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Semester 1 TxWes Updated Fall 2024 > A/P Unit 4 > Flashcards

A/P Unit 4 Flashcards

1
Q

Which NM disease gets worse throughout the day? Why?

A

MG - because we start to run out of ACh as the day goes on

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2
Q

What NM disease gets better with activity?

A

LEMS/ELMS - with more activity, the body develops a temporary workaround, they theory is through more ACh binding to the auto receptor

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3
Q

What drugs can treat LEMS/ELMS?

A

TEA (tetra ethyl-ammonium), 3-4di-aminopyridine and steroids

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4
Q

What smooth muscle is primarily grouped together via gap junctions?

A

Visceral

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5
Q

What smooth muscle gives us good fine motor control?

A

Multi-unit

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6
Q

What advantages does the opposing orientation of smooth muscle myosin heads provide?

A

Greater ability to lengthen and contract. They also need minimal overlap to function. Overall, greater magnitude of shortening.

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7
Q

A pacemaker cell’s Vrm is significantly higher due to which ions?

A

Na and Ca

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8
Q

Define oscillating membrane potential

A

The change in membrane potential as the permeability to ions (for smooth muscle, its Ca and Na) changes. As it increases, it can (but not always) lead to an AP. This creates “waves”, similar in appearance to A. Flutter waves

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9
Q

What is the process of a smooth muscle contraction?

A

Ca enters the cell, which causes release of SR Ca. This binds to calmodulin to form a complex. This complex activates MLCK which phosphorylates the myosin light chain and contraction occurs. When Ca is pumped out, myosin phosphatase removes the phosphate from myosin light chain, causing relaxation.
Ca entry -> SR Ca release -> binds to calmodulin -> activates MLCK -> Phosphorylates MLC -> contraction

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10
Q

What dictates the rate of cross bridge cycling in smooth muscle?

A

The rate of phosphorylation of the MLC and myosin phosphatase (if one is higher than the other, the rate will mimic that, so if MLC is being phosphorylated faster than myosin phosphatase can removed them, then contraction rate will increase).

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11
Q

What are the 3 ways Ca is removed from the smooth muscle cell?

A

1: SERCA pump into the SR
2: PMCA pump into the extracellular fluid
3: Pumped out via the Ca/Na ATP-ase pump (1 Ca our for 3 Na in)
note the SERCA and PMCA (plasma membrane Ca pump) are identical, the only difference is location in the cell

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12
Q

The setup of the smooth muscle most closely mimic what other cell?

A

Heart muscle cell

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13
Q

What is the NO precursor?

A

L-arginine

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14
Q

What are the 3 versions of nitric oxide synthase, and define each

A

iNOS - inducible, meaning its not around all the time and is expressed under specific conditions
eNOS - endothelia version, active pretty much around the clock. Located in the endothelial cells of the blood vessel
nNOS - neuronal, used to communicate between neurons

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15
Q

What meditates NO release from the endothelium?

A

ACh, it binds to the endothelium via mACh receptors, which causes NO release. Done to help improve blood flow to the muscle

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16
Q

Define shear stress

A

Blood flow is normally laminar, if it becomes turbulent or picks up speed, the vessel detects this because the vessel changes shape, and encourages NO release

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17
Q

Define the process of ACh or bradykinin (both can start this process) activating NO release

A

They bind to the GPCR -> Ca release from the ER -> binds to calmodulin -> turns on eNOS -> Arginine turned into NO -> No diffuses from the endothelial cell to the vascular smooth muscle cell -> activates soluble guanylyl cyclase -> cGMP -> activates PKG (protein kinase G) which phosphorylates a Ca channel (which closes the channel) and phosphorylates MLCK (which turns it off, MLC is now not being activated) causing vascular relaxation

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18
Q

What breaks down cGMP? What drugs can inhibit it?

A

PDE (phosphodiesterase), and sildenafil and milrinone

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19
Q

What are the NO donors mentioned in lecture?

A

Nitrates or nitrites, nitroprusside, nitroglycerin

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20
Q

What can start a smooth muscle contraction?

A

An AP causing Ca to get into the cell, or any other method getting Ca into the cell. An AP is not required, as long as Ca gets into the cell, a contraction can occur

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21
Q

Describe the process of smooth muscle constriction via the alpha-1 receptor

A

Agonist binds (such as neo) -> GPCR alpha subunit disassociates, starts phospholipase C -> IP3 and DAG released -> DAG activates PKC which causes contraction, IP3 opens calcium release channels in the SR -> binds to calmodulin -> increase MLCK activity -> phosphorylation of MLC -> contraction

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22
Q

What example of stretch induced relaxation was used in lecture other than blood vessels responding to higher driving pressure?

A

The bladder, as UOP increases, the bladder initially stretches and you don’t feel the need to urinate. It continues this up to a point, then the urge hits.

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23
Q

What is the skeletal response to a neurotransmitter?

A

All or nothing response

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24
Q

What does a skeletal AP resemble?

A

A neuron AP

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25
Q

What does a smooth muscle AP resemble?

A

Variable, depends on the muscle. Uterine looks like a fast heart AP. Normal smooth muscle AP is somewhat reminiscent of a neuro AP

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26
Q

What ions dictate oscillating membrane potential change, what is the main one?

A

Na and Ca, Na being the main one

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27
Q

What, generally, is the pacemaking current?

A

Na

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28
Q

Per lecture, is an example of oscillating membrane potential causing smooth muscle action?

A

Intestinal functions, mainly peristalsis. The APs from them could represent intestinal spasms or cramps

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29
Q

What is the contraction of heart strength highly dependent upon?

A

ECF calcium influx

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30
Q

What is the term for outside calcium releasing internal calcium from the SR?

A

Calcium induced, calcium released

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31
Q

What happens to the myocytes as they stretch from preload?

A

You get better cross bridge alignment, leading to better contraction

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32
Q

In a healthy heart, what is the relationship to blood returning to the heart?

A

The heart pumps out whatever we return to it

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33
Q

What is the Vrm of the SA node? Threshold?

A

-55, -40

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34
Q

What would happen to phase 4 with increased Na permeability? Less?

A

Increased Na = sharper slope = faster HR
Decreased Na = flatter slope = slower HR

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35
Q

What would happen to Vrm with increased K permeability? Less?

A

Increased K = more - Vrm = slower HR, slope of phase 4 not affected
Decreased K = more + Vrm = faster HR, slope of phase 4 not affected

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36
Q

What governs K permeability in the heart?

A

mACH receptors. More ACh = more K permeability = slower HR (vagal stimulation)
Less ACh = less K permeability = faster HR (this is what atropine does, block K channels to raise Vrm)

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37
Q

How does calcium impact threshold potential?

A

Increased Ca = raised threshold = slower HR (takes longer to get to threshold)
Decreased Ca = lowered threshold = faster HR

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38
Q

What phases are in a slow heart AP?

A

Phase 4, 0 and 3

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39
Q

What phases are in a fast heart AP?

A

Phase 0 - 4, though phase 1 is not labeled in lecture

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40
Q

What are the differences between fast and slow cardiac APs?

A

Phase 0 = nearly vertical in fast, more of a slope in slow
Phase 1 = minor in fast, none in slow
Phase 2 = plateau in fast, none in slow
Phase 3 = nearly identical, both are sharp lines down
Phase 4 = flatter in fast, steeper in slow

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41
Q

Which has a longer AP duration, ventricles or nodal AP?

A

Ventricular

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42
Q

What ion dictates a slow AP?

A

Calcium

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43
Q

What is the other term for phase 4?

A

Diastolic depolarization

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44
Q

What drives phase 0 in the fast AP?

A

Na

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45
Q

Why is calcium the ion that drives a slow AP?

A

There are either no fast Na channels, or they don’t work in a slow AP

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46
Q

Why does width of AP change throughout the ventricular tissue?

A

To make sure all the ventricular tissue contracts in a coordinated timely manner

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47
Q

What would happen if the nodal tissue went offline?

A

Eventually, the fast AP of the ventricles would take over, with a rate of 15 - 30

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48
Q

What is five and dime reflex? (Also known as the oculocardic reflex)

A

This is when during ocular surgery you put pressure in the wrong area and get massive vagal output. Can cause can cardiac arrest for 30 - 40 seconds. Name tells you want nerves are compressed, 5 and 10.

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49
Q

Per lecture what happens with an especially strong vagal response?

A

You can take the SA/AV nodes offline, causing complete heart block

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50
Q

In a fast AP, how many more times are we permeable to potassium relative to sodium at rest?

A

Roughly ten times

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51
Q

What are the 3 factors you can change to affect HR?

A

Change Na permeability (changing the slope of phase 4), change Vrm with K permeability, or change threshold (via Ca)

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52
Q

How much of the hearts calcium is internally stored? How much comes from the outside?

A

80 internal, 20 outside

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53
Q

What is a basic difference between cardiac and muscle T-tubules in terms of ions?

A

Cardiac T-tubules let Ca in

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54
Q

How much Ca is pumped back into the SR in cardiac cells? What happens to the other 20% (specify amount and pumps)

A

80% goes into the SR via SERCA pumps, of the last 20%, 15 is pumped out via the NCX pump (1 Ca out, 3 Na in) 5 is pumped out via a Ca-ATPase pump

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55
Q

What acts as the brakes of the SR?

A

Phospholamban

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56
Q

What would happen if you excite phospholamban?

A

Prolongs contraction of the heart, active sites are revealed longer. If inhibited, shortens contraction of the heart, more Ca gets packed into the SR

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57
Q

What are the 3 things that PKA does in the heart?

A

Takes the brakes off the SERCA pump, opens the Ca channels and keeps them open, increase strength of contraction by phosphorylating troponin I

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58
Q

What governs PKA activity?

A

How much cAMP we have

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59
Q

What degrades cAMP and cGMP?

A

Phosphodiesterase

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60
Q

What non drug mentioned in lecture can inhibit PDE in the heart?

A

Caffeine

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61
Q

What does cAMP do in nodal tissue?

A

Increases due to beta stimulation, allows Na in, which would increase HR

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62
Q

What connects heart cells to each other? What is unique about its anatomy?

A

Intercalated disks, and they have many infoldings that allow surface area for gap junctions to allow electricity to easily spread

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63
Q

What is the primary current going through gap junctions?

A

Na current

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64
Q

How many nuclei are present in a heart cell?

A

1 - 3

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65
Q

What is the difference in troponin I in the heart vs skeletal muscle?

A

In the heart, it can be phosphorylated

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66
Q

What do cardiac stem cells and fibroblasts do? What is the difference between them?

A

Both fix the heart, stem cells are slower but will replace cell(s) over time. Fibroblasts are a fast repair system, but don’t replace cells, they’ll just place scar tissue

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67
Q

What condition is associated with too much fibroblast activity?

A

CHF

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68
Q

What slows down fibroblasts in CHF? What condition to you not want to take it?

A

ACE inhibitors, do not take them if you are pregnant

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69
Q

What is the term for the hearts ability to function as a unit by sharing or spreading an electrical current to its neighbors?

A

Syncytial connections

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70
Q

List the layers of the heart, inner to outer

A

Endocardium, myocardium, pericardium, pericardial space, parietal pericardium, fibrous pericardium

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71
Q

According to lecture, what layers make up the pericardium?

A

Epicardium, pericardial space, parietal pericardium and fibrous pericardium

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72
Q

Why is the crisscross pattern of muscle fibers in the heart an advantage?

A

This provides a very efficient and powerful method to pump out blood. Think of how wringing out a towel by twisting it gets out so much water.

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73
Q

What is the difference in T-tubule of a heart compared to a skeletal one?

A

It is 5x wider, and holds 25x volume

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74
Q

What process does the heart use to store calcium in the T-tubule?

A

A network of carbohydrate groups that act like a sponge for calcium

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75
Q

What pumps calcium back into the SR in the heart (be specific)?

A

SERCA2 pump, it is functionally the same as other SERCA pumps, just a different isoform

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76
Q

What does phospholamban do?

A

It functions as a brake for the SERCA pump

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77
Q

What is the Vrm of ventricular muscle? The Purkinje fibers? What is the rate?

A

-80 and -90 to -95 and a heart rate of 15 - 40 bpm

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78
Q

How much longer is a cardiac contraction relative to skeletal?

A

15x

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79
Q

What is the refractory period? When does it occur?

A

A period during the cardiac cycle were the heart cannot be stimulated. Occurs from Phase 0 to halfway through phase 3.

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80
Q

What is the relative refractory period? When does it occur?

A

A period where some of the Na/Ca channels have reset, and with a strong enough stimulus, a cardiac AP can be created (though it will be weaker than normal). Occurs from the middle of phase 3 to the end of phase 3.

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81
Q

What does the R. Vagus nerve innervate in the heart? The left?

A

R = SA node at the right atrium
L = AV node in the middle of the heart

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82
Q

List the segments of the internodal pathway

A

The anterior, middle and posterior internodal pathways, then there is the interatrial bundle (Bachmann’s bundle) that comes off the anterior internodal pathway, wraps around the back of the heart and innervates the left atrium

83
Q

What goes through the small opening in the cartilage insulating the heart chambers?

A

The penetrating bundle of His

84
Q

How long does it take for an AP to reach the AV node? Depolarize the Right and left atrium?

A

SA node = 0.03
R atrium = 0.05 per lecture (diagram says 0.07 for the very last portion)
L atrium = 0.09 seconds

85
Q

What tissue will have a slow AP? Fast AP?

A

Slow = SA and AV node (slope to phase 0)
Fast = all the muscle tissue (vertical slope to phase 0 in ventricles, more of a shark fin appearance in atrial muscle)

86
Q

What is the total time it takes for atrial muscle to be excited? Ventricular?

A

Atrial = 0.09 seconds
Ventricular = 0.22 seconds

87
Q

How long does it take for an AP to reach the septum?

A

0.16 seconds

88
Q

What causes the delay in the AV node? How can this function as a safety mechanism?

A

It has minimal gap junction and is “fatty” which isn’t very conductive. The safety mechanism is making signals going in the opposite direction “slow down” in the AV node. And by the time the signal gets through the AV node, the heart is in the refractory period, and therefore the signal is unlikely to cause an aberrant beat.

89
Q

What are the 2 primary delays in conduction from the SA node to depolarization of the septum?

A

The AV node, and the narrow (therefore high resistance) of the penetrating bundle of His

90
Q

How long does it take to clear the AV node?

A

0.12 seconds

91
Q

What direction will current flow during a depolarization?

A

Towards the positive end of the cell

92
Q

What deflection will be created if an electron is going towards the + lead? - lead?

A

Towards the + lead (away from the - lead) = + deflection
Towards the - lead (or away from the + lead) = - deflection

93
Q

When is the greatest amount of current measureable?

A

When half the cell is depolarized and the other half is still polarized

94
Q

What type of deflections would occur with a depolarization and repolarization occurring in the same order?

A

+ deflection followed by a - deflection

95
Q

What type of deflections would occur with a depolarization and repolarization occurring in opposite order?

A

+ deflection followed by a + deflection

96
Q

In general, where are the electrons going when traveling around the heart?

A

Towards the left foot

97
Q

What is the trend of ventricular depolarization/repolarization in regards to the inner/outer ventricular tissue? Why?

A

The inner depolarizes first and repolarizes last, the outer depolarizes last and repolarizes first. This allows for the muscle to contract near simultaneously. Short version: Inner AP is longer, outer AP is shorter

98
Q

What is amplitude?

A

The difference of the starting point to the highest point of the waveform.

99
Q

What is the average amplitude of the fast AP? What is its starting point?

A

100 mV, -110 mV

100
Q

When does contraction occur in the cardiac cycle?

A

During the plateau phase

101
Q

What is the amplitude of a QRS? What explains the difference of amplitude between the QRS and fast AP?

A

1.5 mV. This is due to all the non-conductive tissue that the signal needs to get through to be seen by the electrode (much of the tissue is high resistance)

102
Q

What 2 conditions have severely lower the amplitude of the QRS?

A

Obesity and COPD

103
Q

What is the time frame for one small box? One large box? Five large boxes?

A

1 small = 0.04 seconds
1 large = 0.2 seconds
5 large = 1 second

104
Q

How long does atrial depolarization last? Amplitude?

A

2 small boxes ish (0.08 seconds) in length, 2 small boxes high

105
Q

What changes in the P-wave indicates a L. Atrial problem? Right?

A

L = longer P-wave
R = increased amplitude
Pneumonic: long left, height right

106
Q

What does a QS wave indicate?

A

Dead heart tissue, usually an ominous sign

107
Q

When should there never be current in the heart, regardless of the condition of the heart?

A

ST segment

108
Q

What is the QRS limit? What condition can lengthen it?

A

0.12 seconds, bundle branch block

109
Q

Why does the T-wave have a + deflection despite the fact it represents repolarization?

A

Because it occurs in opposite order to depolarization

110
Q

What is the other name for the PR interval? Why is PR generally preferred?

A

PQ interval, because you don’t always have a Q wave

111
Q

What is the formula to solve for HR from an EKG?

A

HR = 60 / RR interval (example below, HR is 72, calculate RR interval)
72 = 60 / RR interval (isolate RR, now labeled as X)
72X = 60
x = 60 / 72 = 0.83, so RR interval is 0.83

112
Q

Describe leads in Eindhoven’s triangle in relation to each extremity

A

Lead I = + left arm, - right arm
Lead II = + left lower body, - right arm
Lead III = + left lower body, - left arm

113
Q

What direction is electricity going during the Q wave?

A

Towards to right side of the body, slightly down

114
Q

What direction is electricity going during the R wave?

A

Down and towards the left foot

115
Q

What heart tissue is most prone to damage? Why?

A

The endo-ventricular tissue of the left ventricle. It is deepest and hardest to perfuse. It also contracts longer so the window to get it blood is shorter.

116
Q

What change would occur in the Fast AP if sodium conduction via gap junctions was slowed?

A

The slope of phase 0 would flatten out or take longer

117
Q

What safety mechanism is in place to prevent retrograde signals via gap junctions?

A

Two-fold: a current signal must not be propagating, and the retrograde signal would have to hit when the cell is not refractory

118
Q

Describe the effect on phase 0 if Na channels become blocked

A

The amount of Na current that can come in would be decreased at the cell that is blocked. This would also flatten or elongate phase 0 in all cells downstream of the affected cell

119
Q

What is the mean electrical axis of the heart?

A

+59 degrees

120
Q

What is the normal range of of electrical axis?

A

0 - 90

121
Q

What normal process can shift the electrical axis?

A

The respiratory cycle

122
Q

What angle constitutes a right axis deviation? Left?

A

Right = +90 < (greater than 90)
Left = 0 > (less than zero)

123
Q

What 2 conditions can shift the axis of the heart?

A

COPD, obesity

124
Q

What direction does the P-wave go?

A

Towards the left foot

125
Q

Why can’t you see the T-wave for atrial repolarization? What deflection would it be?

A

It is buried in the QRS, negative because it repolarizes in the same direction as depolarization

126
Q

What is Eindhoven’s law?

A

Lead I + III = Lead II

127
Q

Describe the setup for AVF

A

+ lead is at the base at LL, the negative leads look up at the middle of lead I

128
Q

Describe the setup for AVR

A

+ lead at the RA, and the - lead is at the halfway point of lead III

129
Q

Describe the setup for AVL

A

+ lead at the LA, - lead is at the halfway point of lead II

130
Q

Per lecture, what lead would have the greatest amplitude?

A

V4

131
Q

Which precordial lead would have the greatest negative deflection?

A

V1

132
Q

Where does current go in regards to an injury?

A

Away from the site of injury

133
Q

If the heart shifted it’s axis straight down, which lead would have the greatest + deflection?

A

AVF

134
Q

What happens to the electrical axis as the diaphragm moves up? Down? Relate this to inspiration and expiration

A

Up (deep expiration) = heart is compressed, turns to the left
Down (deep inspiration) = the heart is more “floating” down, and shifts to the right or downwards

135
Q

How would the axis shift with induction of anesthesia?

A

Almost all the air leaves the lungs, heart would shift to the left

136
Q

How would the axis shift of you go supine?

A

Abdominal cavity shifts up, axis shifts to the left

137
Q

How does the axis shift going supine to upright? Upright to supine?

A

Supine -> upright = a right axis shift
Upright -> supine = a left axis shift

138
Q

What shift would likely occur in an obese person?

A

Shift to the left

139
Q

What shift would likely occur in someone tall and skinny?

A

Shift down, or slightly to the right from baseline

140
Q

How would conduction change with LV hypertrophy?

A

Shift to the left, there is much more resting tissue there because of the increased size. This shift would be most noticeable in lead I

141
Q

How would conduction change with RV hypertrophy/dilation?

A

Shift to the right, there is either more resting tissue (hypertrophy) or a longer distance to travel (dilation), in both cases, there will be more + charge on the right side of the heart, creating a right axis shift

142
Q

How does a bundle branch block shift the axis?

A

It creates a delay in conduction with a shift to the same side. So, a RBB = right axis shift, LBB = left axis shift

143
Q

What happens to fast Na channels as Vrm increases?

A

Less are able to reset (we don’t know the exact number, but the cell needs to be very negative for these channels to reset). As we get more +, less of the channels can reset, which will create more slope to phase 0

144
Q

What condition can cause the Vrm to increase and slow down or stop fast Na channel reset (one specific example mentioned in lecture)?

A

Ischemia, the body runs out of energy, which means the Na/K pump won’t run, and we can’t repolarize, and the tissue stays depolarized

145
Q

Describe the safety mechanisms to fast Na channel failure during ischemia

A

The slow (L-type) Ca channels. Their Vrm to reset is much higher (more +) that Na. So they can function and reset even during periods of ischemia. Though conduction will be slower due to the AP now taking on the slow AP shape and Ca not conducting as fast in the cell as Na does. There are also K channels that open in response to ischemia to try and maintain a negative Vrm, but it is unlikely to prevent a rise in Vrm due to ischemia

146
Q

What is the isoelectric point?

A

The J point (right after the QRS)

147
Q

What is the current of injury in ST depression?

A

A positive current of injury (ST segment doesn’t move, but the rest of the cardiac cycle is “higher” or more positive on the strip)

148
Q

What is the current of injury in ST elevation?

A

A negative current of injury (ST segment doesn’t move, but the rest of the cardiac cycle is “lower” or more negative on the strip)

149
Q

What does the Kir (inward rectifying) channel do? Gating mechanism?

A

Inward rectifier channel, maintains high K permeability during phase 4, and it’s decay contributes to phase 4 slope, it is suppressed during phases 0 - 2 (if we lose K, we would repolarize, don’t want this to occur during plateau because it could repolarize the cell too soon)
GM = voltage

150
Q

What is the Nai (Na fast of Nav 1.5) channel? Gating mechanism?

A

Fast Na channel, how it works is self explanatory at this point. Its inactivation may contribute to phase 1
GM = voltage

151
Q

What is the Kto (transient outward) channel? Gating mechanism?

A

This is what contributes to phase 1, the mild repolarization after the fast Na gates slam shut
GM = voltage

152
Q

What is the Cai (slow inward L channels or Cav 1.2) channel? Gating mechanism?

A

The slow Ca channels that primarily contribute to phase 2, enhanced by beta adrenergic stimulation
GM = Both (ligand and voltage)

153
Q

What is the Ki (delayed rectifier) channels? Gating mechanism?

A

Causes phase 3 of the AP, enhanced by increased intracellular Ca
GM = voltage

154
Q

What is the Katp (ATP-sensitive) channel? Gating mechanism?

A

Increased K permeability when ATP is low, Good for ischemia, increasing K permeability would lead to a lower Vrm, lower HR and lesser metabolic demands
GM = Ligand (ATP)

155
Q

What is the KACh (K acetylcholine activated) channel? Gating mechanism?

A

Responsible for the effects of vagal stimulation, decreases diastolic depolarization, and therefore decreases HR. Hyperpolarizes Vrm, shortens phase 2
GM = Ligand (ACh)

156
Q

What is the funny (Pacemaker via HCN) channel? Gating mechanism?

A

The only channel that opens as a result of hyperpolarization and cyclic nucleotides. Contributes to diastolic depolarization (increasing slope of phase 4), enhanced by beta adrenergic agents, suppressed by vagal simulation
GM = Both

157
Q

What lead would have a + deflection for the Q-wave (lead I, II or III)?

A

Lead III

158
Q

What part of the heart is last to depolarize?

A

Superior, anterior lateral side of the left ventricle

159
Q

What view does the standard 3 leads give us of the heart?

A

A coronal view

160
Q

What view does V2 give us of the heart?

A

Anterior/posterior view

161
Q

What view does the augmented leads give us of the heart?

A

Superior/inferior and lateral

162
Q

If the COI is negative, what change would you see in V2? Where does the current originate?

A

ST elevation, meaning the injury is in the front of the heart and the current is moving away from V2

163
Q

If the COI is positive, what change would you see in V2? Where does the current originate?

A

ST depression, meaning the injury is in the back of the heart and the current is moving towards V2

164
Q

Other than COPD and obesity, what specific cause of decrease in QRS voltage was mentioned during lecture?

A

Scar tissue replacing healthy muscle tissue; we lose electrically excitable tissue causing the drop in voltage

165
Q

What are the 2 factors associated with angiotensin II, per lecture?

A

A scar deposition factor and a blood vessel growth factor

166
Q

What is the relationship of the area under the curve of the QRS relative to the T-wave?

A

In theory, they should both equal each other despite the fact their appearances are distinct from each other

167
Q

What is the reason a digoxin OD creates a biphasic T-wave?

A

Digoxin disproportionally affects the epicardial tissue, so with an OD of it, the epicardial repolarization is more likely to be affected then endocardial. So the epicardial T-wave repolarization inverts (and because it repolarizes first, it will show up in the first half of the T-wave) and the endocardial T-wave remains the same, creating the biphasic wave

168
Q

Which current does epicardial tissue rely on more? Endocardial?

A

Epi = more Na dependent
Endo = more Ca dependent

169
Q

What is the main contraindication to digoxin?

A

Bradycardia

170
Q

What are the other names for the activation/inactivation gates for fast Na channels?

A

AG = M gate
IG = H gate

171
Q

What are the other names for the activation/inactivation gates for slow Ca channels?

A

AG = D gate
IG = F gate

172
Q

Per lecture, what is the repolarization point for fast Na channels?

A
  • 65
173
Q

Per lecture, what is the depolarization and repolarization point of nodal tissue?

A

D = -40
R = -55

174
Q

How much longer does the inactivation gate of Ca channels stay open relative to Na?

A

15x

175
Q

Per lecture, what is the repolarization point of slow Ca channels?

A
  • 40
176
Q

What likely effect would hypernatremia have on Vrm?

A

Likely raise it, make it more +

177
Q

What likely effect would hyperkalemia have on Vrm?

A

Raise Vrm, the higher K is, the longer it takes to get phase 3 to get us to phase 4, which (per lecture) could be the mechanism of potassium related bradycardia

178
Q

What are 3 ways we can temporarily reduce ECF K? How do they work?

A

A beta agonist, diuresis and Insulin. Both speed up the Na/K pump, beta agonists do this as a result of their binding to the beta receptor, Insulin’s MOA is unclear for this. Diuresis is easy, give them lasix, and we get rid of K

179
Q

Why is it unsafe to suddenly ramp up exercise while on a BB?

A

Because the beta receptors are blocked, the circulating catecholamines can’t bind. This means we can’t speed up the Na/K pump, and the muscles are releasing K when they contract. If this cycle continues, we could potentially build up a lot of K in the blood

180
Q

Define inotropy, give an example of + and -

A

Strength of contraction
+ = beta agonist, dobutamine
- = BB, metoprolol

181
Q

How does beta stimulation increase HR?

A

The beta receptors at the nodal tissue open HCN channels, leading to faster nodal tissue depolarization

182
Q

Define chronotropy, give an example of + and -

A

Heart rate or pacing rate
+ = beta receptor stimulation at nodal tissue
- = muscarinic ACh receptors at nodal tissue

183
Q

Define dromotropy, give an example of negative (no + example given in lecture)

A

Speed of conduction
- = a caine drug

184
Q

Define lusitropy, give an example of + and -

A

Speed of the resetting process
+ = Serca pump working faster (done via a beta agonist)
- = beta antagonism

185
Q

What is + for inotropy, chronotropy, dromotropy and lusitropy? And what is negative for all 4?

A

a beta agonist is + for all 4, a beta blocker is - for all 4

186
Q

What effect do volatile anesthetics exert on the body?

A

Increase K permeability, lowering Vrm, making it harder to excite

187
Q

What nerves are involved in the five and dime reflex?

A

Trigeminal and Vagus

188
Q

What is the relationship of degree temperature change to heart rate?

A

Per 1 degree Fahrenheit increase is equivalent to an increase in 10 Bpm of heart rate

189
Q

Describe how Neo causes a drop in HR

A

The baroceptors sense the increase in BP, as a reflex, the PNS slows down the HR to try and decrease CO to return to baseline. Since Neo is causing constriction, the vessels don’t relax but HR does slow down

190
Q

What segment is extended with bradycardia?

A

the T-P segment (NOT P-T, be careful there)

191
Q

What are the treatments for SVT?

A

Vagal reflex, beta blocker, digoxin

192
Q

Why is there an inverted P-wave with a sino-atrial block?

A

Since the current starts in the AV node now, the electricity is going in an almost opposite orientation as normal, creating a negative deflection rather than a positive one

193
Q

What are the common causes of an AV block?

A

Ischemia of the AV nodal tissue or bundle fibers, compression of the AV bundle, AV nodal/bundle inflammation, excessive vagal stimulation, excess of digoxin or BBs

194
Q

Why doesn’t the rapid rate of atrial flutter cause a rapid ventricular rate?

A

The AV nodes refractory period manages to block many of those impulses

195
Q

What is the electrical difference in A flutter/fib?

A

With flutter, the electrical signal is going around in a circular pattern that is somewhat coordinated. Generally at a ratio of 2 - 4 atrial excitations to 1 ventricular.
With fib, there are numerous ectopic pace makers all over the atria that are firing in random directions

196
Q

What is the name for a ventricular escape rhythm associated with fainting?

A

Stokes-Adams syndrome

197
Q

Describe electrical alternans and its likely cause

A

This is when you have one normal QRS followed by an abnormal one at a 1:1 ratio, the abnormal looks similar to a PVC. This is generally due to ischemia, particularly in the septum. The heart doesn’t fully recover for the next heartbeat, explaining the change in electrical signal

198
Q

What is the difference between a PAC from the SA node and the AV node?

A

SA-PAC = and ectopic signal, but the p-wave is still normal
AV/bundle source = an inverted p-wave, because the signal starts from the AV node, and the electrical sequence is now backwards

199
Q

How do you differentiate between early and late AV nodal/bundle source PACs?

A

Early = the inverted p-wave shows up earlier on the EKG strip, indicating a high AV junction source
Late = the inverted p-wave shows up later on the EKG strip, indicating a low AV junction source

200
Q

What are common causes of PVCs?

A

Cardiac irritants making the tissue more excitable, caffeine, lack of sleep, stress, nicotine

201
Q

What is a cause of EAD (early after depolarization)? What makes it dangerous?

A

Spontaneous opening of the Ca channels, lengthening the time of contraction. If the QT lengthens enough, it can lead to Torsaddes

202
Q

What kind of current do you want to use when trying to shock a heart out of an unfavorable rhythm?

A

Direct current

203
Q

Describe and name an accessory pathway

A

Bundle of Kent, this is when muscle tissue grows over the insulator creating a pathway for electrical signals to travel. Usually not deadly, if symptomatic, can be fixed with an ablation.

Semester 1 TxWes Updated Fall 2024 (7 decks)

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