Ecg !

3,405 views

Published on

Ecg !

  1. 1. 20 IMPORTANT ECGs NOOR ATIKAH SAINI 080201033
  2. 2. Ecg 1h/o: 60 years old man with 4 hours crushing chest pain
  3. 3. This ECG shows :• Rate = 60/min• Rhythm = sinus rhythm• Axis = normal• P wave = normal• QRS complex = normal• T wave = normal• ST segment = elevated in the anterior leads V1-V6, I and aVL = reciprocal ST depression in the inferior leads ( leads II,III, aVF)• PR interval = normal• QT interval = normalDiagnosis = Acute Anterolateral Myocardial Infarction
  4. 4. Ecg 2 :H/o: A 56 years old man with chest pain and vomiting for 90minutes
  5. 5. This ECG shows :• Rate = 50/min• Rhythm = sinus• Axis = normal• P wave = normal• QRS complex = normal• T wave = normal• ST segment = elevated in the inferior leads II, III, aVF. reciprocal ST depression in the anterior leads ( V1-V4).• PR interval = normal• QT interval = normalDiagnosis = Acute Inferior Myocardial Infarction
  6. 6. Ecg 3 :H/o: A 78 years old lady with chest pain and collapse, BP 60/40
  7. 7. This ECG shows :• Rate = 50/min• Rhythm = sinus• Axis = normal• P wave = normal• QRS complex = tall R wave in leads V1-V3• T wave = tall upwright T wave in leads V1-V3• ST segment = depression in anterior leads V1- V3• PR interval = normal• QT interval = normalDiagnosis = Acute Posterior Myocardial Infarction
  8. 8. Summary : 1. Features of MI based on its site of infarction:Changes Anterolateral Inferior MI Posterior MIof ECG MIST •ST elevetion in •ST elevation ST elevationsegment leads V1-6, I in the leads in leads V1-3 and aVL II, III and aVF •With ST •With ST depression in depression in leads II,III,aVF leads V1-V4R wave - - Tall R wave in leads V1-V3T wave - - Tall T wave in leads V1-3
  9. 9. Progression of Ischaemia to Injury to InfarctionECG changes:• Ischaemia = only T wave abnormalities• Injury = T waves + ST segments abnormalities• Infarction = T waves + ST segments + QRS complexes abnormalities
  10. 10. Ecg 4 :H/o: A 64 years old man with breathlessness and a raised JVP
  11. 11. This ECG shows:• Rate = 120 beats/min• Rhythm = sinus• Axis = normal• P wave = normal• QRS complex = normal• T wave = small or inverted• ST segment = widespread• PR interval = normal• QT interval = normalOther features = alternating high and low voltages of all the ECG waveformsDiagnosis = Electrical alternans of pericardial effusionThe classic example is a pericardial effusion with the heart "swinging" in it and changing its location and proximity to the chest wall (where the electrodes are) from beat to beat.
  12. 12. electrical alternans/low voltage alternans:=>alternate-beat variation in the direction, amplitude, and duration of any component of the ECG waveform (ie, P, PR, QRS, R-R, ST, T, U).Causes :1. Physical : hypothermia2. Infections : myocarditis, pericardial TB3. Neoplasm : pericardial mesothelioma4. Metabolic disorders : obesity, heart amyloidosis,haemochromatosis cardiomyopathy5. Structural disorders : pericardial effusion, cardiac temponade, hydro/hemopericardium,pneumothorax6. Poisoning : chronic alchoholism
  13. 13. 60 year old male with chronic kidney disease onmantainance hemodialysis is brought to emergencywith breathlessness and volume overload
  14. 14.  Findings:-sinus rhythm-small or absent P wave-long PR interval-shortened ST segment-normal axis-broad QRS complexes-tall tented T waves
  15. 15. Hyperkalemia Definition:plasma potassium level of 5.5mM Changes in hyperkalemia:1.mild-prolongation of PR and QRS interval.2.moderate-loss of Pwave and progressive widening of QRS complex3.severe-sine wave sinoaventricular rhythm
  16. 16.  Management:-IV administration of glucose along with insulin to encourage shift of potasium from EC to IC compartment -50ml of 50% glucose plus 10 unit of soluble insulin as bolus -500ml 20% glucose plus 10 unit of soluble insulin as infusion over 6 – 12 hours
  17. 17. -10ml of 10% calcium gluconate IV slowly over 2- 5 min to stabilise myocardial cell-50 – 100ml of 8.4% sodium bicarbonate IV-nebulisation of beta agonist( salbutamol)-if these measure fail hemodialysis is indicated
  18. 18.  Findings:-sinus bradycardia-long PR interval-normal axis-small T wave-Presence of U wave (repolarization of papillary muscles or purkinje fibres)-ST segment deviation-prolonged QT interval
  19. 19.  ECG changes of hypokalemia-increased amplitude and width of Pwave-prolongation of PR interval-T wave flattening and inversion-ST depression-prominent U wave-apparent long QT interval due to fusion of T and U waves
  20. 20.  Hypokalemia-causes:1.Low PTH level:parathyroid agenesis, destruction, reduced function2.High PTH level:vit D deficiency, drugs, PTH resistance syndrome, acute pancreatitis-features1.Asymptomatic2.Paresthesia of fingers ,toes,circumoral regions3.severe:seizure, carpopedal spasm, bronchospasm, laryngospasm
  21. 21. Case 3A 65 year old women with congestive cardiacfailure and on treatment come with the ECG.
  22. 22.  Findings:-Abnormal rhythm-inverted T wave-downward sloping ST segment- reversed tick sign-depressed ST – J point-shortened QT interval
  23. 23.  Digitalis effects-digitalis is a drug used in CCF and to slow the ventricular rate in atrial tachyarrhythmias-digitalis effects is due to early recovery and repolarisation of myocardial cells. 1.coved ST segment depression 2.flattened T wave 3.decreased QT interval
  24. 24.  Digitalis toxicity-due to excessive amount of digitalis >2ng/ml-features: 1.general symptoms-weakness, anorexia, nausea, vomitting, visual effects and mental changes. 2.arrhythmias and conduction disturbance- ventricular arrhythmia,bidirectional ventricular tachycardia,AV junctional rhythm,sinus bradycardia
  25. 25. -treatment: 1.prevention-baseline ECG, serum electrolyte, BUN and creatinine. 2.definitive treatment depend on arrhythmia minor-discontinuation of digitalis and careful observation serious-suppression with IV drugs lidocaine -pacemaker in patient with complete heart block -digitalis binding antibody IV (digoxin immune Fab)-lethal dose
  26. 26. A 40 year old male, asymptomatic came withthe ECG
  27. 27.  Findings :-sinus rhythm-inverted P wave in lead I-increased PR interval-right axis deviation-QRS complexes get progressively smaller from V1 to V6 with small R wave
  28. 28. Dextrocardia It is the condition in which the cardiac apex is in the right side of the chest D/D-accidental reversal of the left and right arm electrodes-situs inversus : congenital condition in which major visceral organs are reversed from their normal position
  29. 29. CASE #1• A 27 year old female, Mrs. Terry, a known case of α₁- a nt i t r y ps i n de f i c i e nc y , c o mp l a i n e d o f f e v e r , i nc r e a s e d br e a t hl e s s ne s s a nd COPD wh e e z i n g s i n c e 3 da y s .
  30. 30. • Rhythm : sinus rhythm• Axis : right axis deviation• P wave : P pulmonale ( >2.5mm in lead II)
  31. 31. D/D for P pulmonale Valvular Pulmonary Congenital disease hypertension heart disease• Tricuspid • COPD • Ebstein’s stenosis • Pulmonary anomaly• Tricuspid embolism regurgitation • ILD • Sleep apnoea • LV systolic dysfunction
  32. 32. EBSTEIN’S ANOMALY-congenital conditionoften associated withWPW syndromeECG findings- ‘Himalayan’ P wave- prolong PR interval
  33. 33. ECG 240 y e a r o l d f e m a l e w i t h h i s t o r y o f c h r o n i c b r e a t h l e s s n e s s
  34. 34. • Rhythm : irregularly irregular• Axis : right axis deviation• P wave : diminished MITRAL STENOSIS
  35. 35. LA enlargement???
  36. 36. CASE #3• A n 83-y e a r -o l d m a n w h o i s a p p a r e n t l y a s y mp t o ma t i c c a me t o O P D .H e i s r e g u l a r l y s e e n b y y o u r c o l l e a g u e . S i n c e y o u r c o l l e a g u e i s o n l e a v e ,t h i s p a t i e n t a s k e d y o u r r e v i e w o n h i s c u r r e n t h e a r t
  37. 37. ECG #3
  38. 38. • Rhythm : sinus rhythm• Axis : left axis deviation• P wave : biphasic (2nd half of wave is –ve)• QRS complex : deep S wave, tall R wave
  39. 39. DIAGNOSING LVH ON ECG• Limb Leads (Low sensitivity, high specificity) – R wave lead I + S wave lead III > 25 mm – R wave aVL > 11mm – R wave aVF > 20mm – S wave in aVR > 14mm
  40. 40. ......• Precordial Leads (High sensitivity, low specificity) – R wave V5 or V6 > 26mm – R wave V5 or V6 + S wave in V1 > 35mm – Largest R wave + largest S wave in precordial leads > 45mm
  41. 41. ........• The Sokolow-Lyon criteriumR in V5 / V6 + S in V1 > 35mm• The Cornell criteriumR in aVL and S in V3 >28 mm in menR in aVL and S in V3 >20 mm in women
  42. 42. ECG #4
  43. 43. CASE #4• A 60-y e a r -o l d f e m a l e , k n o wn c a s e o f I HD, p r e s e n t e d wi t h pa l pi t a t i ons i n t he O P D . O n e x a mi n a t i o n , h e r me a s u r e d s y s t o l i c B P i s 80.
  44. 44. Tor s a de s de Poi nt e s
  45. 45. TORSADES DE POINTES (Polymorphic ventricular tachycardia)• Acute management • Long-term management1)Electrolyte 1)β-blockers2)Drugs 2)Left cardiac sympathetic3)Heart rate denervation4)MgSo₄ 3)Pacemaker5)IV isoprenaline
  46. 46. NUR SHUHAIZA BINTI SUPIAN 080201039
  47. 47. CASE 1A 23 years old male with h/o episodes of palpitation
  48. 48. ECG FINDINGS: Normal rate Sinus rhythm Normal axis Short PR interval Slurred upstroke of QRS complex, best seen in I, V4, V5 Widened QRS complex due to „delta‟ wave WPW SYNDROME
  49. 49.  one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. majority of individuals with WPW remain asymptomatic throughout their entire lives risk of sudden cardiac death associated with the syndrome. caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles Electrical signals travelling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supraventricular tachycardia referred to as an atrio- ventricular reciprocating tachycardia.
  50. 50. CASE 2A 50 years old male with h/o chest pain for 24 hours
  51. 51.  Sinus rhythm with ventricular bigeminy Normal rate and axis Bigeminy : every sinus beat is followed by a ventricular premature beat No preceding P wave The coupling interval is usually constant Usually followed by compensatory pause VENTRICULAR BIGEMINY
  52. 52. Compensatory pause:The R-R interval between the beats directlypreceding and following the VPB is exactlytwice that of regular R-R intervalCommon cause for ventricular bigeminy: May occur in normal individual Ischemic heart disease Digoxin toxicity Left ventricular dysfunction
  53. 53. CASE 3A 40 years old female, bedridden for 48 hours, comewith c/o breathlessness
  54. 54.  Sinus tachycardia Normal rate Normal axis Prominent S wave in Lead I Small Q wave, inverted T wave in Lead III S1 Q3 T3 PATTERN ACUTE PULMONARY EMBOLISM
  55. 55. CASE 4A 60 years old male, recently diagnosed with myocardialinfarction
  56. 56.  Rate increased (>100/min) Sinus rhythm Independent P wave Broad QRS complexes (>0.16s) beat to beat variability of the QRS morphology VENTRICULAR TACHYCARDIA
  57. 57. Fusion beat:When one impulse originating from ventricle and a secondsupraventricular impulse simultaneously activate the ventricularmyocardiumCapture beat:Normal conduction momentarily “captured” control ofventricular activation from VT focus
  58. 58. Brugada Criteria: Lack of an RS complex in the precordial leads Whether the longest interval in any precordial lead from the beginning of the R wave to the deepest part of the S wave when an RS complex is present is greater than 100 ms Whether atrioventricular dissociation is present Whether both leads V1 and V6 fulfilled classic criteria for ventricular tachycardia.
  59. 59.  Immediate cardioversion in synchronised mode IV Amiodarone : given as bolus followed by continuous infusion IV Lidocaine
  60. 60. AV BLOCKS• FIRST DEGREE-All impulses conducted, but delay present (prolonged PR interval)Incoronary artery disease,drug toxicity(digoxin, CCB’s, β blockers)electrolyte disturbances(hyperkalemia) acute rheumatic carditis, congenital heart diseases(ASD, Ebstein’s anomaly)
  61. 61. • SECOND DEGREE- Impulse completely fails to pass through the AV node Mobitz type ll Wenkebach phenomenon/Mobitz type l Causes-o Physiological- atheletes, vagotonic individualso Acute rheumatic carditiso MI (eg inf wall, right ventricular)o Acute diphtheric myocarditiso Drugs- digitaliso Idiopathic fibrosis of the conduction system (Lenegre’s disease)
  62. 62. • THIRD DEGREE- Atrial contraction is normal, but no beats are conducted to the ventricles Causes-o Drugs-o Acute MIo Acute rheumatic carditiso Congenital heart disease(ASD, VSD)
  63. 63. HOW TO DIAGNOSE• LOOK FOR-R-R INTERVALP WAVESP-R INTERVAL
  64. 64. R-R INTERVALREGULAR IRREGULARP-R INTERVAL 2ND DEGREESAME VARIABLE P-R INTERVAL1ST DEGREE 3RD DEGREE CHANGES FIXED MOBITZ TYPE I TYPE II
  65. 65. CASE I• 70 year old male, complains of exercise intolerance
  66. 66. • RATE- normal• RHYTHM- regular( dual rhythm)• AXIS- normal• P WAVE• QRS COMPLEX• T WAVE• PR INTERVAL• QRS INTERVAL
  67. 67. CASE II• 90 year old male, presented with syncope
  68. 68. Rhythm : sinus rhythmAxis : normalP wave :QRS complex : widersR’ pattern (M shaped) in V1, V2•T wave : inversion in V1, V2•wide, slurred S wave in L I and V5, V6ST segment : depression in V1, V2PR interval :QT interval :
  69. 69. CAUSES• acute myocardial infarction,• acute pulmonary embolism,• chronic cor pulmonale• Congenital heart disease(ASD, VSD, Ebstein’s anomaly)• Myocarditis• Cardiac contusion
  70. 70. CASE III• 90 year old male presented with sudden onset of chest pain and was diagnosed to have myocardial infarction
  71. 71. •Rhythm : sinus rhythm•Axis : normal•P wave :•QRS complex :widesmall r waves followed by deep, wide and slurred Swaves in V1, V3;•broad, notched or slurred (M shaped) R wave in L I,aVL, V5, V6;absence of q waves in L I, aVL, V5, V6;•T wave : inversion•ST segment :depression in L I, aVL, V5, V6•PR interval :•QT interval :
  72. 72. CAUSES• Always pathological• acute myocardial infarction,• hypertensive heart disease• dilated cardiomyopathy• Aortic valve disease• Drugs (quinidine).
  73. 73. CASE IV• 90 year old male with a past history of MI, which was complicated by LBBB. He is currently asymptomatic
  74. 74. WHERE IS THE PACEMAKER ?• Atrial pacing spikes- short vertical lines preceding the P waves and best seen in lead III• Ventricular pacing spikes- precede the QRS complex and best seen in lead V2 , V3, V4 & V5

×