Michele Ritter, M.D. Argy Resident – Feb. 2007 EKG Extravaganza! Michele Ritter, M.D. Argy Resident – Feb. 2007

Normal Conduction of the Heart SA node Left/Right atrium Atrial Contraction AV node Bundle of His Purkinjie fibers Endocardium Epicardium Ventricular contraction

Generation of EKG

Generation of EKG P wave: QRS complex: T wave ST segment QT interval = depolarization/contraction of both atria QRS complex: = depolarization/contraction of ventricles T wave = rapid phase of ventricular repolarization ST segment = plateau phase of ventricular repolarization QT interval = ventricular systole

ECG Leads Limb Leads Bipolar Unipolar Precordial Leads V1 V2 V3 V4 V5 Lead I – left arm (+) and right arm (-) Lead II – left leg (+) and right arm (-) Lead III – left leg (+) and right leg (-) Unipolar aVR - right arm potentials aVL – left arm potentials aVF – left leg potentials Precordial Leads V1 V2 V3 V4 V5 V6

Precordial Leads

Reading EKGs Rate Rhythm Axis Hypertrophy Infarction

Rate Large Box = 0.2 seconds Small Box = 0.04 seconds

Rate 300-150-100-75-60-50 Rule Rate = 1500/(mm between R waves) If one box between R-waves, then rate is 300; If two boxes between, then rate 150, etc. Rate = 1500/(mm between R waves)

What is the rate?

Rhythm Is the rhythm regular (distance between QRS complexes equal)? Is there a P-wave before every QRS complex? Is the PR interval normal? 0.12 sec - 0.20 sec Is the QRS duration normal? 0.04 sec to 0.12 sec

Irregular Rhythms Usually caused by multiple, active automaticity sites that causes irregular atrial and ventricular activity Include: Wandering Pacemaker Multifocal Atrial Tachycardia Atrial Fibrillation

Irregular Rhythms Wandering Pacemaker Have P’ waves (not true P waves because pacemaker activity is wandering from SA node to a nearby atrial automaticity foci) Atrial Rate less than 100 Irregular shape to P waves and irregular ventricular rhythm.

Irregular Rhythms (cont.) Multifocal Atrial Tachycardia Think of it as tachycardic wandering pacemaker P’ waves again Atrial rate excees 100 Irregular ventricular rhythm Irregular morphology of P’ waves Occurs in: COPD Heart Disease

Irregular Rhythm (cont.) Atrial Fibrillation No P waves (because there are multiple atrial automaticity foci sending impulses – no single impulse depolarizes atria completely) Irregular ventricular rhythm Caused by: Heart disease (CAD, CHF) Thyroid disease Pericardial effusion Alcohol

Tachy-arrhythmias Rapid rhythms originating in a very irritable foci that paces rapidly. Includes: Rate Range Paroxysmal Tachycardia 150 to 250 Flutter 250 to 350 Fibrillation 350 to 450

Atrial Tachyarhythmias Supraventricular tachycardia Includes paroxysmal junctional tachycardias Paroxysmal Atrial Tachycardia and Paroxysmal Junctional Tachycardia Caused by very irritable automaticity foci that originate above the ventricles. Narrow QRS complex tachycardia Have P’ waves – often get lost in QRS.

Supraventricular arrhythmias

Atrial Tachyarrhythmias (cont.) Torsades de Pointes Rate is usually 250 to 350 beats/min. The amplitude of each successive complex gradually increases and then gradually decreases – “party streamer” Caused by: Severe hypokalemia Medications that block potassium channels Congenital abnormality (Long QT syndrome)

Atrial Tacchyarrhythmia Atrial Fibrillation Rapid Ventricular Response = increased heart rate, putting patient at risk for hypotension.

Atrial Tachyarrhythmias (cont.) Atrial Flutter Extremely irritable atrial focus produces a rapid series of atrial depolarizations (250-350 beats/min.)

Ventricular tacchyarrythmias (cont.) Paroxysmal Ventricular Tachycardia Is like a run of PVC’s Irritable (hypoxic) ventricular focus results in rapid rate that is too fast for heart to function effectively. WIDE QRS COMPLEX tachycardia

Ventricular Tacchyarhythmia (cont.) Ventricular Fibrillation Caused by rapid-rate discharges from many irritable, parasystolic entricular automaticity foci. An erratic, rapid twitching of the ventricles, with ventricular rate reaching 350 to 450 beats/min. Tracing is totally erratic, without identifiable waves.

Tacchyarrhythmia Wolff-Parkinson-White syndrome A ventricular “pre-excitation” arrhythmia An abnormal, accessory AV conduction pathway, the bundle of Kent, can “short circuit” the usual delay of ventricular conduction in the AV node. Results in Shortened PR interval (< 0.12 sec) Widened QRS (> 0.12 sec) Delta waves Can result in several tachyarrhythmias including supraventricular tachycardia, atrial flutter, atrial fibrillation

Blocks Sinus Block AV Block Bundle Branch Block

Sinus Block SA node fails to pace for at least complete cycle. Occurs in: Sick Sinus Syndrome (SSS) SA node dysfunction resulting recurrent episodes of sinus block or sinus arrest Frequently occurs in elderly patients with heart disease. Bradycardia-Tachycardia Syndrome Patients with SSS who develop episodes of supraventricular tachycardia mingled with sinus bradycradia.

AV Block 1° (first degree) AV Block Prolongs AV node conduction Prolonged PR interval (>0.2 sec – one big box) The PR interval is consistently prolonged the same amount in every cycle P-QRS-T sequence is normal in every cycle.

AV Block (cont.) 2° (second degree) AV Block Wenckebach (Mobitz Type I) Gradually prolongs the PR interval , until the final P wave fails to produce a QRS response. This cycle then repeats itself. Usually non-pathologic Mobitz (Mobitz Type II) Totally blocks a number of paced atrial depolarizations (P waves) before conduction to the ventricles is successful. Can be: 2:1 – two P waves to every QRS 3:1 – three P waves to every QRS Usually permanent, and can progress to complete heart block

2° AV Block – “Wenckebach”

2° AV Block - Mobitz 2:1 3:1

AV Block - 2° AV block (cont.) If see 2:1 AV block and uncertain if Wenckebach or Mobitz… Do vagal maneuver If Wenckebach, there is an increase the number of cycles/series (increasing to 2:3 or 4:3) If Mobitz (Type II), it becomes a 1:1 AV conduction.

AV Block (cont.) 3° (third degree) AV block: “Complete Heart Block” Complete block of the conduction to the ventricles, so atrial depolarizations are not conducted to the ventricles. See a sinus-paced atrial (P wave) rate and a totally independent, focus-pased, slow ventricular (QRS rate) – AV dissociation. Can have: Junctional Focus Normal (narrow) QRS Ventricular rate: 40-60/min. Ventricular Focus PVC-like QRS’s Ventricular rate: 20-40/min.

AV Block (cont.) 3° (third degree) AV Block

Bundle Branch Block

Bundle Branch Blocks Caused by block of conduction in the right or left bundle branch. The bundle branch delays depolarization to the ventricles that it supplies. Left Bundle Branch Block (LBBB) Associated with cardiovascular disease! Incidence increases greatly with age. Think – V5, V6!! Right Bundle Branch Block (RBBB) Associated with structural heart disease, increased age, sometimes iatrogenic (cardiac cath.) Think – V1, V2!!

Bundle Branch Block

Left Bundle Branch Block Widened QRS (> 0.12 sec, or 3 small squares) Two R waves appear – R and R’ in V5 and V6, and sometimes Lead I, AVL. Have predominately negative QRS in V1, V2, V3 (reciprocal changes).

Right Bundle Branch Block Widened QRS (> 0.12 sec or 3 small squares) R and R’ in V1 and V2, often with ST depression and T wave inversion. Reciprocal changes (big negative S) in V5,V6, I and AVL.

Right Bundle Branch Block

Bundle Branch Block Final Note: If you have the above changes with R and R’, but a normal (not widened) QRS, it is referred to as an incomplete bundle branch block.

Axis The direction of depolarization as it passes through the heart. A vector towards a lead results in a positive deflection on the ECG, while a deflection away from a lead results in a negative deflection. If hypertrophy is present, the overall vector (axis) points towards the hypertrophied part.

Axis Horizontal Plane Frontal Plane

Axis Normal Axis: QRS vector pointed downard and to the patient’s left, in the 0 to 90° Range. Right axis Deviation: > 100° Left axis Deviation: < 0°

Axis – the nitty gritty QRS net positive in Lead I and AVF: normal axis QRS net positive in Lead I and net negative in AVF: Left axis Deviation QRS net negative in Lead I and net positive in AVF: Right axis Deviation AVF

Axis Left Axis Deviation: Right Axis Deviation: Can occur in: Left Ventricular Hypertrophy (hypertension!) Inferior myocardial infarction Right Axis Deviation: Right ventricular overload (cor pulmonale) Left pneumothorax Lateral myocardial infarction.

Hypertrophy – we’re going to essentials only. Left Ventricular Hypertrophy Important because it is often a sign of long- standing hypertension! Calculation: mm of S in V1 + mm of R in V5 If sum is more than 35 mm, you have LVH!!! Remember, you usually see Left axis deviation with LVH.

Now the most important…. MYOCARDIAL INFARCTION !!!!

EKG in Myocardial Infarction Gives information about: Duration — hyperacute/acute versus evolving/chronic Extent — transmural versus subendocardial Size — amount of myocardium affected Localization (which area of heart affected) Difficult to use EKG in certain situations: Left bundle branch block Paced rhythm

EKG in myocardial infarction Ischemia: T waves Injury: ST changes Necrosis: Q waves

Myocardial Ischemia Represented by inverted T waves. Should be symmetrically inverted. Can be marker of OLD infarction Wellens syndrome: Marked T wave inversion in V2 and V3, which alerts to stenosis of the left anterior descending coronary artery (LAD)

Myocardial Injury Injury = “acute” or “recent” ischemia. ST changes show that the episode is acute. Transmural injury ST Elevation Subendocardial injury ST Depression

ST elevation

ST depression

Myocardial Necrosis Q wave: Diagnostic for myocardial infarction. Can have MI in its absence (non Q-wave MI) Can be acute or old! (Use ST changes to determine if acute) Is significant if at least one small square (1 mm or 0.4 seconds in duration) Is usually at least 1/3 of the QRS amplitude

Location of Infarction Posterior Right Coronary Artery Large R, ST depressions in V1, V2, V3 Inferior R or L coronary artery ST changes/Q waves in II, III, AVF May have reciprocal ST depressions in I and AVL Lateral Circumflex artery ST changes/Q waves in I and AVL, V5, V6 May have reciprocal ST depressions in II, III, AVF. Anterior Left Anterior Descending artery ST changes/Q wave in V1, V2, V3, V4

Where’s the MI?

Where’s the MI?

Where’s the MI?

Final one…

EKG - Conclusion Rate Rhythm Axis Hypertrophy Ischemic Changes Regular, irregular, irregularly irregular? P waves? PR interval? QRS duration? Axis Hypertrophy Ischemic Changes T wave changes? ST changes? Q waves