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CM2001 > PED2007 L12-L15 > Flashcards

PED2007 L12-L15 Flashcards

1
Q

what are sinoatrial node pacemakers

A

the rate of firing of the SA node sets the heart rate
it initiates the cardiac cycle

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2
Q

what is phase 0 of the cardiac cycle

A

calcium ion influx
upstroke of the slow pacemaker action potential
triggered at the threshold potential of -55mV
increase in movement of Ca2+ into cell

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3
Q

what is phase 3 of the cardiac cycle

A

calcium ion channels inactive
delayed potassium ion efflux
increase in potassium efflux
membrane hyperpolarises

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4
Q

what is phase 4 of the cardiac cycle

A

pacemaker sodium ion influx
calcium ion channels recover from inactivation
pumps restore ion gradients

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5
Q

what is the HCN channel

A

found in pacemaker cells
pacemaker cell membranes contain HCN-gated channels (hperpolarisation-activated, cyclic nucleotide-dependent nonspecific channels)

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6
Q

how is the HCN channels involved in phase 4 of the cardiac cycle

A

activated by hyperpolarusation
HCN mediated a funny current - simultaneous potassium ion efflux and sodium ion influx
sodium ion influx dominates causing slow depolarisation of membrane
reaches threshold
upstroke inactivated HCN

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7
Q

what is phase 0 of the ventricular myocyte action potential

A

sodium ion channels open
permeability to sodium ion increases
membrane potential approx -90mV

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8
Q

what is phase 1 of the ventricular myocyte action potential

A

sodium ion channels close; fast potassium ion channels open
permeability to sodium ions decreases
membrane potential approx 20mV

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9
Q

what is phase 2 of the ventricular myocyte action potential

A

calcium ion channels open; fast potassium ion channels close
permeability to potassium ions decreases and permeability to calcium ions increases
membrane potential approx 10mV

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10
Q

what is phase 3 of the ventricular myocyte action potential

A

calcium ion channels close; slow potassium ion channels open
permeability to potassium ions increases and permeability to calcium ions decreases
membrane potential approx -55mV

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11
Q

what is phase 4 of the ventricular myocyte action potential

A

resting potential

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12
Q

how do the sympathetic nerves effect heart rate

A

activation causes release of noradrenaline - binds to beta1-adrenoceptors on the cardiac pacemaker and myocyte cell membranes
increases opening of HCN channels in pacemaker cells - increases sodium ion influx
opens calcium ion channels
increases in slope of pre potential (phase 3)
heart rate increases 75 –>113

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13
Q

what would we give to slow heart rate

A

noradrenaline

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14
Q

what effects does the parasympathetic nerves have on heart rate

A

activation causes release of acetylcholine - binds to muscarinic cholinergic receptors
decreases opening of HCN channels - decreased sodium ion influx
slows opening of calcium ion channels - decreases calcium ion influx
opens additional potassium ion channels - increases potassium efflux
hyperpolarises membrane and reduces slopes of prepotential
heart rate decreased 75 –> 50

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15
Q

what is the vagal tone to the heart

A

intrinsic rate of firing of SAN cells ~100-110 Aps per min
constant tonic activation of some parasympathetic nerves on SA node

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16
Q

when does early after depolarisation occur

A

occur when normal heart rate low - suppressed by high heart rate
occurs when AP prolonged - some calcium channels inactivates during shoulder, reactivate to give EAD, calcium L channels, calcium T channels, need different drugs to Rx

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17
Q

what is delayed afterdepolarisations

A

seen at increased heart rates
associated with elevated [Ca2+]
ca2+ activation of Na/K channels (depolarising)
NaCa exchange 3:1 - electrogenic
toxic doses of cardiac glycosides

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18
Q

what are beta agonists

A

slows heart rate rhythms or bradycardias - need to increase heart rate

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19
Q

what are 2 examples of beta agonists

A

atropine - switch of vagus nerve - muscarinic antagonist drug
isoproterenol - activate beta receptors

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20
Q

what is class 1 of the Vaughan Williams classifications

A

sodium channel blockers
drugs to treat abnormal fast heart rhythms - tachycardia
lidocaine/lignocaine

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21
Q

what is class 2 of the Vaughan Williams classifications

A

beta blockers
atenolol, metoprolol, sotalol

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22
Q

what is class 3 of the Vaughan Williams classifications

A

potassium channel blockers - effect the last bit of the action potential - takes longer to reset so action potential lasts longer
amiodarone

23
Q

what is class 4 of the Vaughan Williams classifications

A

calcium channel blockers
effect upstroke of SA node
effect plateau of ventricular
verapamil

24
Q

what is adenosine used for

A

drugs to treat adnormally fast heart rhythms - tachycardia

25
Q

which drugs are used in the treatment of cardiac arrest

A

systole - adrenaline/epinephrine
ventricular fibrillation - amiodarone, lignocaine

26
Q

what is atropine

A

naturally occurring antimuscarinic alkaloid
blocks vagal inhibition of sinus and AV node
intravenous bolus administration
predominately hepatic metabolism
short half lifer

27
Q

what are the anticholinergic adverse effects

A

dry mouth
mydriasis
postural hypotension

28
Q

what are the 3 drug groups of class 1 drugs

A

class 1a - lengthen action potential duration and refractory period e.g. quinidine, propafenone, disopyramide
class 1b - shorten action potential duration and refractory period e.g. lignocaine/lidocaine
class 1c - no effect on action potential duration and refractory period, delay conduction velocity in purkinje fibres e.g. flecainide

29
Q

what is the action of class 1b drugs

A

e.g. lidocaine
blocks fast sodium channels and slows phase 0 depolarisation
shortens action potential duration
specific effect on rapidly depolarising tissue

30
Q

what are the indication of class 1b drugs

A

ventricular arrhythmias

31
Q

what is the pharmacology of class 1b drugs

A

short half life - must be given a bolus plus IV infusion
not absorbed via oral route (hepatic first pass metabolism)
hepatic clearance decreased in elderly, heart failure, liver disease

32
Q

what are the adverse effects of class 1b drugs

A

hypotension, heart block
neurotoxicity

33
Q

what are the types of class 2 beta blockers

A

non-cardioselective - also blocks beta2 receptors e.g. propranolol
cardioselective - less potent blockers of beta2 receptors e.g. atenolol
others - e.g. beryllium

34
Q

what is the pharmacology of beta blockers

A

can be beta 1 selective (atenolol, metoprolol) or beta1, beta 2 non-selective (propranolol)
oral and IV (metoprolol, propranolol) use
first pass hepatic metabolism, e.g. propranolol
renal excretion e.g. atenolol

35
Q

what is the action of beta blockers

A

beta adrenoceptor antagonists
reduce intrinsic rate in sinus and AV nodes
reduces heart rate, blood pressure and cardiac work
reduces renin secretions

36
Q

what are the adverse beta 1 effect of beta blockers

A

bradycardia
heart failure

37
Q

what are the adverse beta 2 effects of beta blockers

A

exacerbation of asthma
cool peripheries
muscular aches
worsening intermittent claudication

38
Q

what are the other adverse effects of beta blockers

A

fatigue nightmares, sleep disturbances
withdrawal effects (angina, MI)
unawareness of hypoglyceamia

39
Q

what is the action of class 3 drugs - amiodarone

A

prolongs action potential duration and refractory period
lengthened QT interval on ECG

40
Q

what are the indications of class 3 drugs - amiodarone

A

effective for ventricular and supra ventricular tachycardia
first line for treatment of ventricular fibrillation
improves survival in patients with recurrent ventricular tachycardia

41
Q

what is the pharmacology of class 3 drugs - amiodarone

A

long half life
hepatic metabolism

42
Q

what are the adverse effects of class 3 drugs

A

serious adverse effects limit use to high risk patients

43
Q

what are the serious adverse effects of amiodarone

A

thyroid disturbance
pulmonary fibrosis
pro-arrhythmia and torsade de pointes
peripheral neuropathy
hepatitis
blue-grey skin discolouration

44
Q

what are the 3 classes of calcium channel blockers

A

dihydropyridines
benzothiazepines
phenylalkylamine

45
Q

what are dihydropyridines

A

nifedipine, amlodipine
predominately vascular effects (arterial vasodilation)

46
Q

what are benzothiazepines

A

diltiazem
mixed vascular and cardiac effects

47
Q

what are phenylalkylamine

A

verapamil
predominately cardiac effects (negative ionotrope and chronotrope, anti arrhythmic)

48
Q

what is an example of a class 4 drug

A

verapamil

49
Q

what is the action of class 4 drugs

A

calcium channel blockers
slows phase 1 and 2; slow calcium entry
reduces rate and conduction velocity in sinus and AV nodes

50
Q

what are the indication of class 4 drugs

A

supraventricular arrhythmias

51
Q

what is the pharmacology of phase 4 drugs

A

actions on heart&raquo_space; actions on blood vessels
oral and IV use
first pass hepatic metabolism

52
Q

what are the adverse effects of class 4 drugs

A

heart failure, hypotension
constipation
vasodilation, oedema, flushing

53
Q
A

CM2001 (13 decks)

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