week 7 combiIntroduction to ECGs (1)-mergeded.pdf

Introduction to ECGs: Electrodes & Leads Foundations of Critical Care 2024 D.Freer ECG coverage in this course This week (Week 6) Introduction to ECGs, Sinus & Atrial arrhythmias Week 7 (Online due to ANZAC day PH 25 April) Atrioventricular, junctional, and ventricular...

Introduction to ECGs: Electrodes & Leads Foundations of Critical Care 2024 D.Freer ECG coverage in this course This week (Week 6) Introduction to ECGs, Sinus & Atrial arrhythmias Week 7 (Online due to ANZAC day PH 25 April) Atrioventricular, junctional, and ventricular rhythm analysis Week 8 – May 2 12 lead ECG, Bundle branch & fascicular blocks Week 9 – May 9 Differentiation of broad complex tachycardias Heart failure & hypertrophy Week 10 – May 16 Acute Coronary Syndromes & ECG practice How many times have you revised ‘how to interpret an ECG?’ For me, it’s at least annually for the last 20 years, and still, I forget! - Amjid Rehman Learning Objectives - Review the anatomy & physiology of the cardiac conduction system - Understand ECG electrodes and leads - Review the physiology and normal appearance of the basic elements of an ECG - Develop a systematic approach to looking at an ECG Let’s begin Properties of Cardiac Cells Contractility: the ability of a cell to respond to a stimulus to shorten & contract Automaticity: the ability of a cell to spontaneously generate an electrical impulse Conductivity: the ability of cells to transmit an electrical impulse Excitability: the ability of a cell to respond to an electrical impulse Review Sinoatrial (SA) node Located in the upper right atrium Dominant pacemaker in the heart Depolarises between 60-100 times/min Intra-atrial tract known as Bachmann’s Bundle delivers impulses to the Left Atrium Blood supply – RCA 55% or Left Coronary Artery Atrioventricular Junction Only connection between the atria and ventricles…. Consists of: Atrioventricular (AV node) Bundle of His Receives its blood supply from the AV nodal artery Right Coronary Artery (RCA) 85% Left Circumflex (LCx) 15% Functions of the AV node Slows impulse conduction Synchrony. Allows atria to contract and empty contents into the ventricles Represented by PR interval on the ECG Backup pacemaker Depolarises at 40-60 times/min if SA node fails Junctional rhythm Physiological block Blocks impulses if the atrial rate > 200 bpm Protects the ventricles from rapid rates Bundle of His Located at the bottom of the AV node Lies in the upper part of the intraventricular septum Conduction velocity increases Divides in the left and right bundle branches Bundle Branches Rapidly conduct impulses to the ventricles Right bundle branch – right ventricle Left bundle branch – left ventricle Left anterior fascicle Left posterior fascicle Major blood supply – septal branches of the LAD The conduction pathway Depolarization Repolarization Atrial depolarization, initiated by the SA node, causes the P wave. Ventricular depolarization is complete. With atrial depolarization complete, the impulse is delayed at the AV node. Ventricular repolarization begins at apex, causing the T wave. Ventricular depolarization begins at apex, causing the Ventricular repolarization QRS complex. Atrial is complete. repolarization occurs. The ECG What is an electrocardiograph – ECG? What information does an ECG provide? What does it not provide? Why perform an ECG? Electrodes 10 electrodes Sense the heart’s electrical activity at the skin’s surface Usually described as being positive or negative Positive electrode – recording, active or exploring Negative electrode – determines the direction in which the positive electrode records Current moves from negative to positive Electrodes are connected to form leads Principles of wave deflection Principle 1: If an impulse travels towards a positive electrode it will produce a positive or upwards deflection Principle 2: If an impulse travels away from a positive electrode it will produce a negative or downward deflection Principle 3: If an impulse travels perpendicular (at right angles) to a positive electrode it will produce a biphasic deflection (half up, half down) ECG Leads Do NOT refer to the wires connected to the patient 12 leads on an ECG, 10 electrodes An ECG lead records the electrical activity between two electrodes as the current passes through the heart Bipolar – one positive electrode and one negative electrode. Which leads are these? I,II, & III Unipolar – one positive electrode and a reference point. Which leads are these? The other 9 - aVL, aVR, aVF, V1-V6 The 12-Lead ECG International standard 12 leads Gives 12 different “views” of the heart Consists of 6 limb leads that record in the frontal plane 3 standard limb leads (I, II & III) 3 augmented limb leads (aVR, aVL & aVF) 6 precordial leads that record in the horizontal plane Leads V1 – V6 Standard limb leads: I, II & III Are bipolar leads – the ECG designates one electrode positive and one electrode negative depending on the lead Einthoven’s triangle The three limb leads form an equilateral triangle called Einthoven’s triangle Heart centrally located within Important to place four limb electrodes equidistant from the heart! Augmented limb leads: aVL, aVR & aVF Are unipolar Have a single positive electrode – the recording electrode The reference point is the centre of the heart’s electrical field Formed by connecting the two limb electrodes that are not used as the recording electrode The vector recorded is extremely low and is augmented, hence the a Augmented limb leads ‘a’ for augmented ‘V’ for voltage ‘R’, ‘L’ & ‘F’ indicate placement of the recording electrode Right arm Left arm Foot (left) Precordial leads: V1-V6 Are unipolar The positive electrode is placed on the anterior chest wall The reference electrode lies in the centre of the heart’s electrical field Formed by combining the voltages of all three limb leads based on Einthoven’s triangle Frontal plane Horizontal plane The Hexaxial reference system Lead variation: Right sided leads Helps diagnose RV infarction Suspected if ST elevation in V1 ST depression in V2 (reciprocal) ST elevation in III>II Commonly occurs in inferior MI’s Place V1-6 in mirror image position on the R) side of the chest V4R is the most useful lead (ST elevation diagnostic accuracy of 83% of RV infarct) Lead variation: Posterior leads Helps diagnose posterior MI Suspect posterior if see following changes in V1-V3 Horizontal ST depression (reciprocal of ST elevation) Tall, broad R waves (reciprocal of q waves) Leads V7-V9 are placed on the posterior chest wall in the same horizontal plane as V6 V7 – Left posterior axillary line V8 – halfway between V7 and V9 V9 – Left spinal border Re-label these leads What if the patient has dextrocardia? Think about your leads every time you put the electrodes on Introduction to ECGs: Waveforms, Intervals & Segments Foundations of Critical Care D.Freer The backdrop: What is an ECG? It is literally a graph of the electrical activity in the heart X- axis is time measured in seconds Y- axis is voltage measured in millivolts (mV) This is represented on ECG paper: standard speed is 25mm/sec The backdrop Y-axis: Voltage Measured in millivolts (mV) 10mm = 1mV All monitors & ECG’s are ‘standardised’ or ‘calibrated’ so a 1mV signal produces a 10mm deflection. Normal Half Double Calibration spike is 10mV for 0.2 standardisation standardisation sec The backdrop X-axis: Time Measured on the horizontal axis Each small square in 1mm and represents 0.04 sec Each large square in 5mm and represents 0.20 sec Calibration spike is 10mV for 0.2 sec Normal Double speed (25mm/s) (50mm/s) Isoelectric line Horizontal baseline It is flat because no electrical activity is sensed Isoelectric line Basic system for rhythm analysis 1. Calibration, patient details, clinical story 2. Rhythm: regular or irregular 3. Rate: atrial & ventricular 4. P waves: morphology, association with QRS 5. PR interval: measure PR interval 6. QRS complex: measure QRS complex 7. ST segment: elevated or depressed 8. T-waves: upright, inverted, height 9. QT interval – measure it 2. Rhythm: regular or irregular? - Regular or irregular Overall look Measure R-R interval - Where did the action potential start – denotes the cardiac rhythm? 3. Calculating the rate Atrial, ventricular, both What method do you use? There are many ways…… We will go through 2 of them: Large square method – regular rhythms 10 second method – irregular rhythms Rate: Large square method 𝟑𝟎𝟎 Heart rate / min = 𝑹−𝑹 𝒊𝒏𝒕𝒆𝒓𝒗𝒂𝒍 (𝒍𝒂𝒓𝒈𝒆 𝒔𝒒𝒖𝒂𝒓𝒆𝒔) Distance Corresponding Between R Heart Rate waves (Large squares) 1 300 2 150 3 100 4 75 5 60 6 50 7 43 Rate: 10 second method Good for irregular rhythms Most ECG’s record for 10 seconds (4 x 2.5 seconds) Count the number of QRS complexes in the entire rhythm strip and multiply by 6 Heart rate = Number of QRS complexes x 6 Waves and intervals What do you need to systematically assess? P wave PR interval QRS complexes ST segment T waves QT interval P wave Physiology: represents atrial depolarisation In normal sinus rhythm: Polarity: Upright in lead II, inverted in aVR, biphasic in V1 Shape is small and rounded Precedes each QRS complex Consistent shape in the same lead Height 2mm deep (may be a normal variant in leads III and aVR) > 25% of the height of the following QRS Present in leads V1-V3 Essentially, Q waves are abnormal if they’re big Most commonly due to previous myocardial infarction Permanent so cannot tell the age of the infarction R wave Progression R wave is the first upward deflection after the P wave R-wave progression Ventricles depolarise down and toward the LEFT Right sided leads (V1) negative Left sided leads (V6) positive The ‘progression’ just means a smooth transition When R>S this is labelled the transition point Normal transition point is in V3-V4 Abnormal R wave progression in anterior MI Also in LVH, RVH, and other conditions ST Segment Physiology: no electrical activity – ventricles are depolarised Normally Isoelectric (flat) Measured from the end of the S wave (J point) to the beginning of the T wave J point defines where the QRS ends & ST segment begins Sometimes difficult to isulate ‘High take off’ = high J point ST Segment Look for: Elevation Depression Shape Concave up normal Concave down / horizontal abnormal, more indicative of ischemia / infarction Ischemia can cause ST elevation or depression Depression more commonly associated with ischemia Elevation more commonly associated with infarction (STEMI) Many other causes Pericarditis, LBBB, benign early repol, LVH, etc. T wave Physiology: Ventricular repolarisation Shape: rounded, slightly asymmetrical Polarity: normally the same polarity as the QRS Height: not normally > 5mm limb leads or 10mm chest leads Follows the QRS Anything that disrupts depolarisation usually affects repolarisation Abnormal T-waves: - Ischemia / infarction – localised to an area - Bundle Branch blocks, prolonged QRS, hypertrophy T waves Check: Orientation (upright or inverted) Usually inverted in children – adults V1 and aVR Occasionally inverted in V2 Height Peaked T-waves in hyperkaemia Hyperacute T waves an early sign of MI U wave Represents the final stages of ventricular repolarisation Follows the T wave Same polarity as the T wave Normally goes unnoticed because of its low voltage Best known for its presence in hypokalaemia Often seen in bradyarrhythmias QT interval Physiology: Ventricular depolarisation and repolarisation – entire action potential duration Varies with heart rate (decreases as HR increases) Start of the QRS complex until the end of the T wave QT Interval duration As a general rule, the QT should be half the RR interval The key reason for measuring the QT is to see if it is long QT prolongation predisposes to life threatening ventricular arrhythmias – especially torsades de pointes QT interval corrected for HR (QTc) More accurate 𝑄𝑇  𝑅𝑅 𝐼𝑛𝑡𝑒𝑟𝑣𝑎𝑙 Normal QTc should not exceed 0.44 sec for men Normal QTc should not exceed 0.46 sec for women QTc > 0.5 sec is associated with an increased risk of Torsades de Pointes VT Causes of prolonged QTc Class III antiarrhythmics Antipsychotics Low K+, Mg++, Ca++ Bradycardias MI Subarachnoid haemorrhage Congenital Hereditary Basic system for rhythm analysis 1. Calibration, patient details, clinical story 2. Rhythm: regular or irregular 3. Rate: atrial & ventricular 4. P waves: morphology, association with QRS 5. PR interval: measure PR interval 6. QRS complex: measure QRS complex 7. ST segment: elevated or depressed 8. T-waves: upright, inverted, height 9. QT interval – measure it Questions? Atrial Arrhythmias Part 3 Purity Ng’etich  OFFICIAL Objectives Identifying features of atrial arrhythmia's including: – Premature atrial contractions – Wandering atrial pacemaker – Atrial tachycardia – Multifocal Atrial tachycardia – Atrial flutter – Atrial fibrillation Outline their significance & treatment  OFFICIAL Premature atrial complex (PAC)  OFFICIAL Premature atrial complex (PAC) Causes: PAC’s are the result of increased automaticity of cells Increased catecholamine and sympathetic tone Infection Emotional stress Stimulants (Caffeine, Nicotine) Sympathomimetic drugs (Adrenaline, Ventolin) Hypoxia Digitalis toxicity CVD – ACS, Heart Failure Dilated or hypertrophied Atria  OFFICIAL Premature atrial complex (PAC) Rhythm: Irregular due the premature beat Rate: Depends on underlying rhythm P waves: Premature (may be hidden in the T wave) – Different shape to the sinus beat due to the different focus PR: Usually normal but may be prolonged or non- conducted PR QRS: Usually normal but may be aberrantly conducted or absent – Depend on the how premature the beat is Pause: Noncompensatory *  OFFICIAL Length of PR interval If AV node still refractory (absolute), impulses will be non-conducted If AV node has partially repolarised (relative refractory period) impulses will be conducted slowly prolonged PR OFFICIAL  OFFICIAL To determine the type of pause.. Mark off two PP or RR intervals preceding the ectopic beat Compare this to the pause across the ectopic beat OFFICIAL  OFFICIAL Full compensatory pause Sinus rhythm is uninterrupted Seen in PVC’s  OFFICIAL Atrial bigeminy  OFFICIAL Atrial trigeminy  OFFICIAL Non-conducted PAC  OFFICIAL Clinical Significance of PAC’s Isolated: Not really significant, may in fact happen in the healthy heart. Frequent PAC’s (may indicate enhanced automaticity of a cell) may precipitate/warn of other atrial Arrythmia’s Atrial Tachycardia Atrial Fibrillation/Flutter Paroxysmal SVT Consider PAC burden on the patient in regard to Cardiac Output?  OFFICIAL Wandering atrial pacemaker (WAP)  OFFICIAL Causes: May be a normal phenomenon May occur when respiration effects vagus nerve (much like sinus arrythmia) Digoxin Clinical Significance: Not usually clinically significant  OFFICIAL Atrial tachycardia  OFFICIAL Atrial tachycardia Rhythm: Atrial rhythm is regular* Rate: Atrial rate usually 150-250 bpm P waves: Differ in morphology to sinus P waves PR Interval: Usually normal Possibly difficult to measure (rate related) QRS: normal  OFFICIAL Paroxysmal atrial tachycardia  OFFICIAL Terminology PAT Paroxysmal atrial tachycardia (PAT) – Starts & stops abruptly Incessant atrial tachycardia – Less common & lasts for more than half a day – May result in dilated cardiomyopathy Mechanisms Enhanced automaticity Re-entry  OFFICIAL Causes Digoxin toxicity Coronary artery disease Mitral valve disease / rheumatic heart disease / cor pulmonale (Right Heart Failure) Electrolyte abnormalities Chronic lung disease Theophylline administration Stimulants alcohol, caffeine, tobacco Inferior MI with RV dysfunction  OFFICIAL Clinical significance Relatively uncommon Patients present with symptoms of palpitations May present because of haemodynamic compromise – Rapid rate decreases ventricular filling & CO Hypotensive Dizziness, light-headedness, confusion, syncope Dyspnoea & LVF – Rapid rate increases myocardial oxygen demand Chest pain  OFFICIAL Treatment Rate control - digoxin, β blockers, calcium channel blockers Digoxin toxicity - cease digoxin & correct hypokalemia Rhythm control - antiarrhythmic e.g. amiodarone & sotalol DC cardioversion if heamodynamically unstable Identify & treat the cause Vagal stimulation, CSM, Valsalva, adenosine Sedation, reducing anxiety may slow the rate Drug therapies often fail in patients with incessant AT – Radiofrequency ablation & insertion of a PPM  OFFICIAL Multifocal atrial tachycardia (MAT) Also known as chaotic atrial tachycardia Rapid firing of atrial foci from more than two locations Rate faster than 100 bpm Rare  OFFICIAL Causes Primarily seen in the elderly Commonly with acute cardiopulmonary illness or COPD Less commonly causes – Pulmonary infections or embolism, hypoxia – Hypokalemia, hypomagnesaemia – CCF, mitral stenosis – Diabetes is a common co morbidity  OFFICIAL Treatment Directed towards treating the cause – Correct hypoxia – Correct electrolyte abnormalities – Treatment of CCF Rate control - β blockers, verapamil Rhythm control - antiarrhythmics often ineffective Discontinue theophylline  OFFICIAL Atrial flutter http://lifeinthefastlane.com/ecg- library/atrial-flutter/  OFFICIAL Atrial flutter Rhythm: Atrial rhythm is usually regular* – Ventricular rhythm may be regular or irregular Rate: – Atrial rate varies between 250-450 bpm Usually 300 – Ventricular rate varies depending on block at the AV node Usually 150 due to 2:1 AV conduction  OFFICIAL Atrial flutter P waves: F (flutter) waves, regular, sawtooth pattern – One flutter wave usually hidden in the QRS – Best seen in the inferior leads II, III, aVF or V1 PR: May be fixed or variable depending on AV block QRS: Usually normal but aberration can occur  OFFICIAL Atrial flutter AV block – Normal physiological block – AV node usually conducts up to ~ 210 bpm F F F F Atrial flutter with 4:1 block  OFFICIAL Atrial flutter with variable block  OFFICIAL Atrial flutter 2:1 AV conduction Common With 2:1 conduction flutter waves may not be obvious Is this a T wave or a P wave?  OFFICIAL Mechanisms of atrial flutter Re-entry circuit in the RIGHT ATRIUM  OFFICIAL Common causes IHD Atrial dilation of any cause – Hypertensive heart diseases – Rheumatic heart disease – Valvular heart disease Cardiac surgery  OFFICIAL Other causes Cardiomyopathy Cor pulmonale (Right Heart Failure) CCF Pericarditis or myocarditis Thyrotoxicosis / alcoholism Hypoxia  OFFICIAL Clinical significance Potential for haemodynamic compromise Mural thrombi may form as there is no strong atrial contraction – risk similar to atrial fibrillation Persistent atrial flutter is uncommon Risk of persistent atrial flutter – Tachycardia dependant cardiomyopathy  OFFICIAL Treatment Rate control – digoxin, β blockers, calcium channel blockers Rhythm control – restoration of SR – Antiarrhythmic medications Class I flecainide, Class III sotalol & amiodarone – DC cardioversion – Overdrive atrial pacing Anticoagulation usually warranted Radiofrequency catheter ablation – Treatment of choice for recurrent atrial flutter  OFFICIAL Atrial fibrillation (AF) The most common arrhythmia Affects 2% of adult population Affects 5 % of people older than 65 years Affects 10 % of people older than 75 years Incidence higher in men Incidence appears to be increasing  OFFICIAL AF  OFFICIAL Atrial fibrillation Rhythm – Atrial rhythm: no discernible P waves – Ventricular rhythm is irregularly irregular Rate – Atrial rate normally 400-600 bpm – Ventricular rate usually 100-160 if untreated “rapid AF” – Ventricular rate usually 60-100 if treated “controlled AF”  OFFICIAL Atrial fibrillation P waves – no discernable P waves – Fibrillatory (f) waves PR interval: Not measurable QRS complex: Usually normal – Aberration is common with faster rates Conduction – Impulses are blocked at the AV junction & conducted randomly OFFICIAL  OFFICIAL Terminology associated with AF Controlled AF: 60-100 bpm Rapid AF: > 100 bpm Slow AF: < 60 bpm Paroxysmal AF: Duration usually less than 7 days, terminates spontaneously Persistent AF: Duration greater than 7 days, may last indefinitely if not treated. Permanent AF: Duration greater than 1 year, resistant to treatment.  OFFICIAL Atrial Flutter 3:1 AF uncontrolled University of Adelaide 43  OFFICIAL Atrial Flutter Variable block PAC University of Adelaide 44  OFFICIAL AF Controlled University of Adelaide 45 Questions? OFFICIAL  OFFICIAL Rhythm Interpretation Part 2 Purity Ng’etich  OFFICIAL Basic system for rhythm analysis 1. Calibration, patient details, clinical story 2. Rhythm: regular or irregular 3. Rate: atrial & ventricular 4. P waves: morphology, association with QRS 5. PR interval: measure PR interval 6. QRS complex: measure QRS complex 7. ST segment: elevated or depressed 8. T-waves: upright, inverted, height 9. QT interval – measure it  OFFICIAL Sinus Rhythm Rhythm: Regular Rate: 60-100 bpm P wave: Small, round, upright, precedes QRS P-R interval: 0.12-0.20 seconds QRS: