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ECG Notes
This document provides information about electrocardiogram (ECG) rhythms, intervals, abnormalities and their causes and treatments. It discusses normal sinus rhythm and various arrhythmias including sinus tachycardia, sinus bradycardia, supraventricular tachycardia, ventricular tachycardia, atrial fibrillation, atrial flutter, and heart block. It also covers abnormalities of the P-R interval, diseases of the atria and ventricles, bundle branch blocks, myocardial infarctions and localization based on ECG findings. Treatment options are provided depending on hemodynamic stability and the specific arrhythmia or condition.
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Overview of ECG parameters: Rhythm, Rate, and Axis with emphasis on normal ECG findings.
Insights into rhythm types, assessing regularity and methods to calculate heart rate from ECG.
Discusses abnormal rhythms such as sinus bradycardia and tachycardia, their causes, and treatments.
Characteristics of SVT including ECG features and common types like AVNRT.
Management protocols for SVT, focusing on patient stability and treatment options.
ECG characteristics of VT, differences between monomorphic and polymorphic VT.
Management of VT, highlighting the importance of stabilizing the patient and specific drug treatments.
Characteristics and causes of atrial fibrillation, focusing on ECG findings.
Approach to managing atrial fibrillation, stability assessment, and duration considerations.
ECG features of atrial flutter and treatment options based on hemodynamic stability.
Focus on P-R interval abnormalities like short and long intervals with examples and implications.
Details on different heart blocks (1st to 3rd degree), ECG characteristics, and treatment strategies.ECG features indicating atrial (P pulmonale, P mitrale) and ventricular hypertrophy.
Identifying right and left bundle branch block with ECG features and clinical importance.
ECG changes in acute coronary syndrome, differentiating STEMI and NSTEMI with localization.
Criteria for thrombolytic therapy in acute myocardial infarction and contraindications.
Other significant conditions affecting ECG like pericarditis, hyperkalemia, and PE.
Interactive case study assessments regarding ECG interpretations and management.
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ECG Notes
- 2. Content: RRA: RHYTHM , RATE ,AXIS NORMAL ECG RHYTHM ABNORMALITIES ABNORMALITIES OF P-R DISEASES OF ATRIA & VENTRICLE BUNDLE BRANCH BLOCK INFARCTIONS OTHER CASES QUIZZES
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- 5. Notes : Qwave is always negative with the exception of lead 3 and aVR . Abnormal (pathological) Q-wave is more than 0.04 second "one small box' in duration OR more than one third the height of the following R-wave.
- 6.
- 7. Rhythm Sinus ornot Regular or not
- 8. Rate regular 𝟑𝟎𝟎 number oflarge squares between R−R interval
- 9. Rate irregular 20 ×number of QRS complexes in 15 large squares
- 10. Axis We have manyways but the simplest one is: Look for lead 1 and lead 3 , if both QRS complexes are predominantly upward , this mean normal axis If QRS complexes in lead 1 is downward and in lead 2 and 3 are upward , this mean RAD IF QRS complexes in lead 1 is upward and in lead 2 and 3 are downward , this mean LAD
- 11. Normal Axis RAD LAD Lead 1 Lead2 Lead 3
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- 16. Some pathological causes: * MI * Hypothermia * Cholestatic jaundice * Hypothyroidism * Drugs , eg. B-blockers , digoxin , verapamil 1 Sinus bradycardia
- 17. Treatment : “ACLS” Isthe patient hemodynamically stable or not? YES Monitor & observe NO * Give ATROPINE 0.5 mg IV push to repeat every 3-5 minutes If it is ineffective , the next options will be : * DOPAMIN infusion 2-20 mcg /kg/ min EPINEPHRINE infusion 2-10 mcg/ * Transcutaneous pacing
- 18. *Anxiety *Fever *Anemia *Heartfailure *Thyrotoxicosis *Phaeochromocytoma *Drugs , eg, B-agonist Some pathological causes : 2 Sinus tachycardia
- 19.
- 20. 3 Sinus Arrhythmia Itis a normal phenomenon that occurs with changes in intrathoracic pressure .The heart rate increase with inspiration (R-R interval shorten) and decreases with expiration (R-R interval lengthen) , so the rhythm is irregular
- 21. Supraventricular Tachycardia (SVT ) ECGCharacteristics : * Absent P wave , they are often hidden in the QRS complex * Rhythm : regular * Rate : 150 – 250 * QRS complex : NARROW 4
- 22. The most commontype is atrioventricular nodal reentrent tachycardia 'AVNRT'
- 23. Another example ofSVT : Narrow complex tachycardia ~ 220 bpm. No visible P waves.
- 24. Another example ofSVT :
- 25. Treatment of SVT Isthe patient hemodynamically stable or not? NO Synch. DC YES Measures to ↑ vagal tone: A:press on eyeball B:carotid sinus massage C:Valsalva maneuver D:immersing the face in cold water NO EFFECT IV ADENOSIN NO EFFECT B BLOCKER CCB Digoxin NO EFFECT ALTERNATIVE CLASSES : CLASS 1 A CLASS 1 C CLASS 3
- 26. Ventricular Tachycardia (VT ) ECGCharacteristics : *P-wave : usually not seen *Rhythm :regular *Rate : 101 – 250 *QRS complex : WIDE 5
- 27. A ) MonomorphicVT The QRS complexes are of the same shape and amplitude Its like number 7 or 8 in Arabic
- 28. B ) PolymorphicVT The QRS complexes vary in shape
- 29. Treatment of VT Isthe patient hemodynamically stable or not? NO Synch. DC YES * AMIODARONE 300 mg IV over 10-20 min * IV LIDOCAINE Always treat : Hypokalemia Hypomagnesaemia Acidosis Hypoxemia
- 30. NOTES : For preventionof VT : give B blocker ( Amiodarone can be added if additional control is needed ) CLASS 1C anti arrhythmic drugs ( flecainide , propafenone ) should not be used for prevention of VT in patient with coronary artery disease or heart failure . In patients at high risk of arrhythmic death , the use of implantable cardiac defibrillator is recommended.
- 31. 6 Atrial fibrillation 'AF' ECGCharacteristics * P-wave : not seen Rhythm : usually* irregularly irregular
- 32. Some causes : *Coronary artery disease * Hypertension * Valvular heart disease * Hyperthyroidism * Cardiomyopathy * Alcohol
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- 35. Treatment of AF Fullhistory Examination 12 lead ECG Measure the vital signs Is the patient hemodynamically stable or not? NO Synch. DC YES B BLOCKER CCB DIGOXIN ADENOSIN AV node blocking agents : {1st choice in general →1st choice if there is heart failure Continue-
- 36. Then ask aboutthe duration of the symptoms : Less than 48 hrs. more than 48 hrs. We give a cardioverter drug , either CLASS 1C OR CLASS 3 The patient may have a thrombus , so we should exclude it by trans esophageal echo OR we put the patient on anticoagulation for 4 weeks THEN do cardioversion THEN we keep the patient on anticoagulation for at least 3 months following successful cardioversion.
- 37. 7 Atrial Flutter ECGCharacteristics : * P-wave : not identifiable , with saw toothed , flutter waves In : lead 2 , lead 3 , aVF & V1. * Rhythm : usually regular
- 38. NOTE : theatrial rate usually range from 220 – 430 bpm . the ventricular rate is half of the atrial rate.
- 39. Another example ofAtrial Flutter :
- 40. Treatment of AtrialFlutter Is the patient hemodynamically stable or not? NO Synch. DC YES AV node blocking agents : B BLOCKER CCB DIGOXIN ADENOSIN Alternative classes : CLASS 1C CLASS 3 We should give anticoagulation depend on CHADSVAS SCORE & like that of Af as we mentioned.
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- 43. ECG characteristics ofWPW : * Short P-R interval , less than 3 squares *Slurring of the QRS complexes , Called Delta wave * Sometimes wide QRS complexes
- 44. WPW may bedescribed as type A or B Type A Type A has a positive delta wave & there is prominent R in V1
- 45. Type B There isprominent R in V5 & V6 but the R is negative in V1
- 46. Notes : • UsuallyThe presentation of WPW is Either SVT or very rapid AF . ( if SVT the carotid sinus message or IV adenosine can terminate the tachycardia WHILE the very rapid AF may cause collapse , syncope and even sudden death so it should be treated as emergency usually with DC cardioversion). • Usually we can not diagnose WPW During the attack of SVT or AF unless we convert The tachyarrhythmia to sinus rhythm .
- 47. • The drugsthat contraindicated during the attack of tachyarrhythmia : 1) IV digoxin 2) iv Beta blocker 3) IV CCB • Prophylactic anti arrhythmic drugs such as Flecainide or Propafenone , can be used to slow conduction , and prolong the refractory period of the accessory pathway .
- 48.
- 49. 1st degree heartblock ECG characteristics : * Rate : usually within normal range , but depends on the underlying rhythm * PR interval : prolonged more than 0.20 sec ( more than 5 small squares) but constant.
- 50. Causes : 1 :drugs : eg, B Blockers , CCB , digoxin 2 : degenerative changes in AV node 3 : acute inferior MI RX : Usually it need no treatment
- 51. 2nd degree heartblock type 1 (Wenckebach , Mobitz type 1) There is a progressive increase in PR interval , until a P wave appears without a QRS complex , then the cycle is repeated.
- 52. RX : needno treatment
- 53. Another example ofWenckebach cycle : Note the difference in PR interval between the first and last QRS complex of each group.
- 54. Mobitz type 2 ECGcharacteristics : The PR interval of the conducted impulses remain constant but some P waves not followed by QRS complexes
- 55. RX : Thistype of block is more serious and is often progress to third degree heart block , so it should be treated with temporary pacemaker.
- 56. Another example ofMobitz type 2 :
- 57. 3rd degree heartblock ECG characteristics : *AV dissociation ( the atria and ventricles beat independently ) * The Rate is slow ( 25-50 /min ).
- 58. CAUSES: *A: Congenital *B: Acquired,like : *1:Idiopathic fibrosis *2:MI / Ischemia *3:Drugs (eg digoxin) *4 : Inflammation(eg,Chagas disease) Rx : pacemaker
- 59. 3rd degree heartblock.
- 60.
- 61. 1 P Pulmonale * Tall, peaked wave greater than 2.5 mm in height in leads 2,3,aVF an d large posterior initial Positive deflection of the p wave in V1. *It indicate RA hypertrophy due to any causes like tricuspid valve stenosis OR pulmonary hypertension
- 62. 2 P mitrale ＊Broad ,notched and greater than 0.11 sec in duration , best see in lead 2 & V1 * Indicate LA hypertrophy or enlargement ＊It called P mitrale because of the mitral valve disease (mitral stenosis , mitral regurgitation) that are associated with this condition , but it generally indicate LA hypertrophy.
- 64. ECG FEATURES : *Rightaxis deviation *Tall R in V1 , V2 (greater than 7 mm ) *Deep S wave in V6 3 Right Ventricular Hypertrophy
- 65.
- 66. ECG FEATURES : *leftaxis deviation *The sum of S wave in V1 & R wave in V5 or V6 is ˃ 35 mm (7 large squares) . OR R wave in aVL ˃ 11 mm 4 Left Ventricular Hypertrophy
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- 68.
- 69. Right BBB LeftBBB *Normal variant *Right ventricular hypertrophy *Congenital heart Disease (eg. ASD ) *Coronary artery disease *Coronary artery disease *Hypertension *Aortic valve disease *Cardiomyopathy causes
- 70. ECG features ofBBB: Both of them had wide QRS complex ≥ 3 small squares LBBB RBBB Look to the left leads ( lead1 , aVL , V5 & V6 ) , we will find wide & slurred R wave. While in the right leads (V1 &V2) , we will see normal R wave but there is wide & slurred S wave . Look to the right leads (V1 &V2) , we will find wide R with rSR pattern . While in the left leads ( lead1 , aVL ,V5 & V6 ) , we will see normal R wave but there is Deep S .
- 71. LBBB Dominant S wavein V1 with broad, notched (‘M’-shaped) R wave in V6
- 72.
- 73. RBBB Tall R’ wavein V1 (“M” pattern) with wide, slurred S wave in V6 (“W” pattern)
- 74.
- 75. 1 2 Non – ST– Elevation MI OR Unstable angina ST – Elevation MI ECG changes : ST depression and / or T wave inversion . We should differentiate between them by the cardiac enzymes. Acute coronary syndrome
- 76. ECG changes ofSTEMI according to the time of appearance: 1 : Tented T wave 2 : ST elevation (convex ) 3 : reduction of R wave 4 : pathological Q wave 5 : deep T wave inversion
- 77. LocalizationLeads Coronary artery V1 _V6 V1_V4 V4 _V6 V1_V6, lead1,aVL lead1,aVL,V5,V6 lead1 , aVL lead2,lead 3,avf ST depression & prominent R in V1 -V4 Anterior MI Anteroseptal MI Anterolateral MI Extensive anterior MI Lateral MI high lateral MI inferior MI posterior MI LAD LAD LMCA LCX RCA RCX Sites LAD LCX
- 78. What are Thereciprocal changes? Reciprocal ST-segment depression, also known as reciprocal change, is defined as ST - segment depression in leads separate and distinct from leads that reflect ST -segment elevation . Reciprocal change is seen in approximately 75% of patients with inferior wall MI and frequently in lateral STEMI. Reciprocal change is an important ECG concept to consider for two reasons. First, it identifies patients with a high-risk ACS presentation & Second , the presence of reciprocal change is strong confirmatory evidence that STEMI is present.
- 79. Examples on reciprocalchanges : Reciprocal changes (ST depression) Type of MI In lead 1 & aVLInferior MI Lateral MI In lead2,lead3 & aVF
- 80.
- 81. Another example on Anteriorwall MI
- 82. Anterior wall MI Thereare hyperacute T-waves in V2-6 (most marked in V2 and V3) with loss of R wave height.
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- 85.
- 86. Another example on Extensiveanterior MI
- 87. Lateral MI There isreciprocal ST depression in the inferior leads (III and aVF)
- 88.
- 89. Inferior MI There isST elevation in II, III and aVF with Reciprocal ST depression and T wave inversion in aVL
- 90. Important note : Upto 40% of patients with an inferior STEMI will have a concomitant right ventricular infarction. These patients may develop severe hypotension in response to nitrates and generally have a worse prognosis. If the ST elevation in lead III > II with reciprocal change present in lead I ± aVL , It may suggests an associated RV infarction. This patient should have right-sided leads to confirm this. After we did the right sided ECG , if the ST elevation is persist especially in V4 , the patient have right ventricular infarction .
- 91. Another example There isST elevation in II, III and aVF with Reciprocal ST depression. ST elevation in lead III > I
- 92. Posterior MI * Itusually occur in the context of an inferior or lateral infarction. *Isolated posterior MI is less common. *Explanation of the ECG changes in V1-4: The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted : ST elevation becomes ST depression Q waves become R waves Terminal T-wave inversion becomes an upright T wave
- 93. Isolated posterior MI STdepression in V2-4 Tall, broad R waves in V2-3
- 94. Inferolateral MI ,Posterior extension is suggested by: Horizontal ST depression in V1-3 Tall, broad R waves (> 30ms) in V2-3 Dominant R wave (R/S ratio > 1) in V2 Upright T waves in V2-3
- 95. ST depression (leadsI, II, V5-6) it could be Unstable angina or NSTEMI. We differentiate between them by the cardiac enzymes .
- 96. ABC Measurethe vital signs Put the patient on a monitor Give O2 if there is low oxygen saturation Aspirin 300 mg chewable Plavix 300 mg Nitroglycerin, unless hypotensive (sublingual 300 _ 500 mg) Heparin Morphine (2.5 _10mg) & give metoclopramide (10mg) Beta Blocker Then choose Either OR PCI Which is the best RX but it should be given within 2 hours Thrombolytic therapy According to the indication & the absence of C.I
- 97. Indication of thrombolytictherapy : 1 : ischemic chest pain ˂ 12 hour 2 : ECG changes : A : ST elevation ˃ 1 mm in 2 contagious limb lead B : ST elevation ˃ 2 mm in 2 contagious chest lead C : new or presumed new LBBB D : posterior MI
- 98. Some of thecontraindication of thrombolytic therapy : Absolute Relative Previous hemorrhagic stroke at any time Previous ischemic stroke within the past 1 year Suspected aortic dissection Known intracranial neoplasm Previous allergic reaction to fibrinolytic agent Uncontrolled hypertension Recent surgery (within 1 month) Pregnancy High probability of active peptic ulcer Previous subarachnoid or intracerebral hemorrhage
- 99.
- 100. Pericarditis ECG characteristics : *ST elevation with upward concavity * PR interval depression which is a more specific indicator Some refer to the concave upwards ST elevation as the "smily face" of pericarditis compared with the “sad face" of STEMI.
- 101. Widespread concave STelevation and PR depression is present throughout the precordial (V2-6) and limb leads (I, II, aVL, aVF).
- 102. Hyperkalemia The following ECGchanges listed sequentially as K level increase : • Tall , symmetrically peaked T wave • ST depression • P-R prolongation , widening and flattening of P wave • P wave disappearances • QRS widening and fusion with tall T wave • Ventricular tachycardia , ventricular flutter , ventricular fibrillation , ventricular standstill
- 103. Early ECG changes showingPeaked T waves
- 104. Prolonged PR interval Broad,bizarre QRS complexes Peaked T waves
- 105. Hypokalemia ECG characteristics : •Lowering and inversion of T wave • Prominent U wave • ST depression • Prominent P wave and prolongation of PR interval • Atrial & ventricular arrhythmias including ventricular tachycardia & ventricular fibrillation
- 106. ST depression. T waveinversion. Prominent U waves
- 107. Pulmonary Embolism The ECGmay offer some help when assessing patients who are suspected of having PE : • ECG may be normal • Sinus tachycardia , and other transient supraventricular arrhythmias such as atrial fibrillation , atrial flutter . • P Pulmonale • RBBB • ST depression & T wave inversion in the V1 & V2 • RAD • S1 Q3 T3 ( S wave in lead 1 , Q wave in lead 3 , inverted T wave in lead 3 )
- 108. RBBB RAD S1 Q3 T3 T-waveinversions in V1 V2
- 109.
- 110. Case 1 :35 year old patient admitted to ICU because of palpitation & SOB of 1 day duration , he had occasional such attacks since 1 year. He has no history of hypertension or DM. Physical examination revealed rapid heart rate , BP 125/85mmHg with mid diastolic murmur in mitral area. ECG showed the following changes :
- 111. Q1 : Whatare the ECG changes ? Q2 : What is the diagnosis ? Q3 : How you will manage this case ?
- 112. The answer isAtrial Fibrillation
- 113. Case 2 :57 year old patient presented with palpitation , SOB & dizziness . Physical examination revealed rapid heart rate , BP 130/70mmHg. ECG showed the following changes :
- 114. Q1 : Whatare the ECG changes ? Q2 : What is the diagnosis ? Q3 : How you will manage this case ?
- 115.
- 116. Case 3 :60 year old patient admitted to ICU because of severe retrosternal chest pain persisting more than 30 minutes with vomiting & profuse sweating. ECG showed the following changes :
- 117. Q1 : Whatare the ECG changes ? Q2 : What is the diagnosis ? Q3 : How you will manage this case ?
- 118. The answer is extensiveanterior MI
- 119. Case 4 :70 year old patient presented with fatigue , dizziness & impaired exercise tolerance . He is on digoxin treatment. ECG showed the following changes :
- 120. Q1 : Whatare the ECG changes ? Q2 : What is the diagnosis ? Q3 : How you will manage this case ? Q4 : mention 3 causes
- 121. The answer is thirddegree heart block
- 122. Case 5 :70 year old patient presented with retrosternal chest pain , then he developed hypotension , bradycardia & ↑ JVP , the chest was clear with no tachyarrhythmia . ECG showed the following changes :
- 123. Q1 : Whatare the ECG changes ? Q2 : What is the diagnosis ? Q3 : what is the complication in this case ? How to confirm it ? Q4 : How you will manage this case ?
- 124. The answers are: * Dx : Inferior MI * Complication : RV infarction & we confirm it by right sided ECG * Rx : the same RX of STEMI but without nitroglycerine
- 125. Case 6 :45 year old patient presented to the ED with retrosternal chest pain , radiating to lower jaw of 20 minutes duration. ECG showed the following changes :
- 126. Q1 : Whatare the ECG changes ? Q2 : Give 2 differential diagnosis ? Q3 : how to differentiate between them ? Q4 : How you will manage this case ?
- 127. The answer : TheECG shows ST depressions , so the diagnosis will be either NSTEMI or UNSTABLE ANGINA , the cardiac enzymes will differentiate between them .
- 128. References: 1: Davidson's principlesand practice of medicine, 22nd edition 2: The ECG made easy, seventh edition 3: ACLS guidelines 2015 4: ECG for medical students and general practitioners, 1st edition 5: Learn ECG in a day, 1st edition 6: ECG notes interpretation and management guide, 1st edition 7: www.medscape.com www.lifeinthefastlane.com www.ecgpedia.org