2-cardio Flashcards by Emily Liu

what is the role of the sinoatrial node

its the fastest pacemaker and dominates the rhythm normally

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

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

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

the AV node

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what is the role of the purkinje fibres

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

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

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

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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what happens if the SA node impulse is not extinguished

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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what can cause dysrhythmias (general)

when the timing of impulse conduction is disturbed

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what is the definition of arryhthmia

changes in normal cardiac rhythm

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what can cause arrhythmias (4 causes)

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

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what are symptoms of dysrhythmias

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

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can dysrhythmias be fatal

yes

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how do you name dysrhythmias

named after point of origin
ex: atrial dysrhythmias
ventricular dysrhythmias

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

fibrillation>flutter>tachycardia

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

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

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are ventricular dysrhythmias or supraventricular dysrhythmias more dangerous than supraventricular

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

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when do you use AV blocking drugs

for superventricular dysrhythmias

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where are the “fast” cardiac action potentials

purkinje fibres, atria, ventricles

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where are the “slow” cardiac action potentials

SA and AV nodes

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what happens in phase 0 of fast AP

Na+ goes in (rapid depolarization)

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what happens in phase 1 of fast AP

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

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what happens in phase 2 of purkinje AP

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

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what happens in phase 3 of fast AP

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

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what happens in phase 4 of fast AP

Study These Flashcards

pacemaker depolarization

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

what happens in phase 0 of slow AP

Ca++ and Na+ go in

what happens in phase 3 of SA node AP

K+ goes out

what happens in phase 4 of SA node AP

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

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

SA node more Ca++

what is the P wave

atrial depolarization

what is the QRS complex

ventricular depolarization

what is the T wave

ventricular repolarization

what is the PR interval

A-V conduction time

what is the QT interval

duration of ventricular AP

what happens to impulse direction with damaged tissue

normal conduction blocked BUT retrograde impulses propagate slowly

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

when its block normal and slow retrograde

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

dysrhythmia

which adrenergic receptors are found in all parts of the heart

beta1

name 6 effects that beta agonists have on the heart

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

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

``` by Gs (adenylyl cyclase, cAMP, phosphorylation of ion channels via PKA) ```

what causes the positive chronotropic effect (general)

the effect of b1 adrenergics on the heart

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

increase of slope of phase 4 pacemaker in SA node | resting membrane potential gets to threshold sooner

what ion causes the positive inotropic effect

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

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

decreases PR interval (increase AV conduction) | enables high HR but can lead to dysrhythmia

what do b1 agonists do to ventricular AP duration

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

what do b1 agonists do to purkinje fibre (2)

increase its rhythmicity (increases slope of the pacemaker potential) good for emergency pacemaker but can lead to dysrhythmias

when do early after depolarizations occur

in the plateau

when do late afterdepolarizations occur

from resting potential

what causes late and early afterdepolarizations to occur

calcium overload and excess activation of Na/Ca exchanger

what nerve is the main parasympathetic nerves in the heart

vagus nerve

where do sympathetic nerves go to the heart

everywhere

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

M2 receptors (muscarinic), Gi

where are M2 receptors located on the heart?

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

what effects do M2 agonists have on chronotropy?

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

what are 3 main effects of M2 on heart

- negative chronotropic effect - atria shortens AP & refractory - AV node increases PR interval

what does M2 agonists do to the atria

shortens AP duration and reduces refractory period

what does M2 agonists do to AV node

conduction block or delay, increased P-R interval

why does A-V conduction increase with beta adrenergics

because they increase SA node so the ventricles gotta keep up

what does atropine do to heart? why?

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

2-cardio Flashcards

(58 cards)