cardio: arrhythmias Flashcards

1
Q

antiarrythmic drugs: class 1a

A

sodium channel blockers - moderate:
procainamide, quinidine, disopyramide

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2
Q

antiarrythmic drugs: class 1b

A

sodium channel blockers - weak:
lidocaine, mexiletine

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3
Q

antiarrythmic drugs: class 1c

A

sodium channel blockers - strong:
flecainide, propafenone

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4
Q

antiarrythmic drugs: class 2

A

beta blockers, block sympathetic autonomic effects:
metoprolol

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5
Q

antiarrythmic drugs: class 3

A

potassium channel blockers, prolong effective refractory period:
amiodarone, sotalol

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6
Q

antiarrythmic drugs: class 4

A

ccb:
verapamil, diltiazem

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7
Q

antiarrythmic drugs: class 5

A

other MOA:
digoxin, adenosine, magnesium

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8
Q

normal cardiac rhythm

A

originates in SA node (frequency: 60-100bpm) -> spreads through the atria and enters the AV node -> AV conduction is low (~0.15s) -> impulse propagates through His-Purkinje system -> ventricular activation complete in <0.1s

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9
Q

arrhythmia

A

any cardiac depolarisation that deviates from normal rhythm
- abnormality in: site of origin of impulse, rate, regularity, conduction

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10
Q

likely triggers of arrhythmia

A

ischaemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, excessive catecholamine, autonomic influence, toxicity eg. digitalis, cardiac fibre overstretch, scarred/disease tissue

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11
Q

all arrhythmias result from disturbance in:

A

impulse formation/conduction, or both

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12
Q

amiodarone primarily class3, but shares

A

class 1,2,4 properties and additional actions

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13
Q

sotalol primarily class 3, but also

A

class 2

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14
Q

aim of antiarrhythmics pharmacology

A
  • reduce ectopic pacemaker activity
  • modify conduction/refractoriness in re-entry circuits to disable circus activity
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15
Q

MOA of sodium channel blockers

A
  • local anesthesia action blocking sodium channels
  • reduce sodium current, slows upstroke of action potential, hence slows conduction
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16
Q

flecainide moa

A

(class 1c) blocks sodium and potassium channels, no anti-muscarinic effects

17
Q

flecanide use

A

pt w normal hearts with supraventricular arrhythmias
X aflutter, ihd, structural heart disease, hfref, liver disease, crcl<35

18
Q

flecainide toxicity

A

may cause severe exacerbation of arrhythmia in patients with pre-existing ventricular tachyarrythmias or previous MI

19
Q

disopyramide MOA

A

(class 1a)
- blocks sodium channels, slow upstroke of action potential
- nonspecifically blocks potassium channels, prolongs action potential

-> slows conduction
-> directly depresses sa and sv node

extracardiac effects:
- ganglion blocking activities, hence reduce peripheral vascular resistance -> produce hypoTN esp w iv use

20
Q

amiodarone MOA

A

(class 3) prolongs action potentials
- usually by blocking K channels or
- sometimes by enhancing inward current eg. thru sodium channels (block sodium channels)
- also weak adrenergic and ccb

-> prolongs action potential duration
-> slow hr and av node conduction

extracardiac effects: produce peripheral vasodilation

21
Q

dronedarone is a ____ of amiodarone

A

structural analogue, lacks iodine atoms
- less toxic but less effective alternative
- no thyroid and pulmonary toxicity

22
Q

amiodarone use

A

treatment of serious ventricular arrhythmias, effective for supraventricular arrhythmias eg. AF

23
Q

amiodarone toxicity

A
  • bradycardia
  • heart block in pt w existing SA/AV node disease
  • fatal pulmonary fibrosis in 1% of pt
  • hepatitis
  • tissue accumulation: blue-grey skin discoloration, corneal microdeposits
  • hypo/hyperthyroidism (source of inorganic iodine)
24
Q

digoxin MOA

A
  • positive inotropic effects: blocks Na-K ATPase, incr intracellular myocytes Na and hence Ca influx
  • negative chronotropic effects: decreases conduction of electrical impulses through the av node inhibition and increases vagal activity
25
Q

adenosine MOA

A

used iv for terminating SVT
- acts on adenosin receptors (GPCRs) -> influence potassium channels -> ca channels -> inhibit avail of ca in cells -> decr hyperexcitability and propagation of signals involved in AF

26
Q

magnesium sulphate/trimagnesium dicitrate (anhydrous) used for

A

specific arrhythmias eg. torsades de pointes and digoxin-induced

27
Q

moa of magnesium

A

exact unclear: Mg competes with Ca in terms of uptake and distribution of Ca within cells

28
Q

arrhythmias, hr<60

A

Bradycardia: heart block, simple bradycardia
- atropine, adrenaline, dopamine

29
Q

Arrhythmias, hr>100, QRS<120ms

A

Narrow complex (info propogated through AV node into purkinje complex = supraventricular issue):
- AF/flutter: class 3, 1c - or rate control by nodal blocking agents eg. Class 2/4
- Other SVTs: class 2/4
- Sinus tachycardia (MI or anxiety): class 2

30
Q

Arrythmias, hr>100, qrs>120ms

A

Broad complex:
- VF: after 3x defibrillation attempts - vasopressin, adrenaline, amiodarone
- VT: amiodarone, class 1b

31
Q

Supraventricular preexcitation tachycardias of the Wolff-Parkinson-White syndrome

A

AV node inhibitors (class 2/4) or by catheter ablation of the bypass tract

32
Q

Arrhythmias of congestive heart failure

A

Class 2: carvediolol
Class 5: digoxin

33
Q

Sustained ventricular tachycardia especially with infarcted or ischemic zone

A

Cardioversion if persistent or amiodarone

34
Q

Drugs that can cause prolonged QT interval

A

Antiarrythmics: disopyramide, procainamide, quinidine, amiodarone, sotalol
Anaesthetics: halothane
Antibiotics: macrolides, metronidazole with alcohol, moxifloxacin
Antifungals: ketoconazole, fluconazole
Antivirals: nelfinavir
Antimalarials: chloroquine, mefloquine
Antipsychotics
Antihistamines: terfenadine, astemizole
Antidepressants: amitriptyline

35
Q
A