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Cardio > Antiarryhthmics Dr. Roane > Flashcards

Antiarryhthmics Dr. Roane Flashcards

Dr. Roane EXAM IV

1
Q

What determines the duration of cardiac action potentials?

A

opening of ion channels: (Na, Cl, K)
-> followed by depolarization

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2
Q

Terms describing a fast heart rate

A

-Tachycardia
-Flutter
-Fibrillation

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3
Q

Which of the ions have high intracellular and extracellular concentrations?

A

-high extracellular concentration: Na+ and Cl-

-high intracellular concentration: K+

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4
Q

MOA of Lidocaine (Lidoderm)

A

Sodium channel blocker -> prevents action potential from occurring

-used for local and topic anesthesia by preventing nerve conduction
-also antiarrhythmic

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5
Q

Which channel causes the rapid depolarization phase?

A

voltage-gated sodium channels

depolarization: the potential becomes positive

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6
Q

What causes the prolonged plateau of depolarization?

A

slow and prolonged opening of voltage-gated (L-type) Ca2+-channels
+
closing of K+ channels

-> so the potential stays positive

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7
Q

What causes the repolarization phase?

A

Opening of the K+ channels
-> K+ moves out -> potential becomes negative again

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8
Q

Which phase of the action potential does the P-wave refer to?

A

depolarization in the atrium

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9
Q

Which phase of the action potential does the QRS complex refer to?

A

depolarization of ventricles, bc in the ventricles the greatest mass (number of cells is polarized (number of cells)

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10
Q

Which phase of the action potential does the T-wave refer to?

A

repolarization of Purkinje fibers

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11
Q

What initiates the action potential of the pacemaker?

A

Funny Na+ channels [1]
-the more Na+ channels are open the steeper the slope

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12
Q

What causes the Ca+ channels [2] to open?

A

The Ca+ channel opens once the threshold is reached
-once the potential reaches the threshold
-the potential is becoming positive due to the Na+ channel [1] opening

order:
F (Na+)
Transient (Ca2+)
Long-lasting (Ca2+)
K+

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13
Q

How do cardiac cells electrically affect adjacent cells?

A

-through Connexin channels (pores)
-mechanically through Desmosomes

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14
Q

What causes arrhythmias of the heart to occur?

A

malfunction of any (or two or three) of the 13 ion channels (Na+, Cl-, K+) -> ions will not flow as they should and when they should

most common due to:
-tissue damage due to ischemia
-pathological remodeling
-Covid-19
-diabetes
-hypertension
-stress/anxiety

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15
Q

Categories of arrhythmias
Tachycardia

A

Tachycardia
-Atrial fibrillation (Afib): chaotic -> associ. with future stroke
-Atrial flutter: more organized than Afib
-Ventricular fibrillation (Vfib): chaotic ventricles
-Ventricular tachycardia: too fast
-Supraventricular tachycardia: starts above the ventricles

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16
Q

Categories of arrhythmias
Bradycardia

A

-Sick sinus syndrome: damage around the SA node

-Conduction block at the AV node: the conduction of the depolarization slows down in the AV node (bottleneck), it can be blocked in the AV node - AV block

not Bradycardia:
-premature heartbeat: heart beats too soon before it gets filled up, an extra beat -> palpitation

17
Q

What does the term functional syncytium mean?

A

it refers to cells (also muscle cells) being connected to adjacent cells through connexins

18
Q

Automaticity in cells

A

if the SA node doesn’t work, some cells can spontaneously depolarize and take the function of the SA node

19
Q

What is an ectopic cell?

A

cells with the ability to act as the SA node (pacemaker), when they should not

-impulse-conducting tissues are prone to that, especially when K+ levels are low (hypokalemia)
-damage to ventricular cells can induce automaticity

20
Q

What induces the automaticity of cells in the heart?

A

l-ow K+ levels
-damage to ventricular cells

21
Q

QTc prolongation

A

QTc prolongation = triggered event due to altered potassium levels

-DAD = delayed afterdepolarization
-EAD = early afterdepolarization

22
Q

What causes DAD and EAD?

A

DAD: rapid ventricular beats, and high Ca2+

EAD: high influx of Ca2+ or Na+ or failure to get K+ out

-so too many positive ions

23
Q

Conduction abnormalities

A

-Heart block (AV block): impulse doesn’t travel through the AV node as quickly as normal

-Re-entry phenomena: the signal from the SA node travles to the AV node and moves through the outer lining of the heart back to the AV node

24
Q

atrioventricular re-entry tachycardia

A

patients with slow (fast refraction) and fast (slow refraction) pathways of conduction
refraction = time where no impulse is possible

the fast pathway goes down and excites cells of the bundle of his but also cells of the slow pathway -> the fast impulse cancels out the slow impulse

-the next impulse will travel along the slow path first bc the refraction is shorter -> it will excite cells of the bundle of his and also cells of the fast pathway retrograde up to the atrium, but also re-enters the slow pathway again -> continuous circuit, causing simultaneous ventricular and atrial contraction

25
Q

How is the re-entry phenomenon treated?

A

Blocking K+ receptors -> Repolarization phase is delayed (comes down later) -> thereby extending the effective refractory period ERP (it takes longer for the short pathway to start?)

26
Q

Goal of pharmacotherapy

A

-reduce ectopic pacemaker activity

-modify conduction or refractoriness in reentry circuits to disable circus movement

mechanism:
1. sodium channel blockade
2. calcium channel blockade
3. blockade of sympathetic autonomic effects in the heart
4. prolongation of the effective refractory period

27
Q

Class 1A drugs MOA

A

-Block Na+ channels: decreases the slope of Phase 0 which slows impulse propagation

-Block some K+ channels: increases the duration of the action potentials

Quinidine
Procainamide
Disopyramide

28
Q

Class 1B drugs MOA

A

-Block Na+ channels and effectively raise the
depolarization threshold. Treat ventricular
arrhythmias

Lidocaine
Mexiletine
Phenytoin

29
Q

Class 1C drugs MOA

A

-Flecainide
Blocks Na+ channels and some K+ channels and blocks Ca++ release from the smooth endoplasmic reticulum

-Propafenone
Block Na+ channels
Blocks b-receptors
Slows impulse conduction and raises depolarization
threshold

30
Q

What do all Class 1 antiarrhythmic drugs have in common, and practical benefits?

A

-all block Na+ channels

-in practice, the drugs’ efficacy increases as the
frequency of depolarizations increases

31
Q

Class 2 drugs MOA

A

-Beta-blocker (preventing adrenaline, noradrenaline from increase heart rate and force of contraction)
-Blocking b receptors: slows heart rate, slows conduction velocity

Propranolol
Metoprolol
Esmolol (Breviblock) - half-life of minutes, emergency drug IV
Sotalol (this is a class 3 drug) - blocks K channel

32
Q

Class 3 drugs MOA

A

-Block Na+ channels and K+ channels (mostly): this prolongs action potential duration APD

Amiodarone: effective but toxic, analog of thyroid hormone that blocks the conversion of T4 to T3

Dronedarone: safer but less effective

Dofetilide (mostly K-channel activity)

Ibutilide MOA is similar to dofetilide (mostly K-channel activity)

Sotalol (mostly K+ channel)

33
Q

Class 4 drugs

A

Calcium channel blocker
Non dihydropyridines NDH

Verapamil
Diltiazem

34
Q

Other antiarrhythmics

A

-Ivabradine
-Digoxin
-Magnesium sulfate
-autonomic drugs: atropine, isoproterenol

35
Q

Which drug blocks funny Na+ channels?

A

Ivabradine

36
Q

What promotes toxicity in Digoxin therapy?

A

-low bioavailability of digoxin due to microbes in the intestine -> antimicrobes may kill microbes -> higher plasma levels -> TOXIC

Digoxin: use in re-entry conditions

37
Q

Which drug can reverse “Torsade de pointes”?

A

Magnesium sulfate

-blocks Ca++ channels
-Torsade de pointes: ventricular tachycardia caused by prolonged QT

38
Q

Adverse effects of Amiodarone

A

-Extremely lipophilic with a t1/2 of weeks to months
-Can cause fatal pulmonary fibrosis
-Hypothyroidism
-Many others

Cardio (27 decks)

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