Arrhythmias:- treatment Flashcards by Anna Coull

supraventricular arrhythmias?

SVT (junctional)

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ventricular arrhythmias?

Ventricular tachycardia

Ventricular fibrillation

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

Influx of Na+

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describe cardiac action potential

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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what is sinus arrest?

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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Vaughan-Williams classification antiarrhythmic drugs - class IA

moderate Sodium channel blockade

reduce amplitude of AP and conduction velocity

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Vaughan-Williams classification antiarrhythmics - class IB

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

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Vaughan-Williams classification antiarrhythmics - class IC

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

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Vaughan-Williams classification antiarrhythmics - class II

Beta blockers

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Vaughan-Williams classification antiarrhythmics - class III

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

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Vaughan-Williams classification antiarrhythmics - class IV

calcium channel blockade

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Vaughan-Williams classification antiarrhythmics - class V drug

digoxin

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VW class IA drug names (3)

Quinidine
procainamide
dispyramide

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VW class IB drug names (3)

Lidocaine
mexiletine
tocainide

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VW class IC drug names (2)

Flecainide - more commonly used

propafenone

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Class II VW drug names (2) and action

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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class 3 VW drug names (3) and action

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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class IV drug names (2) and action

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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When are class I drugs more effective?

at higher heart rates

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

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

Phases of action potential

phase 0 - Na+ enters the cell. Depolarisation occurs

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

phase 3 - K+ exits the cell. Repolarisation

Amiodarone - class 3:-

use?
interacts with which other drug?
side effects?

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

Digoxin:-
half life
age group used for
toxicity

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

digoxin toxicity (5)

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

treatment if patient has digoxin toxicity

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

what is digibind?

drug that binds with digoxin, forming complex molecules excreted in urine

Adenosine

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

affect of adenosine on SVT:- ECG

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

indications for anticoagulation AF

AF high prevalence in elderly risk of stroke, peripheral emboli

CVS indications for anticoagulation

metallic heart valves DVT/PE

what is the 'ideal' anticoagulant

``` 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 ```

oral anticoagulant examples

warfarin dabigatran rivaroxaban apixaban

How does warfarin work against vitamin K?

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

monitoring warfarin therapy INR

actual prothrombin time over standard prothrombin time time taken for blood to clot therapeutic INR 2.5-4.0 warfarin therapy

normal INR value

adverse effects of warfarin in pregnancy

Teratogenic (chondrodysplasia - malformation of cartilage) (Retroplacental bleeding and fetal intracerebral bleeding). Avoid in first and third trimesters

how do aspirin and sulfonamides increase warfarin activity

decrease binding to albumin

how do cimetidine and erythromycin increase warfarin activity

inhibit degradation of it

how do oral antibiotics increase warfarin activity

decrease synthesis of clotting factors

which enzyme pathway breaks down warfarin

cytochrome P450

drugs that decrease warfarin activity

barbiturates, phenytoin Induction of metabolizing Barbiturates Enzymes (cytochrome P450) Vitamin K, cholestyramine Promote clotting factor synthesis Reduced absorption

other drugs that warfarin interacts with

macrolide antibiotics, antifungals, anti-epileptics

inhibitors of the cytochrome p450

``` Omeprazole Disulfiram Erythromycin Valproate Isoniazid Ciprofloxacin and Cimetidine Ethanol (acutely) Sulphonamides ```

Inducers of the cytochrome p450

``` Alcohol (chronic use) Barbiturates Carbamazepine Phenytoin Rifampicin Sulphonylureas ```

DOACs vs NOACs

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