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1ST YEAR SYSTEMS: Cardiovascular > Arrhythmias:- treatment > Flashcards

Arrhythmias:- treatment Flashcards

1
Q

supraventricular arrhythmias?

A

AF

SVT (junctional)

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2
Q

ventricular arrhythmias?

A

Ventricular tachycardia

Ventricular fibrillation

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3
Q

what causes the fast depolarising phase of the cardiac action potential?

A

Influx of Na+

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4
Q

describe cardiac action potential

A

Leak of Cations into the cardiac cell (and release from intracellular stores)
leads to drift up of the potential.

Once threshold is hit (-40 mV) the voltage gated sodium channels open and the cell rapidly depolarises.

The movement of ions across the cardiac cell’s membrane results in the propagation of an electrical impulse.

This electrical impulse leads to contraction of the myocardial muscle.

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5
Q

what is sinus arrest?

A

medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat.

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6
Q

Vaughan-Williams classification antiarrhythmic drugs - class IA

A

moderate Sodium channel blockade

reduce amplitude of AP and conduction velocity

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7
Q

Vaughan-Williams classification antiarrhythmics - class IB

A

weak Na+ channel blockade ie they have a weak effect on the initiation of depolarization

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8
Q

Vaughan-Williams classification antiarrhythmics - class IC

A

strong affect on the initiation of depolarisation but slow Na+ channel blockade

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9
Q

Vaughan-Williams classification antiarrhythmics - class II

A

Beta blockers

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10
Q

Vaughan-Williams classification antiarrhythmics - class III

A

prolong refractoriness (recovery) so slow K+ flow out of cells

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11
Q

Vaughan-Williams classification antiarrhythmics - class IV

A

calcium channel blockade

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12
Q

Vaughan-Williams classification antiarrhythmics - class V drug

A

digoxin

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13
Q

VW class IA drug names (3)

A

Quinidine
procainamide
dispyramide

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14
Q

VW class IB drug names (3)

A

Lidocaine
mexiletine
tocainide

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15
Q

VW class IC drug names (2)

A

Flecainide - more commonly used

propafenone

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16
Q

Class II VW drug names (2) and action

A

atenolol
bisoprolol - first line for AF

acts via beta 1 receptors to block sympathetic stimulation of the heart
slows SA and AV conduction and reduces excitability in non nodal cardiac tissue

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17
Q

class 3 VW drug names (3) and action

A

amiodarone
bretylium
sotalol

increase AP, prolong repolarisation in phase 3. Prolongs ERP

used for dysrhythmias that are difficult to treat. Sustained ventricular tachycardia or fibrillation etc

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18
Q

class IV drug names (2) and action

A

diltiazem
verapamil

Ca2+ channel blockers- bind to Lcard -type voltage gated Ca channels
Depress phase 4 depolarisation in SA and AV nodes
Slow the heart rate - decrease automaticity and slows AV conduction

Shorten phase 2 Plateau phase (reduce contractility)

Show use dependence (ie. More effective at higher HR)

Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

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19
Q

When are class I drugs more effective?

A

at higher heart rates

20
Q

Class I drugs are divided into IA, IB and IC. Which is the weaker, moderate or strong drug?

A

IA - moderate - increases effective refractory period
IB - weak decreases effective refractory period
IC - strong - effective refractory period remains the same

ERP = time that cell cannot respond to a new stimuli

21
Q

Phases of action potential

A

phase 0 - Na+ enters the cell. Depolarisation occurs

phase 2 - Ca2+ enters the cell, initiation of conraction

phase 3 - K+ exits the cell. Repolarisation

22
Q

Amiodarone - class 3:-

  • use?
  • interacts with which other drug?
  • side effects?
A

used for VT and occasionally in supraventricular tachycardia

interacts with digoxin

side effects:- 
thyroid (hypo or hyperthryoidism) pulmonary fibrosis
slate - grey pigmentation
corneal deposits
Liver function test abnormalities
23
Q

Digoxin:-
half life
age group used for
toxicity

A

half life = 36-48 hours, increased in renal impairment
(50-70% of digoxin is excreted almost entirely unchanged by the kidneys - excretion proportional to GFR)

commonly used in the elderly

monitor potassium levels, conc of digoxin in plasma and for toxicity

24
Q

digoxin toxicity (5)

A

Nausea and vomiting

Xanthopsia - predominance of yellow in vision due to a yellowing of the optical media of the eye

Bradycardia
Tachycardia
Arrhythmias: VT and VF

sign:- reverse tick on ECG - ST segment

25
Q

treatment if patient has digoxin toxicity

A

stop digoxin (long half life though)

if levels very high and risk of significant arrhythmia - give digibind

digoxin toxicity is more serious if potassium levels are low

26
Q

what is digibind?

A

drug that binds with digoxin, forming complex molecules

excreted in urine

27
Q

Adenosine

A

Slows/ Blocks conduction through the AV node

Used to convert paroxysmal supraventricular tachycardia to sinus rhythm

Very short half-life

Only administered as fast IV push

May cause asystole for a few seconds
Other side effects minimal - cardiac arrest rhythm - it is a flatline EKG

28
Q

affect of adenosine on SVT:- ECG

A

irregular, wide complex tachycardia with QRS complexes that are similar but with varying morphologies

29
Q

indications for anticoagulation AF

A

AF high prevalence in elderly

risk of stroke, peripheral emboli

30
Q

CVS indications for anticoagulation

A

metallic heart valves

DVT/PE

31
Q

what is the ‘ideal’ anticoagulant

A 
oral
no need for monitoring
no interaction with food or drugs
once or twice a day/ fixed dose 
as effective as warfarin
safer than warfarin
32
Q

oral anticoagulant examples

A

warfarin
dabigatran
rivaroxaban
apixaban

33
Q

How does warfarin work against vitamin K?

A

Vitamin K normally helps your blood clot so wounds don’t bleed too much.

Warfarin works against vitamin K, making your blood clot more slowly.

it inhibits vitamin K epoxide reductase which causes a reduction in vitamin K and inhibits production of active clotting factors

34
Q

monitoring warfarin therapy INR

A

actual prothrombin time over standard prothrombin time

time taken for blood to clot
therapeutic INR 2.5-4.0 warfarin therapy

35
Q

normal INR value

A

1

36
Q

adverse effects of warfarin in pregnancy

A

Teratogenic (chondrodysplasia - malformation of cartilage)

(Retroplacental bleeding and fetal intracerebral bleeding).

Avoid in first and third trimesters

37
Q

how do aspirin and sulfonamides increase warfarin activity

A

decrease binding to albumin

38
Q

how do cimetidine and erythromycin increase warfarin activity

A

inhibit degradation of it

39
Q

how do oral antibiotics increase warfarin activity

A

decrease synthesis of clotting factors

40
Q

which enzyme pathway breaks down warfarin

A

cytochrome P450

41
Q

drugs that decrease warfarin activity

A

barbiturates, phenytoin

Induction of metabolizing Barbiturates
Enzymes (cytochrome
P450)

Vitamin K, cholestyramine
Promote clotting factor
synthesis
Reduced absorption

42
Q

other drugs that warfarin interacts with

A

macrolide antibiotics, antifungals, anti-epileptics

43
Q

inhibitors of the cytochrome p450

A 
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin and Cimetidine
Ethanol (acutely)
Sulphonamides
44
Q

Inducers of the cytochrome p450

A 
Alcohol (chronic use)
Barbiturates
Carbamazepine
Phenytoin
Rifampicin
Sulphonylureas
45
Q

DOACs vs NOACs

A

new oral anticoagulants, or sometimes called non-vitamin K antagonist

DOACs are direct because they block a single blood clotting factor to treat or prevent blood clots

1ST YEAR SYSTEMS: Cardiovascular (39 decks)

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