Test 4 🩷 Flashcards
Cardiac
How does cardiac muscle contract?
As a unit–similar to smooth muscle
How are cardiac cells connected to eachother?
Intercalated discs
What provides a pathway for neighboring cells to communicate?
Gap junctions
Where are gap junctions located in each cardiac cell?
the border of each cell–curvy/ jagged (intercalated discs)
How do intercalated discs allow for more gap junctions?
The cells fit together with the next cell creating more surface area for gap junctions
What is the pattern of cardiac muscle?
Striated
What does the cardiac muscle pattern correspond with?
alignment of actin and myosin
What type of sarcomeres are similar to cardiac sarcomeres?
Heart sarcomeres look similar to skeletal sarcomeres
How many nuclei per cardiac muscle cell?
one nucleus per cardiac cell
What is the function of stem cells?
slow process to generate new cardiac cells and patch areas where cells have died
Why wouldnt you be able to generate cardiac cells to replace tissue after MI?
Stem cells wouldnt be able to produce new cells fast enough
injury overwhelms the replacement system
What are fibroblasts?
Cells in the heart that deposit scar tissue
When do fibroblasts lay scar tissue in the heart?
usually at a controlled rate
can be uncontrolled in setting of disease processes (CHF)
What is an example of a disease where fibroblasts are overactive?
CHF–excessive scar tissue
What drug can be used to slow down fibroblast activity and prevent unnecessary scar tissure deposition?
ACE inhibitors
How do ACE inhibitors prevent unnecessary scare tissue deposition?
ACE inhibitors block RAAS-prevent growth factor from angiotensin II and prevent excess scar tissue in the heart
Which group should not be prescribed ACE inhibitors?
Pregnant women–angiotensin II is important for development of fetus and ACE inhibitors would block that growth/development
How does scar tissue mess with transduction system in the heart?
Scar tissue doesnt contract or conduct action potentials
What is the arrangement of cardiac ventricular muscle?
Syncytial connections
How many layers does ventricular muscle have?
2
How are the cells oriented in ventricular muscle layers?
The layers have cells oriented in different directions (perpendicular)
How do the ventricle contract?
They squeeze and rotate in opposite directions
What analogy was used in lecture to compare to ventricular contraction?
Wringing water out of a wet towel
What is meant by “top part of heart”?
Atria
What is meant by “lower half of heart”?
ventricles- everything below AV node
What makes up the vast majority of heart cells?
muscle tissue–can produce lots of force
What in the muscle cell is responsible for producing force when stimulated by an action potential?
Myofibrils–lots of myofibrils in each cardiac muscle cell
How is specialized conduction tissue different from muscle tissue?
conduction tissue does not produce force like muscle tissue
What is the main job of specialized conduction tissue?
Send action potentials quickly
How does conduction tissue send action potential quicker than other tissues?
Conduction tissue doesnt have myofibrils inside–less stuff inside so action potential can travel quicker
What is the deepest layer of cardiac muscle?
Sub-Endocardium
In which cardiac muscle layer do most MIs occur and why?
Sub-endocardium
wall pressure are highest in the deep parts of the heart muscle
Where are cardiac wall pressures the highest?
The deeper in the heart= higher wall pressure
Why is high wall pressure a bad thing?
makes it more difficult to perfuse
What are 2 thing that increases chances of cardiac ischemia?
Clogged vessels and really high wall pressures
Where is the endocardium and what is it composed of?
I cell layer thick endothelial layer
deep cardiac muscle
What makes up the bulk of the cardiac muscle wall?
Myocardium
What is the most superficial layer of the heart chambers?
Epicardium
Where do the major blood vessels sit in the heart?
All major BVs sit on top of the epicardium
some penetrate deep in some areas
What is the area directly outside of the epicardium?
Pericardiac space
What is contained in the pericardial space?
filled with a small amount of fluid and decent amount of mucus
what is the function of the pericardial space?
Mucus decreases friction with cardiac movement
What happens if there is friction in the pericardium?
It is very painful
What causes friction in the pericardium?
inflammation of pericardial space or loss of fluid/mucus in this area
What is the name of the connective tissue sack that encloses the heart?
Pericardium
What are the 2 layers of the pericardium?
Parietal pericardium
Fibrous pericardium
What is the difference between the parietal pericardium and the fibrous pericardium?
Parietal pericardium is the inner layer–stretchy
Fibrous pericardium is the outer layer–stiff and difficult to expand
How does the cardiac sarcomere look when the heart is relaxed?
under stretched–no H band because actin filaments are overlapping with each other
How does the cardiac sarcomere look when contracting?
myosin moves to z discs–provides good EF/SV
What is the purpose of the Purkinje fibers?
Conduct action potentials–no contraction
What is Vrm of purkinje fibers?
-90mV
How does the typical action potential of purkinje fiber look?
Extended action potential with plateau phase
What are both purkinje fibers and ventricles permeable to at rest?
slight permeability to Na+–not constantly permeable to Na+
Are purkinje fibers able to self depolarize?
Yes, but it takes them a long time since Vrm is -90mV and threshold is -70mV
Do purkinje fibers usually fire their own action potentials?
they can, but self depolarization rate is very slow
T or F: If things are working normally in the heart, purkinje fibers rely on APs generated from neighbor cells to depolarize
True–neighbor cell generates action potential and spreads to purkinje fibers
What is the threshold of purkinje fibers and ventricular muscle?
-70mV
What happens if there is no action potential from upstream neighbor cell?
Cell would eventually conduct own action potential but there would be a lag time (maybe 30 seconds before 1st AP)
What is Vrm for ventricular muscle?
-80mV
What causes ventricle to contract?
Action potential passing through
If there is a complete heart block at the AV node, would it take 30 second for every beat?
No, It takes a lot longer for the 1st beat to come back but once its gets going it will beat more regular just at a slower rate
What type of surgical manipulation can generate a complete heart block?
eye manipulation–sensors in the eye orbit and body doesnt like when they are messed with
What is V + X (5 and dime) reflex?
pressure in the eye socket sent to cranial nerve V (trigeminal) and eye socket pressure sensors send info to brainstem which sends message to vagus nerve (X) causing massive vagal output (heart rate drop)
What is cranial nerve V and what does it do?
Trigeminal nerve–in control of sensory perception in the eye socket
big nerve on side of face
What happens in response to massive vagal output from the CNS?
Prevents transmission of action potentials at the AV node–HR may go to 0 but come back in 30 seconds
What is necessary for heart cells to spontaneously depolarize?
Time
What does the slight slope in the resting phase between heart beats indicate?
Increased sodium permeability of the cell at rest (sodium leakiness)
Describe phase 4 of the cardiac action potential:
Resting membrane potential
slowly getting more positive with Na+ leakiness
Describe phase 0 in ventricular cardiac action potential:
Action potential is set off by Na+ coming into cell from gap junctions of neighbor cell
fast Na+ channels open briefly
Describe phase 1 of purkinje cardiac action potential:
K+ channels close during action potential
fast T-type Ca2+ channels open
When do K+ channels close during cardiac action potential?
End of phase 0 through phase 1 and 2 for duration of action potential
K+ channels start to open back up at very end of phase 2
What is happening during phase 2 of cardiac action potential?
Plateau phase–L-type Ca2+ channels open for extended period then close
What is happening at phase 3 of ventricular action potential?
K+ channels open back up and reset cell back to phase 4 (Vrm)
How long is the typical cardiac action potential and why is it necessary?
200ms–allows for coordinated contraction
What phase correlates with when the heart is contracting?
Phase 2–longer plateau means longer contraction
Shorter plateau is shorter contraction
Why do we need coordination between superficial and interior parts of the heart?
Allows heart to produce a lot of force and eject a lot of blood
What is the only outward current during a heartbeat?
K+
What is meant by inward rectifying K+ channels?
Current of K+ is still outward, but it is in response to something else coming in (like Ca2+ or Na+)
When is K+ current the highest during cardiac action potential?
K+ current is high at rest and during repolarization
When is K+ current depressed during cardiac action potential?
During duration of action potential
makes sense because K+ channels close
What is the sodium permeability compared to calcium permeability in cardiac action potential?
Large increase in Na+ permeability compared to less significant increase in Ca2+ current
Why is there not as much Ca2+ current compared to Na+ current in cardiac AP?
Not as much Ca2+ coming in because not very many Ca2+ channels in the cell wall
What is Ohms law?
V=iR
Voltage= current x resistance
What does “i” represent?
ionic current
What 2 things does ionic current depend on?
Number of channels open
electrochemical gradient of the ion
What par of the nervous system primarily controls nodal tissue?
Parasympathetic
What innervates the SA node?
Right vagus nerve
What innervates the AV node?
Tips of the left Vagus nerve
What is the main function of the parasympathetic nervous system at the heart?
suppressed activity of pacemaker cells in the nodal areas of the heart
What is the function of sympathetic innervation at the heart?
Wide spread Innervation to the heart primarily the atria and ventricles
Where does the sympathetic chain connect at the heart?
Sympathetic chain has thick connections with atrial and ventricular muscle tissue
What is the primary catecholamine released from sympathetic nerves at the heart?
Norepinephrine
What receptors does norepinephrine interact with in the heart?
Beta receptors
Which areas of the heart have fast action potentials?
Ventricular conduction system (purkinje) and ventricular muscle cells
What is another term for ventricular muscle cell?
Ventricular myocyte
What is the peak of action potentials in ventricular myocyte?
+20mV
What amount of depolarization is happening in the ventricle muscle and ventricular conduction system?
100mV
How is the amount of depolarization in a ventricle determined?
Difference in charge between Vrm and peak of action potential
What does the EKG measure?
Sum of all current flowing between electrodes placed on the body
Which current does the EKG show?
All mV that is making its way around the heart
looking at depolarization or repolarization that is spreading through the heart
What is normal amplitude for QRS deflection?
1.5mV (a little over 3 boxes in amplitude)
How many mV is each small box on an EKG?
+0.5mV
What is the voltage on an EKG like compared to voltage generated with ventricle action potential?
Lower voltage on EKG compared to action potential
Why is the voltage so much lower on EKG compared to action potential?
A lot of the voltage is lost from the action potential in high resistance tissues
What is meant by high resistance tissues in the body?
Parts of the body that impede the flow of electrical current
What are examples of high resistance areas in the body?
Fat and air
What would you expect an EKG for someone with COPD to look like?
Lower QRS complex due to increased air which increases voltage lost
What happens to a tissue as it depolarizes or repolarizes?
There is a charge gradient between the part that has depolarized and the part that is repolarized
What would be the voltage if measured with a voltage meter of a resting cell?
0mV
What would be the voltage of a completely depolarized cell?
0mV
What would be the measured voltage of cell that is half way depolarized starting from the left?
High positive # voltage
What would be the measured voltage of a tissue that is halfway repolarized from left to right?
High negative # voltage
electrodes are traveling toward the anode
At what point is electrical current the highest in depolarization and repolarization?
When the cell has reached the 1/2 way point between depolarized and repolarized
biggest charge difference
If repolarization occurs from right to left, what would you expect the voltage meter to read when the repolarization if half way through?
Very positive #
Where is conduction system?
Conduction system is very deep in the heart wall
How does depolarization travel in the heart?
from inside to outside
Action potential starts in deep areas of the heart then makes its way to the surface of the heart as time passes
What is the first thing in the heart to depolarize?
Inside of ventricles
What depolarizes second to the inside of ventricles?
Outer layer of ventricular muscle depolarizes
How does repolarization in ventricular muscle start and spread in the heart?
Repolarization starts in superficial layers and travels to deeper layers of ventricular wall
Compare depolarization pattern and repolarization patter in the heart:
Repolarization is happening opposite order of depolarization
Explain how repolarization of ventricles is still positive deflection:
Epicardium is repolarizing before endocardium (spreads from outside to inside)
electrons are still coming towards positive electrode
If electrons are traveling toward positive electrode what would you expect on a voltage graph?
Positive deflection
If electrons are traveling away from the positive electrode what would you expect on a voltage graph?
Negative deflection
What electrical event is represented by the P wave?
atrial depolarization
What electrical event is represented by the T wave?
Ventricular repolarization
What electrical event is represented by QRS complex?
depolarization of ventricles
How does current travel through the ventricle?
electrons come from area of depolarization to areas of the heart that are still resting or that have repolarized
What is the first thing to completely depolarize in the heart?
interventricular septum
What happens to electrical current in a cell that has area of injury (ie ischemia)?
Ischemic area cant repolarize
little spot of depolarization creates current at rest when there shouldnt be
What type of current is there when the tissue resets after action potential?
there should be no current
What are examples that can cause and area of the cell to be chronically depolarized?
lack of nutrients–oxygen, glucose
obstruction like a blood clot
anything that leads to ischemia
What happens if part of a tissue cant get the nutrients it needs?
Tissue without enough energy will not be able to repolarize
What types of currents result from infarcted issues that do not electrically reset?
Currents of injury
What are currents of injury?
Current from a sick part of the cell at rest that should not be happening
How are currents of injury/ electrical abnormalities diagnosed?
12 lead EKG
What is the pacemaker of the heart?
SA node
What is the MOA of the SA node being the pacemaker?
Tissue at SA node depolarizes and reaches threshold faster than any other cell in the heart
What does SA nodal cell depolarization rate correspond with?
depolarizes decently fast to produce our normal heart rate of 72bpm
What is a normal heart rate in a health adult?
72bpm
What is the resting membrane potential of SA nodal cell?
-55mV
What is threshold potential in SA nodal cells?
-40mV
What causes the large increase in membrane potential at phase 4 in SA nodal cells?
HCN channels
NA+/Ca2+ leak channels
What allows the SA node to reach threshold quickly
large increase in membrane potential at phase 4 (at rest) so it doesnt take long to go from resting to threshold
What does HCN channel stand for?
Hyperpolarization and cyclic nucleotide channel
What do HCN channels do?
when open, they are non specific cation channels
allow Na+ and Ca2+ through
What is the majority of current through HCN channels?
Na+ primarily then Ca2+
Why is Na+ the primary current for HCN channels?
Na+ is smaller and fits through channel easier than Ca2+
Why doesnt K+ come out through HCN channels?
In theory the channel would allow it out, but there is so much Na+ and Ca2+ coming through it that K+ doesnt really move through it
Why are HCN channels called hyperpolarization?
HCN channels open when the cell reaches Vrm
Vrm in the heart is comparable to hyperpolarization
When do HCN channels open?
When the heart cell reaches Vrm
With increase cAMP/ Increased Beta activity
What does the cyclic nucleotide portion of HCN channels correlate with?
HCN channels can be controlled with cyclic nucleotides like cAMP
How does beta activity influence HCN channels?
Norepinephrine binding to to beta receptors in heart increases adenylyl cyclase which produces cAMP
What does the “A” in cAMP stand for?
Adenosine
With normal amounts of beta receptor activity, what can we expect in regards to HCN channels?
Normal amount of HCN channels operating during phase 4
What phase of the action potential do HCN channels open?
phase 4
What happens to HCN channels when a beta agonist is given?
increases cAMP and opens more HCN channels
What happens to the slope of phase 4 when a beta agonist is given?
more HCN channels open would increase the slope of phase 4 and decrease the time of phase 4
How does a beta agonist increase HR on a molecular level?
-stimulates adenylyl cyclase
-increases cAMP
-opens more HCN channels
-Vrm goes to threshold faster
-earlier AP
-increased HR
What happens to HCN channels with a beta blocker?
Less HCN channels open with phase 4
What happens to heart rate when atenolol is given on a molecular level?
-Less HCN channels open
-Reduced slope during phae 4
-Longer to reach threshold and generate AP
-Slower HR
What happens to the slope in phase 4 when a beta agonist is given?
Slope is steeper and less time in phase 4 leads to earlier APs
How does cholinergic and adrenergic signaling occur in the heart?
They antagonize eachother
What happens to membrane potential with activation of mACh-receptors?
The receptors provide a conduit for K+ to leave the cell so membrane potential is more negative
What happens to membrane potential with increased levels of acetylcholine?
More K+ channels are open so membrane potential decreases
What happens to the slope during phase 4 with increased acetylcholine?
the slope of the line is the same, it will just be a lower starting point and take longer to get to threshold
What does acetylcholine do to the heart?
Decreases HR by increasing K+ leaving the cell
What does beta adrenergic activity do to K+ channels?
increases cAMP and Shuts down K+
What do mACh-receptors do in regards to cAMP?
Decrease cAMP
How do mAch-receptors agonists decrease cAMP?
Inhibitor alpha subunit on adenylyl cyclase
What determines how many K+ channels are open in the heart?
Acetylcholine at the nodal tissue
What would happen in the cell if K+ permeability is reduced?
Vrm would be more positive and would hit threshold faster
What cardiac effects would be seen with slight hyperkalemia?
Increase in HR by increasing Vrm
What does hyperkalemia do to K+ gradient?
Reduces the gradient so less K+ movement and increased Vrm
What is a normal K+ concentration gradient?
30:1
What effect does blood calcium level have on membrane potential in the heart?
Blood calcium levels can change threshold potential in heart tissue
What happens in reasonable hypercalcemia in reference to cardiac cells?
Increases threshold potential (more positive) and lowers HR
What happens to cardiac cells if a patient is hypocalcemic?
Makes threshold potential more negative and increases HR
How does calcium cause changes in threshold potential of myocytes?
unknown how calcium does this
What does the sub-endocardium usually refer to?
Left ventricle
How would depolarization from left to right look?
Positive deflection–moving toward positive electrode
How is the amplitude of the deflections for cardiac action potentials determined?
By how much current
How does repolarization from left to right look?
Negative deflection
How would repolarization that is opposite of original depolarization look?
Positive deflection (double negative)
reason why T wave is positive deflection on EKG
Why do ventricular action potentials have a smaller phase 4 slope?
There are not very many HCN channels or leaky Na+/Ca2+ channels
Are there HCN channels present in ventricular action potentials?
Yes, just not as many
know there are still some because of the slight increase at phase 4
Compare phase 4 slope in ventricular fast APs and slow SA APs:
Slope of phase 4 is much steeper/greater than in ventricular action potentials
more HCN channels
What does phase 0 represent in fast APs and slow APs?
The upstroke of the action potential
How does phase 0 in fast AP look compared to phase 0 in slow AP?
In fast AP–phase 0 is almost straight up and down
slow AP has less slope to phase 0 with longer duration
What causes the steep slope of phase 0 in ventricular AP?
VG Na+ channels are creating fast increase
Are there VG Na+ channels involved in nodal tissue AP?
No, phase 0 is due to L-type Ca2+ channels
What causes the slope in phase 0 of nodal areas in the heart?
L-type slow Ca2+ channels
slower to open and stay open longer
What determines how fast APs move around in the heart?
Slope of phase 0
How would an action potential be traveling that has a steep/ fast phase 0?
AP is starting off fast and is propagated to the next cell very quickly
this is what happens with ventricular current
What is usually involved in action potential propagation?
sodium current
lots of VG Na+ channels opening in fast action potentials that can move Na+ through gap junctions to neighbor cells to fire AP there
How does the action potential travel in nodal tissue if there are not VG Na+ channels?
phase 0 slope is lower so it takes longer to move action potential from one cell to another
Do the atria use VG Na+ channels to propagate action potentials?
Atria do not have many VG Na+ channels–slow for AP to generate and spread to next cell
Why does it take longer for the atria to conduct action potentials and for the action potentials to spread?
Not as many VG Na+ channels
primary current is Ca2+(more difficult for Ca2+ to travel through the gap junctions)
What happens in phase 3 of nodal cells?
L-type Ca2+ channels close and VG K+ channels open to reset the cell
Some people include a phase 2 in nodal cells, where would this be?
Phase 2 would be a “plateau” phase from L-type Ca2+ channels
Dr Schmidt doesnt agree with phase 2
What phase is missing from nodal cells that is present in ventricular cells?
Phase 1
What phases do slow action potentials include?
Phase 4,0, sometimes 2, and 3
Why is the AV node a slower pacemaker than the SA node?
The cells in AV node are not leaky to Na+ and Ca2+ during phase 4
What is vrm of AV node compared to SA node?
AV node vrm is more negative (lower than SA)
What does a lower vrm in AV nodes indicate?
In the AV node it takes longer to generate its own AP
Are there HCN channels in the AV node?
Yes, but not as many as SA node
Which cells have the most HCN channels?
SA nodal cells
Compare the shape of SA and AV node APs:
SA and AV nodal AP have similar shape
Compare Purkinje and ventricular APs:
Both are fast and both have similar shape
What is the duration of ventricular action potentials?
Ventricular action potentials vary in length
Which ventricular tissue correlates with the longest action potential duration in the ventricle?
Deep interior ventricular action potentials are longer
Where would you expect to see the longest duration of ventricular action potential?
Deep–in the sub endocardium
How do action potentials in the deep layers of the heart fire?
Action potentials in the deep parts of the heart get start earlier and repolarize later than superficial tissue
How do action potentials conduct in the superficial ventricular myocyte?
action potential get started a little bit later in the superficial levels because it takes time for AP to move from inside ventricle to outside
What is the duration of AP in superficial ventricular myocyte?
Decreased duration
will depolarize last and repolarize first
What is an example of superficial tissue in the heart?
Epicardium
How does repolarization in epicardial tissue compare to repolarization in sub endocardium?
Repolarization in epicardial tissue is over sooner than in sub endocardium
What is the order of ventricular repolarization?
repolarization travels from outside to inside ventricle
How does ventricular AP length vary based on the layer of ventricular tissue?
superficial ventricular tissue has a shorter AP than deeper tissue
Why do deep tissues in the ventricle have a longer action potential?
It is important to get all of the muscle to squeeze at the same time to get enough force to eject blood
makes sure there is overlap in contracting time so heart muscles contract together
How do atrial action potentials look?
in between ventricular AP and SA nodal AP
What does phase 0 in atrial AP look like?
Straight up and down, similar to ventricular AP
Is there a plateau phase in atria AP?
small plateau phase but doesnt need plateau because atria are only contracting for short period of time and not pumping against a lot of resistance
Is it important to coordinate inner atria muscle contraction with outer like in the ventricles?
Not an issue in the atria because the atria walls are thin
How frequently does SA node generate AP with normal vagal stimulation?
AP every 0.83 seconds
How fast would SA node generate AP without any nervous system influence?
110bpm
How fast would SA Node generate AP if only influenced by sympathetic nervous system (not parasympathetic)?
120 bpm
How many beats does the SNS increase heart rate?
10 bpm
Which nervous system has the greater effect on heart rate?
Parasympathetic
How frequently does SA node generate AP with only simulation from Parasympathetic nervous system?
60-62bpm
Self depolarization at the SA node produces and action potential every _________ seconds.
0.83 seconds
How can we calculate HR from normal self depolarizing rate of SA node?
60 seconds per minute/0.83 seconds= 72bpm
What works as the “breaks” in the resting heart?
Parasympathetic–vagal system
What is the secondary pacemaker cell?
AV node
If AV node becomes primary pacemaker of the heart, how fast would it generate APs?
40-60bpm
What are the purkinje fibers and where is it located?
ventricular conduction system
buried in ventricular muscle mass
What rate would purkinje fibers generate AP if they take over as pacemaker of the heart?
15-30bpm
If the purkinje fibers take over as primary pacemaker, would you be able to survive?
Would be enough to keep us going for a little bit (like to get to hospital)
What does the conduction system of the heart allow for?
coordinated timing of all muscle mass
orderly process where signals get sent on defined pathways and tale defined amount of time
What happens if there is a timing issue in the cardiac muscle?
the muscle tissue is active or inactive at wrong period of time–causes issues with function
If the atria aren’t working, would the ventricles still work?
Technically we dont need the atria to fill the ventricles with blood, but if they aren’t helping then the ventricle wont be as full as normal and output will decrease leading to low BP
What is a crucial element to having a functional heart pump?
Coordinated timing
What makes sure AP can travel from SA to AV?
Conduction tissue
What is the conduction system of the ventricles?
Purkinje fibers
What is the conduction system of the atria?
3 pathways in the right
one to the left atria
Where are the 3 conduction pathways for the RA?
Between SA and AV node
What are the 3 conduction pathways in the RA?
Internodal pathways:
-anterior
-middle
-posterior
Which internodal pathway branched off to conduct the LA?
conduction tissue from anterior internodal pathway
What is the conduction tissue in the LA called than branched from the anterior internodal pathway?
Interatrial bundle
Where does the interatrial bundle create?
pathway for AP between right atria and left atria
What is another term for interatrial bundle?
Bachmans bundle
What is the function of bachmans bundle?
Conduct electrical signals to the left atria and propagate signals from SA to AV node
What is the time it take for AP to move from SA to AV node?
0.03 seconds–now the AP is at the AV node
How long does it take for entire RA to depolarize?
0.07 seconds
Why does it take longer for left atrium to depolarize than right?
AP has to travel further to LA
At what time does the last part of the LA depolarize?
0.09 seconds
What is the point when both atria are fully depolarized?
0.09 seconds
What does atrial depolarization correspond with?
P wave should be 0.09 seconds long
When does the P wave start and end?
P wave starts when AP starts and ends when all atrial tissue is depolarized
Regions in the LA that are closer to the RA depolarize _________.
quicker (0.04 seconds)
What part of LA is furthest away from conduction tissue?
lower lateral part of LA
Why does it take longer for the LA to fully depolarize?
Further away from conduction tissue
AP has to travel through muscle in atria with myofibrils that do not conduct AP very fast
What causes the delay in AP traveling from upper left atria to lower left atria?
AP is traveling through muscle and myofibrils that do not conduct electricity very fast and there is not specialized conduction tissue in this area
What does the top half of the heart include?
Atria, SA, AV
What is the path for AP to take to fully depolarize ventricles
AP moves from SA through right atrium to AV through bundle branches and purkinje to all of the ventricle
How long does it take for action potential to travel from SA to all of the ventricle?
0.22 seconds
Why is delay at AV node a good thing?
Gives atria time to contract before ventricles
Allows AV to function as a filter
allows ventricles to contract
What happens with AP conduction with older hearts?
Older hearts have more tissue–takes longer for AP to travel through all the tissue
How does AV node function as a filter?
AV node can filter out extraneous AP in the atria so we dont end up with fast ventricular rhythms
What happens if there is crazy electrical activity in the atria (ex afib)?
AP in the top half of the heart are not coordinated with the lower half of the heart because AV node is filtering
What is the absolute refractory period of the AP?
point in time if another AP hits before the cell is fully reset from the previous AP–there will not be a new AP
How does AV node filter through extraneous AP?
If AP hits the node during its refractory period there will not be a new AP generated
How is the AV node structured?
Has an area that is Big and fat
What does the fat area of the AV node allow for?
Low conduction–Fat doesnt conduct AP
What makes the conduction in the AV node delayed/slower?
Fat tissue
Low number of gap junctions between conduction cells
How much time does it take for AP to travel from internodal pathway to AV?
0.03 seconds after SA fires
What is the time of the delay for the AP to get through AV node?
0.12 seconds–this is when the AP is traveling through the fat tissue
What is the delay in the AP at the bundle of His (penetrating bundle)?
0.01 seconds
What is another name for the bundle of His?
Penetrating bundle
What area allows for crossover of AP from atria to ventricular septum?
Area just above left and right bundle branch
What is the amount of time it takes AP to get from SA to main bundle branches?
0.03 + 0.13= 0.16 seconds
How long does it take AP to get from AV through bundle of his?
0.12 delay at AV + 0.01 delay at bundle of His= 0.13 seconds
After SA fires, how long until main bundle branches get AP and what does this correspond with?
0.16 second–corresponds with PR interval
What triggers the QRS complex?
initiation of AP in the main bundle branches in the interventricular septum
What happens if there is an abnormal pathway in the atria causing AP that aren’t suppose to be there?
If AP hits AV node during refractory period it will not propagate action potential to ventricles
How does the AV node protect against ventricular tachycardia rhythms?
AV node will not propagate action potential to the ventricle if it is hit with AP during refractory period
What part of the heart depolarized first and why?
ventricular septum–where bundle branches are located
Where are the bundle branches located?
ventricular septum
How does depolarization spread after after hitting the septum?
2 different directions:
-toward left ventricle
-toward right ventricle
What pattern does depolarization of the heart follow?
Pattern where electrical signals are sent toward the left foot
What is the degree of average electrical movement during typical heart beat?
59 degrees
What does EKG show in regards to current?
EKG shows all electrical activity in the heart
What is a typical magnitude of depolarization for ventricular AP?
100mV or more
What would EKG look like if we moved the leads closer to the heart?
Voltage (deflection) to be a lot higher–less tissue getting in the way
What would be expected for QRS deflection if the electrodes are places closer to the heart?
3-4mV instead of 1.5mV
Which leads would we see a larger deflection in?
V1-V6 chest leads–closer to the heart in a 12 lead
What happens to the voltage in a 3 lead EKG?
increased loss of voltage because there is a lot of tissue/structures in the way
is: air in lungs, fat
What does the QT interval correspond with?
length of longest ventricular AP (endocardial)
length of time for ventricular depolarization
Which parts of the heart are depolarized for the duration of the QT interval?
The deeper parts of the heart (endocardium)
Where does the EKG start when the cell is at rest?
0
How big is a normal P wave deflection?
positive deflection–2.5 small boxes long and 2.5 small boxes tall
Why does the P wave show up as a positive deflection?
because movement from SA to AV–AP is traveling toward the foot–toward positive lead
If P wave originates at SA node what deflection do we expect to see?
Positive
If P wave originates in AV node–what deflection do we expect to see
action potential would travel retrograde back to SA node
P wave would be inverted because traveling toward negative electrode
What causes a P wave to be high?
Problem with RA (hypertrophy)
What size on EKG correlates with a high P wave?
greater than 3 boxes high
Why does RA hypertrophy cause increase in height of p wave?
more tissue= larger magnitude of deflection
more tissue= more electrical current for the positive electrode to see
What is happening if the P wave is too long?
Conduction problem with the LA
What happens to the P wave if the left atrium is stretched out?
takes longer for the entire LA to be repolarized (so its depolarized longer) causing longer P wave
What is happening if p wave has a double hump?
electrical block in LA–preventing AP from spreading to LA correctly
What deflection is seen with Q wave?
Negative deflection
Do all leads have Q waves?
No
What does the R wave indicate?
Positive deflection
corresponds with depolarization of ventricles
What does the PR interval measure?
Period from start of atria depolarization to initiation of electrical activity in the ventricle
Why is the PR interval not called PQ?
We do not always have a Q wave
would technically be PQ is Q wave always existed
What is the ideal time for PR interval?
0.16 seconds–time from SA to bundle branches in ventricular septum
What is the time between R waves? (RR interval)
0.83 seconds
What can RR interval be used for?
Reliable way to calculate heart rate
What deflection does the S wave have?
Negative deflection
What does the QRS show us on an EKG?
time source of the AP working through the ventricular conduction system and ventricular muscle
When does QRS complex end?
When all ventricular muscle has been depolarized
How is the end of ventricular depolarization depicted on an EKG?
Point after QRS where entire lower half of heart is depolarized (back to 0 on EKG)
What is the resting point after the QRS called?
J-point
What is the J-point used for?
reference point for currents of injury
How long does it take to get the last part of ventricle fully depolarized
0.22 seconds
How long should the ideal QRS complex be?
0.22 (heart is completely depolarized) - 0.16 (atrial depolarization to bundle branches) = 0.06 seconds
How long is the QRS in most people?
longer than 0.06 seconds
people usually have more heart tissue than what is ideal
Why do ideal number for EKG recording measurements not work for normal people?
Most people have more heart tissue than what is ideal–creating longer time for depolarization wave to spread
What are examples that could increase the size of ventricles?
High blood pressure
drinking too much caffeine over long period of time
What is the typical QRS deflection amplitude?
magnitude of deflection of 1.5mV
positive 1mV and 0.3 mV negative added together for total
How to calculate magnitude of deflection for QRS:
How far above baseline added to how far below baseline= magnitude of deflection
What does magnitude of deflection measure?
total amount of electrical current during QRS
What can cause a high voltage QRS?
Electrodes closer to the heart
heart tissue bigger than normal
What does increased ventricular tissue do to electrical activity in the heart?
extra ventricular tissue will allow for more electrical activity causing enlargement of QRS complex
What do enlarged ventricles do to QRS complex?
widens QRS
increases magnitude of QRS
What does dilated cardiomyopathy do to QRS complex?
ventricle walls are stretched out
widen/prolong qrs complex
When does atrial repolarization occur on an EKG?
Toward the end of R wave
hidden in QRS
What is another term for J-point?
Isoelectric point
What does the J-point show on the EKG?
point where entire ventricles are depolarized
How is the J-point used to identify currents of injury?
look at j-point and compare that to different point in EKG where heart should be completely repolarized
What part of the EKG should the heart be completely repolarized?
right side of T wave
What is J-point useful in determining?
ST elevation and ST depression by comparing to TP interval
T orF: The j point is useful because it shows when ALL tissue is depolarized–including areas of injury
T
Why do we look at area after T wave to compare to J point?
All healthy tissue should be resting after T wave–unhealthy tissue would still be depolarized causing current
What does QT interval show on EKG?
Includes start of depolarization in the septum up until all tissue in ventricle is repolarized
What is typical time period for QT interval?
0.25 to 0.35 seconds
duration of fast action potential in endocardial heart tissue
Where is the ST segment measured?
End of S wave to start of T wave
What is ST segment beneficial for?
useful to look at for areas of injury and ischemia
What is happening that results in the T wave on EKG?
repolarization of the ventricles
Why is the T wave an upward deflction?
repolarization is spreading from superficial to deep layers and repolarization is opposite of depolarization and is moving in an opposite way of depolarization
How does the heart cause a physiologic increase in heart rate?
reduces time before SA node fires
Heart will shorten ST segment and QT segment
What happens to ventricular repolarization if ST and QT segments are shortened?
ventricle repolarizes earlier and body would be able to fire AP sooner–increasing HR
What is Lusitropy?
How fast the resetting of ventricles occurs during an AP
What is meant by positive lusitropy agent?
repolarizes the ventricles faster than normal causing increase in HR
Inotropy
Stronger heart beat (more Ca2+ in heart)
chronotropy
increased heart rate
Dromotropy
speed of conduction of action potential
What is dromotropy dependent on?
Dependent on Na+ current coming in
the more Na+ the faster the AP conduction can be
What is the voltage of each big box on EKG?
0.5mV
What is the voltage of each small box on ekg?
0.1mV
smaller boxes divide larger box up 5 times
Why are the EKG measurements set up how they are?
From the old school paper machines
paper was fed through machine at 25mm/sec
How many big boxes per second?
5 big boxes in one second
How much time is measured by each big box?
1/5 of a second–0.2 seconds
How much time is measured by each small box?
each small box =1/5 of big box
0.04 seconds for each small box
What is a premature action potential?
Smaller than normal AP
What causes premature action potentials?
If the cell is mostly reset but not entirely and an AP is generated
What is the period called when a cell is mostly reset but not entirely?
Relative refractory period
Why dont we want these premature action potentials (early heart beats)?
uncoordinated electrical system with mechanical pumping leads to uncoordinated contraction and decreased pumping performance
How does a relative refractory period AP correspond with heart pumping?
Heart will not pump efficiently
What is a later premature action potential?
Heart has been able to fully reset–generates AP a little early
What is the absolute refractory period?
toward the peak of AP
Can an AP be generated during absolute refractory period?
No, AP would not be generated even if cell was stimulated with outside current
What is the serous visceral pericardium?
Very thin/ clear membrane that sits between parietal pericardium and the heart
How are action potentials propagated in the heart?
Gap junctions
What would cause slower propagation through gap junctions?
Ca2+ will be slower transmission because its bigger–can still generate AP
What is a downside to gap junctions?
Bidirectional current/ synapse
Why would it be safer to have synaptic connections in the heart opposed to gap junctions?
Chemical synapses do not allow for current to back travel
would take much longer
What is the primary thing protecting us from retrograde movement in cardiac cells?
absolute refractory period
How does the heart guard against re-entry rhythms?
By having a refractory period
What plane does a 3 lead EKG display?
frontal/ coronal
What plane do augmented leads use to display EKG?
Frontal/ coronal
How can you tell augmented leads?
Have an “a” in front
Where is aVR located?
augmented right lead
What is the 3 lead EKG measuring?
Electrical movement and direction of movement in the frontal plane
How is lead II set up in a 3 lead EKG?
Positive electrode on left foot
Negative electrode on right arm
What deflection does lead II see with atrial depolarization?
Large positive–SA to AV moved toward left foot
What deflection is seen in lead II with ventricular depolarization?
large positive deflection: current moving toward left foot
Where are the positive and negative connection for lead I for 3 leak EKG?
Positive connection on left arm
Negative connection on right arm
How does lead I view electrical current?
Horizontal plane: left and right movement
Where are the positive and negative connections for lead III on 3 lead EKG?
Positive on left foot
Negative on left arm
How many electrodes on the left foot for a 3 lead EKG?
2 positive electrodes
How many electrodes on the right arm for a 3 lead EKG?
2 negative electrodes
How many electrodes on left arm for 3 lead EKG?
One positive electrode and one negative electrode
Who is the dutch scientist who theorized the electrical triangle for the heart?
Einthoven: theorized Einthoven’s triangle
What equipment is needed to look at electrical activity in the heart?
Recorder and amplifier to turn signals into something that can be processes
What is the typical mean electrical axis for depolarization of the ventricles and the direction?
59 degrees pointed toward left foot
At what degree is lead II oriented in?
60 degree angle from horizontal
What is the term when mean electrical axis is less than 59 degrees (textbook less than 0)?
Left axis deviation
Which direction would the heart rotate for a left axis deviation?
Counter clockwise
How would the mean electrical axis look for a left axis deviation?
Up and towards the left arm from right to left
What is it called when heart is rotated clockwise?
Right axis deviation
How is net electrical axis pointed for a right axis deviation?
Pointed toward right side of the body
What degree is classified as a right axis deviation?
Anything greater than 59 degrees
What are some things in the heart that would cause the electrical axis to change from one way to another?
Bundle branch blocks–depending on which branch is blocked
What type of axis deviation might a person with COPD have?
Lunger are hyperinflated–shifts heart to the right (oriented straight up and down)
right axis deviation
How can ventilation change heart orientation?
When exhaling- heart is oriented more on left side (left axis deviation)
when taking a deep breath in- shifts heart to the right (right axis deviation)
How is electrical activity changed if one side of the heart is much larger than the other?
The larger side has more electrical activity going to that area
What degree of axis does lead II have?
60 degree from horizontal
What would be another way to say mean electrical axis of 300 degrees?
-60 degrees
If mean electrical axis is negative, what direction does it rotate from horizontal?
Counter clockwise
If mean electrical axis is positive, what direction does it rotate from horizontal?
clockwise
Why does it take less time for AP to travel through right ventricle?
Right heart walls are thinner–only pumping against resistance of pulmonary circulation
What happens with AP travel in the left ventricle?
Left ventricle walls are thicker
Takes longer for last sliver of ventricle to depolarize
Why does the left lateral section of the ventricle take longer to depolarize?
It is furthest from the AV node
Where is the first place to depolarize in the ventricles?
Main bundle branch at the inter ventricular septum
Why do we see positive deflection with the p wave?
depolarization in the atria is moving from SA to AV–toward left foot
What would we expect to see if we could see atrial repolarization?
Repolarization of the atria would be a negative deflection heading toward left foot
Why do we not see the repolarization wave of the atria?
Hidden by QRS–atria walls area thin so not a ton of muscle tissue to rise above qrs
What deflection would atrial T wave be?
Negative deflection
Why would the atrial T wave be more spread out than the P wave?
When the conduction system is working in retrograde it doesnt have the same properties as when moving forward
What is the electrical axis for lead I?
0 degrees–horizontal
How can we determine how much current is measures at lead I?
draw a triangle: the amount of current picked up in lead I corresponds with how long the side of the triangle is that is moving on horizontal axis
How would lead I amplitude look compared to lead II during depolarization?
Lead I would be smaller amplitude positive deflection
What would lead I show if mean electrical axis is 90 degrees?
Lead I would show 0—wouldnt see any current moving toward it
What would lead I show if mean electrical axis is toward the right side of the body?
Lead I would be negative deflection–current moving from left to right (toward negative electrode)
What would Lead I show if mean electrical axis is along the same horizontal plane moving left to right?
Very negative deflection
What type of deflection should all electrical events have in lead II during ventricular depolarization?
Large and positive deflection for all events
What would lead II show if mean electrical axis is 90 degrees?
large positive deflection in lead II–still close in line with lead II
What is the normal electrical axis of lead III?
120 degrees from horizontal
What can be accomplished with a 3 lead EKG?
Diagnose any conduction and arrhythmia problems using 3 lead axis
How can a 3 lead EKG be used to figure out what the mean electrical axis is?
Look at how positive or how negative the deflections are in the 3 different leads
What is a benefit of 12 lead EKG compared to 3 lead EKG?
3 lead EKG can figure out what the problem is
12 lead is better for figuring out where the problem is (more eyes on the problem with chest leads)
How does einthovens law look at the heart leads?
As an equilateral triangle
What is Einthoven’s Law?
Net deflection in Lead I + net deflection in Lead III = Net deflection in Lead II
How to find net deflection?
Positive deflection of QRS minus negative deflection of QRS
Does Einthovens law always work?
Yes, works in every situation in the 3 standard leads
If mean electrical axis is 60 degrees, what would be expected in lead I, lead II, and Lead III?
Lead I and Lead II would have similar size that would add up to size of lead II positive deflections
What is expected on 3 lead EKG when only the septum is depolarized?
LI: small positive deflection
L2: a little more positive deflection
L3: small positive deflection
What is expected on EKG when the heart is half way depolarized?
LI: increased positive deflection
L2: Very positive deflection
L3: increased positive deflection
If a vector is draw for lead II what can be said about lead I and lead III?
Vector for lead I and lead III equals lead II
What is expected on EKG when MORE than half of the heart is depolarized?
Current slows down
LI, L2, and L3: still positive but less positive than last plot
What happens to net electrical axis when only superior lateral wall of left ventricle is left to depolarize?
Net electrical axis is shifted and pointing up and to left arm (toward last sliver of resting tissue)
What is expected on EKG when only the upper lateral wall of the left ventricle is resting?
L1: would be slightly positive
L2: Slightly negative
L3: Very negative
What movement shows up as positive deflection in Lead I?
Right to left movement
What creates the S wave during electrical depolarization of the ventricles?
When there is only a little bit of tissue on the left ventricle waiting to be depolarized
Electrical axis shift to the left causes negative deflections in lead 2 and lead 3 (s wave)
During the last stage of depolarization, how does the negative deflection in lead II compare to lead III?
Lead III has more negative deflection
Lead II is only slightly negative
What would the current in the 3 lead EKG look like when the entire heart is depolarized?
No current
Which lead is least likely to have an S wave?
Lead I–never had a negative deflection during depolarization
What is the origin or the Q wave?
The first thing to depolarize in the bundle branches is a part of the septum to the left side of the inter ventricular septum
Where does the depolarization head after the initial part of the septum is depolarized?
To the right
What would the 3 leads on the EKG see during initial spread of depolarization from the septum?
L1: negative
L2: Slight negative
L3: slight positive
What does a big vector indicate?
a lot of electrical activity
What does a smaller vector indicate?
Less electrical current
What angle would be the most electrical activity in regards to each lead?
Parallel with the plane
What do the 3 lead electrodes looks like for the R wave?
Current is pointing down to the left
Large positive deflection in LII
positive deflection in LI
positive deflection in LIII
How is the net electrical axis pointed for a normal S wave in a 3 lead EKG?
Current is up to the left
How would the 3 lead EKG leads look for the S wave?
LI: positive
LII: slightly negative
LIII: more negative than LII
What electrical activity is happening at the ST segment?
should have no electrical activity
Entire heart is depolarized–same charge in all the tissue
Where are the augmented leads located?
Half way between the standard leads
What does the V stand for in the augmented leads?
voltage
What does the last letter in the augmented leads indicated?
Location on the body
How many electrodes do the augmented leads us?
1 positive
average of 2 negative
Where is the positive electrode for aVR?
Right arm
Where does the negative electrode come from for aVR?
between left arm and left leg–average between those 2 electrodes
How are most of the deflection in aVR oriented?
Usually current is heading away from right arm–negative deflections
Which augmented lead is the least used?
aVR
What degree is aVR at?
210 degree from horizontal
Where is the positive electrode in aVL?
left arm
Where is the negative electrode in aVL?
average of right arm and left leg
What is the degree for aVL?
150 degrees
What are normal deflections in a healthy heart for aVL?
everything that is positive in lead II is the same in aVL (P, T, QRS)
What size should the qrs be in aVL?
Same as standard: 1.5mV
Where is the positive electrode in aVF?
left foot
Where is the negative electrode coming from in aVF?
negative electrode is average from left arm and right arm
What orientation is aVF looking?
straight up
What is the purpose of aVF?
resolution to see problems–especially between LII and LIII
What degree is aVF at?
90 degrees
What deflections would we see for depolarization from aVF?
positive deflections for QRS, P, and T wave
What is another name for precordial leads?
Chest leads
How many leads make up the precordial leads?
6 extra leads around the chest
Where are the positive leads located for the precordial leads?
V1-V6 around the heart are positive precordial leads
Where are the negative electrodes for 12 lead ekg?
Negative electrodes are a combination of electrodes on right arm, left arm, and left foot
uses standard leads as the negative leads
Where is V1 placed?
right side of sternum–4th intercostal space
Where is V2 placed?
Left side of sternum–4th intercostal space
What is another name for V1 and V2 leads?
Septal leads
How does QRS look in the V1?
QRS downward deflection
How do the P and T wave look in V1
Inverted
Why is there not alot of electrical current toward V1?
current normally heads toward left foot and off to the side–misses V1
Which precordial lead is the most useful to figure out where a problem in the heart is?
V2
How does the QRS look in V2?
Negative deflection
What is V2 used for?
Figure out anterior and posterior injuries
Why is V2 used to see anterior and posterior issues?
It is situated so it points directly at the front of the heart
How would current move with a posterior infarct?
from back of the heart to the front of the heart
How would V2 read electrical current from posterior infarct?
current coming toward V2–positive electrode
How would current move if an anterior part of the heart is ischemic?
Electrons from anterior part of the heart would move toward positive charged area in posterior part of the heart
How would V2 read electrical current from an anterior infarct?
negative current of injury–current going away from V2
Where is V3 located?
Sandwiched between V4 and V2
What is another term for V3 and V4 leads?
Anterior leads
How does V4 see electrical activity heading toward it?
all electrical activity heading toward V4 is a big positive deflection
Why is V4 a positive deflection?
Situated in line with normal electrical axis of the heart
which precordial lead should have the largest positive deflection in QRS?
V4
What is another name for V5 and V6?
Lateral leads
How does QRS look in V5 and V6?
QRS is smaller because the leads are over on lateral side of the thorax and not as inline with normal cardiac electrical axis
Where are lead V4, V5, and V6 located?
5th intercostal space on left side
How does the electrical activity in the precordial leads compare to electrical activity in a 3 lead EKG?
Precordial electrical activity is larger (bigger deflections) because electrodes are placed closer to the heart
What is happening electrically that shows up as an inverted T wave?
Repolarization is happening in the same way as depolarization
When inside of the heart is resetting before the outside
What happens when ventricular repolarization is happening in the same direction as depolarization?
Positive QRS and inverted T wave
What is a biphasic T wave?
Half up half down
tissue is repolarizing in abnormal way
How can yo figure out mean electrical axis from LI, LII, and LIII?
plot LI and LIII based of net magnitude of QRS
What does a mean electrical axis down to the right indicate?
Potentially right ventricular hypertrophy along with large QRS in lead I and lead III
How does depolarization differ in someone with right ventricular hypertrophy?
Left ventricle would depolarize first then current would shift to the right side of the body
How does ventricular depolarization typically look?
Both ventricles depolarize at the same time
What happens if there is an occlusion in one of the bundle branches?
Higher resistance in that bundle branch–unaffected side would depolarize faster then shift current to resting portion
causes wonky electrical activity
How can we figure out which bundle branch is blocked?
Determine the electrical axis of the heart
up to the left would be LBBB
Why is repolarization hard for the heart compared to depolarization?
To repolarize have to have Na/K pump working to get Na+ out after AP, and other things that require energy for the cell to repolarize
What happens to the heart if there is an energy deficiet?
EX: blocked vessel–some of the tissue isnt getting enough energy and it will be stuck in depolarized state
What is it called if an area in the heart is stuck in a depolarized state?
area of injury
How would current flow around the area of injury?
Current would be from injury toward are of reset heart tissue
When would current of injury be seen?
When the rest of the heart it resting
What type of EKG change would be expected in Lead II from a small area of ischemia in the left ventricle?
TP segment elevated–looks like ST depression
What part of the heart wall is usually impacted by an infarction?
usually the entire wall
How does the electrical current typically look when part of the left ventricle is infarcted?
Large vector up and to the right
What would you expect in Lead II if part of the left ventricle is infarcted?
TP segment dropped down–would make ST look elevated
What type of current is associated with J-point that is higher than TP segment in LI, LII, or LIII?
Negative current of injury
What type of current is associated with J-point that is lower than TP segment?
Positive current of injury
After plotting the the vectorcardiogram for the current of injury, how is the area of injury in the heart determined?
Arrow of mean electrical activity for currents of injury is pointing AWAY from the where the injury is
Which part of the heart is ischemic if the mean electrical current of injury is pointed down to the right?
Left heart issue
What is indicated by J-point that is higher than TP segment in V2?
Negative current of injury
-current would be flowing away from V2–would be an anterior infarct
What is indicated by a mean electrical current of injury that is pointed straight up?
issue in apex of the heart
Why cant computers calculate these different vectors accurately?
Zero point is very difficult for a computer to figure out
Computer cant figure out J point
What has to happen to close M gate and re open H gate on VG Na+ channels?
Cell has to repolarize
What happens to VG Na+ channels if unable to repolarize?
They are stuck in inactive form- cant be used for action potential
What are the 2 gates on the L-type Ca2+ channels?
Activation gate (D gate)
Inactivation gate (F gate)
Where are the 2 gates for the L-type Ca2+ channels located?
D gate: outside
F gate: inside
What has to happen in order for the D gate to open?
Voltage dependent. Has to have enough of a depolarization to open
Compare D gate to M gate:
D gate takes longer to open and is open for a longer amount of time compared to M gate
D gate: CA2+
M gate: Na+
What is the order for resetting L-type calcium channels during repolarization?
activation gate (D) closes then inactivation gate (F) opens
What is the resting state for L-type Ca2+ channels?
D gate is closed
F gate is open
How is Vrm different for L-type Ca2+ channels compared to VG Na+ channels?
Vrm for L-type calcium channels is more positive than VG Na+ channels
Which pacemaker cells has the fastest diastolic depolarization rate?
SA nodal cell: Phase 4 is the steepest
Why are there no VG Na+ channels in nodal tissue? (2 reasons)
1) There might not be any VG channels in that tissue
2) The VG Na+ channels do not function because Vrm in nodal tissue is too positive for them to reset
What is the slope of phase 0 in purkinje tissue related to?
VG Na+ channels
What happens to ventricular action potentials if Vrm is more positive?
Will start to lose VG Na+ channels and slope of Phase 0 decrease
What happens to phase 1 if Vrm in ventricular AP is increased?
Peak of phase 1 might not be as high as normal
What happens to the action potential if vrm in ventricular AP is super positive that there are no VG na+ channels involved?
AP would look like slow nodal AP
Ca2+ would be able to generate decent AP
What issues occur when the VG Na+ channels are not repolarizing?
Conduction issues–sodium is usually required for fast propagation through gap junctions
Why are there conduction issues in the heart when Na+ influx is decreased?
AP is more reliant on Ca2+ to spread AP to other cells
Ca2+ doesnt fit through gap junctions as well as Na+
If Vrm is more positive than -55 what will happen to AP?
Lose VG Na+ and L-type Ca2+ channels–wouldnt have any action potential
What determines the slope if phase 0?
Which ions are involved and how many ions are coming in
What issues cause vrm to be more positive than normal?
elevated K+
Acidosis
Ischemia/ infarction
How does acidosis increase resting membrane potential?
enzymes arent able to function outside pH of 7.4 and cant catalyze chemical reactions needed to reset the cell and provide energy
ultimately the cell can not repolarize
What type of drugs block VG Na+ channels?
-CAINE drugs
How does lidocaine affect ventricular action potentials?
reduced slope of phase 0
Which cells are the most leaky to Ca2+ at rest?
Nodal tissue
Which cells are the least permeable to Ca2+ at rest?
Purkinje
What are the 2 mACh-receptors at the heart?
-mACh-R is associated with potassium channels
-mACh-R with inhibitory alpha subunit
What is the primary way nodal tissue maintains or adjusts Vrm?
Through mACh-r that are linked to potassium channels
What happens when an agonist binds to mACh-r in nodal tissue?
increased K+ permeability reduces vrm and reduces heart rate
What happens if mACh-R in nodal tissue are blocked?
K+ permeability decreases so membrane potential is more positive and heart rate increases
Do mACh-R have beta antagonism?
No, works as a stand alone system
What does the alpha subunit on mACh-R inhibit?
Inhibits adenylyl cyclase
Where is adenylyl cyclase located in the heart?
tethered to the cell wall in the heart
What is the function of adenylyl cyclase?
Turn ATP into cAMP
What does an agonist at mACh-R do to adenylyl cyclase?
Slows down adenylyl cyclase through inhibitory alpha subunit that is activated when the agonist binds to the receptor
What happens with the alpha subunit at the beta receptors in the heart?
alpha subunit is stimulatory at the beta receptors
stimulated adenylyl cyclase causing increase cAMP
What other channels are activated by certain beta receptors?
Some beta receptor cause direct activation of HCN channels
How do beta receptors cause HCN channels to open?
increase cAMP by increasing speed of adenylyl cyclase causes HCN channels to open
What happens when more HCN channels are open?
More Na+ and Ca2+ coming into any pacemaker cell during phase 4
What does cAMP further increase activity of?
Protein kinase A
What are targets for PKA?
L-type Ca2+ channels
Troponin I
Phospholamban
What does PKA do to L-type Ca2+ channels?
Phosphorylates them to make them more sensitive and easier to open
Increases amount of Ca2+ coming in from outside during AP
Why is phosphorylation of L-type Ca2+ channels dangerous?
too much beta adrenergic activity–Ca2+ channels are too sensitive they may open at the wrong time causing EAD or DAD
increase risk for heart attacks with increased activity level
What happens when PKA phosphorylated troponin I?
increases contractile protein sensitivity to calcium and increases cycling rate of cross bridge generating filaments
What effect does PKA have on phospholamban?
increases speed of the SERCA pump increases HR
phospholamban usually inhibits SERCA so by phosphorylating it allows SERCA to reset cell faster
What breaks down cAMP in the heart?
Phosphodiesterase–breaks it down into AMP
What is the outcome of a PDE inhibitor?
increased cAMP and increased PKA
What causes arrhythmias?
Problem with conduction system or the action potential is gong through the muscle outside the conduction system
What usually generates abnormal rhythmicity in arrhythmias?
Abnormal pacemaker in the heart
What happens if a random tissue starts generating action potentials on its own?
Action potentials would probably be out of sequence from normal and can spread through gap junctions
Why do gap junctions allows for inappropriate current to travel through them?
Gap junctions do not filter, they dont care about which way the signal is moving
They are just a pathway for action potentials to spread
What is an ectopic pacemaker?
Area in the heart that is generating action potentials other than the SA node
What happens if ventricular muscle starts generating action potentials?
An arrhythmia will be generated
What happens to areas in the heart that have been blocked from action potentials moving through?
Sometimes the the tissue that is blocked will generate its own action potential
How do normal action potentials differ from arrhythmia action potentials?
Normal action potentials have a defined pathway and speed
Arrhythmia pathways are abnormal
What makes arrhythmia pathways abnormal?
AP from these pathways could hit a tissue causing an AP to fire during relative refractory period or fire early than its suppose to
What can cause ectopic pacemakers in the heart?
Increased VRM
Increased serum K+
Ischemia
How does increase VRM help generate arrhythmias?
If resting membrane potential is closer to threshold potential in the pacemaker cell an AP can be fired earlier
Increased VRM Increases probability of having an action potential generated on its own
What happens if the AV node is ischemic?
If bad enough may halt all AP through AV node
If VRM increases in AV node it may fire AP earlier than normal causing an arrhythmia
What is the issue in abnormal sinus rhythms?
Abnormal firing of SA node
What is happening in sinus tachycardia?
SA node is firing faster than normal
At what rate is sinus tachycardia officially called sinus tachycardia?
> 100bpm
What are some reasons for sinus tachycardia?
-Moderate increase in body temp
-Reflex sympathetic stimulation
-Loss of vagal stimulation
How does increased body temp cause sinus tachycardia?
Increased body temp increases the energy demands of the body
What happens to heart rate initially with massive blood loss?
sympathetic nervous system is trying to pump more blood to replace what is being lost
–increasing heart rate to try to compensate
What happens to hear rate with low blood pressure?
Nervous system can sense low BP if ventricles arent working right–feeds into back to SA node to increase rate to try to improve BP
Why are beta blockers sometimes administered with anti-arrhythmics?
Beta blocker helps to prevent compensatory sinus tachycardia through reflex activation of SA node
What are toxic conditions of the heart that can result in sinus tachycardia?
Conditions that increase VRM
-hyperkalemia
-acidosis
-nicotine
-alcohol
What is the definition of sinus bradycardia?
<60 bpm
Where does sinus bradycardia originate?
SA Node–generating slower rate than normal
What happens to RR interval with sinus bradycardia?
prolonged RR interval
Why do athletes or very healthy/active people have lower resting heart rates (sinus brady)?
Heart is physiologically bigger which increases stroke volume with each beat
nervous system will tell heart to slow down because there is a lot of SV with each beat and we only need 5L/min
What is associated with a higher resting heart rate?
decreased stroke volume
If heart rate is elevated at rest and there is no other reasons why it would be, what could be the reason for this?
Overactive thyroid
What happens to heart rate with increased vagal stimulation?
Bradycardia
Why doesnt taking away sympathetic nervous system drastically decrease HR?
There is only a small amount of SNS input during a resting heart rate so taking it away doesnt do much since there isnt alot to start with
Explain the neural reflexive bradycardia with drugs:
Phenylephrine–arteries squeezing increases BP which baroreceptors sense and respond by feeding back to the heart to reduce heart rate to maintain homeostasis
What does the paroxysmal aspect of paroxysmal atrial tachycardia indicate?
Atrial tachycardia that comes and goes
Where is the problem originating from in paroxysmal atrial tachycardia?
SA node: firing at increased rate
What do P and T waves look like in paroxysmal atrial tachycardia?
rate is sped up so P and T waves are overlapped and hard to distinguish from each other –looks like one notch
combo of atrial P wave and ventricular T wave
What could cause paroxysmal atrial tachycardia?
A drug that block vagal tone in the heart
What is it called when SA impulses are completely blocked?
Sinoatrial Block
What causes sinoatrial blocks?
Severe dysfunction at the SA node
If SA node is ischemic and cant reset any of its ion channels to produce action potentials
What do P waves look like in sinoatrial block?
P waves are either inverted or hidden
Which region of the heart becomes the pacemaker if there is a sinoatrial block?
AV would be next in line if it is healthy
What takes over as pacemaker if SA and AV node are messed up?
Purkinje system–15-30bpm so very compromised output
What determines if we can see an inverted P wave in a sinoatrial block?
Depends on which part of the AV node is generating the action potentials
We can see inverted P wave if pacemaker is set up in early parts of AV node
What causes the inverted P wave?
Retrograde movement from AV to SA
If pacemaker is set up in later parts of the AV node–what happens to P wave?
P wave would still be inverted we just wouldnt see it–would take time to travel backwards through AV node and ventricular electrical activity would mask it
What is decreased with all arrhythmias?
Stroke volume
Under normal circumstances, the atria should contract when the AV valves are __________?
Open
What causes early closure of AV valves?
If something causes the ventricles to depolarize early–causes early closure of the AV valves
Why is early closure of AV valves a bad thing?
Atria are trying to contract and push blood through a closed valve–creates turbulence
What happens with turbulence in the heart?
Creates blood clots and calcifications of the valves
What is categorized as enhanced delay at AV node?
PR interval beyond 0.16
the more increased delay= more abnormal block
What causes an enhances delay at the AV node?
-AV nodal ischemia
-Compression of AV node
-AV bundle inflammation
-Excessive vagal stimulation
-Excess beta blockers
What is occurring with AV node ischemia?
raises Vrm and less VG ion channels participating in AP
How does compression of AV node cause an enhanced delay?
Cells are pressed down and have a smaller diameter–decreased rate of action potential propagation with smaller diameter (increased resistance)
What causes compression of AV node?
Caused by remodeling of heart by fibroblasts
What is blocked with excessive vagal stimulation?
SA and AV nodes are blocked–reliant on ventricular escape to kick in
What is the MOA of digitalis?
Inhibits Na/K ATPase pump
increases vrm–used for extreme heart failure
What happens if Na/K pump is inhibited like with Dig?
-More sodium in the cell
-More calcium in the cell since its usually pumped out by Na/Ca exchanger
Why is dig usually the last med to try for heart failure?
Very dangerous by inhibiting cells ability to reset itself–not completely specific to heart
How do beta blockers enhance delay at AV node?
Reduce speed of conduction at AV node
PR interval greater than 0.2 seconds:
incomplete 1st degree heart block
Characteristics of 2nd degree heart block?
-Dropping QRS
-PR interval increases to >.25 seconds
-P wave doesnt always correspond to QRS
Which part of the heart has a faster rate during second degree heart block?
Atria has a faster rate than the ventricles (losing QRS)
What is another name for Mobitz type 1?
Wenckebach periodicity
What are the characteristics of a wenckebach?
Irregular PR interval
Which mobitz block is more dangerous?
Mobitz type 2
What are the characteristics of Mobitz type 2?
-Fixed P wave to QRS ratios
-regular/fixed PR interval on p and qrs that we have
What is the typical ratio seen of p waves to QRS complexes with mobitz type 2?
2:1
3:2
3:1
Which heart block would need a pacemaker?
Second degree mobitz type 2
complete heart block
What is happening in a complete heart block?
Total AV node block and bundle of His
What does the heart rely on for its pacemaker in a complete heart block?
Ventricular escape–purkinje system (15-30bpm)
What happens to atrial rate during complete heart block?
Cardiac output if reduced–nervous system sees low BP and feed back to heart to increase atrial rate
nervous system telling SA node to fire faster
What do the P waves look like in complete heart block?
-Random P waves all over the place
-no correlation of timing between P waves and QRS complexes because no action potentials are getting through AV node
What is a genetic syndrome that involves complete block of the AV node at random times associated with fainting spells?
Stokes-Adams Syndrome
What happens to ventricular escape rhythm in Stokes-Adams Syndrome?
Delayed ventricular escape 5-30 seconds
-reason why lose consciousness–if ventricular escape was faster wouldnt pass out
What causes a person with Stokes-Adam Syndrome to faint?
Delayed ventricular escape–period of time with no electrical activity in the heart
What arrhythmia causes circular reentry that is separate from SA node?
A flutter
What part of the atria is involved in Aflutter?
The entire atria
How is the atria contracting in a person with a flutter?
Atria are contracting in a way that is separate from SA Node
What predisposes people to a flutter?
Slower conduction rate and atrial hypertrophy
Why does aflutter only occur at a slower conduction rate?
If faster the AP would run into tissue in the refractory period that would stop the circular movement in the atria
How does atrial hypertrophy assist with development of aflutter?
Atria is stretched out there is more space for electricity to travel and less likely for circular movement to hit and area of the atria in refractory period
What can cause refractory period to not be as effective in preventing arrhythmias?
Slow conduction rate and increased distance (atria hypertrophy)
Why is Aflutter not an effective primer for the ventricles?
Part of the atria is contracting and part of the atria is relaxed–net result would be a high atrial rate
Why is atrial rate higher in aflutter?
Not waiting for SA node to fire an action potential
Can there be elevated ventricular rates in a flutter?
Sometimes a few AP pass into ventricles so some elevated ventricular rates
Which is worse: Afib or Aflutter?
Afib
How is afib different from a flutter?
Afib doesnt have a defined pathway that electrical current is taking
Where is the ectopic pacemaker in afib?
There are lots of ectopic pacemakers firing on their own and no coordinated at all
What predisposes someone to afib?
When the atria are stretched out–increases surface area for weird electrical activity
How are the atria contracting in afib?
small bits of the atria have little contraction–shaky muscle that causes turbulence
What is generated in afib that increases risk for blood clots?
Lots of turbulence is generated from all the ectopic pacemakers
What could happen if clots are forming in the right atria?
Could be pushed into pulmonary system–PE
What is the main predisposing factor for afib?
Increased age–atria stretched out over time
Can afib be treated with ablations?
No, since there are multiple sources of pacemaker activity
could ablate a few if they are super problematic
What is the movement in the atria called that is associated with afib?
Circus movement–going nuts
What is shown on ECG in place of p wave for someone in afib?
No pave just fibrillations–no blood being pumped
Would a patient feel if they are in afib?
Depends, but probably would be uncomfortable feeling heart beating at wrong time
What is the main issue in afib and aflutter?
Atria are not coordinated with the ventricles
Why should people with afib/flutter be on an anticoagulant?
Since atria arent coordinated with ventricles at certain points atria are contracting and trying to push blood against closed valves–increases risk for clotting and valve calcification
What type of issue is Alternans?
Incomplete interventricular block
What is the primary issue with alternans?
Problem with resetting in the purkinje conduction system
What could cause increase risk for alternans?
-Ischemic purkinje system
-compressed with scar tissue
-inflammation of purkinje
What does the pattern for alternans look like on an EKG?
irregular QRS that occurs every other beat
alternating between normal QRS and prolonged/low QRS
What is happening to the irregular QRS in alternans?
Conduction speed of irregular QRS is lower than normal because cell wasnt fully reset and takes longer for AP to get through the tissue (wider)
What is the ratio for normal to irregular QRS complexes in alternans?
1:1
What happens if there is an area in the purkinje system that is chronically depolarized?
Slows down purkinje system–can cause Alternans
When is alternans more likely to occur?
with high ventricular heart rate–slower heart rate would allow more time for repolarization and QRS would look normal
What causes premature atrial contractions?
Ectopic tissue in atria that fires action potentials early
What causes premature atrial contractions?
Ischemia, irritation, or calcified plaques
What happens in the ventricle as a result of PACs?
Creates abnormal filling in the ventricles–not as much time for filling and reduces priming ability of the atria
What happens as a result of PACs?
Atria beat is not timed right and not in coordinated manner–lower stroke volume in these premature beats
What happens to the stroke volume with PACs?
Stroke volume is lower
What occurs with PACs as a result of lower stroke volume?
Radial pulse deficit if listening (less noise generated during PAC)
What happens when there are premature contractions originating from AV node or bundle?
Obscure P wave depending on timing when AP moves forward into ventricle
Where does an early and inverted P wave originate?
Originates in high AV
Where does a late and inverted P wave originate?
Low AV source (probably wont see P wave because its hidden by QRS)
What are some things that can cause premature ventricular complexes?
Caffeine, Stress, lack of sleep, nicotine
What is happening at a PVC?
Bigger than normal QRS complex that is happening too quickly
Why are normal qrs complexes smaller than PVCs?
In normal QRS, the ventricles are depolarizing at about the same time–some of the electrical activity cancels out when depolarizations are coordinated
Where does the pacemaker usually start for PVCs?
Ectopic pacemaker in the ventricular muscle tissue–takes longer to get into purkinje system (reason why PVC is longer)
What happens during ventricular depolarization that produces PVCs?
Ventricles are depolarizing independent of each other–not cancelling out any of the current–large deflection in PVCs
How does the T wave look after a PVC?
If depolarization is abnormal would expect repolarization to be abnormal–usually causes inverted T waves
What can PVCs be a precursor to?
Paroxysmal Ventricular tachycardia
Where does paroxysmal ventricular tachycardia originate?
Purkinje system
What is happening in paroxysmal ventricular tachycardia?
Purkinje conduction system is overactive–high voltage prolonged QRS
What causes paroxysmal ventricular tachycardia?
Severe ischemia
What is paroxysmal ventricular tachycardia a precursor to?
V fib
What is happening with ventricular rate in paroxysmal ventricular tachycardia?
Ventricles are firing at a faster rate than AV or SA node
What are early after depolarizations?
When an action potential is fired a little early but before it is fully reset
How do EAD compare to regular action potentials?
EAD are smaller and do not allow for good pumping
Why are contractions from EAD weaker than normal?
Not very much Ca2+ coming in leads to a decreased force of contraction
Why is there a decrease in Ca2+ coming in with EAD?
Less ion channel involvement because cell hasnt fully reset
How do EAD look on an EKG strip?
Look like prolonged QT interval
What predisposes someone to early after depolarizations?
Sensitivity to L-type calcium channels
What can cause and increased sensitivity/ overactive L-type Ca2+ channels?
Increased beta adrenergic activity increases sensitivity of l-type ca2+ channels and they are more prone to fire AP
What do mACh-R antagonists do in the heart?
sensitize L type calcium channels making them more sensitive to firing
How does increased amount of Benadryl affect the heart?
anticholinergic–presents as long QT syndrome because cells are not resetting themselves before the next AP
What are EADs precursors to?
Torsades de pointe
What is torsades de point a precursor to?
Vfib
What happens to coronary blood flow if ventricular output is low?
eventually coronary blood flow is impacted and none of the tissues can repolarize–leads to vfib
What can be attempted to correct vfib?
Shock–direct current to reset the heart
What would prevent the heart from resetting from a shock to correct vfib?
If the ischemia is too severe
What are the abnormal accessory bundles that some people have genetically?
Bundles of kent
What are the bundles of kent and where could they be located?
Electrical connections that bypass the normal
extra tissue that connects High lateral wall of left ventricle to left atria or right ventricle to right atria
What percent of the population has bundles of kent?
0.2%
What is a solution if the extra pathway from the bundles of kent becomes an issue?
ablation–get rid of the tissue to break the electrical pathway
What is an example of a reentry source?
Bundles of Kent
