Basics of ecg interpretation by dr sai

Editor's Notes

• #7: So the limb leads look at the heart along the chest wall and the chest leads look at the heart in cross section.
• #20: The PR interval is used to evaluate heart blocks, the QRS interval helps us ascertain which pacemker site ventricular depolarization occurs in, the ST segment is used to evaluate myocardial oxygen utilizaton and myocardial infarction.Remember ST depression= ischemia and elevation= MI
• #28: First we’ll look at sinus arrhythmias. Criteria of sinus arrhythmias are shown on the slide. We’ll look at tracings for normal sinus rhythm and variants.
• #29: First we’ll look at sinus arrhythmias. Criteria of sinus arrhythmias are shown on the slide. We’ll look at tracings for normal sinus rhythm and variants.
• #30: In normal sinus rhythm the rate 60 to 100.
• #31: Sinus bradycardia can be a normal variant especially in a young person with high vagal tone or in an athlete. It can also be result of medication that slows the heart rate down or severe hypoxia. There are many other causes. If the patient is symptomatic with decreased cardiac output, give atropine and pace as soon as possible. If the patient is stable, then look for an underlying cause.
• #32: Sinus tachycardia is caused by many things such as exercise, fever, or hyperthyroidism. If a patient is symptomatic and/or unstable with sinus tachycardia, look for the underlying cause and slow the rate. Remember that slowing the rate in a tachycardic patient with heart failure may decrease the cardiac output. Patients aren’t usually symptomatic until the rate is greater than 150 bpm. We do not cardiovert sinus tachycardia. It is already a sinus rhythm.
• #33: Sinus arrhythmia is commonly seen in young patients. It is secondary to breathing. Inspiration causes increased blood flow to the right side of the heart. The heart has to beat a little faster to get the blood out.
• #35: Now let’s look at atrial arrhythmias. Take a moment to read the criteria shown on the slide. Then we will look at each of the types also shown.
• #36: Now let’s look at atrial arrhythmias. Take a moment to read the criteria shown on the slide. Then we will look at each of the types also shown.
• #37: In the premature atrial contraction, the QRS complex is narrow, but the RR interval is shorter than the sinus QRS complexes. The P wave has a different morphology than the sinus P wave.
• #38: In ectopic atrial rhythm, notice a narrow QRS complex. The P wave is inverted.
• #39: With wandering atrial pacemaker, there are at least three different P wave morphologies with a ventricular rate less than 100 bpm.
• #40: In multifocal atrial tachydardia, there are three different P wave morphologies with ventricular rate greater than 100 bpm.
• #41: With atrial flutter, the regular ventricular rate is approximately 150. The ratio of F waves to QRS complexes can be 2:1, 3:1, 4:1, or 6:1. The most common ratio is 4:1. The above rhythm shows atrial flutter with 2:1 conduction.
• #42: This tracing shows atrial flutter with 6:1 conduction.
• #43: This tracing shows irregularly irregular rhythm with no P waves. Ventricular rate is usually greater than 100 bpm.
• #44: This tracing shows irregularly irregular rhythm with no P waves. The ventricular rate is 40. Atrial fibrillation with a slow ventricular rate usually means conduction sickness or Digoxin toxicity.
• #45: This tracing shows regular ventricular rate with P waves that are different from the sinus P waves. The ventricular rate is usually 150 to 250 bpm.
• #46: Now let’s look at junctional arrhythmias. Take a moment to read the criteria shown on the slide.
• #47: Now let’s look at junctional arrhythmias. Take a moment to read the criteria shown on the slide.
• #48: We’ll discuss each arrhythmia shown on the slide.
• #49: Sometimes a premature beat occurs earlier than the expected sinus beat. The R-R interval is shorter. A premature junctional beat is early, has a narrow QRS complex and has an inverted P wave. The P wave can also be buried in the QRS complex.
• #50: A junctional escape rhythm satisfies all the criteria of a junctional origin. The rate is 40 to 60.
• #51: Accelerated junctional tachycardia also satisfies the junctional criteria. The rate is 60 to 100.
• #52: Junctional tachycardia satisfies the junctional criteria and the rate is greater than 100 bpm.
• #53: AV nodal reentrant tachycardia (AVNRT) is secondary to a bypass tract within the AV node. A premature atrial contraction (PAC) depolarizes the normal pathway so that when the sinus beat arrives it must take the bypass tract. By the time the sinus beat reaches the bundle of His, the normal tract is repolarized so that the ventricle is depolarized normally and the atria are depolarized backward. The AV node is now able to self-propagate the rhythm until another PAC arrives to reset the AV node.
• #54: Let’s look at a rate summary for the four arrhythmias we’ve already studied.
• #64: The rhythm strip above is an example of a 1st degree AV block. The PR interval is constant and greater than 2 seconds and all impulses were conducted.
• #65: A 2nd degree Type 1 results when the AV node conducts each impulse slower and slower and finally doesn’t conduct the impulse. This results in a PR interval that gets longer and longer until a QRS complex is missing.
• #66: A 2nd degree AV Type 2 block has a constant PR interval, but the AV node just intermittently decides not to conduct an impulse.
• #67: In a 3rd degree AV block, the AV node doesn’t conduct any impulses. The atria and ventricles beat at their intrinsic rates, 80 and 40 respectively. There is no association between the P waves and the QRS complexes.
• #72: Wolf-Parkinsons-White (WPW) is also caused by a bypass tract. This tract runs from the atria to the ventricle totally bypassing the AV node. The AV node causes a delay to allow the atria to contract blood into the ventricle. This delay is seen on the EKG as the PR interval. In WPW, the PR interval is short, less than .11. When the bypass tract is depolarized, it stimulates the ventricles directly. The impulse is propagated in the ventricle from cell to cell through gap junctions until the bundle branch is reached. Once the bundle branch is depolarized, the depolarization of the ventricles occurs very quickly. That delay when depolarization is occurring from cell to cell causes an upsloping to the QRS complex called the delta wave.
• #73: WPW is recognized by a delta wave and a short PR interval.
• #74: Now let’s look at ventricular arrhythmias which are recognized by wide QRS complexes greater than .16 sec, regular rhythm, and no P waves. The rate varies and determines what the ventricular rhythm is called. We’ll look at the types shown on the right side of the screen.
• #75: A premature ventricular contraction (PVC) occurs earlier than the sinus beat, is wide, and has no P wave. PVCs can occur sporadically, every fourth beat, every third beat, every second beat---quadrimeny, trigeminy, bigeminy.
• #76: Idioventricular rhythms meet the criteria to be ventricular. This is an escape rhythm. Its rate is 20 40 bpm.
• #77: Accelerated Idioventricular Rhythm meets the criteria for a ventricular rhythm. Its rate is 40 to 100.
• #78: Ventricular tachycardia meets the criteria for a ventricular rhythm. Its rate is greater than 100.
• #79: Torsades de Pointes is a type of ventricular tachycardia that occurs secondary to a prolonged QT interval.
• #80: Ventricular fibrillation is an unorganized activity of the ventricle.
• #82: Ventricular fibrillation is unorganized activity of ventricle. Here is another tracing showing ventricular fibrillation.
• #84: Now let’s discuss heart chamber enlargements.
• #85: Right atrial enlargement is caused by anything that elevates pressure in the right ventricle, increases the volume in the right atrium, or obstructs atrial emptying. Note the causes shown on the slide.
• #86: Right atrial enlargement is diagnosed by looking at the height of the P wave in any lead. The best is lead II. Note the P wave criteria shown.
• #87: If the height of the P wave in lead II is greater than 2.5 mm, then right atrial enlargement is present.
• #88: Left atrial enlargement is caused by anything that elevates pressure in the left ventricle, increases the volume in the left atrium, or obstructs atrial emptying. Note the list shown on the slide.
• #89: Left atrial enlargement is diagnosed by looking at the duration of the P wave in any lead. The best is lead II. Diagnosis can also be made by looking at the terminal portion of the P wave in V1.
• #90: This is a cartoon of lead II. The P wave is made up of the almost simultaneous depolarization of the right atrium (RA) and left atrium (LA). As you can see, the RA depolarizes a little bit sooner. That is not a big concern unless the LA is large. The LA part of the P wave takes longer making the P wave wider.
• #91: This is an example of left atrial enlargement as shown by the P wave.
• #92: The P wave in V1 is also made of the simultaneous depolarization of the right and left atria. When the LA is enlarged, the end of the P wave widens. Because of the way V1 looks at the RA and LA, left atrial enlargement causes a downward deflection of the end of the P wave in V1.
• #93: The first chamber enlargement we’ll discuss is left ventricular hypertrophy (LVH) which is enlargement of the ventricular wall. The differential diagnosis shows hypertension (HTN), aortic stenosis (AS), aortic insufficiency (AI), hypertrophic cardiomyopathy (HCM), mitral regurgitation (MR), coarctation of the aorta (COA), and physiologic.
• #94: Some things can look like hypertrophy, but are not. False positives can result from thin chest wall, status post mastectomy, race, sex, age, left bundle branch block (LBBB), acute myocardial infarction (MI), left anterior fasicular block (LAFB), and incorrect standardization.
• #97: This cartoon is showing strain. Strain is a repolarization abnormality because the muscle is bigger. In strain, the ST segments and T waves are pushed away from the major deflection of the QRS complex. In RVH, V1 and V2 show strain. In LVH, V5 and V6 show strain.
• #98: Causes of right ventricular hypertrophy are listed on the slide. If the right ventricle (RV) has a difficult time emptying into the lungs due to pulmonary hypertension or pulmonary stenosis, the right ventricle enlarges.
• #100: If the volume to the RV is increased due to tricuspid regurgitation (TR), atrial septal defect (ASD), Tetralogy of Fallot (TOF), or ventricular septal defect (VSD), the RV hypertrophies.
• #101: Right ventricular hypertrophy causes a reversal of the precordial pattern. Usually V1 and V2 have a small R (septal/right ventricular depolarization) wave and deep S (left ventricular depolarization) wave. In right ventricular hypertrophy, the vector moving toward V1 and V2 is larger, creating a bigger R wave.
• #102: This slide depicts right ventricular hypertrophy. The QRS complex is upright in V1 and V2 suggesting increased depolarization from the right ventricle. The ST segment is pushed away from the major deflection of the QRS complex (strain).
• #104: Next we’ll discuss bundle branch blocks.
• #105: There are left and right bundle branch blocks. These blocks can be complete or incomplete.
• #106: Above are causes of a left bundle branch block.
• #107: Above are the criteria for a left bundle branch block (LBBB).
• #108: The cartoon shows the left bundle branch block.
• #110: Above are causes of a right bundle branch block.
• #111: Above are the criteria for a right bundle branch block (RBBB).
• #112: This is a cartoon of a right bundle branch block (RBBB). A complete right bundle branch block has QRS duration of .12 sec or greater and the QRS complex is up in V1. The RSR’ in V1 is the characteristic finding of RBBB.
• #113: Think of this as bunny ears. The first R is caused by septal depolarization. The S wave is left ventricular depolarization. R’ is right ventricular depolarization.
• #115: If the bunny has a septal MI, the first R is lost.
• #116: We’ll now discuss ST segment and T wave changes.
• #117: Now let’s discuss ischemia and infarction.
• #118: The graphic is a reminder about the normal complexes and segments. Remember for ischemia and infarction, we are interested in the ST segment, T wave and the presence of Q waves.
• #119: The J point is where the end of the QRS complex meets the ST segment. Sometimes the J point is sharp and well defined. Other times, it is diffuse.
• #120: We need to measure the elevation or depression of the ST segment. Remember to use the TP segment as the baseline.
• #122: Ischemia causes T wave inversion and ST segment depression. Acute injury is seen as ST segment elevation. Dead tissue is seen as a Q wave.
• #125: This shows the evolution of EKG changes from ischemia to acute injury to infarction.
• #143: One cause of ST segment changes of depression or elevation is strain. Strain is seen with hypertrophy. The ST segment is shifted away from the major deflection of the QRS complex.
• #144: This is an example of strain with left ventricle hypertrophy. Notice how the major deflection of the QRS complex is up and the ST segments are depressed or opposite of the QRS. Remember that strain is a late finding in hypertrophy and places the patient at a higher risk of lethal arrhythmias.
• #145: V1 and V2 are the best leads to look for right ventricular changes. In right ventricular hypertrophy (RVH), the QRS complex will be up. Remember in a normal EKG there is small deflection up, representing septal and right ventricular depolarization, followed by a deep S wave, representing left ventricular depolarization. As the right ventricle enlarges the R wave gets bigger because the right ventricle is bigger. Strain related to RVH is also seen best in V1 and V2 as an ST depression, away from the major deflection of the QRS complex.
• #146: This cartoon shows the difference between ST segment and T changes secondary to strain versus infarction. Notice that in strain the ST segment elevation or depression is not flat, but curved and the T wave is still asymmetric. Whereas in infarction the ST changes are flat and the T waves are symmetric.
• #147: EKG changes consistent with pericarditis are shown in the cartoon. They are diffuse ST segment elevation, PR segment depression and notching of the QRS complex.
• #148: Digoxin causes ST segment changes such as elevation and/or depression. The changes are said to look like a ladle as shown above.
• #149: Ventricular aneurysms are suspected when ST segment elevation remains after an MI is treated. Ventricular aneurysms most commonly occur in the anterior wall.
• #150: Many things can cause T wave changes. Ischemia can cause hyperacute T waves or inverted T waves. Hyperkalemia cause peaked T waves. In the setting of stroke, T waves can invert and/or become very broad.