2-cardio Flashcards
what is the role of the sinoatrial node
its the fastest pacemaker and dominates the rhythm normally
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
what part of the heart protects from excessive electrical activity in supraventricular tissues
the AV node
what is the role of the purkinje fibres
some pacemaker activity, can help if both SA and AV node fail
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
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
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
what can cause dysrhythmias (general)
when the timing of impulse conduction is disturbed
what is the definition of arryhthmia
changes in normal cardiac rhythm
what can cause arrhythmias (4 causes)
delayed after depolarization
abnormal pacemaker activities
heart block (damaged region of the heart)
re-entry
what are symptoms of dysrhythmias
palpatations (racing heart beat, pounding heart, skipping beats), fainting or asymptomatic
can dysrhythmias be fatal
yes
how do you name dysrhythmias
named after point of origin
ex: atrial dysrhythmias
ventricular dysrhythmias
what is the order of flutter tachycardia and fibrillation from most to least impulses per min
fibrillation>flutter>tachycardia
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
are ventricular dysrhythmias or supraventricular dysrhythmias more dangerous than supraventricular
ventricular dysrhythmias, since the ventricles are needed to maintain systolic pressure
when do you use AV blocking drugs
for superventricular dysrhythmias
where are the “fast” cardiac action potentials
purkinje fibres, atria, ventricles
where are the “slow” cardiac action potentials
SA and AV nodes
what happens in phase 0 of fast AP
Na+ goes in (rapid depolarization)
what happens in phase 1 of fast AP
Na+ goes in to a lesser extent and Na+ inactivation causing rapid repolarization
what happens in phase 2 of purkinje AP
-Na+ Ca2+ go through ion channels
-electrogenic NCX operates (3Na+ in 1 Ca2+ out)
“plateau”
what happens in phase 3 of fast AP
K+ goes out (final repolarization) thru K+ voltage gated channels
what happens in phase 4 of fast AP
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
