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History Of ECG : History Of ECG Animal Electricity Bancroft(1769) Electric current for Matteucci(1842) each heart beat(frog) Capillary electrometer G.Lippmann(1872) ( Nobel Prize) Recorded first human ECG A. Waller(1887) Naming of ECG as PQRST W.Einthoven(1895) String Galvanometer W.Einthoven(1901) Why do a 12 lead ECG? : Why do a 12 lead ECG? Monitor patients heart rate and rhythm Evaluate the effects of disease or injury on heart function Detect presence of ischaemia / damage Evaluate response to medications, e.g anti dysrhythmics Obtain baseline recordings before during and after surgical procedures Recording an ECG : Recording an ECG Explain procedure to patient, obtain consent and check for allergies Check cables are connected Ensure surface is clean and dry Ensure electrodes are in good contact with skin Enter patient data Wait until the tracing is free from artifact Request that patient lies still. Push button to start tracing Procedure (cont.) : Procedure (cont.) Before disconecting the leads ensure the recording is - Free from artifact Paper speed is 25mm/sec Normal standardisation of 1mv, 10mm Lead placement is correct ECG is labelled correctly Basic electrocardiography : Heart beat originates in the SA node Impulse spreads to all parts of the atria via internodal pathways ATRIAL contraction occurs Impulse reaches the AV node where it is delayed by 0.1second Impulse is conducted rapidly down the Bundle of His and Purkinje Fibres VENTRICULAR contraction occurs Basic electrocardiography The standard 12 Lead ECG : The standard 12 Lead ECG 6 Limb Leads 6 Chest Leads (Precordial leads) avR, avL, avF, I, II, III V1, V2, V3, V4, V5 and V6 Rhythm Strip Limb leads Chest Leads : Limb leads Chest Leads Limb leads I to III : Limb leads I to III First six leads of the 12-lead ECG come from four electrodes on the patient’s arms and legs called bipolar or standard leads Lead I : Lead I consists of positive electrode on the left arm looking toward the negative electrode on the right arm for electrical energy produces upward deflection of the QRS Lead II : Lead II consists of positive electrode on the left foot, negative electrode on the right arm shows most upright QRS complexes and most prominent P waves is favorite monitoring lead in many ICUs and telemetry units Lead III : Lead III consists of positive electrode on the left foot, negative electrode on the left arm produces upward QRS deflection Limb leads aVR to aVF : Limb leads aVR to aVF Next set of leads use single positive monitoring electrode called augmented or unipolar leads Lead aVR : Lead aVR consists of positive electrode on the right arm--only limb lead on the right side of the body is the only lead with downward deflected QRS (in normal ECG) Lead aVL : Lead aVL consists of positive electrode on the left arm, looks to the right and down produces the least upright QRS among the limb leads Lead aVF : Lead aVF consists of positive electrode on the left leg and looks straight up to the center of the chest has very upright QRS complexes with prominent P waves known as inferior lead (along with leads II and III) because all look upward Chest leads V1 to V6 : Chest leads V1 to V6 Chest (or precordial) leads: lie across anterior chest measure the mean vector in the horizontal plane Chest leads : Chest leads Lead V1 located at right sternal border, fourth intercostal space lies above right ventricle and septum Lead V2 located at the left side of sternum, fourth intercostal space Lead V3 located midway between leads V2 and V4 Chest leads : Chest leads Lead V4 located at the midclavicular line, fifth intercostal space Lead V5 located at the anterior axillary line, fifth intercostal space Lead V6 located at the midaxillary line, fifth intercostal space, above lateral wall of the left ventricle ECG Waveforms : ECG Waveforms Normal cardiac axis is downward and to the left ie the wave of depolarisation travels from the right atria towards the left ventricle when an electrical impulse travels towards a positive electrode, there will be a positive deflection on the ECG if the impulse travels away from the positive electrode, a negative deflection will be seen Slide 23: The P wave represents atrial depolarisation the PR interval is the time from onset of atrial activation to onset of ventricular activation The QRS complex represents ventricular depolarisation The S-T segment should be iso-electric, representing the ventricles before repolarisation The T-wave represents ventricular repolarisation The QT interval is the duration of ventricular activation and recovery. Waveform Description : Waveform Description P Wave atrial depolarization, from the SA node towards the AV node, and spreads from the right atrium to the left atrium. A P wave must be upright in leads II and aVF and inverted in lead aVR to designate a cardiac rhythm as Sinus Rhythm . P duration < 0.12 sec P amplitude < 2.5 mm Slide 25: P wave rate 60-100 pbm with <10% variation. Rate <60= sinus bradycardia Rate >100= sinus tachycardia Variation> 10%= sinus arrhythmia Slide 26: Abnormal P waves :- Right atrail hypertrophy left atrail hypertrophy Atrial premature beat hyperkalaemia Q Waves : Q Waves Non Pathological Q waves Q waves of less than 2mm are normal Pathological Q waves Q waves of more than 2mm indicate full thickness myocardial damage from an infarct Late sign of MI (evolved) Pathological Q waves : Pathological Q waves QRS Complex : QRS Complex corresponds to the depolarization of the ventricles. QRS duration < 0.10 sec QRS amplitude is quite variable from lead to lead and from person to person. Two determinates of QRS voltages are: Size of the ventricular chambers 2. Proximity of chest electrodes to ventricular chamber (the closer, the larger the voltage) QRS Complex : QRS Complex May be too broad ( more than 0.12 seconds) A delay in the depolarisation of the ventricles because the conduction pathway is abnormal A Left Bundle Branch Block can result from MI and may be a sign of an acute MI. Wide QRS (LBBB) : Wide QRS (LBBB) QRS Complex : QRS Complex May be too tall. This is caused by an increase in muscle mass in either ventricle. (Hypertrophy) ST Segment : ST Segment The ST segment represents period between ventricular depolarisation and repolarisation. The ventricles are unable to receive any further stimulation The ST segment normally lies on the isoelectric line. ST Segment Elevation : ST Segment Elevation The ST segment lies above the isoelectric line: Represents myocardial injury It is the hallmark of Myocardial Infarction The injured myocardium is slow to repolarise and remains more positively charged than the surrounding areas Other causes to be ruled out include pericarditis and ventricular aneurysm ST-Segment Elevation : ST-Segment Elevation Myocardial Infarction : Myocardial Infarction A medical emergency!!! ST segment curves upwards in the leads looking at the threatened myocardium. Presents within a few hours of the infarct. Reciprocal ST depression may be present Infarction : Infarction Infarction location - Anterior MI = Q in V1,V2,V3, or V4 - Lateral MI = Q in I and AVL - Inferior MI = Q in II, III, and AVF - Posterior MI = large R in V1, Q in V6 ST Segment Depression : ST Segment Depression Can be characterised as:- Downsloping Upsloping Horizontal Horizontal ST Segment Depression : Horizontal ST Segment Depression Myocardial Ischaemia: Stable angina - occurs on exertion, resolves with rest and/or GTN Unstable angina - can develop during rest. Non ST elevation MI - usually quite deep, can be associated with deep T wave inversion. Reciprocal horizontal depression can occur during AMI. Horizontal ST depression : Horizontal ST depression ST Segment Depression : ST Segment Depression Downsloping ST segment depression:- Can be caused by digoxin. Upward sloping ST segment depression:- Normal during exercise. T waves : T waves The T wave represents ventricular repolarisation Should be in the same direction as and smaller than the QRS complex Hyperacute T waves occur with S-T segment elevation in acute MI T wave inversion occurs during ischaemia and shortly after an MI T waves : T waves Other causes of T wave inversion include: Normal in some leads Cardiomyopathy Pericarditis Bundle Branch Block (BBB) Sub-arachnoid haemorrhage Peaked T waves indicate hyperkalaemia Hyperacute T waves : Hyperacute T waves Inferior T-wave inversion : Inferior T-wave inversion T wave inversion in an evolving MI : T wave inversion in an evolving MI How to read an ECG : How to read an ECG Standardisation Rate Rhythm Axis Chamber enlargement & hypertrophy Arrythmias & conduction delays Ischaemia / infarction The 12-Lead ECG Format : The 12-Lead ECG Format The computer diagnosis is not always accurate!!! The 12-lead ECG Format : The 12-lead ECG Format The computer IS very accurate at measuring intervals & durations Calculating Heart Rate : Calculating Heart Rate 1. Count the R waves registering within 6 seconds and multiply by 10. (quick yet inaccurate method) 2. Count the number of large squares between two R waves and divide by 300. (this loosed accuracy when used to calculate fast heart rates and can only be used with regular rhythms) 3. Count the number of small squares between two R waves and divide by 1500. (most accurate method but can only be used with normal rhythms.) What is the heart rate? : What is the heart rate? (300 / 6) = 50 bpm www.uptodate.com What is the heart rate? : What is the heart rate? (300 / ~ 4) = ~ 75 bpm www.uptodate.com What is the heart rate? : What is the heart rate? (300 / 1.5) = 200 bpm The Rule of 300 : The Rule of 300 It may be easiest to memorize the following table: 10 Second Rule : 10 Second Rule As most EKGs record 10 seconds of rhythm per page, one can simply count the number of beats present on the EKG and multiply by 6 to get the number of beats per 60 seconds. This method works well for irregular rhythms. What is the heart rate? : What is the heart rate? 33 x 6 = 198 bpm The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/ The QRS Axis : The QRS Axis The QRS axis represents the net overall direction of the heart’s electrical activity. Abnormalities of axis can hint at: Ventricular enlargement Conduction blocks (i.e. hemiblocks) The QRS Axis : The QRS Axis By near-consensus, the normal QRS axis is defined as ranging from -30° to +90°. -30° to -90° is referred to as a left axis deviation (LAD) +90° to +180° is referred to as a right axis deviation (RAD) Slide 61: causes of extreme right axis deviation. emphysema hyperkalaemia lead transposition artificial cardiac pacing ventricular tachycardia Slide 62: causes of right axis deviation normal finding in children and tall thin adults right ventricular hypertrophy chronic lung disease even without pulmonary hypertension anterolateral myocardial infarction left posterior hemiblock pulmonary embolus Wolff-Parkinson-White syndrome - left sided accessory pathway atrial septal defect ventricular septal defect Slide 63: causes of left axis deviation left anterior hemiblock Q waves of inferior myocardial infarction artificial cardiac pacing emphysema hyperkalaemia Wolff-Parkinson-White syndrome - right sided accessory pathway tricuspid atresia ostium primum ASD injection of contrast into left coronary artery Determining the Axis : Determining the Axis The Quadrant Approach The Equiphasic Approach Determining the Axis : Determining the Axis Predominantly Positive Predominantly Negative Equiphasic The Quadrant Approach : The Quadrant Approach 1. Examine the QRS complex in leads I and aVF to determine if they are predominantly positive or predominantly negative. The combination should place the axis into one of the 4 quadrants below. The Quadrant Approach : The Quadrant Approach 2. In the event that LAD is present, examine lead II to determine if this deviation is pathologic. If the QRS in II is predominantly positive, the LAD is non-pathologic (in other words, the axis is normal). If it is predominantly negative, it is pathologic. Quadrant Approach: Example 1 : Quadrant Approach: Example 1 Negative in I, positive in aVF RAD The Alan E. Lindsay ECG Learning Center http://medstat.med.utah.edu/kw/ecg/ Quadrant Approach: Example 2 : Quadrant Approach: Example 2 Positive in I, negative in aVF Predominantly positive in II Normal Axis (non-pathologic LAD) The Alan E. Lindsay ECG Learning Center http://medstat.med.utah.edu/kw/ecg/ The Equiphasic Approach : The Equiphasic Approach 1. Determine which lead contains the most equiphasic QRS complex. The fact that the QRS complex in this lead is equally positive and negative indicates that the net electrical vector (i.e. overall QRS axis) is perpendicular to the axis of this particular lead. 2. Examine the QRS complex in whichever lead lies 90° away from the lead identified in step 1. If the QRS complex in this second lead is predominantly positive, than the axis of this lead is approximately the same as the net QRS axis. If the QRS complex is predominantly negative, than the net QRS axis lies 180° from the axis of this lead. Equiphasic Approach: Example 1 : Equiphasic Approach: Example 1 Equiphasic in aVF Predominantly positive in I QRS axis ≈ 0° The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/ Equiphasic Approach: Example 2 : Equiphasic Approach: Example 2 Equiphasic in II Predominantly negative in aVL QRS axis ≈ +150° The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/ Rhythm: Regular / Irregular : Rhythm: Regular / Irregular Distance between the ‘R’ waves Normal Sinus Rhythm : Normal Sinus Rhythm Ventricular rate: 60-100; Regular rhythm Atrial: Same as ventricular P consistent shape – always positive P-R interval: 0.12-0.20 QRS complex: 0.04-0.10 1 P wave for every QRS Dysrhythmias : Dysrhythmias Disorders of electrical impulse: Formation Conduction Named by Site of origin of impulse Mechanism of formation or conduction involved Dysrhythmias : Dysrhythmias Site of origin SA node Bradycardia, Tachycardia Atrial tissue Flutter, fibrillation AV node Blocks Junctional Ventricular tissue Tachycardia, fibrillation Dysrhythmias : Dysrhythmias Mechanism of formation or conduction Normal Bradycardia Tachycardia Flutter Fibrillation Premature complexes Conduction blocks Sinus Tachycardia : Sinus Tachycardia Etiology ↑ CNS response: Anxiety; Pain; Fever; Anemia; Meds; Compensatory: hypovolemia Is client symptomatic? Interventions Identify cause, Select best Treatment Goal: ↓ HR to normal levels ASA, β-blockers, ACE Inhibitors Meds of concern Sinus Tachycardia : Sinus Tachycardia Ventricular rate: > 100 (up to180); Regular rhythm Atrial: Same as ventricular P consistent shape P-R interval: Normal P wave for every QRS QRS complex: Normal Slide 80: Paroxysmal Supraventricular Tachycardia (PSVT) Paroxysmal supraventricular tachycardia” is a term used to describe SVT that starts and ends suddenly Sinus Bradycardia : Sinus Bradycardia Ventricular rate:< 60; regular rhythm Atrial: same as ventricular P consistent shape P-R interval: Normal P wave for every QRS QRS complex: Normal Atrial Flutter : Atrial Flutter Ventricular rate: Variable, Regular rhythm Atrial: 250-300/minute, Regular rhythm P shape – “sawtooth” formation P-R interval: Absent No P wave QRS complex: Normal Atrial Fibrillation : Atrial Fibrillation Premature Ventricular Contractions : Premature Ventricular Contractions Interrupts basic rhythm Occurs early in the R-R cycle No P wave w/ PVC QRS wide and unusual PVC Ventricular Tachycardia (V Tach) : Ventricular Tachycardia (V Tach) Unable to determine rhythm Regular ventricular rate (100-250) No P waves present QRS complex > 0.10 sec Ventricular Fibrillation (V Fib) : Ventricular Fibrillation (V Fib) Coarse Fine Heart Block Overview : Heart Block Overview 1st degree – PR interval > 0.20 seconds All impulses reach the ventricles 2nd degree – (2 types) Mobitz I – each impulses takes longer to conduct until 1 is blocked and a QRS complex is dropped and a pause occurs; then cycle repeats Mobitz II – Impulses are blocked at a regular interval causing dropped QRS complexes 3rd degree – None of the atrial impulses reach the ventricles Activity of the atria and ventricles is ‘divorced’ Results in inadequate cardiac output Requires pacemaker Slide 88: 2nd degree Type 1 1st degree Slide 89: 3rd degree 2nd degree Type II Hypertrophy : Hypertrophy Is an increase in the thickness of the wall of a heart chamber Right atrial hypertrophy…. See diphasic P wave with tall initial component Left atrial hypertrophy…. See diphasic P wave with wide terminal component Hypertrophy : Hypertrophy Right ventricular hypertrophy - R wave greater than S wave in V1 - R wave gets progressively smaller from V1 to V6 - S wave persists in V5 and V6 - Wide QRS Hypertrophy : Hypertrophy Left Ventricular Hypertrophy - S wave in V1 + R wave in V5 add up to more than 35 mm - Left axis deviation - Wide QRS - T wave slants down slowly and returns up rapidly (inverted) Case scenario 1 : Case scenario 1 72 year old man Diabetic with urosepsis Emphysematous pyelonephritis-post nephrectomy Being ventilated in ICU On inotropic support-noradrenaline 5ug/min: BP- 110/60mm Hg Slide 94: On day 3, sudden hypotension Cold clammy extremities BP: 60 sys HR: 140/min CVP:25cms Chest: bilateral crackles CVS: muffled ECG : ECG Slide 96: Serial ECGs and Cardiac enzymes Thrombolysis/ UFheparin/ LMWH Differentials Slide 97: Trop I :12 Thrombolysis contraindicated Progressive hypotension on increasing inotropes Expired Take home message : Take home message Consider myocardial ischemia in every case of sudden hypotension Case scenario 2 : Case scenario 2 20 year old primigravida from Chittoor Fever, jaundice and altered sensorium for 5 days GCS: 12/15 Blood smear positive for plasmodium falciparum Parasitic index 10% Slide 100: Started on Quinine infusion On day 2, Sudden hypotension BP:80 sys HR: 200/min ECG : ECG Slide 103: DC cardioversion Causes Treatment – hemodynamically stable and unstable Monitor QT interval while on quinine! Slide 104: Quinine discontinued, changed to artemether QT interval normalised Delivered fresh stillborn Gradual recovery Take home message : Take home message Monitor QT interval while on quinine! Consider iatrogenic causes of arrythmias - drugs - inotropes - central lines Case scenario 3 : Case scenario 3 55yr old man Sudden onset progressive BOE for 2 days. Sudden worsening of breathlessness today No chest pain, fever, cough No DM, HTN, Smoke Examination : Examination Obese No pallor, edema BP: 110/70mmHg HR:110/min JVP: elevated 3cms Resp : clear CVS: S3, sharp S2 Abd: NAD Slide 108: Sudden hypoxia and hypotension BP: not recordable Slide 111: Admitted to MICU Thrombolysed with STK Improvement over 24 hours Case scenario-5 : Case scenario-5 25 year old man with a history of corrosive acid poisoning presented a day later with a history of chest pain and fever O/E: He was febrile BP100/60 PR 140/minute Case scenario-6 : Case scenario-6 60 year old man with CA stomach underwent a total gastrectomy. Three days later became breathless, was febrile and had multiple ventricular ectopics assosiated with hemodynamic instability. Subsequently he was intubated. Common causes ruled out .He was started on an amiodarone infusion and he settled 24 hours later Take home message : Take home message All anti arrythmics are proarrythmics too All patients on amiodarone infusion once stabilised slowly overlap with oral route & taper infusion Amiodarone half life -prolonged ECG changes in angina : ECG changes in angina Resting ECG typically shows ST segment depression and T wave flattening or inversion during an attacks. Exercise ECG testing is positive in about 75% of people with severe CAD; A normal test does not exclude the diagnosis. Acute anterior MI : Acute anterior MI ST elevation in the anterior leads V1-6,I and AVL Reciprocal ST depression in the inferior leads Acute inferior MI : Acute inferior MI ST elevation in the inferior leads II, III and aVF. Reciprocal ST depression in the anterior leads. Acute posterior MI : Acute posterior MI The mirror image of acute injery in leads V1-3 Tall R rave, tall upright Twave in leads V1-3. Usually associated with inferior and/or lateral wall MI. Old Inferior MI : Old Inferior MI A Q wave in lead III wider than 1mm . A Q wave in lead AVF wider than 0.5 mm A Q wave of any size in lead II. Anteroseptal MI : Anteroseptal MI The QS complexes, resolving ST segment elevation and T wave inversions in V1-2 are evidence for afully evolved anteroseptal MI. The inverted T waves in V3-5, I, aVL are also probably related to the MI. Extensive Anterior/Anterolateral MI : Extensive Anterior/Anterolateral MI Significant pathologic Q-waves (V2-6, I, aVL) plus marked ST segment elevation are evidence for this large anterior/anterolateral MI. The exact age of the infarction cannot be determined without clinical correlation and previous ECGs, but this is likely a recent MI. Postero-lateral MI : Postero-lateral MI The "true" posterior MI is recognized by pathologic R waves in leads V1-2. These are the posterior equivalent of pathologic Q waves (seen from the perspective of the anterior leads). Tall T waves in these same leads are the posterior equivalent of inverted T waves in this fully evolved MI. The loss of forces in V6, I, aVL suggest a lateral wall extension of this MI. Thanks for paying attention.I hope you have found this session useful. : Thanks for paying attention.I hope you have found this session useful. Slide 140: There are 4 steps to interpreting ECG: The first step is to evaluate the P wave. The P wave indicated whether the atrial rhythm is normal. Questions to ask yourself about P waves: Are all the P waves occurring at regular intervals? Do all the P waves have the same appearance on the ECG? Are the P waves visible at all? If any of these questions, you answered “no”; further investigation is needed. P waves occur at regular intervals during normal sinus rhythm. Slide 141: The second step is to determine whether the ventricles are activated from inside the ventricles; or from another location. This can be done by looking at the duration (time) of the QRS complex. A QRS complex of normal duration is 0.04-0.06 seconds. This indicates that waves are going along normal pathways (conduction tissues) A QRS complex longer than 0.6 seconds has left normal pathways and occurs within Ventricular Myocardium. When it takes longer this is called: Ventricular Complex; and causes the QRS complex to have a wide and bizarre appearance on the ECG Ventricular Myocardium: muscular structure of the ventricle. Slide 142: The third step is to determine the relationship between the P wave and the QRS complex. This determines whether the atria and ventricles are working in sync! You must determine whether the P wave is always, never or sometimes associated with the QRS complex. Does the P wave always come before the QRS complex? Where's the P wave? Slide 143: Finally, look for anything abnormal. Arrhythmias Escaped beats And anything else that doesn’t produce the classic PQRST complex. Arrhythmia BAD! Asystole! No heartbeat! Normal ECG waveform : Normal ECG waveform Limb Leads : Limb Leads 3 Unipolar leads avR - right arm (+) avL - left arm (+) avF - left foot (+) note that right foot is a ground lead Limb Leads : Limb Leads 3 Bipolar Leads form (Einthovens Triangle) Lead I - measures electrical potential between right arm (-) and left arm (+) Lead II - measures electrical potential between right arm (-) and left leg (+) Lead III - measures electrical potential between left arm (-) and left leg (+) Chest Leads : Chest Leads 6 Unipolar leads Also known as precordial leads V1, V2, V3, V4, V5 and V6 - all positive Slide 149: Causes of elevation of ST segment:- MI( anterior, inferior) LBBB Normal varients (athletic heart) Acute pericarditis. Causes of depression of ST segment: Myocardial ischaemia Digoxin effect. Ventricular hypertrophy Acute post. MI, pulmonary embolus LBBB Slide 150: Causes of tall T waves:- Hyperkalaemia. Hyperacute myocardial infarction. LBBB Causes of flattened or inverted T waves: Age, race. hyperventilation Anxiety LVH PE Pericarditis, electrolyte imbalance. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.