A&P Test 4 Flashcards
What are the causes of arrhythmias?
abnormal rhythmicity in the pacemaker
* Firing faster/slower
* current sent in a wrong direction
* ectopic pacemaker
Shift of pacemaker from sinus node
Blocks at different points in the transmission
* might cause ectopic pacemaker
Abnormal pathways of transmission in the heart
* normally have a very defined pathway and speed. Ectopic pacemakers might cause AP to go in a different path
Spontaneous generation of abnormal impulses from any part of the heart
* VRM increased
What can cause an ectopic pacemaker in a pacemaker cell?
Increased VRM
Things that increase VRM are things that prevent the heart from _________
Resetting itself
I.e Ischemia in the AV node increase VRM so that the AV node still fires but it is an abnormal beat aka arrhythmia
Anything that increases VRM increases the risk of what
An ectopic pacemaker
Increased K+ levels in the blood leads to an increased ________
VRM
Tachycardia
Abnormal Sinus rhythm where the SA node is firing faster than normal d/t an abnormal SA node. This generates a faster P wave
With sinus tachycardia we should have a normal ____ on the EKG and a short ______
normal looking EKG with a normal P wave
and Short PR interval
What defines Sinus Tachycardia?
HR >100 BPM
What causes ST?
- Increased body temperature
- Reflex stimulation of the heart by the sympathetic system or a loss of stimulation of the vagus system
What toxic conditions did Dr. Smidt mention that increase VRM and can cause ST?
Nicotine
Alcohol
Acidosis
Hyperkalemia
What is the definition of sinus bradycardia?
HR <60 BPM
a normal EKG, just slow
What happens in athletes with a physicological hypertrophy of the heart?
They have a high Stroke volume
Slow heart bc of high stroke volume, don’t need as many BPM
Vagal stimulation to slow down the HR if high HR isn’t needed
What causes sinus bradycardia?
Being an athlete (physiologic hypertrophy)
In general, having a ____ HR is a good thing
Low
If you have a high resting heart rate, your _____ probably isn’t what it is supposed to be
Stroke volume
High resting HR is usually d/t
Hyperthyroidism
Could be a valve problem
Causes for bradycardia
Usually d/t increased vagal
Neural reflex to drugs (increase in HR, baroreceptors see this, phenylephrine increases HR)
Decrease in sympathetic nervous system
Atrial tachycardia that comes and goes
Paroxysmal atrial tachycardia
What does Paroxysmal tachycardia look like in a pt.?
What would cause this?
Sometimes we have normal R-R intervals and sometimes we have fast HR
Something that temporarily blocks vagal stimulus. When the vagus nerve goes back to normal HR goes back to normal
What do the P & T waves look like atrial tachycardia?
T wave goes away, it is hidden under the QRS. They overlap and become indistinguishable.
P wave goes away when the _____
SA node is ischemic
When the SA node is blocked what happens?
The fastest self discharge rate tissue takes over as the pacemaker of the heart
Usually AV node
If AV node isn’t working then
Purkinje fibers take over but gives us a very slow heart rate
If you have a ventricular rate of 20 , what kind of activity can you do?
You can maybe walk around your house but can’t be a professional basketball player
Depending on which part of the AV node is sending out an AP what might happen?
You could have an inverted P wave d/t the AV sending retrograde AP towards the SA node.
What determines if we have an inverted P wave or possibly no P wave at all in relation to sinoatrial block?
Early part of AV node= inverted P wave
Later part of the AV node= retrograde AP takes a while and sometimes it might not be picked up as a negative P wave because electrical activity might be going on in the ventricles that mask the P wave
Why is it that sometimes you have an inverted P wave in sinoatrial block and sometimes you don’t see a P wave at all?
In an AP stimulated in the early part of the AV node it takes a bit for a normal AP to get to the ventricle so it gives the AP time to get to the SA node and provide an inverted P wave but if the AP was stimulated in the later part of the AV node then by the time the retrograde AP hits the SA node, there is electrical activity in the ventricles that mask the inverted P wave.
With all arrhythmias if the timing is off you have a
Decrease in Stroke volume
When the atria contract which valves are open?
The atrioventricular valves(tricuspid & mitral)
so that the atria can prime the ventricles while the ventricles are relaxed
If you have something that causes the ventricles to depolarize early it causes which valves to close?
Why is this a bad thing?
Early closure of the of the atrioventricular valves
Because now the atria contract against a closed valve which causes turbulence.
What does having early closure of the AV valves cause?
causes Damage to the valves and causes them to Calcify
Blood sloshing around and turbulence causes clots
What causes blood clots in the heart?
When atrial contractions are not coordinated with the ventricles. It is like pushing blood into a “brick wall” (closed AV valve) and turbulence results which allows blood to sit and form clots
physiology of a normal AV delay?
A delay at the AV node normally to hold off on firing the ventricles to give the atria time to have a coordinated contraction.
PR interval is .16
>.16 the more the abnormal block.
What causes an enhanced block at the AV node?
- Ischemia= increased VRM
Less voltage ion channels participating in the AP
-we already have slow ion channels here so if VRM gets higher then it takes an even longer period of time for the AP to get through the AV node. - Compression of AV bundle by remodeling after an MI or CHF. Patchwork to prevent the heart walls from blowing out.
If remodeling gets out of control and we have too much scar tissue at the AV node then it can compress the AV node and cause them to have a smaller internal diameter causing increase in resistance = slower AP conduction.
Could be calcifications but usually scar tissue - AV nodal inflammation
- Excessive vagal stimulation (V&X reflex)
- Excess digitalis/beta blockers-impair generation of AP at SA node and reduce speed of conduction at AV node
How does digitalis work?
Inhibits the Na+/K+ pump
Inhibiting the pump =more Na+ in the cell
NCX is a major way Ca++ gets pumped out of the heart cell and it only works d/t Na having a big gradient in the cell
Therefore digitalis results in a slower rate of Ca++ removal. Good if heart is failing as a last resort.
What is a last ditch effort for heart failure?
Digitalis
Why is digitalis dangerous?
It’s messing with something that is very important Na+/K+ pump and VRM.
It works on the Na+/K+ pumps all over the body
PDE inhibitors are not specific to
Just the heart. No absolute specify in any drug.
Incomplete heart block or 1st degree heart block is classified by PR interval being
> 0.20 seconds
Not a true block, it’s just a delay.
Have a P wave in front of every QRS.
Delay from P wave to QRS
2nd degree heart block is classified by
Dropped beats
PR interval increase beyond .25 seconds.
Atria has a faster heart beat than the ventricles in
2nd degree heart block
Mobitz type 1 second degree heart block is classified by:
What is another name for this type of block?
Abnormal amount of time between PR interval
Variable PR interval and sometimes beats are dropped
Wenckebach
“Irregular PR interval on each of the different heart beats”
Mobitz Type 2 second degree heart block is classified by:
Fixed ratio of P to QRS except some beats are dropped after the P wave. Has a fixed PR interval
Which Mobitz type is more dangerous?
Mobitz type 2
When is a pacemaker required in Mobitz type 1
when you get old and decrepit but not required for everyone
When pts haven’t seen the dr in a while and we do an EKG and we sometimes find which heart block?
Mobitz type 2.
Which heart block is cause for a pacemaker?
Mobitz Type 2
P to QRS complex ratio options in Mobitz type 2
P:QRS
2:1
3:2
3:1
Which heart block has some impulses pass through AV node and some do not but is overall very regular
Mobitz type 2
3rd degree or complete heart block is classified by:
Pathophysiology of having so many beats?
R-R interval is consistent
A bunch of random P waves all over the place
Total AV node block, relying on the ventricular escape (15-40 BPM)
Cardiac output is low.
Nervous system sees this and tries to get the heart to increase rate.
Might help the ventricles increase rate a little bit. Also increases the atria rate but AP are not making it past the AV node.
Which heart block has a complete dissociation of QRS from p waves
Complete heart block or 3rd degree
A flutter is defined by:
Circular reentry that is completely separate from the SA node.
A really slow conduction rate in the atria it leads to circular movements that involves the entire atria
What would happen if A flutter AP were at a faster rate?
AP would run into a refractory period which would not allow the conduction to generate an AP. Therefore A-flutter happens at a slower conduction rate.
Causes of A flutter
Atria are all stretched out makes it take longer for the conduction to make it around the heart
what disposes people to A flutter?
Conduction rate is slow
Atria is stretched out so there is more space around the heart (atrial hypertrophy)
In a flutter, the circular movement of AP makes the heart do what?
part of the atria contract and part of the atria relaxed. Does not function as a primer for the ventricle much at all
When looking at the EKG with A flutter you would see
High atrial rate but No P waves.
High ventricular rate if the AP is passed into the ventricle
Follows a predictable pattern
Which is worse, a fib or a flutter?
A flutter
in A fib what is happening in the heart?
A bunch of ectopic pacemakers give a vast variety of AP.
Gives us a very unpredictable pathway which makes little bits of atria contract at different times causes a “shaking” Smidt calls this “fluttering”
what predisposes us to a fib?
Atrial hypertrophy. More surface area to have goofy electrical activity in the heart
Age - main factor. (Heart stretches out with age)
What does the ineffective pumping “shaking” motion of the atria in a-fib cause?
Turbulence
Causes blood clots
Which atria is more likely to have a big clot or embolism and what can this cause?
More likely the r atria d/t it being more likely to be stretched out.
Clot can go into the respiratory vasculature which can turn into a PE
Conduction speed of the irregular QRS complexes in incomplete intraventricular block is lower than normal meaning it takes longer to get through the QRS. How does this look on an EKG?
What is the pattern of QRS complexes in this block?
a short and wide QRS complex
Normal, prolonged, repeat
What can you do for a fib?
Possibly go in and ablate them if they are in a bad spot. But you can’t ablate the entire atria.
What are circus movements?
Screwy movements of AP in the atria
What is a squiggly line where a p wave should be?
Disorganized electrical activity seen in A fib. No blood gets pumped during this
When does a lot of afib get diagnosed?
Older folks going in to get checked out. More likely at 70 years old and may have an uncomfortable feeling
Drugs for afib (A&P)
Blood thinner for forever
Phrase to describe complete AV block that happens at irregular times
Stokes-Adams Syndrome
Symptoms of Stokes-Adams Syndrome
Fainting or syncope
Why do patients faint with Stokes-Adams Syndrome?
Fainting d/t low bp since the heart has stopped beating at the AV node
Reliant on ventricular escape “overdrive suppression” when the Purkinje system kicks in which takes 5-30 seconds. After the Purkinje system kicks in the heart rate will be 15-40BPM
How long can your heart stop beating before you pass out? “threshold for us maintaining consciousness.”
7-8 seconds
What type of block is this?
Incomplete intraventricular block: alternans
slow conduction in the ventricular purkinje system is what type of block?
Incomplete intraventricular block: alternans
Pretty much anything that causes a slow AV node can also cause
Slowing of the ventricular complex
Short and tall alternating QRS complexes are due to
The tissue cannot repolarized itself as fast as it normally would so the ventricles are not repolarized all the way.
More likely to see alternans when?
It is typically d/t a problem resetting the Purkinje system.
you would see this with high ventricular tachycardia d/t the ventricles not being able to reset all the way before the next contraction.
Ratio of short to tall QRS complexes in incomplete intraventricular block?
1:1
In electrical Alternans is there a p wave on the EKG?
no, the P wave is hidden in t wave
Premature ventricular contractions are d/t
Abnormal source of action potential in the atria as a result of ischemia, irritation or calcified plaques in the atria
Not all ectopic AP in the atria make it to the
Ventricles
ectopic atrial beats that make it to the ventricles cause
Abnormal filling of the ventricles
Not an effective primer
What can’t we see on the EKG with PVCs
Abnormal filling d/t both the ventricle not having enough filling time (it happened before the heart was reset) and d/t ectopic AP in the atria not going through the normal pathway making it not a coordinated, regular beat
What is a pulse deficit?
Radial pulse being heard as a quieter sound d/t less SV during that beat
What are the different ways P waves could present on a PVC?
Could be inverted
Could be missing
If the p wave in a PVC is early and inverted it is coming from a _________ AV junction source
If the p wave in a PVC is late and inverted it is coming from a _________ AV junction source
High AV junction source
Low AV junction source
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Me
What is the explanation for why there is prolonged length of QRS complex in PVCs?
If it is prolonged then the AP probably originated in a ventricular muscle and was fed into other muscle before finally making it into the purkinje system.
Why is there a higher voltage deflections in PVCs?
Normal: portion of the electrical activity in the heart obscured d/t both Right and Left ventricles being coordinated.
Left side has more tissue .01 sec longer in the left ventricle.
When you have coordinated tissue that cancels out some of the electrical
Ectopic starts in the lateral wall of L ventricle
L ventricle depolarizes first, takes longer because conduction system is being bypassed.
When it gets to the right side, you would see massive current d/t 50/50 tissue depolarized vs repolarized = high depolarization.
Result of ectopic pacemaker in the lateral walls of a ventricle on the EKG Is a (effects on QRS)
taller and wider PVC
If you have an abnormal depolarization in a PVC you would expect an
abnormal repolarization.
Inverted T wave most of the time
Lateral wall depolarizing outside to in probably means it will repolarize inside to out.
What is a drug that generates a “long QT syndrome” or EAD?
Benadryl d/t mACh-R antagonism
PVCs are
dangerous
In PVCs, the ______ is overly active.
conduction system
Ventricular rate is higher than the typical pacemakers in the heart.
Not sure exactly why
all the problems/stressors of grad school that =PVCs
Caffeine, nicotine, stress and lack of sleep
Ventricular tachycardia: paroxysmal is classified by:
Originating in the ventricular conduction system: accelerated, positive, prolonged (width) QRS with high voltage
R to R intervals are short
P waves usually aren’t visible but might be inverted
Paroxysmal means
“Not a great explanation”
Paroxysmal ventricular tachycardia is the result of_____ or ______ making it very dangerous
severe Ischemia
Infarct
What is the arrhythmia right before vfib?
Paroxysmal ventricular tachycardia
AP right after Absolute Refractory period but before the heart is reset is called _____
How does this effect the output of the heart?
EAD = Crappy AP= crappy pumping performance. Not a ton of Ca++ coming in.
Bunch in a row = severely compromised output of the heart
What determines how much force the heart can generate?
Ca++ coming in through Ca++ channels
Repetitive Premature depolarization in an EKG looks like a
Long QT interval
Predispose to EAD?
- increase in sensitivity to Ca++ channels like d/t lots of Beta stimulation. This increases phosphorylation of L-Type Ca++ channels.
- mACh-R antagonist- atropine given unnecessarily or too high of a dose
mACh-R looks a lot like ______receptors
histamine
Long QT syndrome is a precursor to
Tornadoes de pointes which is a precursor to vfib
If pumping is bad for long enough the heart can’t_____
Perfuse itself.
Output (pumping) is bad leads to the aortic blood pressure being bad and since the coronary arteries have openings in the aorta then coronary blood flow is effected. When coronary blood flow is effected then the heart cells can’t reset itself=vfib
V fib happens when there are a lot of ______ pacemakers in the ventricles. This makes the ventricles ______
ectopic
quiver/flutter
How to reset the heart in v-fib?
pump enough current into the heart to reset the whole thing. (shocking them)
If the heart has been too ischemic too long then shocking the heart to reset it is
not going to do anything- the heart can’t overcome
Typically the atria are separated from the ventricles in depolarization but in this syndrome the high lateral ventricular tissue connects to atria.
Bundles of Kent
What is the physiology of increased body temperature causing increased HR?
Increased temp increases the energy demands of the body trying to keep the body from overheating.
What is the physiology of reflex stimulation of the heart by the SNS or vagal system causing increased HR?
Usually some other problem causes an increase or decrease in SNS or Vagal stimulation.
i.e.
-bleeding out would increase the HR d/t low BP
-Ventricles are slower than normal causing BP to be low. ANS detects this and increases SA node firing.
It is not uncommon to add say a beta blocker to other antiarrhythmics with some arrhythmias to prevent what?
reflex tachycardia
Some people have abnormal electrical pathways from the AV node to the ventricles d/t genetics called_____
The most common one is the
Accessory pathways
Bundle of Kent
What percent of the population has an extra electrical pathway between the atria and ventricles called the bundles of Kent?
0.2%
If the bundle of Kent becomes a problem what can you do?
you can ablate them. Some people live with them and they don’t even know.
What type of arrhythmia is this?
Sinus tachycardia
What type of arrhythmia is this?
Sinus bradycardia
What type of arrhythmia is this?
SVT: paroxysmal atrial tachycardia
What type of arrhythmia is this?
Sinoatrial block
What type of arrhythmia is this?
Incomplete block: 1st degree heart block
What type of arrhythmia is this?
Incomplete Second degree heart block: Mobitz type 1
What type of arrhythmia is this?
Incomplete 2nd degree heart block: Mobitz Type 2
What type of arrhythmia is this?
Complete 3rd degree heart block
What type of arrhythmia is this?
Atrial flutter
What type of arrhythmia is this?
Atrial fibrillation
What type of arrhythmia is this?
Incomplete intraventricular block: alternans
What type of arrhythmia is this?
PVC: atrial source
What type of arrhythmia is this?
PVC: AV node/ bundle source
What type of arrhythmia is this?
PVC
What type of arrhythmia is this?
Ventricular tachycardia: paroxysmal
What type of arrhythmia is this?
Ventricular fibrillation
