Rubery: Arrhythmias 1

Front 1

Sinus node action potential

Back 1

Na+ channels effectively absent
Slow depolarization through voltage-gated Ca++ channels
Automaticity due to continual “leak” during phase 4
Under normal conditions, sinus node automatic rhythm is faster than any other location, which makes the sinus node the dominant rhythm

Front 2

Atrial myocytes

Back 2

Short refractory period
- repolarize quickly
- able to sustain rapid arrhythmias
-- Atrial Fibrillation (>350 bpm)
-- Atrial Flutter (300 bpm)

Front 3

Atrioventricular node

Back 3

Compared to sinus node:
- has similar action potential
- has slower automaticity
Transmits depolarizing current from the atria to the His bundle
AV nodal conduction is slower than atrial, ventricular, His-Purkinje cells
Slower conduction because phase 0 driven by slow Ca++ channels instead of fast Na+ channels
-This is a protective mechanism: atrial fibrillation can be >350 bpm, wouldn't want ventricles to go that fast so AV node slows the impulse

Front 4

His, bundle branches, purkinje fibers

Back 4

His bundle transmits depolarizing current across the “fibrous skeleton” to the bundle branches
Cell structure similar to Bundle Branches and Purkinje Fibers
- Altogether, they are the “His-Purkinje System”
ERP much longer than atrial cells

These bundles of cells conduct each individual heartbeat more rapidly than “regular” contractile myocardial cells
-Have greater density of Na+ channels
--Action potential propagates faster within each cell
-Have greater density of gap junctions between cells
--May also have “better” gap junctions than other cells – better conducting properties
--Current propagates faster from cell to cell

Front 5

Ventricular myocytes

Back 5

Similar to atrial cells, but have longer refractory periods

Front 6

Autonomic effects on AV nodal conduction

Back 6

Sympathetic stimulation increases conduction velocity through AV node
-Positive chronotropic effect (sinus rate increases)
-Positive dromotropic effect (AV nodal conduction enhanced)
-Sympathetic stimulation or parasympathetic blockade (atropine)
Parasympathetic stimulation decreases conduction velocity through AV node
-Negative chronotropic effect (sinus rate decreases)
-Negative dromotropic effect (AV nodal conduction is slowed)
-Parasympathetic stimulation, sympathetic blockade (beta blockers, etc)

Front 7

Chronotropic, dromotropic, inotropic terminology

Back 7

Chronotropic effect
-Alters automaticity
--Usually refers to sinus node automaticity
--Occasionally refers to AV node automaticity
Dromotropic effect
-Alters the speed of propagation of an impulse
--Usually refers to AV node conduction
Inotropic effect
-Alters the strength of myocyte contraction
--Usually refers to ventricular myocytes

Front 8

Bradyarrhythmias

Back 8

2 Primary mechanisms:
Failure of impulse generation
-Abnormal automaticity
Failure of impulse propagation
-Automaticity is normal, but impulse fails to propagate across vital structures

Abnormal Sinus Node automaticity
-Fibrosis, ischemia, metabolic disorders, drugs
-Anything that alters function of the ion channels involved in phase 4 automaticity

SA (sinoatrial) block
-Normal sinus automaticity, but current blocks in perinodal tissue, does not excite the atrium

AV Block
-within the AV node
-Can be physiologic, due only to long refractory periods in presence of abnormally fast atrial rhythms
-Pathologic usually caused by ischemia, fibrosis, or drugs

His bundle Block
-Block within the His Bundle
-Also called “infranodal” block because level of block is below the AV node

Front 9

Escape rhythms: overview

Back 9

Cells which possess normal automaticity:
-Sinus Node (60-100bpm at rest)
-AV Node and His bundle (40-60bpm)
--"Junctional Escape"
--Good reliability, but a little less reliable, more easily suppressed than sinus or atrial rhythms
-Bundle Branches, Purkinje system (30-40bpm)
--"Ventricular Escape"
--Not reliable, easily suppressed
At any given moment, the fastest one wins
-Sinus Node normally fastest, overrides all others
-If sinus node fails to depolarize, or signal fails to propagate, the next fastest rhythm will take over, an “escape rhythm”
--These cells with normal automaticity can also be called “latent pacemakers” – they can assume the role of pacemaker if the sinus node fails

Front 10

Escape rhythms: ectopic atrial pacemakers

Back 10

A number of locations within the atria (mostly the right atrium) have automaticity
Rates are highly variable: 40’s to 90’s
Blur the line between “normal” and “abnormal”
-Probably should be considered normal if ectopic atrial rhythm takes over when sinus rate is very slow
-Probably (mildly) abnormal if ectopic rhythm usurps pacemaker function away from a perfectly normal sinus node
Usually pretty reliable

Front 11

Emergency treatment of bradyarrhythmias: overview

Back 11

In an emergency, it is sometimes possible to “speed up” the heartbeat by:
-Blocking parasympathetic activity
-Enhancing sympathetic activity
Mechanism of either method:
-Increase automaticity of Sinus Node or AV nodal escape rhythm
--Increase chronotropy
-Enhance conduction through AV node
--Increase dromotropy

Increasing chronotropy
-Only works if the problem is “above” the AV node
-Speeding up automaticity of the sinus node or an AV nodal (“junctional”) escape rhythm only helps if the AV node and His bundle transmit the impulse to the ventricles
Increasing dromotropy
-Only works if the problem is within the AV node itself
-Enhancing AV nodal conduction only helps if the His bundle is able to transmit the impulse to the ventricles
-If the level of block is in the His bundle, or within the bundle branches, then improving AV nodal conduction isn’t going to help

Front 12

Speeding up heartbeat with drugs

Back 12

Block parasympathetic activity
-Atropine
Enhance sympathetic activity
-Sympathetic receptors = α-1, α-2, β-1, β-2
-β-1 is the only receptor that affects chronotropy and dromotropy
-A “pure” drug to enhance chronotropy and dromotropy would only affect β-1 receptors
-A drug that stimulates α-1 receptors will act as a vasoconstrictor (should raise BP)

Front 13

Drugs that enhance sympathetic activity

Back 13

Isoproterenol
-β (this is the “purest” one as far as increasing the heart rate is concerned)
Dobutamine
-β (also has a big inotropic effect)
Dopamine
-α, β, and dopamine receptors
Epinephrine
-α and β (a whole lot of both)
Norepinephrine
-Mostly α, but also some β

Front 14

Coronary arteries

Back 14

LCA supplies the left ventricle
-splits into Left Circumflex and Left Anterior Descending
RCA supplies the right ventricle (and usually a portion of the left ventricle)
-Splits into Right Coronary and Posterior descending

Front 15

Sinus and AV nodal arteries

Back 15

Sinus node is supplied by the:
-RCA in about 70%
-LCx (Left circumflex) in about 25%
-Both RCA and LCx share the supply in about 5%
AV node is supplied by the:
-RCA in about 85%
-LCx in about 8%
-Shared by both RCA and LCx in the rest
Don’t memorize these numbers, b/c different books give different numbers
-Just know RCA>LCx>both (for which is more likely to supply the sinus and AV nodes)

Front 16

Non-pharmacologic treatment of bradyarrhythmias

Back 16

Dual chamber pacemaker