CARDIO- Arrhythmias and Anti-arrhythmic drugs

Question 1

what is an arrhythmia

Answer 1

abnormalities of heart rhythm

Question 2

what are the symptoms of arrhythmias

Answer 2

palpitation, dizziness, fainting, fatigue, loss of conscious, cardiac arrest, blood coagulation (stroke, MI)

Question 3

what are the causes of arrythmias

Answer 3

cardiac ischemia (MI, angina), heart failure, hypertension, coronary vasospasm, heart block, excess sympathetic stimulation

Question 4

what are the origins of arrhythmias

Answer 4

supraventricular (above the ventricles - SA node, atria, AV node)

ventricular - tachycardia - bradycardia

Question 5

describe atrial fibrillation

Answer 5

quivering atria activity (no discrete p wave)
irregular ventricular contraction
clot-producing - risk of stroke

Question 6

describe supraventricular tachycardia (SVT)

Answer 6

p waves buried in T wave

fast ventricular contractions

Question 7

describe heart block

Answer 7

failure of the conduction system (SAN, AVN, Bundle of His)

uncoordinated atria/ventricular contractions

Question 8

describe ventricular tachycardia (VT) compared to Ventricular fibrillation (VF)

Answer 8

VT- fast, regular

VF- fast, irregular

Question 9

what are the mechanisms of arrhythmogenesis

Answer 9

abnormal impulse generation due to :
automatic rhythms - increase in SA node activity, ectopic activity
triggered rhythms - early-after-depolarisation (EAD) / delayed-after-depolarisation (DAD)

abnormal conduction due to:
re-entry electrical circuits in heart
conduction block

Question 10

what is ectopic activity in relation to abnormal impulse generation

Answer 10

pacemaker activity is usually initiated in the SAN but other areas of the heart can have pacemaker potentials in case the SAN becomes damaged
these are the AC node, bundle of his, Purkinje fibres
these low frequency pacemaker areas are greatly influenced by sympathetic nerve activity

Question 11

what is the mechanisms of action of EAD/ DAD

Answer 11

EAD - altered ion channel activity, abnormal increase in Na / Ca channel activity

DAD- abnormal levels of Ca in SR, Ca leaks out from RyR into cytosol, stimulates the Na/Ca exchanges, causing an Na influx causing depolarisation

Question 12

explain the concept of reentry

Answer 12

in a normal circulation - action potentials stop conducting because surrounding tissue is refractory - unable to conduct any more action potentials

if there is damage to the myocardium = some areas of the heart are more conductive than others - producing reentry pathways

Question 13

explain the mechanism behind heart block

Answer 13

often AV node issue
first degree - P-R interval >0.2s

second degree - P-R >1s. - atrial impulses fail to stimulate ventricles

third degree- atria and ventricles beat independently of each other

ventricles contract at a slow rate (depending on what sets the pacemaker (e.g., bundle of his))

Question 14

what is the Vaughan Williams classification system of anti-arrhythmic drugs

Answer 14

class system I-IV

Question 15

outline how class I anti-arrhythmic drugs work

Answer 15

na channel blockers (non-nodal tissue)
block Na channels in their activated state
only block Na channels in high frequency firing tissues
fast dissociation drug - comes off the channels in inactive state before the next impulse so no effect on normal firing
used for fast arrythmias - VT, VF

Question 16

outline how class II anti-arrhythmic drugs work

Answer 16

beta blockers (nodal and non nodal tissue)
act at SAN and AVN, atria and ventricles to reduce the excitability of cardia tissue
increase sympathetic activity associated with arrythmias - therefore beta blockers slow the initiation of the pacemaker potentials in the SAN and slow the conduction through the AVN to reduce ventricular firing rate in SVT

Question 17

outline how class III anti-arrhythmic drugs work

Answer 17

potassium channel blockers (non-nodal tissue)
increases the length of the action potential thus increases the length of the refractory period of the heart
inhibits K+ ions channels responsible for repolarisation in the atria / ventricles
thus reduces inappropriate action potential firing and therefore arrhythmias

Question 18

outline how class IV anti-arrhythmic drugs work

Answer 18

calcium channel blockers (nodal and non-nodal)
blocking of L-type voltage gated channels that affect the firing of AV and SA nodes- reduces ventricular firing
these L-type ca channels are also found on vascular smooth muscle and are involved in vasoconstriction - so can produce relaxation of blood vessels to control ventricular response rate in SVT

Question 19

what are some examples of non-classified drugs and what are they useful for

Answer 19

adenosine - decreases activity in SAN and AVN - used for SVT

atropine - muscarinic antagonist, reduces parasympathetic activity, used to treat sinus bradycardia after MI

digoxin - central effects, increases vagus nerve activity, decreases heart rate and conduction, used for atrial fibrillation