Heart Rate and Arrhythmia Basics Kevin Formes D.O. July 27, 2004

Cardiac Cycle Phase 0: Rapid depolarization Sodium moves rapidly into the cell Calcium moves slowly into the cell Phase 1: Early repolarization Sodium channels close Phase 2: Plateau Calcium continues to flow in Potassium continues to flow out Phase 3: Rapid repolarization Calcium channels close Potassium flows out rapidly Active transport Na/k pump Phase 4: Resting Cell membrane is impermeable to sodium Potassium moves out

Ventricular Action Potential & EKG QRS T 0.2 sec

Heart Physiology: Sequence of Excitation Figure 17.14a

Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse approximately 0.1 second Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

Electrocardiography Electrical activity is recorded by electrocardiogram (EKG) P wave corresponds to depolarization of atrium QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex

The 8-Step method Determine the rhythm Determine the rate Determine the axis Evaluate the p wave Determine the duration PR interval Determine the duration of QRS complex Determine the duration of QT interval Evaluate ST segment and T wave

Methods To Determine Rate Distance between the R-R interval (300/#large blocks) 1 large block 300 2 large blocks 150 3 large blocks 100 4 large blocks 75 5 large blocks 60 6 large blocks 50

Lead Systems: In 1902, Willem Einthoven recorded the first EKG. He determined that the heart lies at the center of the electrical field determined by the axis of three standard “Limb” electrodes. Different “leads” or views of the electrical patterns produced were obtained by electrodes placed on the Left Arm, Right Arm, and Left Leg.

Electrocardiogram (EKG): Electrical Activity of the Heart Einthoven's triangle P-Wave – atria QRS- wave – ventricles T-wave – repolarization Figure 14-20: Einthoven’s triangle

Cardiac Axis by different Leads Carr and Brown Figure 8-2

Pathological Conditions Mean Electrical Axis (mark changes in current flow) Left Axis Deviation (hypertrophy of left ventricle) 1. Hypertension (muscle mass on left side of heart) 2. Aortic Valvular stenosis 3. Aortic Valvular regurgitation 4. Several congenital heart conditions Right Axis Deviation 1. Hypertrophy of right ventricle (pulmonary stenosis) 2. Tetralogy of Fallot (congenital right to left shunt )

Precordial (chest) Leads - V6 V5 V4 V3 V1 V2

Electrocardiogram (EKG): Electrical Activity of the Heart ≤100 msec 120-200 msec ≤ 450 msec

Normal Sinus Rhythm Sinus node is the pacemaker, firing at a regular rate of 60 - 100 bpm. Each beat is conducted normally through to the ventricles One P wave for each QRS PRI: .12-.20 seconds and constant QRS: .04 to .1 seconds

Arrhythmias Bradycardia Tachycardia 1st degree AV block 2nd degree AV block 3rd degree AV block Premature Ventricular Complex (PVC) Atrial Fibrillation Ventricular Tachycardia Ventricular Fibrillation

Pathological Conditions That Lead to Arrhythmias Ischemia Intracellular Ca2+ overload Stress: adrenergic stimulation Genetic defects- especially in ion channels Anatomic defects Drug effects

Bradycardia: Rate less than 60 Disorders of impulse formation Sinus bradycardia Sinus node dysfunction (sick sinus syndrome Junctional and ventricular escape rhythms Disorders of impulse conduction (heart block) 1,2,3 degree AV block

Sinus Bradycardia Rate less than 60 Normal P waves, PR interval Causes: Overmedication Inferior wall MI Increased intracranial pressure Hypothyroidism Carotid Sinus hypersensitivity Normal Variant Treatment: Atropine, external or tranvenous pacing if symptomatic, EP of no value diagnosis is derived from Clinical Hx, clinical judgement, and monitoring and correlation with symptoms

1st Degree A-V Block Not really “block” Just P-R interval longer than normal (> 0.2 sec) Treatment: none

2nd Degree AV Block Mobitz type 1 Some action potentials fail to get through the A-V node Normal Sinus Rhythm 2nd degree A-V block Treatment: none or ventricular pacing

2nd Degree AV Block Type I Progressive PR interval lengthening Dropped QRS AV nodal delay

2nd Degree AV Block Type 2 Constant PR interval Dropped QRS Infra-nodal delay- Treatment pacemaker

3rd Degree A-V Block No action potentials from the SA node/atria get through the A-V node Normal Sinus Rhythm 3rd degree A-V block Treatment: ventricular pacing

Junctional Rhythm Originate from the area in and around the AV junction. Inherent rate is 40-60 Enhanced automaticity may causes more rapid rates. Electrical impulses are conducted backward (retrograde) to depolarize the atria and forward (antegrade) to the ventricles. Makes the p-wave inverted in lead II.

Where are those P waves? Impulse from AV junction depolarizes atria before ventricles - p waves will be in front of QRS Impulse from AV junction depolarizes ventricles before atria - p waves will be after QRS Impulse from AV depolarizes atria and ventricles simultaneously - p wave will be hidden in the QRS

Tachycardia: Rate Greater Than 100 Causes Increased automaticity: atrial, junctional and ventricular premature complexes Accelerated junctional rhythm Accelerated idioventricular rhythm Ectopic atrial rhythms Some forms of VT Triggered activity Some forms of VT, long QT Digoxin toxicity (Late after depolarizations) Reentry AV nodal reentrant tachycardia AV reentrant tachycardia (WPW) Atrial fibrillation Atrial flutter Most forms of VT

Delayed Afterdepolarization (DAD) Occurs only after a “triggering” action potential Intracellular Ca2+ overload ischemia digitalis intoxication adrenergic stress Na/Ca exchange generating depolarizing current -50 200 msec Action potential

Normal Action Potential Conduction -50 200 msec Action potential Purkinje fibers 20 msec Conduction times (1 mm/msec): A-C 10 msec A-B 10 msec C-B 10 msec A 10 mm 10 mm 10 mm B C Ventricular Muscle

Re-entry Circuits as Ectopic Foci and Arrhythmia Generators Atrio-Ventricular Nodal Re-entry supraventricular tachycardia Ventricular Re-entry ventricular tachycardia Atrial Re-entry atrial tachycardia atrial fibrillation atrial flutter Atrio-Ventricular Re-entry Wolf Parkinson White supraventricular tachycardia

Differential Diagnosis of Tachyarrhythmias Narrow complex: Regular-sinus tachycardia, ectopic atrial tachycardia, atrial flutter, junctional tachycardia, AVNRT, AVRT Irregular- Atrial fibrillation, multifocal atrial tachycardia, atrial flutter with variable conduction Wide complex Regular- Ventricular tachycardia, supraventricular tachycardia with aberrancy Irregular-Atrial fibrillation with aberrancy

Sinus Tachycardia Sinus node is the pacemaker, firing regularly at a rate of greater than 100 times per minute. Each impulse is conducted normally through to the ventricles Almost always occur as a response to some physiological stimulus (fever, exercise, volume depletion, thyrotoxicosis, hypotension If symptomatic use AV nodal blocking agents (CCB,BB, Dig)

Atrial Flutter Reentrant circuit around tricuspid valve Flutter waves at 250-400 (avg 300/min) AV conduction ratio 4:1, 3:1 ect “Saw-toothed” waves Treatment with ablation works around 99% of the time

Atrial Fibrillation Irregular irregularity R-R interval variablity Rate greater than 400-600 Two types-bad atrial tissue secondary to HTN, ischemia or bad pulmonary vein tissue young patients

Causes of Atrial Fibrillation Pulmonary disease Ischemia Rheumatic heart disease Anemia, atrial myxoma Thyroid Electrolytes Sepsis

Atrial Fibrillation Treatment Try to restore normal rhythm (cardioversion) only within 48 hrs vagatonic maneuvers (carotid massage, Valsalva maneuver, gagging) adenosine If persistent rhythm: control ventricular rate (calcium channel blocker, beta blocker) anticoagulant therapy (coumadin)

Multifocal Atrial Tachycardia Multiple P wave morphology Multiple PR intervals Irregular irregularity Associated with COPD, hypoxia, and theophylline toxicity Treat underlying cause, or AV node ablation with pacemaker

AV Nodal Reentrant Tachycardia Results from a small micro-reentrant circuit within the AV node itself Is usually initiated by a premature atrial beat EKG tachycardia with no p waves or p waves after the QRS complex Treatment is AV nodal-blocking drugs (CCB,BB,Dig)

Atrioventricular Reentrant Tachycardia Involves a large reentrant loop with one limb of the circuit including the AV node and the other being an abnormal connection between the atria and ventricles (WPW) Usually initiated by PVC Two types- Orthodromic (narrow complex QRS) 90%, Antidromic (wide complex QRS) 10% IF AV nodal blocking agents are given with a-fib and avrt could cause V-fib

Ventricular Tachycardia Usually associated with symptoms Rate: 140-220 (200±50); at least 3 ectopic QRS in row QRS: normally wide and bizarre Usually associated with MI or other organic HD; unusual in normals Often serious requiring quick treatment if sustained Mechanism? Reentry or rapid firing ectopic?? Treatment: cardioversion, lidocaine

Ventricular Fibrillation Multiple foci in the ventricles become irritable and generate uncoordinated, chaotic impulses that cause the heart to fibrillate rather than contract. Treatment: cardioversion

Asystole The heart has lost its electrical activity. There is no electrical pacemaker to initiate electrical flow. Treatment: ACLS protocol, transcutaneous pacing, epinephrine 1mg IVP q3 to 5, atropine 1mg q 3 to 5

Premature Atrial Contraction Early beat that originates in the atria as an ectopic pacemaker Etiology Usually caused by enhanced automaticity in atrial tissue May be a single or multiple ectopic sites Shape of the p-wave depends on the location of the ectopic beat

Premature Atrial Contraction P-wave configuration Usually different from the underlying p-wave QRS configuration Usually similar to the underlying rhythm If very early, the bundle branches may not have repolarized sufficiently for normal conduction. (usually conducted left and blocked right)

Non-compensatory pause * measurement between the R-wave preceding the PAC to the R-wave following the PAC is less than two R-R cycles of the underlying rhythm

Compensatory Pause * measurement between the R-wave preceding the PAC to the R-wave following the PAC equals two R-R cycles of the underlying rhythm

Antiarrhythmic Drugs Class I: Local anesthetic action, reducing Na channel current Lidocaine, Quinidine Class II: b-Adrenergic antagonists Propranalol Class III: action potential prolongation Amiodarone Class IV - Ca channel antagonists Verapamil

Quiz Name the Rhythm # 1:

Answer: Atrial Flutter

Name the Rhythm #2:

Sinus Bradycardia

Name the Rhythm #3:

Third Degree Heart Block

Name the rhythm # 4:

Ventricular Fibrillation

Name the rhythm #5:

Normal Sinus

Name the rhythm #6:

AV Block 2 Degree (type 1)

Name the rhythm # 7:

Atrial Fibrillation

Name the rhythm # 8:

Ventricular Tachycardia

Name the rhythm # 11:

Sinus Tachycardia