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Flashcards in L17- Arrhythmia Deck (34)
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How are propagation blocks created?

Decreased resting membrane potential/depolarization 


OR infarct


How does ischemia lead to depolarization?

Ischemia leads to increased extracellular [K] which depolarizes the cell because 1) Phosphate and lactate that normally accumulate in the cell leave and K follows, and 2) ATP depletion activates I-kATP which is protective short term but depletes intracellular K long term 


Change in Ek is primary determinant of Vm 


How does depolarization lead to propagation block?

Na channel inactivation and so slowing the rate of rise and the amplitude of Na current --> Total amount of Na current reduced and get slowed propagation [*significant in reentry] 


When AP propagates slowly, more likely to get block  


How do the PKJ prevent backward propagation?

Longer duration of distal PKJ inmpulse than with ventricular fiber impulse and so the PKJ are refractory for longer 


What are the 3 conditions necessary for reentrant propagation?

1) 2 parallel conduction pathways that are anatomically or physiologically distinct

2) unidirectional block

3) slowed or delayed conduction - required for refractoriness to disappear and enable effective reentry


Antidromic vs orthodromic 

Antidromic - V to A 


Orthodromic - A to V 


Where are the extra beats coming from?

Atrial premature beats 


What are the general categories of anti-arrhythmic drugs that I need to know?

Na channel blockers = Quinidine, Procainamide, Lidocaine, Flecainde, Propafenone

Beta-Blockers = Metoprolol, Atenolol, Esmolol

K-Channel Blockers = Amiodarone, Sotalol, Ibutilide or Dofetilide 

Ca-Channel Blockers = Verapamil and Diltiazem






What are the general actions and characteristics of Class 1 Anti-arrhythmics?

Fast Na channel blockers - decrease Na current and rate of rise of Phase 0 in AP 

Reduce excitability of non-nodal tissues where inward Na current in important - working fibers of the heart 




What are the Class 1a drugs? What is their mechanism/effect? How are they used?

Class 1a drugs = Quinidine and Procainamide

Lower Na current and rate of AP

INCREASE AP DURATION - block K channels and prlong ventricular effective refractory period


Not really used except Procainamide is used acutely 


1A = Broaden AP 


What are the Class 1b drugs? What is their mechanism/effect? How are they used?

Class 1b = Lidocaine

lower Na current and rate of rise of AP modestly

DECREASE AP DURATION!!! no effect on conduction velocity


Administered IV for acute treatment ofventricular arrhythmias 

1B = narrows AP 


What are the Class 1c drugs? What is their mechanism/effect? How are they used?

Class Ic drugs = Flecainide and Propafenone 

Lower na current and the rate of rise of AP strongly


1C = no change in AP 


What are the Class 2 drugs? What is their mechanism/effect? How are they used?

Class 2= Beta Blockers

Propanolol = non-specific beta blocker avoided now for use 

Beta-1 Antagonists = Metoprolol, Esmolol, ATenolol

Non-selective Beta and A1 blocker = Carvedilol

Non-selective Beta and A blocker = Labetalol 


Reduce excitability and decrease conduction velocity in the AV node



What are the Class 3 drugs? What is their mechanism/effect? How are they used?

Class 3 = K+ Channel Blockers

Amiodarone, Dronedarone, Sotalol* 

Ibutilide* (IV) and Dofetilide* (oral) - *tend to produce Long QT and Torsade

Prolong duration of AP without altering rate of rise of AP or resting membrane potential - Increase refractory period 



What are the Class 4 drugs? What is their mechanism/effect? How are they used?

Class 4 Drugs = Ca Channel Blockers

Verapamil and Diltiazem

Block L type Ca channels and so block slow, non-inactivating Ca crrent 

SLOW AP INITIATION, conduction and increase refractoriness  in SA and AV node


Multiple targets of Quinidine

Blocks Na channels

Moderately blocks K channels

Low block on M2 and A/B adrenergic


Multiple targets of Amiodarone

Moderate block K channel

Low Na channel block

Low Ca channel block

Moderate A/B adrenergic block

*rarely causes Torsade


What is a prolbem with Potassium channel blockers?

Reverse Use Dependence:

K channel blockers, like Sotalol, bing in a resting, closed state and can promote long QT and Torsade with slow HR 

Risk with use during bradycardia 


Multiple targets of Sotalol 

Blocks K channels and blocks Beta-adrenergic 


Multiple targets of Digoxin

Na-K Exchange pump inhibitor

Muscarininc M2 agonist to activate vagal input 


Metabolism and side efects of 1a drugs

Liver metabolism to NAPA metabolite which is also a K channel blocker

High incidence of Torsade with thse drugs


Also can cause Nausea and Diarrhea


Metabolism and Side Effects of Amiodarone

High Iodine content 

Long half life as it partitions into liver and fat so delayed onset 



Can cause Pulmonary Fibrosis, Hypo or Hyperthyroidism bc Iodine, Liver toxicity, neuropathy, skin discoloration to blue, photo-sensitivity, corneal deposits and optic neuritis 


MEtabolism and Side effects of Dronedarone

Amiodarone derivatie that is NOT iodinated 

Acts more quickly (within hours) and shorter half life

Hepatic metabolism and elminated in feces

Less side effects but also not as effective

Used for Atrial Fibrillation


Metabolism and side effects of Digoxin

Small therapeutic index so plasma lvels must be monitored

Kidney ecretion - Toxic levels can cause kidney damage!!!

Long half life

Acts to shorten refractory periods BUT can enhance excitability in some fibers so DO NOT GIVE TO SOMEONE WITH ACCESSORY PATHWAY!


What are the anti-arrhythmics that cross the BBB and what are their CNS side effects?

Lisa's Poop causes Mental Death = L, P, M, D

Lidocaine - congition changes and seizures

Propaniolol - nightmares and sedation

Metorprolol - anti-anxiety

Digoxin - cognitive and vision effects 


Atrial Flutter - Mechansm, Clinical Presentation

Atrial Flutter = rates of 250-350 bom 

Mechanism = can be triggered by atrial Premature beats; Reentry loop within the RA, high rates of firing blocked at AV node bc refractory so ventricles beat regularly for every 204 atrial beats

Clinical = Can be transient or persistent, asymptomatic or like palpitations

(Can deteriorate into AFIB)

Risk of thrombi from pooling in Atrial appendages and can lead to stroke - anti-coagulate 



Atrial Flutter - Treatment and drugs

Anti-coagulate!! for >3 weeks bc greatest risk is thrombi formation!!

First - Ventricular Rate Control with Beta blockers or Ca channel blockers to reduce AV node excitability 

Second - Convert back to Sinus rhythm with Class 3 drugs (like IV ibultilde, Amiodarone etc)  or electrical cardioversion 

- Class 3 for effective for atrial flutter bc block K current and increase AP duraion and refractory period to help maintain sinus rhythm

- Class 1c drugs like Flecainide or Propafenone lower Na current and increase Relative Refractory Period may slow propagation and improve AV following 1:1


Atrial Fibrillation - Mechanism, Clinical Presentation

AFib = 350-600 discharges/min (ventricular 100-120)

***Irregularly Irregular*** ventricular beating where high frequency atrial impilses encounter refractory AV node and irregular pattern of propagation 

one or more ectopic pacemaker sites initiating erratic pattern usually from pulmonary veins region and SA node no longer initiating impulse

RISK of blood stasis (esp in LA appendage!) leading to Stroke or PE

Rapid ventricular rate reduces CO for Hypotension and pulmonary congetsion (mre severe in people with LV hypertrophy) 



Atrial Fibrillation - treatment 


Control Ventricular rate - with Beta blockers or Ca channel blockers to reduce AV node propagation 

If no heart disease but still symptomatic after ventricular rate control  - Class Ic = flecainide [or can try class 3 Amiodarone but less reliable due to multiple reentr loops] 

*IF asymptomatic, pts do not need long term treatment so long as ventricular rate is controled!!


AVNRT - mechanism and what's happening

AV node has 2 functionally distinct conduction pathways and 1 is slower than the other

Atrial Premature Beta goes down slow while the fast is refractory from normal beat and then by the time it reaches bottom of the loop can go up fast which has recovered