Garcia, Cholson Banjo E.

 Conduction disturbance  Originate from: ◦ sinus node ◦ AV node ◦ bundle branch

 Sinoatrial Block  Atrioventricular Block  Bundle Branch Block  Fascicular Block

 Impaired conduction from the SA node to the atria  No depolarization of the atria  Absence of PQRST complex

 Etiology ◦ Increased vagal tone ◦ Inferior wall MI ◦ Age related degeneration ◦ Drugs (digoxin, beta blockers, ccb, class IA- antiarrythmic) ◦ Hyperkalemia ◦ myocarditis

 RR interval: irregular (creating a pause, atria is blocked so it never depolarized  PP interval surrounding the pause is commonly multiple of the previous PP interval

 1 st degree AV block  2 nd degree AV block, Type 1 (Mobitz or Wenkebach)  2 nd degree AV block, Type 2 (Mobitz II)  3 rd degree AV block (CHB)

 Prolonged conduction between the atria and the ventricles  Partial block within the AV node  Prolongation of the PR interval and preservation of the underlying rhythm

Etiology – Drugs – Increased vagal tone – Hyperkalemia – MI (inferior wall) – Myocarditis – Degeneration of conducting pathways assoc. with aging – Idiopathic cause

 PR interval: > 0.20 seconds  Length of PR interval is constant  P wave is followed by a QRS complex

 Mobitz type I or Wenckebach  Intermittent conduction between the atria and ventricle  Found with the AV node

Etiology – Digitalis – Escessive vagal tone – MI (inferior wall) – Ischemic heart disease – Myocarditis – Normal variant

 Progressive lengthening of the PR interval until a QRS complex is dropped; P wave appears on time, but no QRS follows  RR interval: irregular owing to drop beats causing the QRS complex to appear clustered together (narrow)  “Grouped Beating”  PP: constant

 Mobitz type II  Intermittent and sudden loss of conduction between atria and the ventricles  Found below the bundle of his  Can proceed to complete heart block  Ventricular rate tends to be slower and cardiac output diminishes

Etiology – Acute Myocardial Infarction (anterior wall) – Drugs (digitalis, beta blocker, ccb) – Degeneration of electrical conduction system (assoc. with aging)

 PR interval: constant or fixed  QRS: wider than normal because of associated conduction block in ventricles  Conduction ratio varies (1:1, 2:1; 3:1)  PP: regular  RR: irregular

 Complete heart block  Complete absence of conduction between atria and ventricles

Etiology – Drug toxicity (digoxin, beta blocker, ccb) – Excessive vagal tone – Acute MI – Age-related Degeneration of electrical conduction system – Myocarditis – Endocarditis – Cardiac Surgery – Congenital origin

 Atrial and ventricular rates are different  No relationship between P waves and the QRS complex  P waves appear but no QRS  PP and RR interval: constant

 Look for 3 ECG patterns 1.Look for the RR interval. Regular or irregular? 2.Look at the P wave. Is there one or more P wave for every QRS 3.Look at the PR interval. Stay the same or change?

 If REGULAR (1 st degree or 3 rd degree) ◦ Only 1 P wave for every QRS ◦ PR interval stay the same  1 st degree ◦ more than 1 P wave ◦ PR interval changes  3 rd degree

 IRREGULAR ( 2 nd degree) ◦ PR interval change: 2 nd degree AV block, TYPE I ◦ PR interval stay the same: 2 nd degree AV Block, TYPE II

 Defect in the intraventricular conduction  Supravetricular impulse: from the unblocked branch depolarizes one ventricle  Blocked branch: impluse spread slowly through the ventricular muscle resulting in abnormal depolarization  Hallmark: abnormal wide QRS complex

 Conduction Delay in the right bundle branch Etiology – RVH – Right ventricular strain – ASD – Wolf parkinson -white – Coronary artery disease – Myocarditis – Cardiac contusion – Idiopathic cause

 QRS complex: 0.12 or more in width  QRS is wide and positive assumes in lead V1  rSR: leads V1 and V2  Wide or Deep I, avL V5 and V6  Down slopping of ST segment V1 and V2

Etiology – LVH – Cardiomyopathy – HPN – Wolf parkinson -white – Coronary artery disease – Myocarditis

 QRS complex: 0.12 or more in width  QRS is negative V1 and V2  rSR (rabbit ear) in I, avL, V5, V6  Wide or deep S V1 and V2  Down slopping of ST segment I, avL, V5, V6

Right Bundle Branch BlockLeft Bundle Branch Block QRS wide and predominantly positive V1 QRS wide and predominantly negative V1 rSR in lead V1rSR in lead V6 Deep S in lead V6Deep S in lead V1 Late intrinsicoid deflection in lead V1 Late intrinsicoid deflection in lead V6

 Hemiblocks  Disturbed conduction in either the anterior or posterior division, or fasicle, of the left bundle branch

 Delay in the conduction through the anterior fascicle of the LBB  Anterior fascicle long thin and has a single blood supply, making it vulnerable to block

Etiology – Coronary artery disease – MI – Congenital Heart disease – Cardiac surgery – Aging process – Normal variant

 QRS: prolonged ( )  Left axis deviation QRS axis (-45 and -90)  Small q wave and a tall R wave in lead I and avL  Small r wave and deep S wave in lead II, III and avF

 Delay in the conduction through the posterior fascicle of the LBB  Posterior: short, thick and has double blood supply  Appearance implies large amount of Myocardial injury has occurred

Etiology – Coronary artery disease – MI – Congenital Heart disease – Cardiac surgery

 QRS: prolonged ( )  Right axis deviation QRS axis (+90 and +180)  Small q wave and a tall R wave in lead II, III and avF  Small r wave and deep S wave in lead I and avL

LAFBLPFB LADRAD qR in lead IqR in lead III rS in lead IIIrS in lead I