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Autonomic Drugs N Stuff > L17- Arrhythmia > Flashcards

L17- Arrhythmia Flashcards

1
Q

How are propagation blocks created?

A

Decreased resting membrane potential/depolarization

OR infarct

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2
Q

How does ischemia lead to depolarization?

A

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

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3
Q

How does depolarization lead to propagation block?

A

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

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4
Q

How do the PKJ prevent backward propagation?

A

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

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5
Q

What are the 3 conditions necessary for reentrant propagation?

A

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

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6
Q

Antidromic vs orthodromic

A

Antidromic - V to A

Orthodromic - A to V

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7
Q

Where are the extra beats coming from?

A

Atrial premature beats

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8
Q

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

A

**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 **

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9
Q

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

A

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

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10
Q

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

A

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

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11
Q

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

A

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

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12
Q

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

A

**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

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13
Q

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

A

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

T**ARGET THE AV NODE **

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14
Q

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

A

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

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15
Q

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

A

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

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16
Q

Multiple targets of Quinidine

A

Blocks Na channels

Moderately blocks K channels

Low block on M2 and A/B adrenergic

17
Q

Multiple targets of Amiodarone

A

Moderate block K channel

Low Na channel block

Low Ca channel block

Moderate A/B adrenergic block

*rarely causes Torsade

18
Q

What is a prolbem with Potassium channel blockers?

A

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
Q

Multiple targets of Sotalol

A

Blocks K channels and blocks Beta-adrenergic

20
Q

Multiple targets of Digoxin

A

Na-K Exchange pump inhibitor

Muscarininc M2 agonist to activate vagal input

21
Q

Metabolism and side efects of 1a drugs

A

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
Q

Metabolism and Side Effects of Amiodarone

A

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
Q

MEtabolism and Side effects of Dronedarone

A

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
Q

Metabolism and side effects of Digoxin

A

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
Q

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

A

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
Q

Atrial Flutter - Mechansm, Clinical Presentation

A

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
Q

Atrial Flutter - Treatment and drugs

A

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
Q

Atrial Fibrillation - Mechanism, Clinical Presentation

A

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
Q

Atrial Fibrillation - treatment

A

**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
Q

AVNRT - mechanism and what’s happening

A

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

31
Q

Treatment for AVNRT

A

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
Q

AVRT - mechanism and what’s happening

A

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
Q

Treatment for AVRT

A

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
Q

WHAT SHOULD BE AVOIDED IN PEOPLE WITH BYPASS TRACT??

A

**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!!

Autonomic Drugs N Stuff (19 decks)

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