Ecg !
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Ecg ! Ecg ! Presentation Transcript

  • Ecg 1h/o: 60 years old man with 4 hours crushing chest pain
  • 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
  • Ecg 2 :H/o: A 56 years old man with chest pain and vomiting for 90minutes
  • 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
  • Ecg 3 :H/o: A 78 years old lady with chest pain and collapse, BP 60/40
  • 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
  • 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
  • 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
  • Ecg 4 :H/o: A 64 years old man with breathlessness and a raised JVP
  • 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.
  • 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
  • 60 year old male with chronic kidney disease onmantainance hemodialysis is brought to emergencywith breathlessness and volume overload
  •  Findings:-sinus rhythm-small or absent P wave-long PR interval-shortened ST segment-normal axis-broad QRS complexes-tall tented T waves
  • 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
  •  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
  • -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
  •  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
  •  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
  •  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
  • Case 3A 65 year old women with congestive cardiacfailure and on treatment come with the ECG.
  •  Findings:-Abnormal rhythm-inverted T wave-downward sloping ST segment- reversed tick sign-depressed ST – J point-shortened QT interval
  •  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
  •  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
  • -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
  • A 40 year old male, asymptomatic came withthe ECG
  •  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
  • 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
  • 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 .
  • • Rhythm : sinus rhythm• Axis : right axis deviation• P wave : P pulmonale ( >2.5mm in lead II)
  • 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
  • EBSTEIN’S ANOMALY-congenital conditionoften associated withWPW syndromeECG findings- ‘Himalayan’ P wave- prolong PR interval
  • 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
  • • Rhythm : irregularly irregular• Axis : right axis deviation• P wave : diminished MITRAL STENOSIS
  • LA enlargement???
  • 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
  • ECG #3
  • • Rhythm : sinus rhythm• Axis : left axis deviation• P wave : biphasic (2nd half of wave is –ve)• QRS complex : deep S wave, tall R wave
  • 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
  • ......• 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
  • ........• 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
  • ECG #4
  • 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.
  • Tor s a de s de Poi nt e s
  • 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
  • CASE 1A 23 years old male with h/o episodes of palpitation
  • 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
  •  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.
  • CASE 2A 50 years old male with h/o chest pain for 24 hours
  •  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
  • 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
  • CASE 3A 40 years old female, bedridden for 48 hours, comewith c/o breathlessness
  •  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
  • CASE 4A 60 years old male, recently diagnosed with myocardialinfarction
  •  Rate increased (>100/min) Sinus rhythm Independent P wave Broad QRS complexes (>0.16s) beat to beat variability of the QRS morphology VENTRICULAR TACHYCARDIA
  • 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
  • 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.
  •  Immediate cardioversion in synchronised mode IV Amiodarone : given as bolus followed by continuous infusion IV Lidocaine
  • 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)
  • • 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)
  • • 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)
  • CASE I• 70 year old male, complains of exercise intolerance
  • • RATE- normal• RHYTHM- regular( dual rhythm)• AXIS- normal• P WAVE• QRS COMPLEX• T WAVE• PR INTERVAL• QRS INTERVAL
  • CASE II• 90 year old male, presented with syncope
  • 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 :
  • CAUSES• acute myocardial infarction,• acute pulmonary embolism,• chronic cor pulmonale• Congenital heart disease(ASD, VSD, Ebstein’s anomaly)• Myocarditis• Cardiac contusion
  • CASE III• 90 year old male presented with sudden onset of chest pain and was diagnosed to have myocardial infarction
  • •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 :
  • CAUSES• Always pathological• acute myocardial infarction,• hypertensive heart disease• dilated cardiomyopathy• Aortic valve disease• Drugs (quinidine).
  • CASE IV• 90 year old male with a past history of MI, which was complicated by LBBB. He is currently asymptomatic
  • 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