Exam 4 - Cardiac Flashcards
What type of muscle cell is the heart?
Visceral smooth muscle
What is the name of this stucture?
Where is the only place it is found?
What is it’s purpose?
- Intercalated discs
- Heart
- Increases the surface area between neighboring cells allowing a greater number of gap junctions to be present
What is the appearence of the heart muscle fibers?
What causes this?
- Alternating red and white bands (striated)
- The organization of actin and myosin filaments
How are cardiac cells nucleated?
They contain a single nuclei
What type of cells regenerate cardiac muscle?
How quick is this process?
- Stem cells
- It is a very slow process
Describe the role of fibroblasts in the heart?
They lay down scar tissue in the heart in areas that die faster than stem cells can replace them (usually at a controlled rate)
In what condition is there excessive fibroblast activity?
What problems does this cause?
What drug can be used to treat this and its MOA?
- CHF
- Fibroblast lay down scar tissue that do not conduct action potentials or participate in contraction
- ACE inhibitors - blocks production of Angtiontensin II which is a growth factor leading to fibroblast activity.
Why do we not give pregnant women ARB’s or ACEi?
They block the RAAS system which produces growth factors. If given during pregnacy, will deplete the fetus of these growth factors.
What is the term used to describe the organization of cardiac muscle layers on the left?
How does this arrangement work?
- Syncytial
- The layers squeeze and rotate in opposite directions, like wringing out a towel, leading to high efficency under high pressures.
Describe the conduction tissue in the heart and how it’s different than skeletal muscle?
This includes SA, AV, Bundle of His, and Purkinjie fibers
* It is highly efficent at conducting AP and does not produce much force.
* It is able to do this because it is not full of myofibrils and other tissues like skeletal muscle.
What is the deepest layer of the heart called that is made of endothelial tissue?
- Endocardium
What is the name of the heart layer containing the bulk of the muscle tissue?
Myocardium
What is the most superficial layer of the heart tissue?
What else is found in this layer?
- Epicardium
- The major blood vessels are superficial to this layer
What is the name of the heart layer that is superficial to the epicardium?
What is contained within this layer and it’s function?
- Pericadial space
- Mucous and fluid that allows the heart to move with low friction. If this area is inflammed or didn’t have enough fluid it would be very painful.
What is the name of the 2 most superficial layers of the pericardium?
Describe its texture?
- Parietal pericadium
- Fibrous pericardium - similar dura, very stiff and leather like
What does the term subendocardium mean?
Muscle in the LEFT heart wall that is very deep, usually in the myocardium or endocardium
Why are MIs usually in the subendocardium?
Because this is where wall pressures are the highest, and are the most likely to become ischemic
Describe the resting condition of sarcmeres in the heart?
The sarcomeres are typically understretched, evidenced by overlapping actin molecules which means there is no H band
Describe the difference in Vrm between purkinje fibers and ventricular muscle?
What is their threshold potential?
- Purkinje fibers: -90mV
- Ventricular muscle: -80mV
- Threshold potential: -70mV
Describe Na+ permeability in ventricular muscle/purkinje fibers at rest?
What is the effect of this?
- They are slightly permeable to Na+ at rest, causing a small upslope in the AP.
- Can generate a depolarization without an AP (but this takes a long time, >30 seconds for first deplarization).
Describe the V + X reflex?
- Named “Five and dime” reflex
- Occurs during manipulation of the eye leading to temporary complete HB/asystole
- Pressure sensor information is sent from the trigeminal nerve (V) to the brain stem
- The brain stem then sends a stimulus via the vagus nerve (X) leading to a massive increase in vagal output that will inhibit APs at the AV node
- This should resolve with spontaneous depolarization of the ventricles
Describe the phases of the cardiac AP and the contributing factors?
- Phase 4 - Resting Vrm, slight up stroke due to Na+ permeability via gap junctions
- Phase 0 - upstroke from fast Na+ channel opening
- Phase 1 - Fast Na+ channels close, Fast T-type Ca++ channels open, and K+ channels close and do not open until the beginning of Phase 3.
- Phase 2 - Slow L-type Ca++ channels open
- Phase 3 - K+ reopen
What is Ohm’ Law?
V= IR
Voltage = current x resistance
What is the ionic current (i) dependent on?
- The number of channels open
- The electrochemical gradient of that ion
Describe parasympathetic nerve location and function in the heart?
- Right vagus nerve is at the SA and the left vagus nerve is at the AV, it also extends a little further past the nodes
- Vagus nerve supresses pacemaker cells in the heart by releaseing ACh that binds to mACh
Describe sympathetic nerve location and function in the heart?
- Innervates atria and ventricles
- Releases NE that binds to beta receptors
What is the amount of depolarization we get in ventricular myocytes?
~100 mV
How much depolarization do we get during the QRS on a ECG?
Why is this so much lower than voltage inside the heart?
- ~1.5 mV or 3 big boxes (0.5 mV/large box)
- The voltage is being conducted through air and fat (non-conductive) to the electrodes
Why do COPD patients have a lower voltage ECG?
They have more air trapped in their lungs which the voltage has to travel through and weakens the signal strength
When a cell is at rest, what would a 2 electrode voltmeter read?
0, because there is no difference in charge between the postive and negative electrode.
What deflection on a voltmeter would you expect for this cell that is just beginning depolarization?
The meter would be just slightly moved to the positive end
Which direction does an ECG wave deflect based on electron movement?
- Electrons moving toward the positive lead creates a positive deflection
- Electrons moving towards the negative lead creates a negative deflection
What volmeter reading would you expect this cell that is half depolarized?
There would be a strong positive reading because it has the greatest difference in charge. (half depolarized, half not depolarized).
This causes a strong current from the negative side to the positive side.
What reading would the voltmeter have with this cell that is almost completely depolarized?
There would be a small slightly positive deflection.
This is because current is reduced due to the smaller positively charged area drawing the electrons towards it.
But electrons are still moving towards the positve electrode.
Describe why depolarization leads to this reading on a non cardiac ECG?
The entire deflection is positive because the electrons are always moving toward the positive electrode.
It is strongest in the middle because this is when the greatest difference in charge occurs (half depolarized, half at rest)
The beginning and end are zero because there is no difference in charge - all negative and all positive.
Here, a cell beginning to repolarize in the same direction as depolarization. What deflection would you expect?
A slightly negative deflection, because the electrons or negative charge are moving only a little towards the small area of positve charge.
This movement is away from the postive electrode, creating the negative deflection.
What deflection would you expect in this half repolarized cell?
A strong negative deflection because this is the largest diffence is charge between the electrodes.
The electrons current towards the positive charge is the greatest.
What deflection would you expect at this point during repolarization?
A small negative deflection
The electons are still moving away from the positve electrode, but current is low due to the small area of negative charge
Explain why we get this ECG in a non cardiac tissue when repolarization occurs in the same direction as depolarization?
Because the electron current is opposite of depolarization. The repolarization is happening from left to right, but the electrons are moving right to left, towards the positive charge and towards the negative electrode.
Here, repolarization is in an opposite direction from depolarization. What deflection should we expect?
What about when half is repolarized in this manner?
A slightly positive deflection
This is due to electrons moving towards the small area that is repolarized and the positive electrode
When half is repolarized, there would be a strong positive deflection due the greatest difference in charge between electrodes
In what manner do depolarizaton and repolarization occur in the ventricles?
How is this evidenced on an ECG?
- Depolarization moves from the septum/deep structures to more superficial tissue (in to out)
- Repolarization starts on superficial tissues and then moves inward to the deeper strucures
- This creates a positive defelction for ventricular repolarization (T wave)
Explain what happens with electrical conduction in ischemic myocytes?
Ischemic tissues cannot repolarize so they stay depolarized.
This causes currents to occur when there shouldn’t be (during repolarization on an ECG).
In healthy adults, why is the SA the pacemaker of the heart?
What is the rate at which is fires action potentials?
- The SA node cells depolarize and reach threshold faster than other areas of the heart, making it the pacemaking center
- Fires AP at a rate of 72 bpm
What is the resting and threshold potential in an SA nodal cell?
- Vrm = -55 mV
- Threshold = -40 mV
Describe the phase 4 slope in SA nodal cells compared to ventricular muscle?
What causes this?
- The phase 4 slope in SA nodal cells is much steeper, allowing them to reach threshold potential much faster than the ventricles.
- This is due to permeability of Ca++ and Na+ via leak and HCN channels.
Describe the function of HCN channels in SA pacemaker cells.
- When the cell reaches Vrm, HCN channels begin to open slowly increasing the rate of depolarization, opening more HCN channels until threshold is reached and phase 4 begins.
- They are non-specific for positive ions K+, Na+, and Ca++. Primarily Na+ and then Ca++. K+ doesnt really move through because of the wave of Na+ influxing.
HCN channels stand for Hyperpolarization and Cyclic nucleotide, how did it get this name?
- Hyperpolarization: because the channels open up when the cell is a Vrm/hyperpolarized
- Cyclic nucleotide: changes activity based off the amount of cAMP
How does increasing/decreasing cAMP directly affect HR?
- cAMP is increased with beta agonism via increased activity of adenylyl cyclase
- Increased cAMP causes opening of more HCN channels
- This increases the slope of phase 4 leading to an earlier AP which increases HR.
-Beta agonism also shuts down K+ channels - Beta antagonism inhibits cAMP production, reducing the opening of HCN channels which decreases the slope of phase 4
- A decreased slope means the AP will take longer to reach threshold, which equals a decreased HR
How do mACh-R affect SA node AP?
- Activation of mACh-R leads to opening of K+ channels - this decreases Vrm, making it take longer to get to threshold, decreasing the number of AP fired and HR
- Antagonism of mACh-R causes more K+ inside the cell, increasing Vrm, allowing the cell to reach threshold quicker, incresing the firing of AP and HR.
Explain what affect slight hyperkalemia has on HR?
Hyperkalemia reduces the electrochemical gradient, causing K+ to stay inside the cell more, increasing Vrm, decreasing the time it takes to reach threshold, increasing the HR.
What does serum Ca++ level do to SA node action potentials?
Increased ECF Ca++ increases SA node cells threshold potential, decreasing HR
Decreased ECF Ca++ decreases threshold, increasing HR
This mechanism is unknown
Why is the phase 4 slope of SA nodal tissue much steeper than the phase 4 slope in ventricular muscles?
- In ventricular muscles, there is not as much permeability to Ca++ and Na+ during phase 4
- There are also not as many HCN channels
What is the other name for phase 4?
What does the speed of this determine?
- Diastolic depolarization
- The faster the depolarization, the faster the HR (takes less time to fire an AP)
Describe the differences in phase 0 slope of SA node and ventricular muscles?
- The SA node phase 0 does not have as steep of an upstroke
- This is because the upstroke of the action potential is almost entirely due to slow L-type Ca++ channels as opposed to fast Na+ channels in the ventricles.
Describe the cause of phase 3 in SA nodal tissue?
What about phases 1 and 2?
- Phase 3 is caused by slow L-type Ca++ channels closing and VG-K+ channels opening
- There is no phase 1 in nodal tissue
- There is no phase 2 per Dr. Schmidt (no discernable plateau phase)
What causes the AV node to have slower automaticity than the SA node?
- Resting Vrm is more negative
- It is “fatter” not conducting AP very well
- Phase 4 slope is not as steep due to decreased permeability to Na+ Ca++
- Fewer gap junctions
Describe the AP’s in the subendocardium and the epicardium?
Correlate this to ECG findings?
(F)Subendocardium: Depolarizes first and has a longer AP
(G)Epicardium: Depolarizes last but repolarizes first, having a shorter AP
-This set up allows coordinated contraction of the inner and outer ventricular muscles
Because the epicardium repolarizes first, repolarization moves from the epicardium to the endocardium. This is why we have a postive deflection during ventricular repolarization (T wave)
Describe why the atrial depolarizations have this apperance?
- They have a short plateau phase because the atria are not producing a large amount of force or pumping against a high resistance
- Atrial walls are thin, so its not as important for the inner and outer muscles to have coordinated contraction
What is the normal firing time of the AP in SA node?
How can this be determined from and ECG?
- Fires an AP every .83 seconds = 72 bpm
- Count the R-R interval, then divide 60 secs by the interval
How fast will AP be generated if the SA node acted without the ANS?
SA node with only SNS input?
SA node with only PNS input?
Correlate this information to priority of ANS innervation.
- 110 bpm
- 120 bpm
- 60-62 bpm
- The PNS/vagus nerve has a much greater effect on the heart than the SNS
What is this structure?
What is its purpose?
Interatrial bundle or “Bachman’s Bundle”
Spreads AP from SA to the left atria
What are the circled structures called?
Internodal pathways
-Anterior (closest to septum)
-Middle
-Posterior (closest to right atrial wall)
How long does it take for the AP to move from the SA to the AV node?
.03 seconds
How long does it take for right and left atria to depolarize?
Describe the lag in time from interatrial bundle deploarization to entire left atrial depolarization?
- Right: .07 seconds
- Left: .09 seconds
- The interatrial bundle does stops at the superior left atria and the remainder of depolarization must be carried out in the tissue by fast Na+ channels
How long does it take for the AP to depolarize the entire heart ideally?
Why is there such a long delay from the AV node to the last ventricular depolarization?
- .22 seconds
- The AV node delays the SA node AP and filters out extraneous AP’s
How long is the delay at the AV node and what contributes to it?
How long does it take for an AP to get from the SA to the bundle branches?
What does this relate to on the ECG?
- 0.13 seconds
- 0.12 s delay at AV node and 0.1 s delay at the Bundle of His
- .16 s from SA to bundle branches (.03 SA to AV, .13 AV to bundle branches)
-This equates to the time for the PR interval, as well as time to start of QRS
What is the direction and degree is electrical depolarization in the heart?
- Depolarized toward left foot
- At an angle of 59 degrees
What is the name of this point on an ECG?
What state is the heart in at this point?
J-point or isoelectric point
All of the ventricles should be completly depolarized
What state is the heart in at this point on the ECG?
What might cause abnormalities here?
All of the heart muscle should be repolarized
Any unhealthy tissue will not be repolarized and can cause abnormal currents
Describe the relative refractory period and what an AP would be like if fired during this period?
Time at the very end of an AP where most but not all of the cell is reset
Since most of the cell is reset, and AP can propigate but it will be much weaker due to some of the cell not having repolarized
What is the absolute refractory period?
The point on the AP close to the beginning of repolarization where an AP cannot be propigated because not much of the cell has repolarized.
What problems can the bidirectionality of gap junctions in the heart cause?
What protects this from happening often?
- The AP could spread retrograde creating an ectopic action potential - these are usually weak AP which in turn leads to weak contraction
- This is prevented by the refractory period of the cells in which an AP cannot be propigated
What plane is the 3 lead ECG looking at?
What leads are involved in these planes?
- Frontal or coronal plane
- Lead I, II, II, aVF, aVR, aVL
What lead has the best view during depolarization?
Why?
How is this lead set up?
- Lead II
- Lead II looks at the heart from a 60 degree angle and the mean electrical current of heart is 59 degrees. This registers as a strong deflection because it is almost directly in line with lead II.
- Positive electrode on left foot, negative electrode on right shoulder
How is lead I set up?
- Negative electrode on right shoulder and positive electrode on left shoulder
- Looks at current at a 0 degree angle
How is lead III set up?
- Negative electrode on left shoulder and positive electrode on left foot
- Looks at current from a 120 degree angle
Describe a left axis deviation?
- A shift in net depolarization to < 59 degrees, towards the left arm
Describe a right axis deviation?
A shift in net electrical current to > 59 degrees
Describe the orientation of degrees regarding cardiac electrical movement?
Movement counterclockwise can be measured as negative numbers
Moving clockwise is positive
Describe depolarization and repolarization in the atria and the corresponding ECG findings?
- Both depolarization and repolarization occur in the same direction, typically towards the left foot similar to QRS wave
- Depolarization creates a positve deflection (p wave) and repolarization creates a negative deflection that is hidden by the QRS
Why is the magnitude of lead I on the ECG much lower than lead II and lead II?
Lead I only is picking up the current moving horizontially.
During depolarization there is not large amount of left to right current leading to smaller magnitude of deflection.
What deflection would be seen in lead I if the mean electrical axis what the red arrow shown below?
There would be a small negative deflection with a strength corresponding to the amount of horizontal current (side B)
What is Einthoven’s Law?
How is it measured?
- Deflection magnitude of lead I + lead III = lead II
- The overall positive deflection is the peak positive deflection - peak negative deflection
What would leads I, II, and III show if only the septum is depolarized as shown below?
Positive deflection in all 3 leads. Magnitude being II>III>I
What would leads I, II, and III show if 50% of the ventricles are depolarized as shown below?
A stronger positive deflection in all 3 leads because the differnce in polarity is at the greatest point and the mean electrical current is in the same plane.
What would be shown in leads I,II, and III at this point during depolarization if more than 50% of the ventricles were depolarized?
The net electrical movement is still towards the left foot, so there is still a positve deflection, but with a decrease in magnitude because more than 50% is depolarized.
A decrease in the vector does not equal a negative deflection. A negative deflection would be below baseline.
What would you see in leads I, II, and II at this point when only the last part of the ventricle has not depolarized?
- The net electrical axis has shifted now up and to the left arm (towards that last area that needs to be depolarized)
- Lead I: positve deflection because the current is moving right to left
- Lead II: Small negative deflection, the current is pointed slightly towards the negative lead.
- Lead III: stronger negative deflection because the current is moving almost directly away from the positive lead, but there is not much space for the current to move
This is the source of the s wave
What would be seen in leads I, II, and III if all the ventricle is depolarized as shown below?
All leads should be at baseline because there is no movement of current.
Why do we get a Q wave? What would this look like in leads I, II, and III?
The initial depolarization of the septum starts on the left side of the heart and then moves rightward and down. This causes a strong negative deflection in lead I, small negative deflection in lead II, and small positive deflection in lead III.
Describe the set up of the augmented leads?
The negative electrodes are comprised of the avereage of the 2 standard leads opposite the positive augmented lead.
aVR: positve lead right arm, negative lead in between LA and LL (lead III)
aVL: positve lead left arm, negative lead between RA and LL (lead II)
aVF: positive lead left leg, negative lead between RA and LA (lead I)
Describe the set up of the deconstructed augmented leads?
There are 30 degree angles between standard leads and augmented leads
aVF: 90 degrees
aVR: 210 degrees or -150 degrees
aVL: -30 degrees or 330 degrees
Where on the body are the chest leads placed?
- V1: 4th ICS, RSB
- V2: 4th ICD, LSB
- V3: in between V2 and V4
- V4, V5, V6: 5th ICS progressing to axilla
Describe the normal EKG seen in V1?
Negative p wave, QRS, and t wave (even though pic is not showing it)
What would a posterior current of injury in V2 show on the ECG and why?
- Would see a positive deflection when the rest of the heart should all be repolarized (between t and p wave)
- This is because current is moving toward positive electrode, or toward V2 lead
What would a anterior current of injury show in V2 and why?
- Would see a negative deflection when the heart should be completely repolarized (between t and p wave)
- The current is moving away from the positive lead or V2
Why do we see a larger magnitude of delfection in the precordial leads?
Which lead is the largest magnitude and why?
- They are placed much closer to the heart.
- V4 because it is almost directly in plane with the mean electrical axis
How were ECG originally read?
Oscilloscopes - showed direction of electrical movement with a continuous line
Describe the physiology of an inverted T wave?
This occurs when the ventricles repolarize in the same direction as depolarization (in to out)
Determine mean electrical axis and possible causes of any abnormalities in the following ECG?
This is a left axis deviation
Potential BBB or leftward heart orientation
Determine mean electrical axis and possible causes of any abnormalities in the following ECG?
This is a right axis deviation
This could be caused by right ventricular hypertrophy making it take longer to depolarize the RV
Determine mean electrical axis and possible causes of any abnormalities in the following ECG?
This is a left axis deviation caused by a left BBB
Determine mean electrical axis and possible causes of any abnormalities in the following ECG?
This is a right axis deviation
Right ventricle taking longer to depolarize, likey due to RV hypertrophy bc of the large QRS seen in lead III
What is occuring in this EKG?
ST segment depression due to a positive current of injury, this is typically seen in ischemia
What is occuring in this EKG?
ST segment elevation due to a negative current of injury, this is typically seen in infarction
Draw the vector cardiogram based off the ECG below.
Determine location of injury based off of vectorcardiogram.
Lead I: small negative current of injury
Lead II: no current of injury
Lead III: small positive current of injury
V2: negative current injury
This is a left anterior current of injury
Describe what ECG findings you would see with an area of ischemia as below?
Most of the heart here is repolarized except for the area of injury. Normally, the voltage on the ECG would be at baseline because all of the tissue is resting. But, because this area is constantly depolarized, it creates a positve deflection between the TP segment (where there should be no deflections).
This is ST segment elevation and characteristic of ischemia.
The ST segment is not actually lower, its that the TP segment is elevated!
Describe what ECG findings you would see with an area of infarction as below?
An infarction usually causes a current of injury oppositie to ischemia. Here the TP segment would have a negative deflection as shown by the blue arrow, showing ST segment elevation. There also would be a larger magnitiude of deflection because the area of injury is large.
Draw the vector cardiogram based off the ECG below.
Determine location of injury based off of vectorcardiogram.
Lead I: no current of injury
Lead II: negative current of injury
Lead III: negative current of injury
V2: positive current of injury
This is a posterior apex current of injury
What happens to the AP in ventricular myocytes when Vrm is slightly increased?
- No all of the fast Na+ channels are reset and the slope of phase 0 is less steep
What happens to the AP in ventricular myocytes when Vrm is high enough that no fast Na+ channels can repolarize?
Explain the mechanism and it’s effects?
The AP appears alot like a slow AP
This is because Ca++ is being used to propigate the AP between gap junctions instead of Na+ and it takes longer for calcium to move through because of its large size.
This leads to a reduction in the speed of conduction
What would happen if the Vrm was so high that Ca++ channels cannot reset?
There would not be any propigation of an AP
