Exam 4 - Cardiac Flashcards
(174 cards)
1
Q
What type of muscle cell is the heart?
A
Visceral smooth muscle
2
Q
What is the name of this stucture?
Where is the only place it is found?
What is it’s purpose?
A
- Intercalated discs
- Heart
- Increases the surface area between neighboring cells allowing a greater number of gap junctions to be present
3
Q
What is the appearence of the heart muscle fibers?
What causes this?
A
- Alternating red and white bands (striated)
- The organization of actin and myosin filaments
4
Q
How are cardiac cells nucleated?
A
They contain a single nuclei
5
Q
What type of cells regenerate cardiac muscle?
How quick is this process?
A
- Stem cells
- It is a very slow process
6
Q
Describe the role of fibroblasts in the heart?
A
They lay down scar tissue in the heart in areas that die faster than stem cells can replace them (usually at a controlled rate)
7
Q
In what condition is there excessive fibroblast activity?
What problems does this cause?
What drug can be used to treat this and its MOA?
A
- 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
8
Q
Why do we not give pregnant women ARB’s or ACEi?
A
They block the RAAS system which produces growth factors. If given during pregnacy, will deplete the fetus of these growth factors.
9
Q
What is the term used to describe the organization of cardiac muscle layers on the left?
How does this arrangement work?
A
- Syncytial
- The layers squeeze and rotate in opposite directions, like wringing out a towel, leading to high efficency under high pressures.
10
Q
Describe the conduction tissue in the heart and how it’s different than skeletal muscle?
A
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.
11
Q
What is the deepest layer of the heart called that is made of endothelial tissue?
A
- Endocardium
12
Q
What is the name of the heart layer containing the bulk of the muscle tissue?
A
Myocardium
13
Q
What is the most superficial layer of the heart tissue?
What else is found in this layer?
A
- Epicardium
- The major blood vessels are superficial to this layer
14
Q
What is the name of the heart layer that is superficial to the epicardium?
What is contained within this layer and it’s function?
A
- 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.
14
Q
What is the name of the 2 most superficial layers of the pericardium?
Describe its texture?
A
- Parietal pericadium
- Fibrous pericardium - similar dura, very stiff and leather like
15
Q
What does the term subendocardium mean?
A
Muscle in the LEFT heart wall that is very deep, usually in the myocardium or endocardium
16
Q
Why are MIs usually in the subendocardium?
A
Because this is where wall pressures are the highest, and are the most likely to become ischemic
17
Q
Describe the resting condition of sarcmeres in the heart?
A
The sarcomeres are typically understretched, evidenced by overlapping actin molecules which means there is no H band
18
Q
Describe the difference in Vrm between purkinje fibers and ventricular muscle?
What is their threshold potential?
A
- Purkinje fibers: -90mV
- Ventricular muscle: -80mV
- Threshold potential: -70mV
19
Q
Describe Na+ permeability in ventricular muscle/purkinje fibers at rest?
What is the effect of this?
A
- 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).
20
Q
Describe the V + X reflex?
A
- 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
21
Q
Describe the phases of the cardiac AP and the contributing factors?
A
- 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
22
Q
What is Ohm’ Law?
A
V= IR
Voltage = current x resistance
23
Q
What is the ionic current (i) dependent on?
A
- The number of channels open
- The electrochemical gradient of that ion
24
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
25
Describe sympathetic nerve location and function in the heart?
* Innervates atria and ventricles
* Releases NE that binds to beta receptors
26
What is the amount of depolarization we get in ventricular myocytes?
~100 mV
27
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
28
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
29
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.
30
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
31
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
32
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.
33
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.
34
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.
35
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.
36
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.
37
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
38
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.
39
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
40
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)
41
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).
42
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**
43
What is the resting and threshold potential in an SA nodal cell?
* Vrm = -55 mV
* Threshold = -40 mV
44
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.
45
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.
46
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
47
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
48
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.
49
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.
50
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
51
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**
52
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)
53
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.
54
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)
55
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
56
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)
57
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
58
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
59
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
60
What is the automaticity of the AV node?
Purkinjie fibers?
* AV: 40-60 bpm
* Purkinjie: 15-30 bpm
61
What is this structure?
What is its purpose?
Interatrial bundle or "Bachman's Bundle"
Spreads AP from SA to the left atria
62
What are the circled structures called?
Internodal pathways
-Anterior (closest to septum)
-Middle
-Posterior (closest to right atrial wall)
63
How long does it take for the AP to move from the SA to the AV node?
.03 seconds
64
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
65
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
66
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**
67
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
68
What is the direction and degree is electrical depolarization in the heart?
* Depolarized toward left foot
* At an angle of 59 degrees
69
How would the ECG be affected if the AP were originating in the AV node?
The p wave would be inverted because the signal is travel retrograde back to the SA node, causing a negative deflection
This could occur before the p wave if the pacemaker is high in the AV node, or after the QRS if lower in the AV node
70
What is the normal p wave size on ECG?
What would cause the p wave to be too high?
What would cause the p wave to be too long?
* 2.5 x 2.5 small boxes
* Right atrial hypertrophy (more tissue)
* Left atrial dilation (stretched)
| "Height Right, Long left"
71
Describe the Q, R, and S wave?
* Q wave: negative deflection prior to R wave (not always seen depending on lead orientation)
* R wave: positive deflection correlating to ventricular depolarization
* S wave: negative deflection following R wave
72
How long should the PR interval be?
0.16 seconds
.03 s from SA to AV, .12 s AV to Bundle of His, .01 Bundle of His to bundle branches
73
How long should the duration of the QRS be?
What causes it to be longer?
.06 seconds
.22 s (last ventricular depolarization) - .16 s (time to start of QRS)
Increase in amount of ventricular tissue (chronic caffeine use)
74
What would cause a larger magnitude of deflection the QRS?
What would prolong the length of the QRS?
* Electrodes placed close to the heart or increased ventricular tissue (hypertrophy)
* Dilated cardiomyopathy (stretched out ventricles)
75
Where does atrial repolarization occur on ECG?
During the QRS wave, hidden
Would be a negative p wave bc atria repolarize in the same direction as depolarization
76
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
77
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
78
What does the QT interval relate to?
How long should it be?
* Start of ventricular depolarization to end of ventricular repolarization
* Correlates to length of endocardial AP because it depolarizes first and repolarizes last
* 0.25-0.35 seconds
79
What happens to the ECG when we have a physiologic increase in HR?
What is the name for this process?
QT interval shortens or repolarizes faster, allowing time to fire more AP, and increasing HR
Lusitropy: Rate of cardiac muscle repolarization
80
What do the large and small boxes equate to on the Y axis of an ECG?
Large boxes: 0.5 mV
Small boxes: 0.1 mV
81
What do the large and small boxes equate to on the X axis of an ECG?
5 large boxes per second
Each large box: 0.2 seconds
Each small box: .04 seconds
82
How did the grid pattern timing get its organization?
Paper was feed through the ECG maching at 25 mm/sec
83
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, an AP can propigate but it will be much weaker due to only part of the cell participating
84
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.
85
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
86
What plane is the 3 lead ECG looking at?
What leads are involved in this plane?
* Frontal or coronal plane
* Lead I, II, II, aVF, aVR, aVL
87
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
88
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
89
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
90
Describe a left axis deviation?
* A shift in net depolarization to < 59 degrees, towards the left arm
91
Describe a right axis deviation?
A shift in net electrical current to > 59 degrees
92
What are some causes of axis deviations?
* Bundle branch block
* Increased cardiac tissue
* Heart orientation in the chest
-COPD: chest is full of air and restricts heart movement, pointing the axis straight down
-Exhalation: axis tilts to the left
-Inhalation: axis tilts to the right
93
Describe the degrees obtained when moving around the frontal plane leads?
Movement counterclockwise can be measured as negative numbers
Moving clockwise is positive
94
What is the last part of the heart to depolarize?
Why?
* Left lateral wall of left ventricle
* The left ventricle is much larger than the right ventricle, so it take more time to depolarize and the left lateral wall is furthest from the conduction system.
95
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
96
In what lead would we see that largest deflections for all 3 main events?
Lead II, all are occuring almost parallel to lead II axis
97
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.
98
What would lead I show on the ECG if the mean electrical axis was pointing straight down?
There would be no deflection because current is perpendicular to the axis
99
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)
100
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
101
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
102
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.
103
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.
## Footnote
A decrease in the vector does not equal a negative deflection. A negative deflection would be below baseline.
104
What would you see in leads I, II, and III 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**
105
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.
106
In what lead would you expect to not have an S wave?
* Lead I - the movement of current during the s wave is towards the positve electrode of lead I resulting in a positive deflection.
107
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.
108
How are the augmented electrodes named?
a = augmented
V= voltage
R, F, L = location of the positve electrode
109
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)
110
Which augmented lead is used least and what direction are its deflections?
aVR: should always have negative deflections, current always should be moving away from RA
111
Describe the set up of the deconstructed augmented leads?
There are 30 degree angles between standard leads and augmented leads
aVF: 90 degrees
aVR: -150 degrees or 210 degrees
aVL: -30 degrees or 330 degrees
112
Describe where to positive and negative end are for the precordial/chest leads?
What are the names given to the leads?
* V1-6 are the positive electrodes
* The negative electrode is an average of the 3 standard leads
* V1, V2: septal leads
* V3, V4: anterior leads
* V5, V6: lateral leads
113
Where on the body are the chest leads placed?
* V1: 4th ICS, RSB
* V2: 4th ICS, LSB
* V3: in between V2 and V4
* V4, V5, V6: 5th ICS progressing to axilla
114
Describe the normal EKG seen in V1?
Negative p wave, QRS, and t wave (even though pic is not showing it)
115
Describe the normal ECG for V2, and the usefulness of this lead?
* Positive p wave and t wave
* Negative QRS
* Used to diagnose anterior or posterior currents of injury because it is looking directly at the middle of the heart.
116
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
117
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
118
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
119
How were ECG originally read?
Oscilloscopes - showed direction of electrical movement with a continuous line
120
Describe the physiology of an inverted T wave?
This occurs when the ventricles repolarize in the same direction as depolarization (in to out)
121
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
122
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
123
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
124
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
125
What is occuring in this EKG?
ST segment depression due to a positive current of injury, this is typically seen in ischemia
126
What is occuring in this EKG?
ST segment elevation due to a negative current of injury, this is typically seen in infarction
127
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
128
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 depression and characteristic of ischemia.
## Footnote
**The ST segment is not actually lower, its that the TP segment is elevated!**
129
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.
130
How do we determine where a current of injury is occuring?
* Compare the J point to the TP segment.
-If the TP segment is lower than the j point = negative current of injury
-If the TP segment is higher than the j point = positive current of injury
* If V2 is given:
-a negative current of injury = anterior
-a positive current of injury = posterior
* The mean electrical axis points **away** from where the current of injury is coming from
131
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
132
Describe the names and locations of the gates on fast Na+ channels and L-type slow Ca++ channels?
* Fast Na+ channels:
-inactivation gate (h gate) is inside the cell
-activation gate (m gate) is outside the cell
* L-type slow Ca++ channels:
-inactivation gate (f gate) is inside the cell
-activation gate (d gate) is outside the cell
133
Describe the process of opening and closing of the fast Na+ channel?
At rest the m gate is closed and the h gate is open, the AP opens the m gate and the h gate closes very quickly.
In order for the m gate to close and the h gate to reopen, the cell must be repolarized.
If they are not repolarized they are stuck in an inactive form and cannot respond to another AP.
134
Describe the process of opening and closing of the L-type Ca++ channel?
At rest the d gate is closed and the f gate is open. The d gate opens in response to a voltage, but it opens much slower than the fast Na+ channel. The f gate also closes slower than fast Na+ channel.
As in the fast Na+ channels, the cell must be repolarized to close the d gate and reopen the f gate in order to be used again.
135
What are the 2 theories as to why there isn't much fast Na+ channel involvement during the SA node AP?
1. There are no fast Na+ channels in the nodal tissue
2. The fast Na+ channels are non-functional because the Vrm is not negative enough to repolarize the channels (Vrm = -55 mV)
136
Describe the amount of repolarization needed for fast Na+ and L-type Ca++ channels?
L-type Ca++ channels need a lower voltage to repolarize (~-55 mV) than the fast Na+ channels.
137
What does the slope of phase 0 directly relate to?
The number of fast Na+ channels
The steeper the slope the more channels and vice versa
138
What happens to the AP in ventricular myocytes when Vrm is slightly increased?
* Not all of the fast Na+ channels are reset and the slope of phase 0 is less steep
139
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
140
What would happen if the Vrm was so high that Ca++ channels cannot reset?
There would not be any propigation of an AP
141
What would increase the Vrm of the heart cells?
* Hyperkalemia
* Acidosis: if pH < 7.4, the enzymes that catalyze chemical reactions no longer function at an optimum speed, leading to an energy defecit and inability to repolarize.
* Ischemia or infarction: not enough nutrients are making it to the cell, also causing and energy defecit and inabilty to repolarize.
142
Describe -caine drugs effects of the myocardial AP?
Blocks Na+ channels, lowering the slope of phase 0.
143
Describe ionotropic mACh-R function and location in the heart?
* Found at the nodal tissue and when bound releases potassium from a nearby channel
* This is the primary way the heart maintains and changes Vrm (increases and decreases HR)
144
Describe the function of metabotropic mACh-R in the heart?
* When activated causes inhibition of adenylyl cyclase via GPCR
* This decreases production of cAMP leading to decreased action of PKA and reduction in HR
145
Describe the metabotropic beta receptor function in the heart?
* When bound increases the activity of adenylyl cyclase via Gs GPCR
* This increases production of cAMP and therefore PKA
146
Describe the ionotropic beta receptor function in the heart?
* This beta receptor is bound to the HCN channel and directly opens the channel when bound
* The HCN channel function is also increased by the increased production of cAMP
* HCN activation leads to influx of Na+ and Ca++ during phase 4 in the pacemaking cells
147
What are the effects of PKA activation?
* Phosphorylates L-type Ca++ channels making them more sensitive and increaseing the amount of Ca++ influx
* Phosphorylates troponin I and increases its sensitivity to ca++ leading to increased rate of cross bridge cycling
* Phosphorylates phospholamban, inhibiting it, increasing the function of the SERCA pump, decreasing time to repolarize, allowing for an increase in HR
148
What effect of beta adrenergic stimulation can be dangerous?
* The phosphorylation of L-type Ca++ channels
* If they become too sensitive they can generate an AP at the wrong time leading to a heart attack(old person shoveling snow)
* They also contribure to delayed afterdepolarizations (DAD) and early afterdepolarizations (EAD)
149
Describe the function of PDE and what inhibition of it would cause?
* Breaks down cAMP into AMP, reducing the activity of PKA
* If inhibited by a phosphodiesterase inhibitor, there would be more cAMP and increased activity of PKA
150
What can cause generation of an ectopic pacemaker?
* Increased Vrm: caused by things that prevent repolarization like ischemia of AV node or hyperkalemia
* if Vrm is closer to threshold it can excite an early action potential
151
What is this rhythm?
What are the causes?
Sinus tachycardia, HR > 100 BPM
**Causes:**
* Increased body temperature (increased metabolic demands)
* SNS stimulation or loss of PNS stimulation (blood loss)
* Toxic conditions: increased Vrm by things like hyperkalemia, acidosis, nicotine, EtOH
152
What is this rhythm?
Causes?
Is this good or bad?
Sinus bradycardia, HR < 60 BPM
**Causes:**
* In patients with physiologically large hearts (athletes) have higher SV and dont need as many BPM to maintain CO
* Increase in vagal stimulation
* Neural reflex to drugs - reflexive bradycardia due to increased BP seen with phenylephrine
* Generally, the lower you HR the better your health
153
What are the 2 primary causes of an increased resting HR?
1. Hyperthyroidism
2. Valve issues
154
What is the rhythm?
Identifiers?
Causes?
Treatments?
SVT or Paroxysmal Atrial Tachycardia
* P and T waves may overlap
**Causes:**
* Driven by abnormal atrial excitation
* Comes and goes, not usually dangerous
**Treatments**
* Drugs that block vagal tone such as beta blockers or digoxin
* Vagal maneuvers
155
What is this rhythm?
Identifiers?
Causes?
Sinoatrial Block
* Causes cessation or inverted p waves due to AV node becoming pacemaker
* AV node fires slower causing slower HR (40-60)
* Caused by severe dysfunction at the SA node (ischemia)
156
During an SA block, what determines whether we see an inverted p wave or not?
Determined by where in the AV node the new AP are firing from
* Early AV node: should see inverted p wave BEFORE QRS d/t retrograde depolarization of the atria
* Late AV node: inverted p waves AFTER QRS or no p wave becuase hidden by ventricular depolarization
157
Describe what occurs when the ventricles contract early and close the AV valves out of sequence?
If the AV valves close early due to ventricular contraction, the atria may still be contracting and now forcing blood against the closed valves.
This causes turbulence of blood can cause clots and calcifications.
158
What are the causes of AV node blocks?
* *AV node ischemia* leading to increased Vrm, decreasing the number of ion channels involved in the AP, increasing the time it takes to fire
* Compression of AV bundle caused by fibroblastic remodling, smaller diameter = incresaed resistance = slower AP propigation
* Inflammation
* Excessive vagal stimulation (V & X reflex)
* Beta blockers - reduce firing of AP and speed of conduction
* Digatalis - increases Vrm by Na/K pump inhibition
“I Can’t Believe I Didn’t Vaccinate”
159
What is the rhythm?
Identifiers?
Incomplete HB, 1st degree block
Increase in PR interval >.20 seconds
160
What is this rhythm?
Identifiers?
Incomplete HB, 2nd degree, Mobitz Type I
Also called Wenckebach
PR interval > .25-.45 seconds
Variable length of PR interval until drop in QRS
| May or may not need a pacemaker
161
What is this rhythm?
Identifiers?
Incomplete HB, 2nd degree, Mobitz Type II
Fixed PR interval and ratio of beats to dropped beats
| Usually need a pacemaker
162
What is this rhythm?
Identifiers?
Complete HB, 3rd degree
Complete dissociation of the atria and ventricles
Reliant on ventricular escape beats at 15-40 BPM
Atrial rate elevated d/t decreased CO which increases firing at SA node
163
What is this rhythm?
Identifiers?
Causes?
Atrial Flutter
* No visible p waves or normal p waves
* Ectopic *coordinated circular* reentry conduction seperate from SA node conduction
* Parts of the atria are contracting while others are not, leading to poor timing with ventricles
**Causes:**
* Stretched out atria and slowed conduction
164
What is this rhythm?
Identifiers?
Causes?
Adverse effects?
Atrial Fibrillation
* No discernable p waves
* Uncoordinated atrial contraction
**Causes:**
* Dilated atria
* Multiple ectopic pacemakers
* Decreased rate of conduction (more cells repolarize before next AP and can be excited by ectopic AP)
* Decreased length of refractory period (more cells are repolarized earlier than normal and can be excited by ectopic AP)
**Adverse effects:**
* Generates a lot of turbulence leading to clots that can lead to pulmonary embolism
165
Describe stokes-adams syndrome?
Genetically inherited condition caused by irregular and untimed complete AV block
Fainting is common because heart does not beat until ventricles self depolarize
Usually faint after 7-8 seconds without a heart beat
166
What is this rhythm?
Causes?
Identifiers?
Incomplete Intraventricular Block; Alternans
* Slowed conduction through the Purkinjie system
* Abnormal small and wide QRS complexes every other beat
* Due to partial repolarization of ventricles leading to increased length and decreased magnitude of QRS
**Causes:**
* Same as AV node block causes
167
What is this rhythm?
Causes?
Adverse effects?
Premature Atrial Contraction
Early ectopic action potential
**Causes**: ischemia, irritation, calcified plaques
**Adverse effects:** decreased filling time of heart leading to decreased SV - can be heard at the radial pulse
168
What is this rhythm?
Identifiers?
Premature AV node/Bundle Contraction
Obscured p waves - may be missing or inverted depending on where in the AV node AP is generated
169
What is this rhythm?
Causes?
Premature Ventricular Contraction
These are typically dangerous
Has prolonged QRS, Higher voltage QRS, and inverted T wave
**Causes:**
* Prolonged QRS due to AP starting in the ventricular muscle instead of purkinjie system
* Higher QRS voltage: ventricles are not depolarizing at the same time, creating a higher difference in amount of tissue that is depolarized and not depolarized
-Normally, the ventricles depolarize basically at the same time and obscure the current created by each ventricle seperately
* Due to caffeine, nicotine, lack of sleep, and stress
170
What is this rhythm?
Concerns?
Paroxysmal Ventricular Tachycardia
QRS originates within the ventricular conduction system
P waves may be inverted or not visible
Usually happens with infarction and may lead to V fib
171
Describe premature ventricular depolarizations?
ECG findings?
Causes?
Concerns?
AP fired during refractory period leading to weakend AP, contractions, and decreased CO
May appear like a prolonged QT interval
**Causes:**
* B- agonist - increase Ca+ sensitivity on L type Ca channels leading to early depolarization
* mACh-R antagonists - atropine, Benadryl
**Concerns:**
* Precursor to torsades de pointes and v fib
* These beats reduce CO and blood flow to coronary arteries, leading to inability of heart to repolarize
172
Describe the bundles of kent?
Found in 0.2% of the population
Accessory pathway between the atria and ventricles
May require ablation later in life
173
What is lusitropy?
The time it takes for ventricular repolarizations. Positive lusitropy = faster ventricular repolarization.
