ABC of clinical ECG Magnus Lauritzen Goal with this seminar • Learn a systematic approach for analysing ECGs:” 5+1” • Recognize and understand normal ECGs • Interpret abnormalitets in ryhtm, conduction or morphology Anatomy Physiology • The sinoatrial node (SA node) contains the fastest physiological pacemaker cells of the heart; therefore, they determine the heart ratedetermine the heart rate • SA-node initiates depolarization, first atria, than ventricles by help of specialized conduction system • Repolarization follows depolarization • Depolarization og myocardial cells causes pos. electrical charges which can be measured be electrodes • Electrical charges moving• Electrical charges moving towards an electrode causes positive deflection relative to the isoelectric line • Electrical charges moving away from an electrode causes negative deflection Electrical axis of heart• The electrical heart axis is an average of all depolarizations in the heart. • The depolarization wave begins in the right atrium and proceeds to the left and right ventricle. • Because the left ventricle wall is thicker than the right wall, the arrow indicating the direction of the depolarization wave is directed to the left. Placements of electrodes (leads) Limb leads (Vertical plane) • Info from limb electrodes are combined to produce six limb leads • Try to look at the leads as eyes ”looking” at the heart from different angles • Group the leads together into right, left and inferior- posterior Chest leads (horizontal plane) Normal ECG intervalls• The PQ interval starts at the beginning of the atrial contraction and ends at the beginning of the ventricular contraction (0,12 – 0,20 seconds) • The QRS duration indicates how fast the ventricles depolarize (normal < 0,10 seconds)seconds) • The normal QTc (corrected) interval indicates how fast the ventricles are repolarized, becoming ready for a new cycle. (below 0.45 seconds in men and below 0,46 in women) Normal ECG – ”Sinus ryhtm” • A P-wave (atrial contraction) precedes every QRS complex • The rhythm is regular, but varies slightly during respirations • The rate ranges between 60 and 100 beats per• The rate ranges between 60 and 100 beats per minute • The P waves maximum height at 2.5 mm in II and/or III • The P wave is positive in I and II, and biphasic in V1 Normal ECG Arrhytmias Classifications based on heart rate: 1. Tachycardia (HR > 100 bpm) 2. Bradycardia (HR < 60 bpm) Classification based on origin of impulse:Classification based on origin of impulse: 1. Supraventricular – ”Narrow QRS complex” (< 0.12 ms) 2. Ventricular - ”Wide QRS complex” (> 0.12 ms) Tachyarrhytmias An overview of pathological supraventricular arrhythmias and their origin Re-entry mechanism Sinustachycardia Atrial frequency 100 – 180 bpm Ventricular frequency 100 – 180 bpm Regularity Regular Origin Sinus node P-wave Positive in II, aVF Effect of Adenosine No (can lead to temporary AV block Sinustachycardia Causes: • Exercise, anxiety, alcohol, caffeine, drugs • Fever •• Hypoxia • Bleeding • Anemia • Hyperthyroidism • +++++ Atrial tachycardia Atrial frequency > 100 Ventricular frequency >100 Regularity Regular Origin Ectopic foci in atrium (re-entry) P-wave Negative in I, aVF (different morphology) Effect of Adenosine / Vagal stimulation Slow down rythm (AV-conduction) Atrial fibrillaton (AF) Atrial Fibrillation (AF) Atrial frequency 400-600 bpm Ventricular frequency 75-175 bpm Regularity Irregular Origin Atria (SVT) P-wave Absent Effect of Adenosine Reduces heart rate Atrial Fibrillation (AF) Atrial flutter Atrial flutter Atrial frequency 250-350 bpm Ventricular frequency 75-150 bpm (3:1 or 2:1 block) Regularity Regular Origin Atria (SVT) P-wave Negative sawtooth in lead II Effect of Adenosine Temporary reduced AV conduction Atrial flutter AV-nodal re-entry tachycardia (AVNRT) AVNRT Atrial frequency 180-250 bpm Ventricular frequency 180-250 bpm Regularity Regular Origin AV-node P-wave Inside or right after QRS-complex Effect of Adenosine Terminates arrhytmia AVNRT Atrioventricular Re-entrant Tachycardia (AVRT)• Also called ”Wolf-Parkinson-White-syndrome” (WPS) and is a part of ”Preexitation syndromes” • Caused by an abnormal accessory conduction pathway between atria and ventriclespathway between atria and ventricles • Ventricles might be stimulated prematurely, resulting in an atriventricular re-entry tachycardia • Can also cause diffuse ECG-changes resembling ischaemia Wolf-Parkinson-White- Syndrome Wolf-Parkinson-White syndrome Ventricular tachycardias Premature ventricular contractions (PVC) • Most common of ventriuclar arrhytmias Ventricular tachycardia (VT) • Regular, HR 110-250 Ventricular fibrillation (VF) • Irregular, HR 400-600 bpm Torsade de pointes • Regular, HR 150-300 Bradyarrhytmias • AV-block 1st degree • AV-block 2nd degree (Wenckebach and Mobitz type II) • AV-block 3rd degree (complete AV-block) • AV-blocks • Sick sinus syndrome AV-blocks • AV-block type 1 • AV-block type 2 – Mobitz I (Wencheback) • AV-block type 2 – Mobitz II • AV-block type III (complete block) • No relation between P-waves and QRS complexes • Atrial rythm 60-100 bpm (or AF)• Atrial rythm 60-100 bpm (or AF) • Ventricular ryhtm might be nodal, ventricular or absent Conduction system Left bundle branch block (LBBB) • Slowed conduction in left bundle, causing delayed depolarization of left ventricle • QRS > 0,12 sec • Deep S-waves in V1-V3 • Late R-waves in V5-V6 • ST-segment depression in lateral leads (I, aVL, V5-V6) • Always a pathological finding in patients! Right bundle branch block (RBBB) • Conduction in right bundle branch is slow, causing late depolarization of right ventricle • QRS > 0,12 sec• QRS > 0,12 sec • rSR (”rabbit ears”) in V1-V2 • Late deep S-waves in lateral leads (I, aVL, V5-V6) • Commonly a physiological finding in patients! Myocardial ischemia and infarction Evolution of ECG changes in Myocardial infarction Diagnosis of myocardial infarction• Elevated cardiac enzymes in blood (Troponin T, C and CKMB) AND on of the following: • Typical symptoms (chest• Typical symptoms (chest pain > 20 min) • ECG changes (ST elevation, ST depression or pathological Q-waves) ECG-changes ST-elevation (STEMI) • Men > 0.2 mV in V2-V3, and/or > 0.1 mV in other leads • Women > 0.1 mV in two or more leads ST-depression •• New horizontal or downsloping ST-depression > 0.05 mV in two contiguous leads T-wave inversion • > 0.1 mV in two contiguous leads Q-wave (old infarction, develops after hours/days) New LBBB!! Location of ECG-changes Location of ECG-changes Where is MI located? Where is MI located? PAUSE! How to read ECG ”5+1”: 1. Rhytm 2. Rate 3. Conduction (PQ, QRS, QT)3. Conduction (PQ, QRS, QT) 4. Heart axis 5. Morphology (P wave, QRS, ST-segment) 6. Compare current ECG with a previous one 1. Ryhtm • Is it sinus ryhtm? • Regular or irregular?• Regular or irregular? • Prolonged recording from one lead is used to provide a rhytm strip (usually lead II) 2. Heart rate • Determine the time between two QRS complexes (RR) • IF paper speed is 25 mm/second, count number of big squares and divide with 300 (only in regular ryhtm) • If paperspeed is 50 mm/second, divide with 600 (only in regular ryhtm) • ”ECG-rulers” 3. Conduction• The PQ interval starts at the beginning of the atrial contraction and ends at the beginning of the ventricular contraction (0,12 – 0,20 seconds) • The QRS duration indicates how fast the ventricles depolarize (normal < 0,10 seconds)seconds) • The normal QTc (corrected) interval indicates how fast the ventricles are repolarized, becoming ready for a new cycle. (below 0.45 seconds in men and below 0,46 in women) 4. Heart axis • Look at lead aVF and I, should normally be positive • Lead II is also postive,• Lead II is also postive, lead III can be pos. or neg. • In normal axis both has predominant positive deflections 5. Morphology • Normal p wave? • No pathological Q-waves? • Prolonged QRS?• Prolonged QRS? • Normal R-wave progression in V1-V6? • ST elevation or depression? • Abnormal T-wave? 6. Compare to old ECG • Are the presenting ECG-changes new? • Remember that new LBBB is treatet as STEMI.. For more ECG traces click: http://ecg.bidmc.harvard.edu/maven/maven main.asp