ECG Made Easy. 1. Evaluate ECG quality and calibration. ECG trace should be entirely within the paper (see example of unreadable trace below)

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1 ECG Made Easy Introduction ECG (EKG) is the recording of the electrical activity of the heart from electrodes placed on the surface of the body. It is commonly used in veterinary practice to: diagnose and monitor cardiac arrhythmias and conduction disturbances evaluate and monitor the effects of some cardioactive drugs monitor cardiac function before, during and after surgery assess the heart rate when the femoral pulse is not easily appreciable (i.e. hypotensive shock) or when counting the heart beats is made difficult by tachycardia or an abnormal rhythm Furthermore, some ECG variations may be suggestive of cardiac chamber enlargement, pericardial/pleural effusion, hypoxia, acid/base or electrolyte disturbances (especially those involving potassium abnormalities). ECG interpretation Follow the following 5 steps: 1. Evaluate ECG quality and calibration 2. Determine the heart rate 3. Evaluate P-QRS-T complex morphology 4. Determine the mean electrical axis (MEA) in the frontal plane 5. Identify disorders of cardiac rhythm 1. Evaluate ECG quality and calibration ECG trace should be entirely within the paper (see example of unreadable trace below) Avoid artifacts (purring, muscle tremors, respiratory movements, motion, electrical interference) muscle tremors and movements

2 Take note of paper speed and calibration (new machines do it automatically) Speed 1 small box = 1mm Sensitivity 1 small box = 1mm 25 mm/sec 40 ms (0.04 sec) 10mm/mV 0.1 mv 50 mm/sec 20 ms (0.02 sec) 5mm/mV 0.2 mv 10 mm/sec 100 ms (0.1 sec) 20mm/mV 0.05 mv 2. Determine the heart rate Average rate: if paper speed 25 mm/sec, 6 seconds cover 150mm (approximately the length of a biro pen). Count the number of complete ECG complexes in that length and multiply x10 if paper speed 50 mm/sec, 3 seconds cover 150mm (approximately the length of a biro pen). Count the number of complete ECG complexes in that length and multiply x20 Instantaneous rate: count the n. of small boxes (mm) between 2 R waves (R-R interval); divide 1500/number of small boxes (if 25 mm/sec) or 3000 number of small boxes (if 50 mm/sec) 3. Evaluate P-QRS-T complex morphology Determine duration/width of complexes in lead II. Count number of small boxes (mm) that make up the duration of the complexes (horizontal axis) multiply by 20 (if paper speed 50 mm/sec) multiply by 40 (if paper speed 25 mm/sec) Normal values for dogs and cats are reported in the appendix. Note: All the following traces are recorded at 25mm/sec and 1cm/mv (unless stated otherwise) P wave = atrial depolarisation; usually positive (upright). A. Prolonged (and often notched): may be suggestive of L-atrial enlargement ("P mitrale") B. Tall (voltage increased): may be suggestive of R-atrial enlargement ("P pulmonale"). A B P-Q Interval = the electrically silent (at the body surface) delay of conduction of the impulse through the A-V node and along the His-Purkinje system to the myocardial cells. Prolonged (=1st degree A-V block) by increased vagal tone (including digitalis glycosides), other drugs (ie. b-blockers) and myocardial disease. Shortened where congenital aberrant conduction pathways exist ("pre-excitation": rare).

3 QRS complex= ventricular depolarisation; shape varies depending on ECG lead in use. Prolonged and tall: suggests left ventricular enlargement (A) Deep Q and/or deep S waves suggests right ventricular enlargement (B) 0.5cm/mv Voltages decreased by pleural or pericardial fluid, obesity, hypothyroidism ST-T wave= ventricular repolarisation - very variable: T wave often negative in normal canine lead II, positive in cats. ST segment can be elevated or depressed (in relation to the baseline) in case of electrolyte imbalance, acid/base imbalance or hypoxia. T wave voltage may be increased by ventricular enlargement or hyperkalaemia 4. Determine the mean electrical axis (MEA) in the frontal plane This gives a very crude estimate of the average direction of orientation of the ventricular depolarisation wave fronts during the whole of the QRS interval. Its derivation is based on many assumptions (many of which are false!) but it is occasionally useful. The M.E.A. in the horizontal plane can usually be estimated simply by inspection in the following manner: Find the limb lead in which the QRS complex is isoelectric (i.e. Q/S and R waves of equal magnitude) The M.E.A. must lie perpendicular to this isoelectric lead axis, ie. if lead I is isoelectric the M.E.A. must lie along the avf lead axis (+90 ). See hexaxial lead system in the appendix. The M.E.A. may deviate outside the normal range due to marked ventricular hypertrophy (e.g. right ventricular hypertrophy gives a right axis deviation) and with anomalous conduction (e.g. right bundle branch block gives a right axis deviation). 5. Identify disorders of cardiac rhythm Answer the following questions a) Is there a P wave for every QRS complex? b) Is there a QRS complex for every P wave? c) Are the P-waves similar to each other? d) Are the QRS complexes similar to each other? e) Are the P waves associated with the QRS-complexes? f) Is the rhythm supraventricular or ventricular? g) Is there any pattern in the arrhythmia?

4 a. Is there a P wave for every QRS complex? NO: ventricles depolarise without atrial depolarisation (ectopy) define the origin of the ectopic QRS complex supraventricular QRS is normal ventricular QRS wide and bizarre define the timing of the ectopic QRS complex premature coming earlier than expected (R-R interval < R-R interval) escape coming later than expected (R-R interval > R-R interval) b. Is there a QRS complex for every P wave? NO: atria depolarised without conduction through the AV node (AV block) intermittent failure of conduction (2 nd degree). To be further classified in Type I or II no AV conduction (3 rd degree or complete) c. Are the P-waves similar to each other? NO: P waves originate from different sites negative in lead II (possible origin from atrial myocardium or AV-node) different morphology (wandering pacemaker; morphology depends on site of origin) hidden in QRS or after QRS complexes (retrograde activation of the atria) d. Are the QRS complexes similar to each other? NO: QRS complexes originate from different areas in the ventricles positive (possibly originating from the right ventricle) negative (possibly originating from the left ventricle) e. Are the P waves associated with the QRS-complexes? NO: Atrio-ventricular dissociation slow HR (3 rd degree AV block) fast HR (Ventricular Tachycardia, Non-paroxysmal Junctional Tachycardia) e. Is the rhythm supraventricular or ventricular? Supraventricular Question Ventricular Narrow Is the QRS complex narrow or wide? Wide Yes Does the premature complex look 90% No like a sinus beat? Yes Are P waves associated with the QRS? No No Are fusion beats present? Yes h) Is there any pattern in the arrhythmia? regularly irregular rhythm: sinus or respiratory arrhythmia (physiologic in dogs)

5 irregularly irregular: rule-out atrial fibrillation

6 Sinus tachycardia Premature Complexes and Tachycardias Supraventricular premature complexes (SVPCs) SVT (sudden onset) Sustained SVT

7 Atrial fibrillation (AF) Single VPCs (3 rd and 8 th complexes in the trace) Ventricular Couplets Ventricular Triplets

8 Ventricular bigeminy Ventricular trigeminy Accelerated idioventricular rhythm (Slow v-tac) at approximately 100 bpm Sustained fast ventricular tachycardia at approximately 400 bpm

9 Sinus arrhythmia Bradyarrhytmias Wandering pacemaker Sinus bradycardia (the P wave, although very small, is always present) Sinoatrial block/ arrest/ sinus pause First degree A-V block

10 Second degree AV block Type 1 (progressive prolongation of the PQ interval) PQ PQ Second degree AV block Type 2 (non-conducted P waves; PQ interval unchanged) P P Third degree (complete) AV block with jucnctional escape beats Atrial standstill

11 APPENDIX Normal ECG values for dogs and cats (*) Parameter Unit DOG CAT Heart rate bpm (puppies <220) Sinus rhythm Yes/No - - P wave duration sec P wave amplitude mv P-Q interval sec QRS duration sec R wave amplitude mv < <0.9 S-T segment depression mv <0.2 0 S-T segment elevation mv < Q-T interval sec Mean electrical axis (MEA) º *Reference ranges from Tilley (1992) Hexaxial lead system P-QRS-T complex morphology Clinical significance of the most common morphological abnormalities (*) Abnormality Possible (*) significance Prolonged P waves left atrial enlargement Tall P waves right atrial enlargement Prolonged PQ interval 1 st degree AV block Short PQ interval pre-excitation (accessory conduction pathways) Prolonged QRS left ventricular enlargement Deep S waves right ventricular enlargement Short (low voltage) QRS obesity, hypothyroidism, pericardial or pleural effusion Short QT interval hypercalcaemia or hyperkalaemia Prolonged QT interval hypocalcaemia or hypokalaemia Tall and spiked T waves hyperkalaemia Right-axis deviation R-side enlargement; RBBB Right-axis deviation L-side enlargement; LBBB (*) sensitivity approximately 50%, specificity approximately 80%

12 Terminology Arrhythmia or Dysrhythmia: any abnormality of the cardiac rhythm Bradycardia: cardiac rhythm characterised by SLOW heart rate Tachycardia: cardiac rhythm characterised by FAST heart rate Paroxysmal tachycardia: episodic tachycardia characterised by an abrupt onset and termination Sustained tachycardia: tachycardia that lasts for 15 seconds (or more) Tachycardiomyopathy: myocardial damage caused by a sustained tachycardia (heart rate > bpm) lasting for 2-3 weeks Vagal manoeuvre: diagnostic test sometimes useful for differentiating supraventricular from ventricular tachycardias. It consists in a carotid sinus massage or ocular pressure to increase the vagal tone of the patient. Should be performed while recording an ECG. Ventricular tachycardias usually do not respond to vagal manoeuvre. Atrial tachycardias may gradually and progressively terminate Supraventricular tachycardia may terminate abruptly General Guideline Supraventricular arrhythmias can be secondary to: atrial dilation atrial masses (i.e. haemangiosarcoma) systemic illness (i.e. hyperthyroidism, digitalis toxicity) Ventricular arrhythmias can be secondary to: primary cardiac disease (cardiomyopathy, myocarditis, endocarditis) systemic disorders (GDV, pancreatitis, splenic masses, electrolyte imbalance, uraemia, hypoxia, pyometra) drug toxicity (digitalis, atropine, anaesthetics)