11/7 Cardiac Arrhythmia: Mechanism - Coromilas

Question 1

great powerpoint - look at it first

Question 2

graphic representation of electrical info in EKG

attach picture

Answer 2

note:

SA node and AV node APs are different from cardiomyocytes

• SA/AV nodes: Na/Ca influx [check]
  
  • beta blockers and Ca blockers have more effect here
• cardiomyocyte: rapid Na influx

Question 3

electrical activation of the heart

relative speed of SA node, AV node, conduction pathways

Answer 3

SA node conduction approx 50-60cm/s

AV node conduction approx 5cm/s

• diff is important bc it allows ventricles time they need to fill before contraction and also filters out aberrant rapid signalling

conduction pathways approx 100-200cm/s

Question 4

major cardiac ion channels/currents

attach image

Answer 4

inward depolarizing currents

• I_Na: fast Na current
• I_Ca,L: Ca current
• I_Na/Ca: Ca out, Na in (NCX)

outward repolarizing currents

• K currents

Question 5

refractory period

Answer 5

absolute: no AP can be triggered

relative: fewer Na channels available, so only small AP can be triggered

supranormal: back to normal, regular AP can be triggered

Question 6

types of cardiac arrhythmias

Answer 6

1. bradycardias (< 60bpm)
2. tachycardias (> 150bpm)

• supraventricular (originate in atria or AV node → have narrow complexes)
• ventricular (originate in ventricles → have wide complexes)

Question 7

mechanisms of arrhythmias

just look at pic

Answer 7

can be FOCAL (arising from one area of heart) or REENTRANT (travelling/circulating around heart)

1. abnormal impulse generation

• incr automaticity of SA node
• enhanced automaticity of latent pacemakers
• abnormal automaticity
• triggered automaticity
  
  • early afterdepolarizations
  • delayed afterdepolarizations
• decr automaticity of SA node (brady)

2. abnormal impulse conduction

• decremental conduction and block (brady)
• reentry

Question 8

normal mechanism of automaticity

AV node

Answer 8

-60mV at RMP (-90 in myocardiocytes)

• slow depol via funny current
  
  • HCN channels: hyperpol-activated cyclic nucleotide-gated channels: slow inward Na current
  • rapid depol via Ca current
• repol via K current

Question 9

autonomic modulation of SA node

Answer 9

HCN channels have SNS, PSNS receptors

• adrenergic (beta1) → incr cAMP → incr activity
• muscarinic → decr cAMP → decr activity

Question 10

overdrive suppression

Answer 10

hyperpolarizing net current: Na/K pump → 3 Na out, 2 K in

depolarizing durrent: If (funny current)

• non-SA node cells receive their trigger for depol from SA node
• increased Na influx → greater expression of Na/K ATPases that hyperpolarize, prevent depolarization at intrinsic rate (unless conduction block knocks out the pacemaker signal)

Question 11

hierarchy of pacemakers

Answer 11

sinus node (SA node) : 60-100bpm

>

AV jx (AV node) : 40-60bpm

>

ventricular (myocytes) : 20-40bpm

Question 12

arrhythmias due to normal automaticity

Answer 12

alteration in normal automaticity

• sinus tachycardia or bradycardia

escape rhythms

• junctional/ventricular escape complexes
• escape rhythms

Question 13

abnormal impulse generation

Answer 13

enhanced automaticity of latent pacemakers

• jxal premature complexes
• jxal tachycardia
  
  • catecholamines
  • myocardial infarction
  • digitalis toxicity
• abnormal automaticity (cells that generate automaticity, evidenced by acquisition of slow depol potential)
  
  • ventricular premature complexes
  • ventricular tachycardia
  • atrial premature complexes
  • atrial tachycardia
• triggered activity
  
  • early afterdepolarizations: depols that occur prior to full repolarization, poss due to long AP duration and influx of Ca during plateau phase
    
    • ex. Torsades de Pointes ventricular tachycardia
  • delayed afterdepolarization
    
    • digitalis induced tachycardias
    • catecholaminergic polymorphic ventricular tachycardia
    • RV outflow tract tachycardias
    • repetitive monomorphic VT

Question 14

summary: automaticity

Answer 14

Question 15

abnormal impulse conduction

decremental conduction and block

Answer 15

• fibrosis (Lev-Lenegre Syndrome) → affects SA/AV nodes
• MI → scar tissue with slow conduction
• hyperkalemia

electrophysiologic mechanisms:

• Na channel inactivation
• gap jx abnormalities
• prolonged refractoriness

Question 16

gap jx, connexons, connexins

Answer 16

gap jx exist at intercalated discs

• ion channels between adj cells comprised of 2 connexons apiece (one on either side of the jx)
• each connexon composed of 6 connexins w 4 transmembrane domains

Question 17

reentry

Answer 17

combination of unidirectional block and slow conduction

• unidirectional block: prevents progression of signal that would normally be conducted through soon-to-be-reentrant-circuit tissue
• slow conduction: allows the refractory period of the signal that WAS conducted (before being blocked) to expire, such that reentrant signal can proceed through the circuit

circle videos at approx 1:07

Question 18

arrhythmias due to reentry

Answer 18

• monomorphic ventricular tachycardia after MI
• atrio-ventricular reentrant tachycardia
• AV nodal reentrant tachycardia
• atrial flutter
• atrial tachycardias post-op for congenital heart disease

Question 19

summary: reentry

Answer 19

Question 20

ventricular pre-excitation

Answer 20

aka “WPW” (Wolff Parkinson White Syndrome)

• short PR interval
• delta wave
• blurred upstroke
• wide QRS