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PMCOL 343 > 2-cardio > Flashcards

2-cardio Flashcards

1
Q

what is the role of the sinoatrial node

A

its the fastest pacemaker and dominates the rhythm normally

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2
Q

what is the role of the atrioventricular node node (3)

A

secondary pacemaker, takes over if SA node is damaged
protects ventricles from excessive electrical activity in supraventricular tissues

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3
Q

what part of the heart protects from excessive electrical activity in supraventricular tissues

A

the AV node

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4
Q

what is the role of the purkinje fibres

A

some pacemaker activity, can help if both SA and AV node fail

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5
Q

what are the 6 steps of cardiac activity starting from SA node to ventricular contraction

A 
1-impulse from SA node
2-atrial contraction
3-AV node
4-bundle of His
5-Purkinje fibres
6-ventricles contract
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6
Q

what does “extinguish by collision” mean and why do you need it

A

impulses from SA node divide and pass through the heart, will cancel out any two AP that come together and collide

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7
Q

what happens if the SA node impulse is not extinguished

A

then there may be extra beats or dysrhythmias, since the haert has more time to repolarize and be receptive to stimuli

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8
Q

what can cause dysrhythmias (general)

A

when the timing of impulse conduction is disturbed

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9
Q

what is the definition of arryhthmia

A

changes in normal cardiac rhythm

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10
Q

what can cause arrhythmias (4 causes)

A

delayed after depolarization
abnormal pacemaker activities
heart block (damaged region of the heart)
re-entry

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11
Q

what are symptoms of dysrhythmias

A

palpatations (racing heart beat, pounding heart, skipping beats), fainting or asymptomatic

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12
Q

can dysrhythmias be fatal

A

yes

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13
Q

how do you name dysrhythmias

A

named after point of origin
ex: atrial dysrhythmias
ventricular dysrhythmias

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14
Q

what is the order of flutter tachycardia and fibrillation from most to least impulses per min

A

fibrillation>flutter>tachycardia

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15
Q

what do supra ventricular dysrhythmias do to the heart (where affected)

A

ventricular contraction is affected but the issue is from places above (supra) the ventricles

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16
Q

are ventricular dysrhythmias or supraventricular dysrhythmias more dangerous than supraventricular

A

ventricular dysrhythmias, since the ventricles are needed to maintain systolic pressure

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17
Q

when do you use AV blocking drugs

A

for superventricular dysrhythmias

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18
Q

where are the “fast” cardiac action potentials

A

purkinje fibres, atria, ventricles

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19
Q

where are the “slow” cardiac action potentials

A

SA and AV nodes

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20
Q

what happens in phase 0 of fast AP

A

Na+ goes in (rapid depolarization)

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21
Q

what happens in phase 1 of fast AP

A

Na+ goes in to a lesser extent and Na+ inactivation causing rapid repolarization

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22
Q

what happens in phase 2 of purkinje AP

A

-Na+ Ca2+ go through ion channels
-electrogenic NCX operates (3Na+ in 1 Ca2+ out)
“plateau”

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23
Q

what happens in phase 3 of fast AP

A

K+ goes out (final repolarization) thru K+ voltage gated channels

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24
Q

what happens in phase 4 of fast AP

A

pacemaker depolarization

  • Na K dependent
  • activation of HCN channels
  • NaK pump restores ionic gradient
25
Q

what happens in phase 0 of slow AP

A

Ca++ and Na+ go in

26
Q

what happens in phase 3 of SA node AP

A

K+ goes out

27
Q

what happens in phase 4 of SA node AP

A

Ca++ dependent pacemaker, regenerating heart beat and causing further depolarization

28
Q

does purkinje or SA node have a more Ca++ dependent action potential

A

SA node more Ca++

29
Q

what is the P wave

A

atrial depolarization

30
Q

what is the QRS complex

A

ventricular depolarization

31
Q

what is the T wave

A

ventricular repolarization

32
Q

what is the PR interval

A

A-V conduction time

33
Q

what is the QT interval

A

duration of ventricular AP

34
Q

what happens to impulse direction with damaged tissue

A

normal conduction blocked BUT retrograde impulses propagate slowly

35
Q

what is worse - no conduction in heart or a blocked normal conduction and slow retrograde

A

when its block normal and slow retrograde

36
Q

what happens with a one way conduction block (what does it cause)

A

dysrhythmia

37
Q

which adrenergic receptors are found in all parts of the heart

A

beta1

38
Q

name 6 effects that beta agonists have on the heart

A

positive chronotropic, positive inotropic, increased AV conduction, shortened ventricular AP duration, increased purkinje fiber rhythmicity, generation of EAD and DADs

39
Q

describe the mechanism of action of beta 1 receptors in the heart

A 
by Gs
 (adenylyl cyclase, cAMP, phosphorylation of ion channels via PKA)
40
Q

what causes the positive chronotropic effect (general)

A

the effect of b1 adrenergics on the heart

41
Q

how do beta 1 agonists have a positive chronotropic effect in terms of ECGs

A

increase of slope of phase 4 pacemaker in SA node

resting membrane potential gets to threshold sooner

42
Q

what ion causes the positive inotropic effect

A

increase ca influx through L type Ca2+ channels in phase 2 = more forceful contraction

43
Q

what happens to AV conduction with b1 agonist and what does it cause

A

decreases PR interval (increase AV conduction)

enables high HR but can lead to dysrhythmia

44
Q

what do b1 agonists do to ventricular AP duration

A

shortens the ventricular AP duration enables due to Ca2+ influx (high HR but can lead to dysrhythmia)

45
Q

what do b1 agonists do to purkinje fibre (2)

A

increase its rhythmicity (increases slope of the pacemaker potential)

good for emergency pacemaker but can lead to dysrhythmias

46
Q

when do early after depolarizations occur

A

in the plateau

47
Q

when do late afterdepolarizations occur

A

from resting potential

48
Q

what causes late and early afterdepolarizations to occur

A

calcium overload and excess activation of Na/Ca exchanger

49
Q

what nerve is the main parasympathetic nerves in the heart

A

vagus nerve

50
Q

where do sympathetic nerves go to the heart

A

everywhere

51
Q

what types of receptors mediate parasympathetic effects on heart? what GPCR are they?

A

M2 receptors (muscarinic), Gi

52
Q

where are M2 receptors located on the heart?

A

exclusively on supraventricular tissue (SA/AV nodes and atria)

53
Q

what effects do M2 agonists have on chronotropy?

A

negative chronotropy (SA node slows, M2 hyperpolarizes SA node (activates GIRK), decreased slope of pahse 4 pacemaker)

54
Q

what are 3 main effects of M2 on heart

A
  • negative chronotropic effect
  • atria shortens AP & refractory
  • AV node increases PR interval
55
Q

what does M2 agonists do to the atria

A

shortens AP duration and reduces refractory period

56
Q

what does M2 agonists do to AV node

A

conduction block or delay, increased P-R interval

57
Q

why does A-V conduction increase with beta adrenergics

A

because they increase SA node so the ventricles gotta keep up

58
Q

what does atropine do to heart? why?

A

tachycardia and increased AV conduction
caused by the fact that the heart is under continual parasympathetic tone

PMCOL 343 (31 decks)

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