beat-to-beat until a P wave is not conducted.

Second degree type II AV block

In 2nd degree AV nodal block Mobitz Type II, 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. The PR interval may be normal or prolonged, however it is constant in length, unlike in 2nd degree AV block Mobitz Type I (Wenkebach) in which the PR interval progressively lengthens until a P wave is not conducted.

Premature Atrial Contractions

A Premature Atrial Contraction (PAC) occurs when a focus in the atrium (not the SA node), generates an action potential before the next scheduled SA node action potential. There are four main characteristics of PACs: 1) They are premature. That is they occur earlier than you would expect if you were to measure the previous P to P intervals. 2) They are ectopic. Meaning originating outside of the SA node. Thus the P wave morphology would be different than the normal sinus P wave. 3) They are narrow complexes. Since they come from the atrium, they will eventually travel through the AV node and use the normal conduction system to spread to the ventricules. Unlike a premature ventricular contraction, which is wide-complexed since it does not use the normal ventricular conduction system. 4) There is a compensatory pause after the PAC. The extra atrial action potential causes the SA node to become refractory to generating its next scheduled beat. Thus it must "skip a beat" and it will resume exactly 2 P to P intervals after the last normal sinus beat. When every other QRS complex is a PAC, then the rhythm is referred to as "atrial bigeminy".

Atrial fibrillation
Atrial fibrillation occurs when many sites in the atria rapidly fire action potentials. The result is a VERY fast atrial rate (about 400-600 beats per minute). Since the atrial rate is so fast and the action potentials produced are of such low amplitude, P waves will NOT be seen on the ECG in patients with atrial fibrillation. The atrial action potentials all attempt to conduct through the AV node, however the AV node becomes intermittently refractory and will only allow a certain number of atrial action potentials to reach the ventricles. This is why the ventricular rate is NOT also 400-600, but rather around 100-200 beats per minute. Since the AV node is intermittently (and not regularly) refractory, the QRS complexes that are produced when an atrial action potential does reach the ventricles will occur in an irregular pattern.

Thus an ECG showing atrial fibrillation will have NO visible P waves and an irregularly irregular QRS complex. The ventricular rate is frequently fast unless the patient is on AV node blocking drugs (such as beta-blockers). When the ventricular rate is greater than 100 in the presence of atrial fibrillation, the person is said to have atrial fibrillation with a "rapid ventricular response" or "RVR". Atrial fibrillation is sometimes abbreviated as "Afib". Thus a "rapid afib" or atrial fibrillation with RVR is sometimes abbreviated as "afib with RVR".

Atrial Flutter
Atrial flutter occurs when a "reentrant circuit" is present causing a repeated loop of electical activity to depolarize the atrium at rate of about 300-400 (remember the atrial rate in atrial fibrillation is 400-600). This produces a characteristic "sawtooth" pattern of the P waves, unlike atrial fibrillation in which the atrial rate is so fast that the P waves are not identifiable. Just as in atrial fibrillation, not all of the P waves are able to conduct through the AV node. Thus the ventricular rate will not be as fast as the atrial rate. Typically, the atrial rate will be about 300 per minute and only every other atrial depolarization will be conducted through the AV node. In this situation, the ventricular (QRS) rate will be exactly 150 beats per minute. Clinical Pearl: A narrow comlpex tachycardia at a ventricular rate of exactly 150 beats per minute is very commonly atrial flutter. Atrial flutter with variable conduction of the P waves can also occur. In this situation there may be 3 P waves to 1 QRS complex, then a quick change to 2 P waves to 1 QRS complex etc. Any combination of P waves to QRS complexes can occur.

Premature Ventricular Contractions

A Premature Ventricular Contraction (PVC) occurs when a focus in the ventricle generates an action potential before the next scheduled SA nodal action potential. There are four main characteristics of PVCs: 1) They are premature. That is they occur earlier than you would expect if you were to measure the previous R to R intervals. 2) They are ectopic. Meaning originating outside of the SA node. Thus the QRS morphology would be different than the normal QRS morphology when the action potential travels through the normal conduction system.. 3) They are wide complexes. Since they come from the ventricles and do notuse the normal ventricular conduction system, the action potential needs to travel from myocyte to myocyte instead which is much slower, thus the QRS complex is wide. Unlike a premature atrial contraction, which is usually narrow-complexed since it uses the normal ventricular conduction system (unless a baseline right or left bundle branch block is present). 4) There is a compensatory pause after the PVC. The extra action potential causes the SA node to become refractory to generating its next scheduled beat. Thus it must "skip a beat" and it

will resume exactly 2 P to P intervals after the last normal sinus beat. Ventricular bigeminy occurs when every other beat is a PVC.

Ventricular Tachycardia
Ventricular tachycardia (VT) occurs when multiple ectopic ventricular beats occur in succession. If all of the QRS complexes appear the same or very similar, then it is termed monomorphic VT. If the QRS complexes appear different from beat-to-beat, then it is termed polymorphic. Another name for polymorphic VT is "Torsades de Pointes". VT can be hemodynamically unstable resulting in syncope and can degenerate into the universally fatal rhythm ventricular fibrillation. When describing ventricular tachycardia, the following should be mentioned: 1) Monomorphic versus polymorphic (Torsades) 2) Sustained versus non-sustained (sustained defined as > 30 seconds in duration or symptomatic) 3) The heart rate at which it is occurring (electrophysiologist use the "cycle length" or the number of milliseconds between the QRS complexes) The Brugada Criteria for determining if the rhythm is indeed VT is below, only 1 is required to establish a diagnosis of VT: 1) The absence of an R-S complex on ALL of the precordial leads (aka "concordance"). Meaning all of the QRS complexes are either all positive or all negative, no in betweens. 2) R-S interval > 100 ms in ANY precordial lead 3) The presence of atrioventricular dissociation (try to identify P waves amongst the QRS complexes going at a different rate, if present then you have AV dissociation and VT is the rhythm) 4) Specific morphology criteria for the QRS complexes

Ventricular Fibrillation
Ventricular fibrillation is often a fatal arrhythmia. It occurs when the ventricular rate exceeds 400. In this setting, virually no forward cardiac output occurs. Advanced Cardiac Life Support (ACLS) should be instituted immediately.

Asystole
Asystole occurs when no electical activity of the heart is seen. Obviously, this may be a fatal arrythmia. Emergent implementation of Advanced Cardiac Life Support (ACLS) is crucial.

Pericarditis

Pericarditis, or inflammation of the pericardium, has typical ECG findings. These findings occur in progressive stages, all of which are seen in about 50% of cases of pericarditis. 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 elecation 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 EKG is back to normal. Note: The EKG changes of pericarditis must be distinguished from those of early repolarization. The ST elevation seen in early replarization 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 repolatization 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 replarization, unlike pericarditis, is a benign ECG finding that should not be associated with any symptoms.