Cardiac Muscle Flashcards
Exam 3
What makes up a cardiac muscle cell? Gap junctions? Intercalated Discs
Cardiac Muscle Anatomy Overview
Nuclei, Sarcomeres (in relaxed state…?)
Intercalated Discs: Jagged, convaluted, curvy lines; borders between the cardiac cells. One cell fits into the next cell. This creates more surface area, allowing for more gap junctions. Not a term used anywhere else in the body
Gap Junctions: Pathway between two adjacent cells in cardiac muscle to allow action potentials to travel quickly between cells
Cell Nuclei: One nucleus per cardiac muscle
Sarcomeres: Similar to skeletal muscle. Under normal conditions, heart is not relaxed to an optimal degree. Actin & myosin are always overlapping
Stem Cells, Fibroblasts, Synctial Connections
Cardiac Muscle Anatomy
Muscle tissue, Conduction Tissue, Role of ACE in fibroblasts?
Stem Cells: Capable of regenerating areas with cell death. Very, very, very slow process that happens over time with regular wear and tear. Not capable of repairing acute damage
Fibroblasts: Cells that form scar tissue. This is what happens with acute damage when stem cells are over-whelmed. Cardiac remodeling after MI. This also happens in CHF; excessive scar tissue formation. Scar tissue does not contract as well as cardiac muscle, does not conduct action potential.
ACE plays a role in growth factor production, which increases the activity of fibroblasts. Taking an ACE inhibitor will reduce the activity of fibroblasts in the heart. Not good for pregnant women though, fetus needs growth factor
Syncytial Connections: Describes the arrangement of cardiac muscle. Two different layers, squeezing/rotating in two different directions. Think; wringing water out of a towel.
Can also refer to the top half of the heart and the lower half of the heart (atria/ventricles)
Muscle tissue: Lots of myofibrils to produce force
Conduction tissue: Has no myofibrils. Transmits action potentials very quickly, but does not produce force. Purkinje Fibers
Endo, subendo, myocardium
Cardiac Muscle Anatomy: Muscle Layers
Epicardium, pericardium (space, parietal, fibrous)
-Endocardium: Cardiac Endothelial Layer (one cell thick layer). Deepest portion of cardiac muscle
“Subendocardium” muscle layer that is very deep in the wall of the heart. Super deep parts of the myocardium or endocardium. MI usually takes place here because the pressures are the highest.
-Myocardium: Bulk of the heart muscle wall
-Epicardium: Outermost/outside layer of the heart muscle
-Majority of our blood vessels sit on top of the epicardium and penetrate deep in a couple of areas
-Pericardial Space: Very small amount of fluid, large amount of mucus in this space just outside of the epicardium. Reduces friction on the heart muscle. Friction is extraordinarily painful (inflammation, loss of fluid or mucus)
-Pericardium: Connective tissue sac that the heart is enclosed in
-Parietal Pericardium: Innermost layer. Stretchy
- Fibrous Pericardium: Outermost layer. Similar to dura layer of CNS in the sense that it is stiff and leathery. Very difficult to expand
Cardiac Action Potential: Ventricles & Purkinje Fibers
Vrm, threshold, what kind of tissue is each? AV node block?
Ventricles:
-Syncytial tissue
-Vrm is about -80mv
-Action potential plateaus
Purkinje:
-Conductive tissue, does not produce force.
-Vrm is about -90mV
Both:
-At Vrm, slightly permeable to Na+. This is not constant. This gives us a slight slope on the Vrm potential axis. PNa+ is causing our Vrm to slowly become increasingly more positive
-Threshold here is ~ -70mV. Ventricles typically don’t self-depolarize because they receive an action potential from our pacemaker tissue.
-If there is a complete block of the AV node, it will take 30+ seconds for the ventricles to reach threshold and self-depolarize for the first initial escape beat. Should be slightly quicker after that
V & X Reflex
5 & Dime
-Pressure sensors in the orbit of the eye
-Pressure is sent to the brainstem via cranial nerve V (trigimenal nerve, fat nerve on the side of the face)
-Brainstem sends a message to the heart via the vagus nerve –> massive vagal output–> causing a complete AV block (temporary).
Heart rate can drop to zero, but should come back in about 30 seconds or so
Cardiac Action Potential: Ventricular Electrical Phases
Phase 4: Vrm. Should be a slight slope here
Phase 0: Na+ coming from the cell immediately upstream via gap junctions cause an action potential to spread –> Fast Na+ channels open, inward rectifying K+ channels close at the end of phase 0
Phase 1: Fast Ca++ current through T-Type Ca++ channels. Typically reach +20mV here
Phase 2: Slow L-type Ca++ channels open–> causing plateau phase. K+ channels begin to reopen halfway through Phase 2. Contraction happens here
Phase 3: All K+ channels open –> repolarization
Length of the action potential is much longer in the heart (~200ms)
What happens here?
Ohm’s Law
V=IR
Voltage is dependant on current crossing over a resistance
i= current
Ionic current is dependant upon how many ion channels are open and the electrochemical gradient of those ions
PNS innervates what? Main NT?
Myocardial ANS
NT for SNS?
PNS:
-Right vagus nerve innervates the SA node; extends just past the SA node out into the heart
-Left vagus nerve innervates the AV node; extens just past the AV node out into the heart
-ACh is released and binds to muscarinic receptors.
-PNS is the most predominant in the heart
SNS:
-Norepi is released and binds to B cells
Amplitude of the QRS (lead II) on EKG vs true depolarization?
Amplitude
Why does this happen? How do we measure amplitude?
-The deflection of the amplitude of the QRS complex is typically about 1.5mV (whereas; in a true AP, the magnitude of depolarization is ~ 100mV)
-Why does this happen? We lose a lot of the voltage that is taking place within our heart because of the high resistance in our tissues
-Amplitute of QRS Complex: The positive deflection above baseline + the negative deflection below baseline
What does the voltage meter show in different phases of AP?
EKG- 2 Electrode System
How do we determine if it is a postive or negative deflection?
-One (+) cathode, one (-) anode
-When we have a positive intracellular charge moving towards a positive cathode –> positive deflection
-This means our cell is depolarizing, and a negative charge is running down the outside of the cell
-When we have a negative intracellular charge moving towards a positive cathode --> negative deflection -This means our cell is repolarizing in the same pattern that it depolarized
-When we have a negative intracellular charge moving towards the negative anode –> positive deflection
-Peak activity on our voltage meter will be when the cell is half depolarized or half repolarized because that is when the charge gradient is at it’s greatest
-When there is no charge difference (resting cell or recently repolarized) our voltage meter will show zero
-Just beginning to depolarize or repolarize, will have slight movement on the meter
What is it?
Current of Injury
-Ischemia in the heart damages the cell, meaning that the cell cannot repolarize and remains depolarized.
-We will have abnormal current of injury in an area where we shouldn’t be having any current
Vrm, threshold. Other names for phase 4? Phase 0 What phase is absent?
Cardiac Action Potential: SA Node
How does phase 4 slope differ here?
-Reaches threshold faster than any other tissue in the heart
-Vrm is ~ -55mV
-Threshold is -40mV
-Large slope in Phase 4 in comparison to our fast action potential in the ventricles due to increased permeability to Ca++ & Na+, partly because of leak channels, but also because of the opening of HCN channels
Phase 0: Duration of action potential is due to L-type Ca++ channels. Not quite straight up and down like the fast action potential, this is due to no fast Na+ channels
Phase 4 also referred to as diastolic depolarization
No phase 1 here.
Maybe a phase 2
What does the name mean? This is a way the heart controls what?
HCN Channels
What happens when beta agonist & antagonists are given?
Hyperpolarizatio & Cyclic Nucleotide channels: Open when the nodal tissue returns to Vrm or in response to hyperpolarization
Non specific for positive ions. The majority of the current that flows through is 1) Na+ and 2) Ca++
The cyclic nucleotide in the name indicates that these channels are responsive to cyclic nucleotides. Cyclic AMP is one.
Beta Agonist –> increases activity of cAMP in the nodal tissue
–>increases the number of HCN channels that are open–> increased inward current of Na+ and Ca++
Beta Antagonist –> decreased activity of cAMP –> less involvement of HCN channels–> decreased slope in Phase 4
We know that the presence of HCN channels is there if there is any slope at all to Phase 4
This is another mechanism that the heart uses to do what?
mACh-r
What do these changes do to the phase 4 slope? 2 types of mACh-r
- ACh binds to mACh-r (GPCR) –> opening K+ channels
–> hyperpolarizing the cell, taking longer to reach threshold
Primary mechanism for nodal tissue to maintain Vrm. The amount of ACh in the nodal tissue directly correlates to K+ permeability. High amount of ACh binding to mACh-r, higher Pk+. If we block this receptor, our cells become less permeable to K+
- mACh-r (GPCR) that is inhibitory to adenylyl cyclase in the cell wall –> reduces the activity of cAMP
Beta Receptors
- GPCR that is stimulatory
-When an agonist binds this receptor, adenylyl cyclase is stimulated, and cAMP production is sped up - Beta receptor that can somehow interact directly with HCN channels. The increase in cAMP also causes the HCN channels to open. These allow more Na+ and Ca++ to enter
What causes an increase of PKA?
Targets of PKA
-Increased cAMP increases PKA (protein kinase A)
-PKA phosphorylates our L-Type Ca++ channels –> causing them to be more sensitive, and therefore open easier. This can contribute to EAD, DAD
-PKA phosphorylates Troponin I, increasing contractile protein sensitivity to Ca++ –> resulting in increased rate of cross-bridge cycling
-Phospholambam (SERCA pump inhibitor): PKA phosphorylates phospholambam –> inhibiting it –> should result in faster cycling due to faster reseting of the cell
cAMP- How does it degrade?
-It can degrade on its own, however that takes time.
-Phosphodiesterase is an enzyme that breaks down cAMP into AMP. Can give drugs to inhibit PDE if we want to keep cAMP around longer –increasing the activity of PKA
Normal HR for A&P
72 bpm
Potassium & It’s Effects on Nodal Tissue
What do these changes do to the phase 4 slope?
-Reducing K+ permeability will cause the VRM of the cell to be more positive
-Minor hyperkalemia (less gradient, less K+ movement); will see an increase in HR
-Major hyperkalemia: we’ll see something different
Not related to PCa
Ca++ & it’s effects on nodal tissue
Hint: reason is unknown
-Ca++ can change the threshold potential.
-Mechanism of action is unknown
-Reasonable Hypercalcemia; increases threshold potential (slows down the heart rate).
-Reasonable hypocalcemia: Reduce threshold potential (increase in heart rate)
What does the steepness of the slope mean?
Phase 0
Phase 0 in Ventricles vs Nodal Tissue
The slope of Phase 0 is important in determining how fast an action potential is going to propagate around the heart.
If we have a very steep, straight up and down Phase 0, that means that the action potential is occurin very, very, very quickly. This usually occurs when fast Na+ channels are involved and that Na+ is moving through gap junctions.
Steeper Phase 0 in ventricular action potential, due to higher number of fast Na+ channels
Sloped Phase 0 in nodal tissue because AP is primarily due to L-type Ca++ Channels.
Slower or faster than SA node? HCN Channels?
AV Node Action Potential
-Slower than the SA node, generates an AP at a rate of 40-60bpm
-Not as permeable to Na+ and Ca++ during phase 4.
-Vrm is slightly lower, and we have a smaller slope
With and without PNS, SNS input
Nodal Tissue & Speed of Action Potential Generation
-In a healthy person, without any influence from the PNS or SNS, the SA node will generate an AP rate of 110 bpm
-With both SNS and PNS input, the SA node generates an AP at a rate of 72 bpm
-Only PNS input, SA will fire at a rate of 60-62 bpm
-The SNS increases HR by about 10 beats per minute. If we have only SNS input, the SA would generate an AP at a rate of 120 bpm
Firing rate of SA, AV, Purkinje
Intracardiac Conduction System
Internodal pathways do what? Where are they?
-SA node is the origin of pacing
-AV node causes a slight delay
-Purkinje fibers can fire an AP at a rate of 15-30 bpm (not ideal, could be worse)
-Three internodal pathways in the right atrium. Anterior, middle, and posterior
-The anterior internodal pathway branches off and reaches over to the left atrium. This is called the interatrial bundle (Bachman’s Bundle)
-This system allows for the action potential to arrive at the AV node at the correct time
-Bundle of His
Intracardiac Timing; Top Half
-Timing is super critical to maintain an efficient pump
SA –> AV via internodal pathways takes 0.03 seconds
SA –> Depolarize entire R atrial muscle tissue ~ 0.07 seconds
SA –> Depolarize entire L atrial muscle 0.09 seconds (duration of P wave, P wave ends here)
Intracardiac Timing; Lower Half
-In a perfectly healthy heart, the AP should be able to make it from the SA node –> AV node –> Bundle of His–> L/R Bundle Branches–> Purkinje Fibers –> to the last portion of the ventricles in 0.22 seconds
-Conditions are not always ideal
AV Node delay? Refractory period does what?
Intracardiac timing; AV Node
The timing from SA node to interventricular septum
-The AV node causes a delay between atrial depolarization and ventricular depolarization. This is a good thing, allows the atria to have time to contract
-AV node also functions as a filter; filters extraneous action potentials in the atria so that they are not reaching the ventricles (a. fib, stretched out L atria). This is due to the AV node’s refractory period. This helps protect us from ventricular arryhthmias that originate in the atria (v tach)
-AV node (fat blob) also doesn’t have very many gap junctions.
-Delay at the AV node is about 0.12 seconds
-Delay at the Bundle of His is ~ 0.01 second –> Total delay beinf 0.13 seconds
-If you add the 0.03 seconds it takes for the AP to reach the AV node, the total time to reach the interventricular septum is 0.16 seconds
Where is the current heading?
-The interventricular septum here is depolarized
-The arrows point to the direction of the current. One wave of depolarization moving towards the left ventricle, one towards the right
-The negative charges on the tissue can either move towards repolarizing already depolarized tissue, or depolarizing resting tissue
-The pattern of the electrical current shows that this activity moves in the direction of the left foot.
-Positive electrode on L foot, negative on R arm
How long is it?
Normal EKG; P Wave
How many boxes tall/wide? What does it mean if too tall or long?
-P wave should be 0.09 seconds long
-Start of the P wave is SA node generating AP. Should be 2.5 boxes long and 2.5 boxes tall. This is a positive deflection
-If the AP began at the AV node and travel retrograde to the SA node, the P wave would be a negative deflection
-If the P wave is too tall, we are dealing with an issue in the right atria such as right atrial hypertrophy or the right atrium is stretched out
-P wave is too long, we have an issue in the left atrium
Causes for a tall QRS? QRS too long? What is Q? What is S?
Normal EKG: P-R Interval, QRS
QRS time length? How to calculate what QRS complex time should be?
-Q wave is the negative deflection before an R wave. Not everyone will have a Q wave depending on how the leads are positioned. Because of that, we measure P-R interval instead of P-Q.
-P-R interval should be 0.16seconds
-R wave is a postive deflection that corresponds with ventricular depolarization
-S wave is the negative deflection following the R wave
-QRS complex should have a length of 0.06 seconds. This is ideal. People typically have a little extra heart tissue, and this causes the QRS complex to be longer
-To determine this, we subtract the time it takes for the ventriles to depolarize - the PR interval
-If we have a tall QRS, means the electrodes are either very close to the heart or we have extra ventricular tissue
-A longer QRS probably due to dilated cardiomyopathy/systolic HF
J Point/Isoelectric Point, T wave, & Current of Injury
-The point on the EKG where the all ventricular tissue should be depolarized and the QRS complex has ended
-This gives us an idea if there is a current of injury
-All tissue should be repolarized by the end of the T-wave. If we see that some tissue is still depolarized, then we know we have an area of injury
How does the heart increase heart rate?
Normal EKG: Q-T, S-T
-Q-T interval is the length of time that we have depolarization happening in the ventricular tissue. The deeper the tissue, the longer it takes to depolarize.
-If we have a physiologic increase in heart rate, the heart shortens the Q-T interval by shortening the S-T segment
-This takes approximately 0.25-0.35 seconds, includes depolarization and repolarization of the ventricle
-S-T Segment; end of the S wave and start of the T-wave. This area helps us determine if there is an area of injury
-T Wave is repolarization of the ventricles. This is a positive deflection because this repolarization travels retrograde to the depolarization wave
Normal EKG: R-R Interval
-Normal R-R should be about 0.83seconds
-Can divide 60 seconds by the R-R interval and that will give us the heart rate
Cardiac Refractory Period
-Refers to the period after the action potential where the heart needs to reset
-An AP cannot be generated in the absolute refractory period
-In the relative refractory period, the cell is reset enough to generate an AP. This AP is weaker and is considered an early premature contraction.
-Affects filling time and strok volume
-Later premature can happen after the cell is completely reset but not quite ready for a full depolarization
If we move in the counterclockwise direction, we are moving towards the negative
If we move in the clockwise direction, we are moving toward the positive
0 degrees is also referred to as 360 degrees, no one calls it that
What is happening in this picture? Pattern of ventricular depolarization
Why does the L side take longer to depolarize?
-Both ventricles share the interventricular septum
-This image is showing the depolarized interventricular septum
-Right ventricle is typically thinner than the left, takes less time to depolarize
-Left heart is thicker, pumps against more resistance. Takes 0.22 seconds to depolarize the furthest point of the left ventricle
-Depolarization begins deep in the heart, in the endocardium. It then proceeds through the lateral walls (myocardium) as well as spread from deep to superficial. So endocardiam –> epicardium
What happens during atrial depolarization?
Repolarization of the atria in a healthy heart?
-The net depolarization wave is still heading in the direction of the left foot
-This means that because there is current heading towards the eyeball on the L foot, we will see a positive deflection (P wave)
-Repolarization of the atria, in a healthy heart, happens in the same manner that the tissue depolarized. This will give us a negative deflection
-We don’t see atrial repolarization on an EKG typically. It is masked within the QRS complex. Small amount of tissue= smaller repolarization wave
-Lead III will have the worst view, and therefore, the smallest P wave
If positive deflection in II.. should show..? A/V stand for what?
Where are the positive and negative electrodes? aVR is typically what?
(+) electrode for aVR is on the R arm. (-) electrode is the average of LA, LF
(+) electrode for aVL is on the L arm. (-) electrode is the average of RA, LF
(+) electrode for aVF is the LF. (-) electrode is the average of RA, LA
A= augmented
v=voltage
aVR is typically negative because we do not typically have current moving towards the RA. Most useless lead
aVL and aVF should have the same positive deflections as lead II
Names for them? Placement? Positive and negative electrodes?
12 Lead EKG; Precordial Chest Leads
Deflections should be what size in comparison to other leads?
V1 + V2- Septal Leads
V3 + V4: Anterior Leads
V5 + V6: Lateral Leads
These are all positive electrodes. They use a combination of the RA, LA, and LF as the (-) electrodes.
V1 and V2 are placed on either side of the septum/sternum in the 4th intercostal space. V4, V5, V6 are placed in the 5th intercostal space on the patient’s left lateral side. V3 is sandwiched between 2 & 4
Because these leads are directly on top of the heart, the deflections should be larger
