HEART BLOCKS AND CARDIAC PACEMAKERS

Arun AbbiJason MitchellJan 21, 2010

OUTLINE

SINUS NODE DYSFUNCTION ATRIOVENTRICULAR BLOCKS INTRODUCTION TO CARDIAC PACEMAKERS INSERTION OF TRANSVENOUS CARDIAC

PACEMAKER

HEART BLOCK

RELEVENT ANATOMY Conduction: SA > Atrium > AV Node > His >

Purkinje Network AV node highly innervated

Responsive to sympathetic and vagal stimuli RCA blood supply

His bundle less responsive Dual blood supply

SINUS NODE DYSFUNCTION

Abnormal sinus impulse formation and propagation

AKA Sick Sinus Syndrome Umbrella term for:

Sinus bradycardia Sinus arrest Sinoatrial exit block Tachy-brady syndrome

SINUS NODE DYSFUNCTION

ETIOLOGY Unclear Fibrosis (most common) Structural heart disease Medications Electrolyte imbalances (HypoK, HypoCa) Endocrine (HypoTSH, HypoT)

SINUS NODE DYSFUNCTION

SINUS ARREST Absent sinus P waves > 2 – 3 seconds

Result of absent sinus impulse formation Duration of pause is not a function of the P-P

interval

SINUS NODE DYSFUNCTION

SINOATRIAL EXIT BLOCK Conduction delay between sinus node and

atrium Three types

SINUS NODE DYSFUNCTION

SINOATRIAL EXIT BLOCK First Degree

Conduction delay between sinus node and atria Cannot be identified on ECG ?Clinical significance

SINUS NODE DYSFUNCTION

SINOATRIAL EXIT BLOCK Second Degree

Intermittant conduction block Type I (Wenkebach) – Progressive shortening of P-P

intervals – Pause duration less

than twice the P interval – Grouped P waves

SINUS NODE DYSFUNCTION

SINOATRIAL EXIT BLOCK Type II – Pause duration that is a multiple of

the P-P interval

SINUS NODE DYSFUNCTION

SINOATRIAL EXIT BLOCK Third Degree

Complete conduction block from sinus node to atrium Cannot be distinguished from sinus arrest on ECG Typically results in an escape rhythm

SINUS NODE DYSFUNCTION

TACHY-BRADY SYNDROME Bradycardia alternating with brief episodes of

SVT Usually Afib ???Cause

ATRIOVENTRICULAR BLOCK

ETIOLOGY Congenital Acquired – Extensive DDX

Medications Hyperkalemia (>6.3 mEq/L) Hypoxia Increased vagal tone Ischemia/Infarction (~40%) Fibrosis (~50%) Infection/Inflammation Vascular Disease Idiopathic

Usually never identified

ATRIOVENTRICULAR BLOCK

FIRST DEGREE AV BLOCK Prolongation of PR > 200 ms Location of block

AV node, His bundle, His-Purkinje system Correlate with QRS complex

Prognosis Framingham: More likely to develop Afib, require

permanent pacemaker, and increased all-cause mortality Locate source of block

If AV node, generally benign and no further Ix If infranodal, may require His-bundle electrocardiogram No specific intervention required for stable 1st degree block

ATRIOVENTRICULAR BLOCK

FIRST DEGREE AV BLOCK

ATRIOVENTRICULAR BLOCK

SECOND DEGREE AV BLOCK Type I (Wenckebach/Mobitz I) - Normal

Gradual prolongation of the PR interval followed by dropped QRS

Atrial impulses reach AV node while it is partially refractory

Location usually the AV node

ATRIOVENTRICULAR BLOCK

SECOND DEGREE AV BLOCK Type II – Never normal

PR interval constant Usually a result of underlying structural disease Location typically His-Purkinje system

High Grade Second Degree 2 or more consecutively blocked P waves

ATRIOVENTRICULAR BLOCK

SECOND DEGREE BLOCK Different sites of involvement/prognoses Type I: Generally involves AV node and is

benign Type II: Almost always infranodal and may

progress to 3rd degree (slow unreliable escape)

Difficult to distinguish type in 2:1 conduction block

ATRIOVENTRICULAR BLOCK

THIRD DEGREE BLOCK Complete AV node failure to conduct Block may be anywhere in conduction system Constant P-P and R-R intervals but no

relationship Variable PR intervals, Atrial HR > Ventricular

HR May be hemodynamically unstable Slow heart rate may produce Torsade ,

especially in women

HEART BLOCK

ECG PRACTICE

ECG 1

SSS (Tachy-Brady)

ECG 2

Type II Second Degree AV Block

ECG 3

Sinus Arrest

ECG 4

3rd Degree AV Block

ECG 5

Type II Second Degree SA Node Exit Block

ECG 6

First Degree AV Block

ECG 7

Type 1 Second Degree AV Block

HEART BLOCK INITIAL ASSESSMENT

Hemodynamic Instability Fatigue, Dizziness, NV, Diaphoresis Hypotension Syncope Dyspnea Chest Pain

ACLS Guidelines for Symptomatic Bradycardia Medications

Β- Blockers Ca2+ Channel Blockers Digitalis Amiodarone

HEART BLOCK

INITIAL ASSESSMENT Investigations

Stabilize first! ECG Bloodwork

Electrolytes Dig level Troponin

HEART BLOCK

MANAGEMENT O2, IV, Monitors Transcutaneous pacing Transvenous pacing

> 30 minutes transcutaneous pacing Unable to obtain capture

Consider atropine Consider catecholamines (be cautious)

HEART BLOCK

CARDIOLOGY CONSULTATION Outpatient

New, asymptomatic Type I 2nd Degree (while awake)

Inpatient Any symptomatic block New, asymptomatic Type II 2nd Degree Asymptomatic 3rd Degree Concomitant MI/Ischemic symptoms High Grade AV Block

CARDIAC PACING

INDICATIONS Temporary

Any symptomatic AV block Asymptomatic, but associated with Torsade

Permanent ACC/AHA/HRS 2008 Guidelines:

Divided into Class Based Recommendations

CARDIAC PACING

CARDIAC PACING INDICATIONS AV Block

Class I 2nd and 3rd Degree

Bradycardia with symptoms (C) Associated arrhythmias and medications that produce

symptomatic bradycardia (C) Asymptomatic, but asystole >3 sec or escape < 40 bpm or

wide QRS escape or Afib and bradycardia with systole >5 seconds (C)

After ablation of AV node or unresolving post-op block (C) Associated with MD, Kearns-Sayre syndrome, Erb

dystrophy (B) Associated with exercise w/o MI (B)

CARDIAC PACING

INDICATIONS AV Block Class IIa

Asymptomatic persistent 3rd degree with escape > 40 (C) Asymptomatic 2nd degree with intra or infra-Hisian block

(B) Symptomatic 1st or 2nd degree block (B) Asymptomatic 2nd degree block with narrow QRS (B)

Class IIb 1st or 2nd degree with MD, Erb dystrophy, peroneal

muscular atrophy +/- symptoms (B) AV block in setting of drug toxicity when block expected

to recur (B)

CARDIAC PACING

INDICATIONS AV Block Class III

Not indicated for asymptomatic 1st Degree (B) Not indicated for asymptomatic Mobitz I with block at

AV node (C) Not indicated for AV block that is expected to resolve

and unlikely to recur (drug toxicity, Lyme disease, transient increased vagal tone) (B)

Also not indicated in: PEA Arrest Traumatic cardiac arrest

Some Things Just Won’t Work

CARDIAC PACING

PACING MODES 5 Position Nomenclature First 3 Positions most common in pacemaker

description Position I: Chamber being paced

Atrium (A), Ventricle (V), Both (D), None (O) Position II: Chamber being sensed

Atrium (A), Ventricle (V), Both (D), None (O) Position III: Pacemaker’s response to sensing

Triggers (T), Inhibits (I), Both (D), None (O)

CARDIAC PACING

PACING MODES Position IV: Programmability and Rate Control

Hierarchical Rate Modulation (R), Communicating (C),

Programmable (P), (O) Position V: Antitachydysrrhythmia Function

Pacing (P), Shocking (S), Both (D)

CARDIAC PACING

PACING MODES Most pacemakers encountered are:

AAIR – Useful for sinus node dysfunction with intact AV node

VVIR – Useful for chronically ineffective atria (AF, AFlutter)

DDD – Most common. Preserves AV synchrony Reduces risk of AF, reduces signs/symptoms HF,

improves QOL No significant mortality benefit over single-

chamber pacing

CARDIAC PACING

ECG MANIFESTATIONS Depends on Pacing Mode Atrial Pacing

Small pacemaker spike prior to P wave with normal morphology

Ventricular Pacing LBBB-like and prolonged, inverted QRS (V5/6)

and LAD

CARDIAC PACING

CARDIAC PACING

CARDIAC PACING

TEMPORARY PACING Goal: Restore effective myocardial contraction

to increase adequate cardiac output Transcutaneous vs. transvenous pacing

modalities

CARDIAC PACING

TRANSCUTANEOUS PACING Temporary stabilization of symptomatic

bradycardia Most patients tolerate pacing for < 15 minutes Pain directly related to current and inversely

related to pad size

CARDIAC PACING TRANSCUTANEOUS PACING

Technique Apply pads front/back or left/right

Front/back preferred Sedate Set HR to 60-80 Set current to 0 mA Choose mode

Synchronous vs. asynchronous Turn pacemaker on Increase current by 10 mA increments until capture obtained

Manifested by wide QRS relating to palpable carotid pulse If unconscious, start at 200 mA and decrease to lowest current

CARDIAC PACING

TRANSVENOUS PACING Placement of electrode into R Ventricle Pacer is VVI mode Allows for asynchronous vs synchronous

CARDIAC PACING

TRANSVENOUS PACING Equipment

Introducer Kit Introducer sheath Pacing catheter

External pacing generator Cardiac monitor

CARDIAC PACING

TRANSVENOUS PACING External Pacing Generator

Delivers electrical current (mA) Output Control Dial

Regulates current from 0.1 – 20 mA Rate Control Dial

Selects pacing rate Sensitivity Control Rate

Threshold suppression of pacer based on native R wave

Asynchronous pacing when sensitivity control turned down

CARDIAC PACING

TRANSVENOUS PACING Transvenous Pacing Catheter

3 types: Flexible, Semifloating, Rigid/Non-floating

Risk of cardiac perforation with rigid catheters Two electrodes attached: + and –

Introducer Sheath Facilitates central venous access

CARDIAC PACING

TRANSVENOUS PACING Technique

Seldinger technique for central venous access R IJ or L Subclavian shown to be most successful

Secure introducer sheath Introduce pacing electrode Inflate balloon when electrode passed through the 20 cm

mark Moot if no pulse

Set pacing generator to max current Set rate between 60-80 Asynchronous sensitivity

CARDIAC PACING

TRANSVENOUS PACING As cath is advanced, monitor will show pacing

spikes Pacing spikes followed by wide QRS indicating of

RV placement Electrical capture

Assess for pulse Mechanical capture

Deflate balloon and secure cath in place Set pacing threshold

CARDIAC PACING

TRANSVENOUS PACING Complications

Inherent to central venous access Arterial puncture, PTX, infection

Right heart catheterization Failure to capture, failure to sense,

dysrrhythmias Cardiac perforation Lead displacement Electrode coiling