Exam 4 Flashcards
the heart (152 cards)
1
Q
what is the function of intercalated discs between the cardiac cells?
A
cardiac myocytes have “jagged borders” which increases surface area for more gap junctions and faster conduction (communication)
2
Q
what is the only type of cell with multiple nuclei?
A
skeletal muscle cells
3
Q
what are fibroblasts?
A
these are cells that lay down scar tissue if the stem cells are overwhelmed by cell damage.
4
Q
How does scar tissue exacerbate CHF?
A
messes with the electrical conduction system and the heart doesn’t contract as well
5
Q
With CHF, what is the number one drug class to limit scar tissue development?
A
ACE inhibitors to inhibit angiotensin II (growth factor in the heart) from putting down too much scar tissue (fibroblasts)
6
Q
What do syncytial connections do for cardiac muscle?
A
Ventricular muscle has two layers with different orientation and can contract in different directions and rotate a little bit. Like wringing water out of a towel. Efficient way to pump blood out of the heart.
7
Q
List the layers of the cardiac muscle in order from most proximal to most distal…
A
Subendocardium (deepest)
endocardium
myocardium
epicardium
pericardial space (between the myocardium and the pericardium, pericardial fluid here)
parietal pericardium (inner stretchy layer)
fibrous pericardium (similar to dura, outer layer)
8
Q
Where is the most common area of the heart where you will experience ischemia (an MI)?
A
The sub endocardium. The deep tissue of the heart.
9
Q
resting sarcomeres in the heart are unique why?
A
The actin overlaps slightly even at rest, the sarcomeres are “under stretched”
Therefore there is no H band
10
Q
What is the difference in resting membrane potential between Purkinje fibers and ventricular muscle cells?
A
Purkinje Vrm: -90mV
Ventricular Vrm: -80mV (slightly more positive)
11
Q
What type of procedure most commonly causes a conduction system issue leading to a complete heart block?
A
Ocular surgeries. There is a five and dime reflex that gets triggered. Pressure sensors in the eye socket send sensory info to the CNS via CN V (trigeminal nerve) the brainstem then sends a message to the vagus nerve (CN X): vagal response
12
Q
What is unique about the resting membrane potential of nodal tissue cells compared to other cell types?
A
They are self depolarizing. The resting membrane potential is slightly sloped (due to a slight increase in Na+ permeability) and will eventually reach a threshold which stimulates an action potential.
13
Q
why do the Purkinje fibers take so long to depolarize if we are in complete heart block?
A
phase 4 slope is shallow. This area of the heart usually relies on an action potential being sent from an upstream neighbor (SA/AV node).
14
Q
What is the threshold potential for Purkinje and ventricular depolarization?
A
-70mV
15
Q
If you don’t have an upstream signal (say from the AV node) to fire at the Purkinje fibers, how long could it take to fire an AP?
A
about 30+ seconds. There is an extremely long lag time for the Purkinje fibers to self depolarize.
16
Q
What is Ohm’s Law
A
voltage = current x resistance (V=IR)
17
Q
What is happening at phase 4 of a ventricular action potential?
A
This is the resting membrane potential mostly dictated by K+ leak channels. Has a slight positive slope, due to some permeability to Na+ and Ca2+ and mostly hovers around -80mV.
18
Q
What is happening at phase 0 of a cardiac action potential?
A
Depolarization phase, voltage gated fast Na+ channels open. K+ channels close at the END of this phase.
19
Q
What is happening at phase 1 of a cardiac action potential?
A
Na+ channels close, K+ channels are closed. A few fast T type Ca2+ channels open.
20
Q
What is happening at phase 2 of a cardiac action potential?
A
Plateau phase, slow L type Ca2+ channels open. K+ channels still closed.
21
Q
What is happening at phase 3 of a cardiac action potential?
A
Repolarization phase, K+ channels open.
22
Q
What nerve innervates and suppresses the SA node? What NT does it use?
A
Right Vagus nerve. ACh.
23
Q
What nerve innervates and suppresses the AV node? What NT does it use?
A
Left Vagus nerve. ACh.
24
Q
What is the predominant system affecting the nodal tissue?
A
Parasympathetic innervation
25
What is the predominant system affecting ventricular muscle contractions?
Sympathetic innervation
26
What are HCN channels and how do they open?
Hyperpolarization cyclic nucleotide mediated channels. These open when the cell reaches Vrm or is slightly hyperpolarized. They are controlled by cAMP.
27
What are the primary and secondary currents that flow through HCN channels?
Mostly Na+ and a little Ca2+ can flow through these channels.
28
How do beta receptor agonists increase the slope (make more steep) of phase 4?
beta agonist binds the beta1 receptors which leads to more cAMP. cAMP opens more of these HCN channels, increasing the slope of phase 4, causing the cell to depolarize faster. This would lead to a faster heart rate.
29
How do beta blockers slow the HR down?
These block beta receptors so cAMP cannot open the HCN channels. This makes the resting cell less permeable to Na+ and makes the phase 4 slope more shallow. It will then take longer to reach threshold potential so the HR is slowed.
30
How do antimuscarinics like atropine effect phase 4?
atropine blocks mACh-R leading to less K+ current. This makes Vrm more positive, so it takes less time to reach threshold leading to an increased HR.
31
how would a muscarinic agonist (like vagal stimulation) effect phase 4?
it releases ACh which binds mACh-R that open K+ channels. K+ efflux decreases Vrm and therefore HR slows.
32
How does mild hyperkalemia effect HR?
It decreases the K+ gradient so less K+ flows out, causing Vrm to be more positive, increasing the HR slightly.
33
How does Ca2+ effect HR?
We don't know the exact mechanism but we do know Ca2+ increases threshold potential, which decreases HR. So a Ca2+ deficiency would lower threshold potential and result in a higher HR
34
Why do the T waves show up as a positive deflection on the EKG?
The cell is repolarizing in the opposite direction towards the negative electrode (double negative) expect to see a positive deflection
35
What are a few key differences between ventricular action potential phases and slow nodal action potentials?
In slow action potentials (nodal areas)
phase 4: more sloped
phase 0: upstroke of AP less sloped and longer
no phase 1 and probably no phase 2.
36
what causes phase 0 to be less sloped and longer in the nodal cells as compared to fast action potentials?
L type Ca2+ channels are slower to open and slower to close.
37
Why is the pace set by the AV node slower than the SA node?
Two reasons:
1. the Vrm of the AV node is slightly more negative than the the SA node Vrm.
2. There are less HCN channels therefore the AV node is less permeable to Na+
38
What is the pace of the heart if only controlled by the SA node?
110 bmp
39
If the SNS is stimulating the SA node what would you expect the HR to be?
120 bmp
40
Including vagal input to the SA node without SNS input what would you expect the HR to be?
60-62 bmp
41
If there is an upstream block and only the AV node is working, what pace would you expect?
40-60 bmp
42
If there is a complete heart block and you only have the pacemakers of the Purkinje fibers working what would you expect the HR to be?
15-30 bmp
43
What are the three sources of input that generate a normal resting HR of 72 bmp in a healthy human?
1. SA node pacing
2. Vagal input
3. SNS stimulation
44
What does the QT interval correspond to?
The total length of time for an action potential in the ventricular tissue to occur (depolarization and repolarization)
45
What are the three internodal pathways from the SA node to the AV node?
anterior, middle and posterior
46
What is the name of the conductive branch between the SA node (R atrium) and the L atrium?
interatrial bundle or Bachman's bundle
47
How long does it take for the entire R atrium to depolarize?
0.07 seconds
48
How long does it take for the entire top half of the heart to depolarize? (Both right and left atria)
0.09 seconds. This corresponds to the P wave on EKG.
49
How long does it take the entire heart to depolarize?
0.22 seconds (in an ideal world, perfectly healthy heart)
50
How long does it take the AP to go from the SA node to the AV node
0.03 seconds
51
How long does it take to depolarize the entire heart?
0.22 seconds
52
What delays are responsible for the major delay between the AV node and the interventricular septum at the start of the two main bundle branches?
0.12 s delay at the AV node (due to less gap junctions)
0.01 s delay at the bundle of His to the bundle branches
53
How long does it take for the AP to get from the SA node to the start of the bundle branches/ interventricular septum?
0.16 seconds
54
What direction (angle) does the depolarization of the heart travel to?
59 degrees from a horizontal axis at the heart, towards the L foot.
55
What is the voltage measured at the heart tissue itself? And on a 3 lead? A 12 lead? Why?
the heart tissue: 100 mV
3 lead: 1.5 mV QRS
12 lead: 3-4mV QRS (in leads 1-6)
There is a difference in magnitude of deflection related to how much tissue (resistance) there is between the heart and the lead itself.
56
What would cause an exaggerated or taller P wave?
Enlarged R atrium
57
What would cause a longer P wave?
A stretched out L atrium
58
If there is a really big issue (probably an electrical block) in the L atrium you will see what?
double humped P wave
59
What does the PR interval measure and how long is it?
the time between the start of the P wave and initiation of contraction of the ventricle. Should be 0.16 seconds.
60
In an ideal patient how long is the PR interval?
0.16 seconds
61
In an ideal patient how long is the QRS?
0.06 seconds (0.22s - 0.16s)
62
If we have an exaggerated QRS or a taller QRS what could cause this?
1. Lead is placed closer to the heart
2. Hypertrophy (enlarged ventricles)
63
What would prolong the length of a QRS?
dilated cardiomyopathy
64
What is the J point?
The point at which ALL of the ventricles should be depolarized. This point serves as a reference to determine if there is any ST elevation or depression
65
How long is the QT interval?
0.25- 0.35 seconds
66
What does the T wave correspond to?
repolarization of the ventricles
67
If you run a marathon and your heart rate speeds up, what is shortening?
Shorter ST segment (which also shortens the QT interval) --> Lusitropy
68
What is Lusitropy?
resetting of the ventricles (repolarization)
69
What is Dromotropy?
Speed of conduction, dependent on Na+ current
70
What ion is responsible for inotropy?
Ca2+ channels (force of contraction)
71
How do we calculate an ideal HR of 72 bmp?
60 seconds / typical R-R interval (0.83 seconds)
72
What is another name for the J point?
The isoelectric point
73
How many big boxes equals one second on a paper EKG? How long is each big box?
5 big boxes = 1 sec
1 big box = 0.2 sec
74
How long is one small box in seconds? How many small boxes in a big box?
0.04 sec. 5 small boxes in one big box.
75
What is the resting membrane potential and the threshold potential for nodal tissue at the SA node? At the AV node?
(SA node) Vrm: -55mV
(SA node) Threshold: -40mV
The AV node is slightly more negative (Vrm) which is why they have a slower pace
76
What is the resting membrane potential and the threshold potential for the Purkinje fibers?
Vrm: -90 mV
Threshold: -70 mV
This is why the pace (firing of AP's) is slowest at the Purkinje fibers
77
If you have an ischemic injury to the heart (like an infarct) what happens to that area of tissue and what happens to the rest of the heart?
The area of injury remains depolarized which sets off abnormal current (should be able to view this current change in a 12 lead)
78
What is the upside and downside of using gap junctions for AP propagation?
Upside: super fast (using Na+)
Downside: can be bidirectional
79
What safeguard can the heart use against re-entry rhythms (APs at inappropriate times)?
Refractory periods (absolute and relative)
80
What does the "a" in aVF, aVR or aVL stand for?
Augmented
81
On a 3 lead EKG where is the negative electrode placed and the positive electrode placed for lead I?
Negative: R arm
Positive: L arm
82
On a 3 lead EKG where is the negative electrode placed and the positive electrode placed for lead II?
Negative: R arm
Positive: L foot
83
On a 3 lead EKG where is the negative electrode placed and the positive electrode placed for lead III?
Negative: L arm
Positive: L foot
84
For our class, what would be considered a left axis deviation of the heart?
Anything less than 59 degrees
85
For our class, what would be considered a right axis deviation of the heart?
Greater than 59 degrees
86
What is Einthoven's Law?
Lead I + Lead III = Lead II
Net upward deflections of QRS complexes
87
Which lead is the best to discern if we have an injury in the posterior or anterior part of the heart?
Lead V2
88
Which lead is the best to discern if we have an injury in the posterior or anterior part of the heart?
Lead V2
89
Which lead on a 12 lead would you expect to have the largest positive deflection?
Lead V4
90
Which area of the ventricles is depolarized first? In what direction?
The septum from L to R. This explains the negative Q wave in leads
91
If you have a positive deflection in lead V2 what type of problem do you think you would have? A negative deflection?
Positive: posterior
Negative: anterior
92
What causes an inverted T wave?
The inside of the heart resets before the outside of the heart
93
What are inward rectifying K+ channels and how are they different?
These are k+ channels in cardiac myocytes that close with the movement of positive ions (instead of open). This happens at the end of phase 0 and helps contribute to a longer action potential
94
Why is it physiologic to have L type slow Ca2+ channels in ventricular cells?
To generate a longer action potential in the heart to generate enough force to cause a contraction.
95
Which Phase is responsible for "how fast an AP is"?
The slope of phase 0.
Steeper = faster
96
Which nodal cell has the fastest diastolic depol?
SA node
97
fast Na+ is only involved in which AP's of the heart?
Purkinje fibers and ventricular cells. (Not nodal tissue)
98
What are the two theories of why there is no fast Na+ channel involvement in nodal cell AP propagation?
1. No VG fast Na+ channels
2. Vrm is too positive for the fast Na+ channels to function
99
Fast Na+ channels and slow L type Ca2+ channels have similar gate anatomy, what is a key difference between these two types of channels?
It takes more repolarization to reset the fast Na+ channels than the slower L type Ca2+ channels
100
Where is the highest density of HCN channels and which nodes are most permeable to Ca2+?
SA node (most HCN and most permeable to Ca2+)
AV node (2nd most permeable to Ca2+ and HCN channels)
Purkinje fibers (least amount of HCN channels and least permeable to Ca2+)
101
when you see "rabbit ears" in a QRS, what does that mean?
a bundle branch block
102
why do you only need to plot two leads on a vectorcardiogram?
because of Einthoven's Law
103
If the arrow points Left where is the current of injury likely coming from? If it is pointing right?
Arrow pointing left: Right sided injury
Arrow pointing right: Left sided injury
Arrow points away from the current of injury
104
How can you tell if it is an anterior or posterior ischemic injury?
Look at V2 lead. It is positioned directly superior to the heart.
105
Positive current of injury is a _____ problem?
posterior
106
Negative current of injury is a ______ problem?
anterior
107
Calcium channel blockers target which Ca2+ channels?
"slow" L-type calcium channels
108
What would happen to the equilibrium potential if extracellular K+ is increased? To resting membrane potential?
K+ concentration outside the cell increases (say from a BL of 4 mEq to 5 mEq) This would make Ek+ less negative and Vrm would follow suit
109
Would the cell be more excitable or less excitable with a resting membrane potential of say -84mV? -65mV?
At first the slight increase in Vrm would make the cells more excitable. But if the resting membrane potential increases too much, fast Na2+ cannot reset and the cell would actually become less excitable.
110
Can the sympathetic nervous system increase HR enough to cause tetany? Why or why not?
No, the refractory periods prevent individual twitches from occurring so closely together that they could summate into tetany
111
When considering abnormal EKGs and plotting vectorcardiograms what is the key difference between an ischemic injury or infarct and axis deviations or ventricular hypertrophy?
Ischemia and infarct will show up on repolarization of the heart muscle. Hypertrophy and conduction pathway blocks or axis deviations can be seen with depolarizations.
112
Why are infarcts and ischemia not seen with cardiac depolarization?
these areas are already depolarized and have their own current of injury but you won't be able to see it until the heart repolarizes.
113
A common type of antiarrhythmic are Na+ channel blockers. What affect do they have on PR interval and the QRS complex.
These block fast Na+ channels, which slows the rate of conduction. Making phase 0 less steep. This would register as a longer PR interval and the QRS would be wider
114
What can cause ectopic pacemakers?
The closer Vrm is to the threshold potential, the more likely it is to fire (this can happen in the nodes or the ventricles). Things that increase Vrm are things that prevent the heart from resetting itself (like hyperkalemia, ischemia or infarct)
115
An athlete discovers he has unifocal PVC's, what would most likely predispose him to these arrythmias?
Premature ventricular contractions originate from ventricular pacemaker cells in the Purkinje system. The intrinsic rate of the Purkinje system is usually 15-40 bmp. These cells are usually reset with each heartbeat, but if the athlete's HR is less than 40 bmp, they might have enough time to reach threshold and produce a ventricular contraction.
116
What is Supraventricular Tachycardia and how can we treat it? How does it look on an EKG?
Also called paroxysmal atrial tachycardia. Is a high HR driven by abnormal atrial excitation that frequently comes and goes. We can treat it by vagal reflex or beta blockers. On the EKG it looks like super fast tachycardia and you can't make out P waves or T waves. QRS is narrow.
117
What happens if there is a sinoatrial block?
The AV node takes over. There are no P waves or sometimes inverted P waves. HR will be 40-60 bpm.
118
Why do you usually have to be on anticoagulants with atrial fibrillation?
Atrial contractions happening asynchronously from ventricular contractions and sometimes the atria contract when the AV valves are closed causing turbulence. This increases clot formation.
119
What usually causes AV block (there are a few we talked about)?
Ischemia from an MI. Cardiac remodeling via fibroblasts d/t CHF or ischemia. The AV bundle gets compressed by the scar tissue or calcification. Inflammation. Too much beta blockade or digitalis toxicity. Anything that increases Vrm.
120
If your PR interval exceeds 0.2 seconds, what type of rhythm is this?
1st degree heart block
121
What is the major difference between Mobitz type I and Mobitz type II heart block?
both have dropped QRS complexes but type I has varying PR intervals (Wenckebach periodicity) and type II has a fixed PR interval and fixed ratio of p waves to QRS complexes.
122
What are some hallmarks of third degree heart block?
There is complete dissociation between the QRS complexes and P waves due to block of the AV node or bundles of His. Rely on ventricular escape to give us a ventricular HR (so HR 15-40 bmp).
123
What are some characteristics of atrial flutter and how does it look on an EKG?
Caused by stretched out atria (hypertrophy) and slowed conduction. A flutter has circular reentry pathways and is disorganized with the ventricles. Expect to see high atrial rate and high ventricular rate. No defined P waves.
124
What are some of the differences between a flutter and a fib?
A fib has multiple ectopic pacemakers and is not coordinated at all. It is irregular.
125
Why do we normally prescribe anticoagulants for a fib?
The circus movements of the ectopic pacemakers create turbulent flow when the atria try to contract with closed AV valves. Turbulence can cause clots.
126
What is Stokes Adams Syndrome?
go into complete heart block randomly from time to time. When in complete heart block it can take up to 30 seconds for ventricular escape to kick in and this can lead to syncope.
127
How many seconds without a heartbeat can we usually withstand before passing out?
7-8 seconds
128
What is incomplete intraventricular block or Alternans?
usually, a result of a slowed conduction in the ventricular Purkinje system and occurs every other heartbeat. This arrythmia increases risk of v tach. Can be caused by ischemia or digitalis.
129
What symptoms do you often see with premature atrial contractions?
atria fire a premature heartbeat. This causes a pulse deficit at the radial artery due to a lower stroke volume.
130
What will you see with the P waves with premature atrial contractions at the AV node? If new pacemaker is at the beginning of the AV node? At the end of the AV node?
The P waves are usually inverted. If the pacemaker is early on in the AV node, you will see an inverted P wave before the QRS. If it's at the end of the AV bundle/ bundle of His, you could see a QRS first and then an inverted P wave.
131
What are some hallmarks of premature ventricular contractions?
They are wider than normal QRS complexes and taller. There is usually an inverted T wave. Things like caffeine, nicotine, stress and lack of sleep can contribute to PVCs.
132
Why are PVC's wider?
They are wider than normal QRS complexes especially if the abnormal QRS complex is initiated by an AP that originates in the ventricular muscle and can spread to other muscle tissue before making it into the Purkinje system.
133
Why are PVC's taller?
They are also higher voltage or taller. This is because some of the coordination occurring in the right side of the heart "cancels out" what's happening in the left. With PVC' there is less of this obscuring as the problem originates in one of the ventricles.
134
What is paroxysmal ventricular tachycardia?
QRS originates in the ventricle, but we don't really know why. This is dangerous and often is the precursor to v fib.
135
What predisposes us to premature ventricular depolarization? And how does it look on the EKG?
This is caused by early or delayed afterdepolarization. Sensitive Ca2+ channel predisposes us to EAD or DAD. This looks like a long QT interval on an EKG.
136
What medications make our Ca2+ channels more sensitive and can cause prolonged QT syndrome?
Beta agonists, mACh-R antagonist, Benadryl
137
What is a precursor to Torsade de pointes?
EAD, pro-longed QT interval.
138
What is the one reentry source we talked about in class and where are they?
The Bundles of Kent are accessory bundles that provide an extra pathway between the ventricles and the atria. About 0.2% of the population has this.
139
How do -caine drugs work like Lidocaine?
They block fast Na+ channels reducing the slope of phase 0.
140
Describe the anatomy of a fast Na+ channel...
These channels have an "M" gate or activation gate on the outside of the cell wall and an inactivation gate or "H" gate on the inside of the cell wall. At rest "M" gate is closed and "H" gate is open.
141
Describe the anatomy of a slow "L-type" Ca2+ channel...
These channels have a "D" gate or activation gate on the outside of the cell wall and an inactivation gate or "F" gate on the inside of the cell wall. At rest "D" gate is closed and "F" gate is open.
142
What are two things that could cause reentry issues with circus movements?
Slowed conduction and reduced refractory periods.
143
Why should we think twice before giving lidocaine if we don't need it? What other condition can cause this to happen?
-caine drugs slow down the conduction system in the heart increasing the chances of reentry causing circus movements. Hyperkalemia.
144
Why is digitalis especially dangerous and often used as a "last resort" medication for treating HF?
It shuts down Na+/K+ ATPase pumps. More Na+ remains in the cell and more K+ outside the cell. This decreases electrochemical gradients for both of these ions and increases Vrm. If Vrm gets too high we knock out fast Na+ channels. If it gets higher still, we knock out slow Ca2+ channels and can no longer generate action potentials or cause contraction.
145
How does too much beta-adrenergic activity lead to increased risk of pro-longed QT interval and arrythmias?
Beta-1 agonists are GPCRs with stimulatory alpha subunits that increase activity of adenylyl cyclase which increase cAMP production. cAMP increases protein kinase A (PKA) which phosphorylates L type Ca2+ channels and makes them easier to open. This causes early afterdepolarizations which looks like a prolonged QT interval on an EKG and is a precursor to Torsades which will eventually cause v fib arrest.
146
What is the primary way the nodal tissue adjusts or determines the resting membrane potential?
via the m-ACh-R associated with K+ channels.
147
What are two things cAMP can do in cardiac cells?
it can open HCN channels and allow more Na+ and Ca2+ into the cell to get to threshold faster. It can also increase PKA which phosphorylates things.
148
What three things does PKA phosphorylate?
1. L-type Ca2+ channels --> making them easier to open
2. Troponin I--> increases the cross-bridge cycling rate
3. Phospholamban --> inhibits the phospholamban from inhibiting the SERCA pump (cell can reset faster)
149
What could you say about the state of depolarization/repolarization of the TP interval with a current of injury?
At the TP segment, the entire ventricle is repolarized except for the area of injury (damaged cardiac muscle)
150
Which structure of the cardiac sarcomere contributes mostly to the passive stiffness of the cardiac muscle?
titin
151
Propagation of an action potential through the heart is fastest at which part of the heart?
the Purkinje fibers or the bundle of His
152
What is one protein that we talked about you will find in vascular smooth muscle that is not in cardiac muscle cells?
calmodulin
