arrythmia Flashcards
what is arrhythmia
when the heart is beating out of rate or rhythm or both
normal heart rate
60- 100
HR < 60 - bradyarrythmia
HR> 100 - tachyarrythmia
defects in conducting pathway of heart causing bradyarrythmias
- sick sinus syndrome - defect in SAN - reduced impulse generation
- AV node block / bundle branch block - reduced impulse conduction
DOC - atropine
definitive treatment - artificial pacemaker
tachyarrythmias
100-200: tachycardia- till 200, may be physiological
200-350: flutter
>350: fibrillation
flutter and fibrillation are always pathological
types of tachyarrythmias
sympathetic tachycardia - sympathetic stimulation on beta 1 receptor of SAN- increased activity of SAN
may be caused by fear, fever, anxiety, hyperthyroidism
treatment - beta blockers
damage of heart (eg: post MI) - atrial muscles create more impulses (ectopic) - AF (fluster/fibrillation) or SVT - have to prevent VT - treatment: AVN blockers
VF/ VT(vent tachycardia) - more dangerous than SVT
if pt is hemodymanically unstable - give DC shock –iv adrenaline + fluids — VF - Amiodarone (DOC) and Na+ channel blockers
AVN blockers
ABCD
Adenosine
Beta blocker
CCB like Verapamil
Digoxin
electrophysiology of heart
2 types conducting fibres
- slow - SAN, AVN - do not have Na+ channels (depolarised by inflow of Ca2+)
- fast - atrial muscle, ventricular muscle - have Na+ channels
action potential of slow conducting fibres of heart
depolarisation by calcium influx
repolarisation by potassium efflux
sympathetic nerve stimulation –> stimulates beta 1 receptors –> opening of calcium channels
parasympathetic nerve stimulation –> stimulates M2 receptors –> opening of potassium channels
to block SAN/AVN
block beta - beta blocker
block calcium- CCB like Verapamil
open K+ - adenosine
stimulate M2(vagus) - Digoxin (vagomimetic)
action potential of fast conducting fibres of heart
have fast sodium channels also
phase 0- inward entry of Na+
phase 1- efflux of potassium
phase 2- efflux of potassium and entry of calcium
phase 3- efflux of potassium
class of drug which is DOC for various types of arrythmias
VF , AF - sodium channel blocker
SVT to prevent VT - AVN blocker
bradycardia - atropine
sympathetic tachycardia - beta blocker
action of sodium channel blocker
inhibits depolarisation –> reduces slope of phase 0
action of potassium channel blocker
inhibits repolarisation - affects phase 1,2,3 - increase action potential duration - prolongs QT interval on ECG (Q wave - vent depolarisation starts and T wave - ventricular repolarisation)
the increase AP duration is the relative refractory period (Na+ channels recover and are ready to open again) so if during this RRP there is a triggered impulse the action potential could start again and if this is repeated it could leadtp Torsades de pointes (QT prolongation caused by potassium channel blockers)
drugs causing Torsades de pointes
- anti arrythmics 1A+3
- Bedaquiline
- Cisapridw
- TCA, SARI
- Astemizole, Terfinodine - antihistaminics
William Vaughan Singh classification of anti arrythmic drugs
class 1- sodium channel blocker - 1A: blocks potassium, 1B: opens potassium, 1C: no effect on potassium
class 2- beta blockers (all except Sotalol which is class 3 as it potassium channel blocker)
class 3- potassium channel blockers
class 4- calcium channel blockers
class 5- miscellaneous - atropine, Digoxin, adenosine, MgSO4
which beta blocker prolongs QT interval or causes Torsades de pointes
Sotalol - class 3
potassium channel blocker
Class 1a agents
sodium channel blockers (blocks both closed and resting channels) for 1-10 seconds - reduces phase 0 slope
block is intermediate
blocks potassium channels (SE- increases QT interval and causes Torsades de pointes)
increases APD
used in SVT and VT
Quinidine
Procainamide
Disopyramide
class 1b agents
sodium channel blocker - reduces phase 0 slope
block is rapid (only blocks closed channels; half life is less than 1 sec)
opens potassium channels
increase AP duration
used in VT only (not effective in SVT as in atria sodium channels open for very brief duration)
Lignocaine
Phenytoin
Mexilitine
Tocainide
class 1C agents
sodium channel blocker - reduces phase 0 slope
block is slowest
blocks both closed and resting sodium channels t1/2>10 secs
no effect on potassium channels
no change in AP duration
treatment of SVT and VT (resistant cases)
Encainide
Flecainide
Propafenone
Moricizine
these drugs are used for treatment of WPW syndrome
these drugs indicate mortality in MI patients in Cast Trial
Quinidine
d isomer of quinine ( anti malarial and obtained from bari of cinchona plant)
1st anti arrythmic drugs
increase AVN conduction and SAN conduction
SE
1. diarrhoea most common
2. blocks acetylcholine receptor (antimuscarinic/atropine) - tachycardia
3. blocks alpha receptor - hypotension
4. blocks potassium channel- prolong QT interval and insulin release from pancreas causing hypoglycemia (always given in 5% dextrose)
5. cinchonism (ototoxicity - tinnitus, deafness & neurotoxicity - seizures)
Procainamide
additional beta blocking action - blocks SAN/AVN - SE- bradycardia
metabolised by acetylation
SE - DLE, agranulocytosis (fall in WBC)
Disopyramide
atropine derivative - SE - tachycardia
other SE - dry eye/mouth, mydriasis, constipation
Lignocaine
class 1b
also called Lidocaine or Xylocaine
also local anesthetic
Tx of ventricular Fibrillation after MI/due to Digoxin (Lignocaine) - pure form of Lignocaine has to be used (don’t use LA formulation - many chemicals)
iv only - not oral( has high FPM in liver)
cardiotoxic - bradycardia
neurotoxic -
1st excitation (suppresses inhibitory neurons) : nystagmus(most common), seizures ——-> suppression (suppresses all neurons) - respiratory depression
phenytoin
class 1b AED
Tx of VF due to Digoxin
Mexilitine
class 1b
oral prodrug of Lignocaine
maintenance or prevention of VF
approved for diabetic neuropathy pain
class 2 agents
beta blockers (except Sotalol)
- DOC sympathetic tachycardia (increased HR - ECG short R-R)
- treatment of SVT - to prevent VT (blocks AV)
- intraoperative tachycardia - iv Esmolol (shortest beta blocker)
- treatment of VF - beta blockers taht block sodium channels (membrane stabilizing action ) - Propranolol, Metopeolol, Labetalol, Atenolol, Pindolol
SE - bradycardia (antidote for beta blocker toxicity is glucagon)
class 3 agents
potassium channel blockers
used for treatment of clutters or fibrillation
not used on prolonged QT/Torsades de pointes
Beautiful DIVAS
Bretylium - medical defibrillator
Dofetilide (oral) , Ibutilide (iv) - pure potassium channel blocker - only increases APD, no effect on Phase 0, only in SVT (AF)
Vernakalant, Amiodarone, Sotalol - multi ion channel blockers - blocks sodium, potassium, calcium beta blocker
used in all SVT or VT
Sotalol is non selective beta blocker
CI in renal failure
purple syndromes
purple man syndrome - Amiodarone - smurf syndrome
purple toes syndrome - warfarin
purple glove syndrome - amiodarone
drug induced vortex keratopathy
Amiodarone
Amiodarone
all types of arrythmias (VT or SVT) except Torsades
most effective anti arrythmic drugs
VF after MI - DOC is Amiodarone (best mortality benefits)
longest drug - Amiodarone (t half is 60 days) - thus, it requires loading dose
metabolised by CYP3A4 (rest all drugs by CYP2D6)
SE
1. Amiodarone contains 37% iodine
hypothyroidism (iodine inhibits release of T3/T4) - Wolf Chaikoff effect»_space;> hyperthyroidism ( increases synthesis of T3 or T4) - Jod Basedow effect
[new modified form is Dronaderone which does not contain iodine]
- pulmonary fibrosis or interstitial lung disease - most dangerous
- purple man syndrom / smurf syndrome - skin discoloration
- peripheral neuropathy
- cirrhosis or liver damage
- cornea microdeposit (reversible) - cornea vernicallata or vortex keratopathy
longest and shortest drug
longest is Amiodarone (t half is 60 days)
shortest is Adenosine (t half is 10 seconds)
