Arrhythmias:- treatment Flashcards
supraventricular arrhythmias?
AF
SVT (junctional)
ventricular arrhythmias?
Ventricular tachycardia
Ventricular fibrillation
what causes the fast depolarising phase of the cardiac action potential?
Influx of Na+
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.
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.
Vaughan-Williams classification antiarrhythmic drugs - class IA
moderate Sodium channel blockade
reduce amplitude of AP and conduction velocity
Vaughan-Williams classification antiarrhythmics - class IB
weak Na+ channel blockade ie they have a weak effect on the initiation of depolarization
Vaughan-Williams classification antiarrhythmics - class IC
strong affect on the initiation of depolarisation but slow Na+ channel blockade
Vaughan-Williams classification antiarrhythmics - class II
Beta blockers
Vaughan-Williams classification antiarrhythmics - class III
prolong refractoriness (recovery) so slow K+ flow out of cells
Vaughan-Williams classification antiarrhythmics - class IV
calcium channel blockade
Vaughan-Williams classification antiarrhythmics - class V drug
digoxin
VW class IA drug names (3)
Quinidine
procainamide
dispyramide
VW class IB drug names (3)
Lidocaine
mexiletine
tocainide
VW class IC drug names (2)
Flecainide - more commonly used
propafenone
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
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
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
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
1
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
