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.
- ARB - block binding of angiotensin
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 SA and AV node
- This should resolve with spontaneous depolarization of the ventricles, may take up to 30 seconds
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 - L-type Ca++ close, 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 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
- cAMP levels also impact the effects of PKA
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 the automaticity of the AV node?
Purkinjie fibers?
- AV: 40-60 bpm
- Purkinjie: 15-30 bpm
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
What causes delay at the AV node?
- The node is large and does not conduct AP efficently
- Has a low number of gap junctions
- Has a more negative Vrm
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 0.01 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