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Flashcards in L17- Arrhythmia Deck (34):
1

How are propagation blocks created?

Decreased resting membrane potential/depolarization 

 

OR infarct

2

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 

3

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  

4

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 

5

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

6

Antidromic vs orthodromic 

Antidromic - V to A 

 

Orthodromic - A to V 

7

Where are the extra beats coming from?

Atrial premature beats 

8

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

Adenosine

Digoxin 

 

 

9

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 

 

 

10

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 

11

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 

12

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

NO CHANGE TO AP DURATION

1C = no change in AP 

13

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

TARGET THE AV NODE 

14

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 

 

15

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

16

Multiple targets of Quinidine

Blocks Na channels

Moderately blocks K channels

Low block on M2 and A/B adrenergic

17

Multiple targets of Amiodarone

Moderate block K channel

Low Na channel block

Low Ca channel block

Moderate A/B adrenergic block

*rarely causes Torsade

18

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 

19

Multiple targets of Sotalol 

Blocks K channels and blocks Beta-adrenergic 

20

Multiple targets of Digoxin

Na-K Exchange pump inhibitor

Muscarininc M2 agonist to activate vagal input 

21

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

22

Metabolism and Side Effects of Amiodarone

High Iodine content 

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

NO RENAL EXCRETION!

 

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

23

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

24

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!

25

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 

26

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 

 

27

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

28

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) 

 

29

Atrial Fibrillation - treatment 

Anti-coaggulate!!! 

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!!

30

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 

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31

Treatment for AVNRT

Vagal Maneuvers - carotid sinus massage or valsalva to interrupt reentry by slowing AV node conduciton

Adenosine IV - reboots heart completely for a second through Ik-adenosine (most effective)

Verapamil - slows conduction and block reentry

 

Long-term wth Beta-Blockers, Ca channel blockers, or Ablation of reentrant limb 

32

AVRT - mechanism and what's happening 

WPW - propagation down a bypass tract from atria to ventricle 

Triggered by atrial premature beat and accessory pathway which has faster conduction velocity than AV node 

 

Atrio-Ventricular Reciprocating Tachycardia 

33

Treatment for AVRT

Same as for AVNRT

Vagal manuevers to slow AV propagation, Adenosine (nost effective) and Ablattion of the Bypass tract 

 

DO NOT GIVE CCG OR DIGOXIN WITH ACCESSORY PATHWAY!!! 

34

WHAT SHOULD BE AVOIDED IN PEOPLE WITH BYPASS TRACT??

Digoxin or Ca channel blockers (Diltiazem or Verapamil) 

 

Shortened impulse in accessory pathwya reduces refractoriness and can lead to A-fib and can precipitate V-Fib

Avoid anything that will shorten impulses when you have a bypass tract!!