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Sem 5 > Pharmacology 10: Drugs affecting heart and heart rhythm > Flashcards

Pharmacology 10: Drugs affecting heart and heart rhythm Flashcards

1
Q

what are class I anti-arrhythmic drugs?

A 
Na+ ion channel blockers e.g.class Ia- quninidine and procainamide
class Ib- lidocaine
class Ic- flecainide
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2
Q

what are class II anti-arrhythmic drugs?

A

beta blockers e.g. atenolol, bisoprolol, metoprolol

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3
Q

what are class III anti-arrhythmic drugs?

A

inhibitors of repolarisation so prolong AP, K+ channel blockers e.g. amiodarone, sotalol

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4
Q

what are class IV anti-arrhythmic drugs?

A

Ca2+ channel blockers e.g. verapamil- a phenylalkylamine and diltiazem- a benzothiazepine

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5
Q

at which phase of the ventricular AP do class I anti-arrhythmics act?

A 
phase O= block fast inward Na+ channels
class Ia produce a weak K+ block- prolong repolarisation so increase effective refractory period, e.g. procainamide
main effect is to decrease conduction velocity through cardiac tissue by decreasing upstroke velocity of phase O, and this stops re-entry loops*
also increase threshold for depolarisation ,and reduce automaticity in SA node by shifting threshold to more +ve potentials, and decrease slope of phase 4 depolarisation, which decreases HR
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6
Q

why is lidocaine only given IV?

A

subject to extensive 1st pass metabolism

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7
Q

ADRs of lidocaine?

A 
nystagmus
seizures
dizziness
drowsiness
-vly inotropic- CI in HF
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8
Q

ST ADRs of amiodarone?

A

hypotension and phlebitis with IV administration

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9
Q

LT ADRS of amiodarone?

A 
hypo/hyper thyroidism
pulmonary fibrosis
hepatic dysfunction
peripheral neuropathy
slate grey skin/photosensitivity
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10
Q

what does the PR interval on an ECG represent?

A

length of time for AP conduction through AV node

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11
Q

what does the QT interval represent?

A

ventricular depolarisation and repolarisation

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12
Q

what does the ST segment represent?

A

period during which ventricles are depolarised, corresponds to plateau phase of ventricular AP= Ca2+ voltage-gated channels open- delayed opening and slow to close, Ca2+ entry and K+ also being moved out of cells.

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13
Q

define an arrthymia

A

heart condition where disturbances in pacemaker impulse formation, or contraction impulse conduction, or combination of the 2.

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14
Q

how do Na+ channel blockers decrease likelihood of re-entry?

A

decreasing conduction velocity by decreasing upstroke of ventricular myocyte AP in phase 0
and
increase refractory period of ventricular myocytes

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15
Q

what is the problem with AP conduction in AF?

A

re-entrant AP conduction through atrium**
chaotic, irregular atrial rhythm= irregularly irregular
AV node responds intermittently, so irregular ventricular rate

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16
Q

2 ways in which AF can be managed (what are drugs targeting)?

A

control ventricular rate

attempt to restore and maintain sinus rhythm

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17
Q

how can ventricular rate be controlled with drugs for AF patients?

A

beta blocker
of Ca2+ channel blocker e.g. diltiazem, or verapamil
digoxin only effective for controlling ventricular rate at rest
if ventricular rate can’t be controlled with single drug, combine digoxin and other drug e.g. beta blocker

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18
Q

how can sinus rhythm be restored in AF using drugs?

A 
class IC Na+ channel blocker e.g. flecainide, shifts SA node AP threshold to more +ve potential and reduces upstroke of phase 4 depolarisation
or K+ ion channel blocker e.g. amiodarone or sotalol
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19
Q

how do beta blockers affect the heart in arrhythmias?

A

diminish phase 4 depolarisation and automaticity at SA and AV nodes, reduced slope of phase 4 AP at SA node part. important, so reduce sympathetic stimulation to SA node and AV node, inhibit If Na+ channels producing pacemaker current.
also prolong repolarisation- reduce K+ currents at AV node, increase effective refractory period so decrease incidence of reentry, slow ventricular rate as prolonged AV node repolarisation means longer time period before another AV node AP can be transmitted to cause ventricles to contract. increase AP duration

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20
Q

term used to describe heart as it can contract spontaneously without outside nervous stimulation?

A

myogenic

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21
Q

most frequently used anti-arrhythmic drugs in supraventricular and ventricular arrhythmias precipitated by sympathetic stimulation?

A

beta blockers

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22
Q

ADRs of beta blockers?

A 
bradycardia
hypotension
heart block
bronchospasm
cold extremities
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23
Q

effects on heart of K+ channel blockers used in arrhythmias?

A

prolong AP by prolonging repolarisation, increasing effective refractory period and decreases incidence of re-entry
also reduce phase 0 and conduction, increase threshold, reduce speed of AV conduction, reduce phase 4

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24
Q

why do Ca2+ channel blockers act preferentially on SA and AV nodal tissues?

A

these pacemaker tissues depend on Ca2+ currents for depolarisation phase of AP (phase 0)

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25
Q

main action of class IV antiarrhythmic drugs (Ca2+ blockers)?

A

slow AP upstroke in AV nodal cells (phase 0 depolarisation) causing slowed conduction velocity through AV node.

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26
Q

why must a patient be closely monitored if receiving an IV infusion of a K+ channel blocking agent?

A

prolongs QT interval, so risk of torsades de pointes which can go into VF and then cardiac arrest

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27
Q

major ADRs of amiodarone?

A

reduce AV or SA node function, hypotension
pneumonitis, leading to pulmonary fibrosis
hyper or hypo thyroidism
elevated liver enzymes
peripheral neuropathy
corneal microdeposits
slate grey skin

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28
Q

why is a beta blocker not used in patients with insulin-dependent diabetes mellitus?

A

in hypoglycaemia adrenaline acts to produce symptoms of episode but a beta blocker will stop adrenaline from acting so patient won’t experience hypoglycaemic symptoms.

29
Q

drugs which affect automaticity?

A

beta blockers- decrease slope of phase 4 pacemaker potential

adenosine- opens a GPC K+ channel, inhibiting conduction, especially at AV node

30
Q

examples of automatic and triggered rhythms?

A 
automatic= ectopic focus, enhanced normal automaticity
triggered= delayed afterdepolarisation, early afterdepolarisation
31
Q

what causes abnormal conduction in heart?

A

re-entry loops
conduction block- 1st, 2nd and 3rd degree
accessory tract pathways e.g. bundle of Kent

32
Q

what 2 things are required for reentry loops?

A

unidirectional block

slowed retrograde conduction velocity

33
Q

what happens in reentry loops?

A

2 pathways: impulse can only pass down 1 as unidirectional block in other pathway- their effective refractory period is prolonged so anterograde conduction prohibited. impulse then travels along to junction where it can now travel in retrograde fashion along pathway which was blocked as cells no longer refractory but this conduction is slowed as cells still refractory or cell damage so when reaches initial point, cells in normal pathway have had time to repolarise so AP can continue down, causing tachyarrhythmias.

34
Q

what is the bundle of Kent and what can it result in in patients?

A

an accessory electrical pathway that conducts impulses directly from atria to ventricles, bypassing AV node. Conduction via this pathway is quicker than through AV node, so setting up conditions for re-entrant tacharrhythmias as differing conduction velocities.
reexcitation cause Wolf-Parkinson-White syndrome

35
Q

why might conduction block produce bradycardia?

A

removes overdrive suppression from SA node, so cardiac myocytes free to beat at their intrinsically slower frequency.

36
Q

if abnormal impulse generation, what 2 ways can drugs act to treat this?

A

reduce slope of phase 4 depolarisation in pacemaker cells (pacemaker potential) e.g. Na+ channel blockers
raise threshold for AP e.g. Na+ channel blockers

37
Q

if abnormal impulse conduction, what 2 ways can drugs act to treat this?

A

reduce conduction velocity by decreasing slope of phase 0 depolarisation e.g. Na+ channel blocker, or Ca2+ channel blocker
increase effective refractory period so cell won’t be excited again e.g. K+ channel blocker

38
Q

3 functions of anti-arrhythmic drugs?

A

decrease conduction velocity
change the duration of the effective refractory
period (ERP)
suppress abnormal automaticity

39
Q

effects on ECG of class IA anti-arrhythmics?

A

increase QRS
increase QT
may effect PR

40
Q

when is quinidine used?

A

maintain sinus rhythms in AF as decrease slope of phase 4 depolarisation (pacemaker potential) and flutter, and prevent recurrent tachycardia and fibrillation.

41
Q

when is procainamide used?

A

acute tment of supraventricular and ventricular arrhythmias

42
Q

ADRs of class IA anti-arrhythmics?

A 
hypotension, reduced CO
proarrhythmia e.g. torsades de pointes
dizziness, confusion, insomnia, seizure
GI effects
lupus-like syndrome- espec. procainamide
43
Q

how does lidocaine act?

A

No change in phase 0 in normal tissue (no tonic block)
APD slightly decreased (normal tissue)
increase threshold (Na+)
decrease phase 0 conduction in fast beating or ischemic tissue

in fast beating or ischaemic tissue increases QRS

44
Q

why are class IB antiarrhytmics better than IA in terms of their SEs?

A

class IB aren’t as pro-arrhythmic as don’t effect QT as much

45
Q

uses of lidocaine?

A

Ventricular tachycardia and fibrillation (esp. during

ischemia)

46
Q

effects on cardiac activity of flecainide?

A

Substantially decrease phase 0 (Na+) in normal
reduce automoticity (increase threshold)
increase APD (K+) and increase refractory period, esp in
rapidly depolarizing atrial tissue
increase PR, QRS and QT on ECG

47
Q

uses of class IC anti-arrhythmics?

A

Used for supraventricular arrhythmias (fibrillation and
flutter)
Premature ventricular contractions (caused problems)
Wolf-Parkinson-White syndrome

48
Q

why is ratio of atrial to ventricular firing rate in atrial flutter typically 2:1?

A

atrial firing so rapid that some impulses reach AV node when its refractory so these not transmitted to ventricles.

49
Q

ADRs of class IC blockers?

A

Proarrhythmia and sudden death especially with chronic
use (CAST study- cardiac arrhythmia suppression trial), so don’t give if coronary disease or poor LV function
increase ventricular response to supraventricular
arrhythmias
CNS and gastrointestinal effects like other local anaesthetics

50
Q

effects on ECG of beta blockers?

A

increase PR

decrease heart rate

51
Q

uses of beta blockers in arrhythmias?

A

treating sinus and catecholamine dependent tachy
arrhythmias e.g. supraventricular tachcardia
converting reentrant arrhythmias in AF, slow ventricular rate
protecting the ventricles from high atrial rates (slow AV
conduction)

52
Q

T1/2 of amiodarone?

A

3 months
distributed into fat
long time for recovery once drug stopped

53
Q

effects on ECG of amiodarone?

A

increase PR
increase QRS
increase QT
decrease HR

54
Q

effects of amiodarone on heart (mainly class III, but can act as other classes)?

A

reduce phase 0 and conduction (Na+ block)
increase threshold
reduce speed of AV conduction
reduce phase 4 (beta block and Ca2+ block)

55
Q

cardiac effects of sotalol?

A

APD and refractory period in atrial and ventricular tissue increased
Slow phase 4 (β blocker)
Slow AV conduction

increase QT and decrease HR on ECG

56
Q

uses of sotalol?

A

supraventricular and ventricular tachycardias

57
Q

SEs of sotalol?

A

proarrhythmia
fatigue
insomnia

58
Q

ECG effects of Ca2+ blcokers?

A

increase PR
increase or decrease HR (depending of blood pressure
response and baroreflex)

59
Q

uses of class IV agents?

A

control ventricles during supraventricular tachycardia

convert supraventricular tachycardia (re-entry around AV)

60
Q

SEs of class IV agents?

A

Caution when hypotension, decreased CO or sick sinus

Some gastrointestinal problems

61
Q

describe the use of adenosine

A

Rapid i.v. bolus, very short T1/2 (seconds)
binds A1 receptors and activates K+ currents in AV and SA node – so increases APD, hyperploarization → decrease HR
decrease Ca++ currents- increase refractory period in AV node
Slows AV conduction
Uses
convert re-entrant supraventricular arrhythmias and in hypotension during surgery, diagnosis of CAD

62
Q

use of digoxin, atropine and magnesium?

A

Digoxin (cardiac glycosides)
enhances vagal activity (increase K+ currents, decrease Ca++ currents, increase refractory period
slows AV conduction and slows HR
Uses
treatment of atrial fibrillation and flutter
Atropine- selective muscarinic antagonist
block vagal activity to speed AV conduction and increase HR
Uses
treat vagal bradycardia
Magnesium
treatment for tachycardia resulting from long QT

63
Q

drugs used in AF?

A

control ventricular rate= beta blockers and Ca2+ channel blockers
restore sinus rhythm= Na+ channel blocker e.g. flecainide, or K+ e.g. amiodarone

64
Q

which IV drug first for ventricular tachycardia?

A

lidocaine, can give amiodarone- must do so via central line so don’t cause thrombophlebitis

65
Q

should flecainide be used alone for atrial flutter?

A

no
must also use beta blocker or Ca2+ blocker aswell or can result in 1:1 conduction
can use Na+ blocker alone if AV node disease

66
Q

best drug fro WPW?

A

flecainide

67
Q

drugs in re-entrant SVT?

A

adenosine

beta blocker

68
Q

drugs for ectopic atrial tachycardias?

A

beta blocker
class IC Na+ blocker
class III
Ca2+ blocker

69
Q

drugs for sinus tachycardia?

A

beta blocker

or Ca2+ blocker if asthamtic

Sem 5 (35 decks)

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