Anti Arrhythmic Drugs

Question 1

NORMAL CARDIAC CONDUCTION

i) which node is the pacemaker of the heart? what does it initiate?
ii) which structure delivers excitation to the apex?
iii) what is the only pathway for the action potential (generated by the SA node) to reach the ventricles
iv) when is there slow conduction when is there fast conduction?

Answer 1

i) SA node > initiates each wave of excitation with atrial contraction
ii) bundle of his delivers the excitation to the apex
iii) AV node is the only pathway for AP to enter the ventricles

iv) slow cond - complete atrial systole before ventricular systole starts
fast cond - bundles of his and purkinje fibres (ventric depol and contrac)

Question 2

CARDIAC ARRHYTHMIAS

i) what are they?
ii) what may happen to the SA/AV node to cause an arrhythmia?
iii) which type of tissue can become an ectopic pacemaker? what does this lead to?
iv) name two things that can cause arrhytmias

Answer 2

i) abnormal rhythms causing the heart to pump less effectively
ii) changes in automaticity of the natural pacemakers (AV/SA)

iii) hypox/ischaemic tissue can undergo spont depol > ectopic pacemaker
- leads to interruption of normal conduction pathway

iv) electrolyte disturbances and drugs

Question 3

CARDIAC RE-ENTRY

i) what is it?
ii) what is it the most common cause of?
iii) where may it occur?
iv) what is anatomically defined re-entry? give three examples
v) what is functionally defined re-entry? give two examples

Answer 3

i) when a propogating impulse fails to die out after normal activation of the heart and persists to reexcite the heart after refractory period has ended
ii) most common cause of clinically important arrhythmias
iii) can occur in any heart region where there is a region of non cond tissue and htereogenois conduction around that tissue

iv) anatomical - re-entry that involves impulse propagation by more than one anatomical pway between two points in the heart
- WPW (extra pway bet A+V), atrial flutter (extra pway in atria), parox SVT (AVRT and AVNRT)

v) functional defined - can occur in the absence of anatomically defined pathways
- AF and VF, torsades de points (VT big>small>big)

Question 4

ANTI ARRHYTHMIC DRUG ACTION

i) what is the goal of treatment? (2)
ii) how do all AA drugs work?
iii) what three ions are the most important?
iv) hich classification system is used for AA drugs?

Answer 4

i) goal is to reduce ectopic pacemaker activity and modify critcally impaired conduction
ii) all work by altering ion fluxes in exciteable tissues in the myocardium
iii) Na, Ca, K
iv) Vaughn williams system used to classify

Question 5

VAUGHAN WILLIAMS CLASSIFICATION

i) what channel do all Class I drugs work on?
ii) which receptor do class II block?
iii) which ion channel do class III block? what does this cause for the AP?
iv) which channel do class IV block? what does this cause?

Answer 5

i) class I - sodium channels
ii) class II > block beta adrenergic receptors

iii) class III block K+ channels
- prolongs the AP and refractory period (supresses re-entrant rhythms)

iv) class IV block calcium channels - impair impulse propagation in nodal and damaged areas

Question 6

CLASS 1A AGENTS

i) give two examples? which one can worsen HF
ii) what are they useful for? (2) what does a patient need to have?
iii) which two channels does it block? how does it affect QRS? what negative effect may it also have
iv) what side effect can cause AV block?

Answer 6

i) quinidine and disopyramide (worsens HF)

ii) useful in SVT and ventricular arrhythmias
- patient must have good LV func due to negative ionotropic effects

iii) blocks sodium and potassium
- prolongs QRS duration and can be pro arrhythmic

iv) anti cholinergic SEs can cause AV block

Question 7

CLASS 1B AGENTS

i) name a class IB agent and its route of admin?
ii) what is the orally active sister? what effect does it have on the QT interval?
iii) name three most common side effects

Answer 7

i) lidocaine (lignocaine) > used IV because of its first pass metabolism

ii) mexiletine - lidocaine orally active sister
- doesnt prolong QT interval > can be used in patients with history of VT

iii) common side effects are CNS - tinnitus, seizures, hallucinations, drowsy

(only a short term solution but its good in emergency)

Question 8

CLASS 1C AGENTS

i) which channels do they block? do they affect the duration of the AP?
ii) do they affect QRS length?
iii) what is the most widely used class IC agent? how does it work? why is it not a first line agent?
iv) which type of patients is the above drug most commonly used in? give two instances where it should not be used/used with caution

Answer 8

i) block sodium channels
- no effect on AP duration

ii) doesnt affect QRS length

iii) flecanide
- fast inward soidum channel blocker used to treat SVT arrhythmia
- not used first line as it can be pro arrhythmic
- cant be used in pts with impaired ventricular function

iv) most commonly used in young fit patients
- cant give if patient has had an MI
- use with caution if pacemaker or ICD

Question 9

CLASS II AGENTS

i) give an example of a drug and three therapeutic uses it may have
ii) how do they affect heart rate and why is this useful? how does it affect force of contrac? what condition is this not good in?
iii) what is the most used class II agent? what is it useful for
iv) in what condition should they not be given in? what should be used instead?
v) which drug is good in HF? what is good in arrhythmia?
vi) name four side effects? what should be done in overdose (3)

Answer 9

i) beta blocker > IHD, HTN, glaucoma, hyperthyroid

ii) reduce heart rate - useful as it increases diastolic filling time and inc coronary perfusion
- reduced force of contraction (not good in acute HF)

iii) Bisoprolol is most used
- useful to prevent arrhythmia post MI and SVT/ventric arrhythmias

iv) dont give if asthmatic as they cause bronchospasm - use ivabradine instead
v) carvedilol - HF, esmolol - arrhytmia
vi) SE - bronchospasm, hypotension, brady, cardiac fail, impotence, exac of PVD

In OD - give glucagon to reverse the beta blocker,
temporary pacing if brady
ionotropic support if BP is low

Question 10

CLASS III - POTASSIUM CHANNEL BLOCKERS

i) how do they work? what are they useful in?
ii) what is the best known drug - how is it given?
iii) which drug is good for paroxysmal AF?
iv) which two class effects does sotalol have? what does it do? what is it useful in?
v) name three instances when sotalol is contraindicated

Answer 10

i) prolong repolarisation phase by blocking outward potassium flux
- anti fibrillatory agents > useful in re-entry tachyarrhythmias

ii) amiodarone - kills all known arrhythmias
- given IV usually through a central line or a big cannula in emergency

iii) sotalol is good for pAF

iv) sotalol - class II and class III effects > beta blocking effects and prlongs the action potention
- combination of effects makes it good in atrial and ventricular arrhythmias

v) contraindicated in patients with QT prolong, bradycardia, torsades, hypomagnesium/kalemia, bronchospasm

Question 11

AMIODARONE

i) what hormone is it structurally related to?
ii) how does it affect the QT interval? is it a good anti arrhythmic?
iii) is amiodarone good for chronic use? why?
iv) what is the mean drug half life?
v) name a pulmonary, liver, thyroid, CNS, skin side effect

Answer 11

i) struc related to thyroid hormone

ii) prlongs QT interval but is less pro arrhythmic than other class III agents
- good because consistently has decreased mortality in trials

iv) mean half life is 53 days - takes a while to clear

v) SEs
- pulm - fibrosis/interstit pneumonitis - need to do 3monthly CXR
- liver - hepatox, 30% of patients have elevated liver enzymes so do 3 monthly LFTs
- thyroid - can cause hyper and hypo thyroid as it is struc sim to thyroid hormone and containts lots of iodine
- CNS - periph neuropathy
Skin - can cause photosensitivity

Question 12

CLASS IV - CALCIUM CHANNEL BLOKCERS

i) how do they work? what are they mostly used for?
ii) name two commonly used agents
iii) name three adverse effects
iv) does amlopidine have cardiac effects? what is it usually used for? give a side effect

Answer 12

i) prolong repol phase by blocking inward calcium current (vdil and cardiac slowing)
- mostly used for treating atrial arrhythmias . SVT arrhythmias

ii) verapamil and diltiazem
iii) bradycarida, hypotension, constipation

iv) amlodpine - usually used to lower BP
- vasodilation but no cardiac slowing
- SE - constipation and peripheral oedema

Question 13

ADENOSINE

i) what is it given as a rapid bolus to treat?
ii) how does it work? how long does this take? what is its half life?
iii) name three short lived common SEs
iv) what is it principally used for?

Answer 13

i) rapid IV bolus to treat paroxysmal SVT

ii) blocks AV nodal conduction within 10-30 secs of admin
- short half life of 1.5-10 seconds

iii) SEs - facial flushing, dyspnoea, chest pressure
iv) principally used to terminate arrhythmias - blocks re-entrant pway and slows HR down (easier to read ECG)

Question 14

DIGOXIN

i) what is it? which channel does it work on?
ii) what is it used for? how does it do this?
iii) what may it exacerbate? why? does it have a wide or narrow therapeutic window?

Answer 14

i) cardiac glycoside that acts by inhibiting Na/K ATPase

ii) used to control ventricular rate in patients with atrial tachy
- increases vagal tone > inhibiting AV nodal conduc

iii) may exacerbate atrial arrhytmias because it can cause calcium overload
- narrow therapeutic window

Question 15

MAGNESIUM SULPHATE

i) what is it used for the treatment of?
ii) name three side effects

Answer 15

i) treats arrhytmias - torsades de pointes
iii) bradycadria, resp paralyis, flushing, headache

Question 16

TACHYARRHYTHMIAS

i) is a wide or narrow QRS more concerning? what is classed as wide?
ii) name a narrow QRS regular and irreg rhythm
iii) name a wide QRS reg and irreg rhythm
iv) what is abbherancy?
v) name four tachyarrhytmias

Answer 16

i) wide QRS is most worrying (>3 boxes)
ii) narrow - regular = sinus tach/SVT, irreg = AF, MAT, a flutter
iii) wide - regular = V tach, sinus tach w abbherancy, irreg - AF w BBB, VF
iv) aberrancy is when there is tachy in atria but BBB lower down
v) SVT, AF, atrial flutter and ventricular tachycardia (mono or polymorphic)

Question 17

SUPRAVENTRICULAR TACHYCARDIA

i) what is it? what type of complex tachycardia do they normally produce?
ii) what is paroxysmal SVT?
iii) what three things may they be classified on? give an example of each?

Answer 17

i) any tachyarrhythmia arising from above the level of bundle of his (umbrella term) > usually produce narrow complex tachy on ECG
ii) SVT with abrupt on and offset (re-entrant tachys involving the AV node such as AVNRT and AVRT)

iii) classified by
sinus node dependent - sinus tachy, sinus node reentry
AV node dependent - AVNRT (re-entrant tachy, extra pway in AV node), AVRT (pway outside node between atria and ventricle)
atrial dependent - atrial tachy, flutter, fibrillation

Question 18

SINUS TACHYCARDIA

i) how is it defined? is it more common in F or M? what is peak incidence age?
ii) what happens? name three clinical features
iii) what does the ECG show - rate, P wave?
iv) how should it be managed?

Answer 18

i) increase in HR >100bpm
- most common in females (90%) and peak age is 38

ii) increased automaticity due to sympathetic activ or psym inhib
- palpitations, chest pain, SOB, light head

iii) ECG - rate >100bpm and visible P waves
iv) mx by treating underlying cause of removing offending agent (can use beta blocker or ivabradine if chronic)

Question 19

ATRIAL FIBRILLATION

i) how is it defined? what are the three types? 10% of people over which age have it?
ii) give four causes? what is the pathphys?
iii) name three clinical feautres
iv) what is seen on ECG? rhythm and P waves

Answer 19

i) irregularly irregular heart rhythm with no P waves on ECG
- paroxysmal, persistent, permanent
- 10% over 70yrs have it

ii) alcohol, caffeien, thyrotox, rheum ever, IHD, pulm fibrosis, electrolyte distub
- pathophys = micro re-entrant circuits

iii) clinical features = asymp, palpitations, SOBOE, ligh head, irreg irreg pulse
iv) ECG = irreg irreg rhythm and absent P waves

Question 20

AV NODE RE-ENTRY TACHYCARDIA

i) what is it? what is it the most common cause of? do males or females predominate?
ii) what is the pathophysiol? name three clinical features
iii) what is seen on ECG? complexes, P waves
iv) how should it be managed? - pharma, compromised, recurrent

Answer 20

i) type of SVT caused by an aberrant circuit in the AV node
- most common cause of parox SVT
- female predom

ii) pathophys - re-entrant circuit occurs within the AVN, usually in struc normal hearts and most commonly involves dual pathways of different velocities
- sudden onset rapid palp, dizzy, breathless, syncope

iii) ECH - regular narrow complex tachy, P waves may not be visible

iv) manage - some can be terminated with vagal manouevre (carotid sinus massage)
IV adenosine/rate limit CCB
cardioversion if compromised
catheter ablation if recurrent

Question 21

WOLF PARKINSON WHITE

i) what is it?
ii) what may be seen on ECG? (3)
iii) what can ECG be used for?
iv) what class of drugs are used to supress it?
v) what should be done if the patient becomes hypotensive?

Answer 21

i) ventricles recieve partial normal signal and partial from an accessory pathway (normally in AF - AV node will block some of the atrial impulses but in WPW it doesnt block any > vent rate also quick)
ii) tachycardia, short PR interval, delta wave (slurred upstroke of QRS) and prolonged QRS
iii) to identify the reentrant pathway and the location of the accessory pathway
iv) class III drugs
v) cardiovert immediately

Question 22

AV RE-ENTRANT TACHYCARDIA

i) what is it? what can lead to it?
ii) what is the aetiology?
iii) what is the pathophysiol? name three clinical features
iv) what is seen in ECG? (3)
v) how is it managed? (3) name two drugs which shouldnt be given

Answer 22

i) type of SVT caused by an anatomically defined re-entrant circuit involving one or more accessory pathways
- WPW is a pre excite syndrome that can lead to AVRT

ii) congenital

iii) accessory pways (bundle of kent in WPW) result in an anatomical re entrant circuit which compromises normal AV conduction and the accessory pathway
- palpitations, chest pain, syncope

iv) see short PR interval, broad QRS and delta wave

v) manege first with vagal manoeuvres, then IV adenosine, flecanide, amiodarone, cardiovert, cathether ablation of accessory pathway
- dont give beta blocker or CCB

Question 23

BROAD COMPLEX TACHYCARDIA

i) is this more or less of an emergency than narrow complex?
ii) name a regular ventricular BCT? name an irregular ventricular BCT
iii) name a supreaventricular BCT’?
iv) if it is broad complex and fast - what should it be treated as?

Answer 23

i) more of an emergency

ii) reg ventricular - monomorphic VT
irreg ventricular- TDP

iii) SVT - bundle branch block with abherrant conduc

Question 24

VENTRICULAR TACHYCARDIA

i) how do the complexes look?
ii) is there typical RBBB/LBBB morphology? is there axis deviation
iii) what is the link between the atria and ventricles? how is this reflected in P and QRS?
iv) what is a capture beat?
v) what is a fusion beat?
vi) what is concordance?

Answer 24

i) very broad
ii) absence of typical BBB morphology and there is extreme axis deviation
iii) there is AV dissociation > P and QRS complexes are completely different rates
iv) capture beat - SA node transiently captures the ventricles to produce a normal QRS
v) fusion beat - sinus and ventricular beat coincide to produce a hybrid complex
vi) everything points the same way - likely to be VT

Question 25

TORSADES DE POINTES

i) how does it look on ECG?
ii) what is it usually caused by? (3) what happens to the QT interval?
iii) how is it managed acutely? (2)
iv) how is it managed chronically? what if the patient has a slow HR? or a fast HR?

Answer 25

i) small then big them small waves

ii) usually caused by medication (quinidine, disopyramide, sotalol), hypokalemia or bradycardia (espec after MI)
- QT interval gets longer

iii) acute - remove the offending medication and shorten the QT interval with magnesium, lidocaine

iv) chronic - may need pacemaker if slow HR or ICD if fast HR
- can also give amiodarone or beta blockers

Question 26

VENTRICULAR FIBRILLATION

i) when is it most common? name three other things that can precip it?
ii) what is there absence of?
iii) what is the rate of recovery?
iv) what drug can be used if refractory to cardioversion

Answer 26

i) most common in acute MI
- also seen in drug OD, anaesthesia, hypothermia, electric shock

ii) no ventricular complexes
iii) low rate of recovery
iv) amiodarone

Question 27

what is it?

Answer 27

sinus tachycardia

Question 28

what is it? why?

Answer 28

atrial fibrillation - absence of P waves

Question 29

what is it? why?

Answer 29

wolff parkinson white
- short PR interval, delta wave (sloped up QRS), prolonged QRS

Question 30

what feature is seen here? what is it likely due to?

Answer 30

concordance (everything points the same way) > likely to be VT

Question 31

what is circled?

Answer 31

capture beat - SA node is able to capture the ventricle in the middle of AV dissociation > normal QRS

Question 32

what is this?

Answer 32

monomorphic VT

Question 33

what is this?

Answer 33

torsades de pointes

Question 34

what is this?

Answer 34

ventricular fibrillation