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CardioPulm2 > Physiology > Flashcards

Physiology Flashcards

1
Q

What is prepotential?

A

Slow polarization of cell that leads to action potential

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2
Q

What is the path of conduction? Please include depolarization

A

SA node –> AV node and Atrial myocytes -> Bundle of His –> Bundle branches –> Purkinje system –> Ventricular myocytes

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3
Q

Why is there a delay between atria and ventricle depolarization? How does the delay happen?

A

So atria can completely depolarize and top off ventricles befor ethey depolarize and contract.
The Cardiac Skeleton helps keep the depolarization away from ventricles until the signal can go down the AV node (which is way slow)

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4
Q

Describe the channels in conductance of ventricular muscle action potential?

A

Phase 0: Depolarize: Fast Na+ channel opens
Phase 1: Dip: Fast K + channels open, Na gates close
Phase 2: Plateau. Ca++ open and K + close. They equilibriate.
Phase 3: Repolarize: Ca++ close, K + open
Phase 4: Resting: K+ closes

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5
Q

Describe the channels in conductance of the SA nodes?

A

Phase 4: Na (f) channels open slowly as to not start a depolarization.
Phase 0: Ca++ open. Since there’s already Na in there, it’s easier for the SA to start a depolarization here.
Phase 3: Close of Ca++, Open special K +

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6
Q

What are importnat difference between SA node and Muscle action potentials?

A

SA Node is:

  • Automatic
  • Uses Ca ++ instead of Na for depolarization
  • Unstable resting potential
  • No phase 1 or 2
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7
Q

What increases conduction velocity?

A

Higher inward of Na
Slower inward of Ca
Larger fiber is faster (AV has smaller fibers)

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8
Q

What does chronotropic mean?
Dromotropic?
Inotropy?

A

Chronotropy: Changes rate of depolarization of SA node
Dromotropic: Speed of conduction
Iontropy: Contractility

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9
Q

Know your Excitation steps: 1) How does Ca++ get into the cell?
2) What happens upon entering?

…..

A

1) AP moves along sarcolemma innto T tubules and opens voltage gated calcium channel
Dihydrophyridine receptors (DHP) which are L type Ca channels
2) Calcium binds to Ryanodine (RYR) receptors, which releases a calcium stored in the cell.
3) Ca binds troponin C
4) Tropomysin moves
5) Myosin actin crossbridges
6) tension is prodcued

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10
Q

What effects the amount amount of tension?

How can it be increased?

A

Depends on Calcium stores ICM.

CaATPase sucks Ca back up and reuses it. So the Ca ATPase and the NXC (Na Xchange Ca) increase Ca stores.

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11
Q

What does cardiac muscle have that is different from skeletal muscle?

A
  • Intercalated discs
  • Gap junctions
  • T tubules are larger. Contain more calcium.
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12
Q

What is the gap junctions role in syncing contraction?

How does it do this?

A

Gap junctions allow RAPID conduction, allowing simultaneous and coordinated contraction.
Decreases the internal resistance of the cell so that the action potential can go super fast.

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13
Q

What is the role of extracellular calcium in muscle contraction?

A

Higher calcium influx = higher calcium released into the cleft = higher calcium uptake from ATPase and NXC = more stored Ca2+ = more released on the next action potential = more tension = increased strength in muscle contraction

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14
Q

How does the heart keep the output of the left and right ventricles equal? Explain Starling’s Law.

A

In general, as pre-load increases, so does stroke volume

To increase pre load, increase venous return. Venous return = Stroke volume.

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15
Q

How does preload affect contractility and ventricle force?

A

As the blood spills into ventricle, it stretches the ventricle’s muscle fibers to the optimal length for contraction. That’s when we get maximum ventricle force. This allows the heart to use less energy by using elastic energy of the optimally stretched fibers

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16
Q

In a single cardiac cell, what is the length tension relationship?

A

In general As the length increases, so does the tension. (there is a limit)
In diseased states, there is a limit to this increasing length in which the tension gets weird after a certain length.

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17
Q

What is preload? and End-Diastolic volume?

A

Preload: The ventricles filling up.
EDV: Maximum blood volume in the ventricle just before ejection

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18
Q

How can we estimate Preload? Which is most reliable?

A

Ventricular End Diastolic Pressure – Higher the pressure higher the preload
Atrial Pressure – if atrial pressure is high before diastole, higher preload (??)
Venous Pressure – Vasodilation decreases pressure = decrease in preload

VEDP is most reliable because it’s a direct correlation.

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19
Q

What is afterload? How does arterial pressure affect this?

A

Aortic Pressure.

If arterial pressure increases =

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20
Q

How do the following affect cardiac performance (stroke volume/Cardiac output)
Preload?
Afterload?
Contractility?

A

High Preload: Increases.
High Afterload: decreases
High Contractility: Increases

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21
Q

What are the phases of the cardiac cycle?

A
  1. Isovolumetric contraction
  2. Systolic ejection
  3. Isovolumetirc relaxation
  4. rapid filling
  5. Reduced filling
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22
Q

What happens in Isovolumetric Contraction?

A

Phase 1 –> 2
Blood has filled the ventricle. Volume is high, so pressure is low.
Mitral valve closes.
Then ventricle contracts, so volume decreases, pressure is way high - higher than systemic circulation.

Lots of O2 consumed here.

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23
Q

What happens in Systolic Ejection?

A

Phase 2 –> 3
When the ventricle contracted, volume decreased, pressure became way high - higher than systemic circulation..
blood wants to flow high to low, so Aortic Valve opens.

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24
Q

What happens in Isovolumetric Relaxation?

A

Phase 3–> 4

Ventricle relaxes. Volume increases, pressure decreases. All valves are closed.

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25
Q

What happens in Rapid Ventricle filling?

A

Pressure falls to below left atrial pressure. Causes mitral valve to open. Blood flows high to low pressure into the left ventricle.

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26
Q

What happens in Reduced ventricle filling?

A

Pressure is increased in the L ventricle due to all the blood, so less wants to go in there.

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27
Q

What changes in pressure-volume when preload is increased?

A

End Diastolic volume increases = increased stroke volume

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28
Q

What changes in pressure-volume when afterload is increased?

A

Increased aortic pressure, decreased stroke volume, increased ESV.
see card 49 for explanation

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29
Q

What changes in pressure-volume when contractility is increased?

A

Increased Stroke volume
Increased Ejection Fraction
Decreased End Systolic Volume

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30
Q

What is the equation for stroke work?

A

Stroke work = Stroke volume x Aortic pressure

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31
Q

What is stroke volume? Where is this on a pressure -volume graph?

A

The amount of blood ejected from one ventricular contraction.
Subtract the max volume from min volume. Check the LOs for a pic

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32
Q

Where is stroke work on a PV loop graph?

A

Area of the loop

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33
Q

What is the Fick Principle?

A

Conservation of O2 in the body

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34
Q

How do you calculate stroke volume, give End Diastolic volume and End Systolic volume?

A

SV = EDV - ESV

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35
Q

How do you calculate ejection fraction, given End Diastolic volume and End Systolic volume?

A

EF = SV/ EDV

SV = EDV - ESV
so

EF = (EDV - ESV)/ EDV

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36
Q

What does a low EF indicate?

A

Heart Failure.

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37
Q

How to calculate O2 consumption with the Fick principle?

A

O2 consumption = (Maximum O2) - (O2 used up in the body)
How to find these numbers?
Maximum O2 found in pulmonary veins.
O2 used up found in Pulmonary arteries.
O2 consumption = (Cardiac Output x [O2]pulm veins) -
(Cardiac output x [O2]pulmarteries)

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38
Q

How do you calculate cardiac output?

A

Cardiac output = O2 consumption/(O2 pulm veins - O2 pulm arteries)

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39
Q

How is cardiac output (oxygen levels) maintained in exercise?

A

Increase Heart rate and stroke volume.

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40
Q

How does a reflex arc work?

A

stimulus → afferent sensory neuron → enters spinal cord via dorsal root → synapse with interneuron → synapse with motor neuron → efferent motor neuron stimulates muscle

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41
Q

Efferent nerves have how many motor neurons?

Afferent nerves have how many sensory neurons?

A

Efferent: Primary and secondary
Afferent: Tertiary, Secondary, Primary

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42
Q

What is the hypothalamus responsible for?
Pons?
Medulla?

A 
Hypo: 
Water balance
temperature 
hunger
Pons: 
Respiration and Cardiac 
Vasculature
Medulla: 
Respiration
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43
Q

Describe 5 general metabolic stances when the parasympathetic is active?

A 
Plenty of oxygen,
heart beats slowly
BP is low
Blood flow to GI
Absorb fuel from GI
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44
Q

Describe 4 general metabolic stances when the sympathetic is active?

A

More oxygen intake and delivery
HR increase
Conserve energy from GI
increase metabolism for fuel.

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45
Q 
Generally describe what these receptors do and where they're located. 
a1
a2
b1
b2
b3
A

a1: Contract/Decrease (Vasculature, Lungs, eye, GI)
a2: Inhibits (GI)
b1: Contracts (heart) Lipolysis (GI)
b2: Dilation (Vasculature, lungs, eye lens, GI: glycogenolysis)
b3: Metabolism: Lipolysis.

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46
Q

Describe Sympathetic system.

A 
Short pre-ganglion
Long Post- ganglion with branching
Adrenergic - uses epi and NE
Alpha and beta receptors
Found in thoracosacral
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47
Q

Parasympathetic

  • Pre-gang, short or long?
  • Post- gang, shortor long?
  • Types of receptors at pre? post?
  • Ligand at pre? Post?
  • Where found?
A 
Long Pre
Short post
pre: Nicotinic recptors for ACh
post: Muscarinic receptors for ACh
Found in craniosacral
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48
Q

What sympathetic receptors act on the heart?

Parasympathetic?

A

b1 and b2 to increase heart rate and contractility

M2: decrease HR and contractiility

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49
Q

What sympathetic receptors act on the Vasculature?

Parasympathetic?

A

A1 Vasoconstrict
B2 Vasodilate

Does zero things

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50
Q

What sympathetic receptors act on the lungs?

Parasympathetic?

A

A1 decrease secretion
B2 Bronchodilate. decrease secretion

M3 Bronchoconstrict. Increase secretions

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51
Q

What sympathetic receptors act on the eye?

Parasympathetic?

A

A1 Dilate Pupil (on radial muscle)
B2 Relax ciliary muscle (Allows for far sightedness)

M3 Pupillary sphincter muscle contraction (constrict pupil)

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52
Q

What sympathetic receptors act on the GI?

Parasympathetic?

A

A1 Contract sphincters
A2 Decrease secretions
B2 Relax smooth muscle

M3 Increase secretion and motility

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53
Q

What sympathetic receptors act on the Metabolism?

Parasympathetic?

A

B1 All increase lipolysis
B2 Also increases glycogenolysis
B3

M3 Promotes insulin and storage

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54
Q

What sympathetic receptors act on the bladder?

Parasympathetic?

A

A1 Sphincter contraction

M3 Contracts detrusor muscle and relaxes sphincter

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55
Q

What is lusitropy?

A

Relaxation

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56
Q

What happens during atrial systole?

Pressures, where is blood.. etc

A

Atrial pressure goes up due to contraction
Blood flows from atria to ventricle.
Ventricles have less pressure than atria
(Just after P wave)

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57
Q

What happens during Isovolumetric contraction?

Pressures, where is blood.. etc

A 
Ventricle depolarization and contraction
All valves are shut
Ventricle pressure rises
Atria pressures goes up a little bc of bulging valve
(QRS)
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58
Q

What happens during Ventricular ejection?

Pressures, where is blood.. etc

A

Ventricle pressure becomes higher than afterload pressure - semilunar valve opens
(ST segment)

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59
Q

What happens during Reduced Ejection?

Pressures, where is blood.. etc

A

Ventricular repolarization
VEntricle pressure decreases until aortic valve closes
(T wave)

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60
Q

What happens during Isovolumetric relaxation?

Pressures, where is blood.. etc

A

All valves close
ventricle relaxes until pressure falls below atrial pressure and mitral opens
Slight increase in aortic pressure due to blood hitting closed valve

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61
Q

What happens during Rapid ventricular filling?

Pressures, where is blood.. etc

A

Ventricular pressure is lower than atrial, so blood is flowing through it.

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62
Q

What happens during Reduced ventricular filling?

Pressures, where is blood.. etc

A

Pressure is growing in ventricle as blood flows in, so less and less blood wants to go in.

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63
Q

What is venous pulse?

A

The veins trying to get back into the right atria

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64
Q

What are 3 pressure differences in venous pulse?

A
  1. When the R atria contracts and blood spills back into them (no valve)
  2. Ventricular contraction - causes atria to bulge and put more pressure on veins
  3. Pressure increase as the veins come back to the heart but can’t enter ventricle bc its full
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65
Q

How does laminar flow work?

A

Blood next to the walls not moving, blood in the center moving very fast.

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66
Q

What can cause turbulent flow?

A
  • Branch points in large arteries
  • Diseased arteries
  • Stenotic arteries
  • Stenotic heart valves
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67
Q

What is the consequence of turbulent flow?

A

Requires more pressure/harder heart work to push through

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68
Q

What effects velocity of blood?

A

Vessel size: large vessel, low velocity.

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69
Q

What is the Volumetric Flow Rate Equation?

What will you more than likely be asked to find using this equation?

A 
Q = V*A
Q = Flow
V = Velocity
A = Area =  π*r^2

Velocity.
V= Q/A

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70
Q

An increase in pressure has what effect on flow?

An increase in resistance has what effect on flow and pressure?

A

↑Pressure =
↑ Flow Rate

↑ Resistance =
↑ Pressure
↓ Flow Rate

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71
Q

What is the Resistance equation?

What factor has the largest influence on resistance?

A

R = (V*L)/r^4

Resistance = viscosity * length/ radius

Radius has largest effect on resistance.

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72
Q

What effect does viscosity have on resistance?

What can increase viscosity?

A

↑ Viscosity = ↑ Resistance
Viscosity is dependent on hematocrit.
Anemia ↓ Hematocrit (↓ Viscosity ↓resistance)

Hyperproteinemia ↑ Hematocrit

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73
Q

What is the relationship between radius, resistance, and flow?

A

↑ Radius = ↑ Flow = ↓ Resistance

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74
Q

What is the relationship between area, velocity, and flow?

A

↑ Area =↓ Velocity =

Q = v*A
or
v=Q/A

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75
Q

How does the cross sectional area differ between arteries, capillaries, and veins?

A
  • Aorta has smallest area, increasing until Capillaries, which have the most.
  • Veins have the 2nd most area.
  • Vena Cava has a bit more area than the aorta
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76
Q

How does the blood volume differ between arteries, capillaries, and veins?

A

Aorta has little blood volume
Arteries have 2nd highest blood volume to veins.
Capillaries have 3rd highest blood volume.
Veins have highest blood volume.

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77
Q

What is resistance?

What is conductance?

A

Resistance - Resistance to flow

Conductance - Permeability

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78
Q

Equation for resistance of vessels in a series?
What are vessels in a series?
If you add resistance, what happens to the total resistance?

A

R1+R2+R3=Rt

artery –> arteriole –> capillary

Rt increases

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79
Q

Equation for resistance of vessels in parallel?

When are vessels in parallel? If you add resistance, what happens to the total resistance?

A

1/R1+1/R2+1/R3=1/Rt

in organs.

Decreases resistance

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80
Q

If there is a complete occlusion, what happens to the Resistance?

A

Resistance becomes infinite.

In parallel, this would increase the resistance.

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81
Q

What is the relationship between resistance and flow?

A

Increase resistance, decrease flow.

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82
Q

What is shear?

Where is shear highest?

A

This occurs when blood next to each other is traveling at different velocities.
Blood Vessel wall

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83
Q

What is Reynold’s number? What is the equation?

What number is the limit?

A 
an indicator of whether blood is going to be turbulent or not. 
Nr = pdv/n
Nr = Reynolds
p = density
d= diameter
v= velocity 
n = viscosity

N = 2000+ will be turbulent

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84
Q

What is a bruit? What are bruits caused by?

A

abnormal sound generated by turbulent flow in an artery

Partial obstruction
Localized high rate of flow
Increase in blood velocity by fever, anemia, hyperthyroidism

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85
Q

How does resistance differ between arteries, capillaries, and veins?

A

Arterioles - greatest resistance.
Capillaries - high resistance
Veins - low resistance

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86
Q

What is compliance? What does it mean for a vessel to have high compliance

A

How stretchy/willing to hold a large volume of blood.

High compliance means a larger amount of blood can be held. So veins have high compliance and can hold a lot of blood.

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87
Q

How can stroke volume affect arterial systolic pressure?
diastolic pressure?
Mean pressure?
Pulse Pressure?

A 
↑  in stroke volume: 
ASP:  ↑ 
DP: ↓
MP: ↑ 
PP: ↑
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88
Q

What is the equation of total peripheral resistance?

A

TPR = (Aortic pressure - vena cava pressure) / CO

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89
Q

What the method of action of arteriosclerosis?

A

stiffening of vessels - decreases compliance.

Increased systolic pressure, pulse pressure, increase mean arterial pressure

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90
Q

What effect does aortic stenosis have on pressures? Stroke volume?

A

Decrease SV
Decreases systolic pressure,
pulse pressure and mean arterial pressure

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91
Q

What is pulmonary vasculature like?

A

25/8
Low pressure, low resistance
High compliance

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92
Q

What is the pulse pressure?
Where is pulse pressure located?
How do you calculate?

A

Difference between systolic pressure and diastolic pressure. same as stroke volume
Arteries only.
Pulse pressure = systolic - diastolic

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93
Q

What is systemic vasculature like?

A

120/80
High pressure, high resistance,
low compliance

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94
Q

How does age affect vessels?

A

Increase stiffness of arteries, which decreases compliance

Arterial pressures increased due to this compliance.

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95
Q

What are the equations for cardiac output in regards to..

  • heart rate and stroke volume?
  • Pressure?
  • Venous Return?
  • Flow?
A

CO=SV*HR

CO=(input pressure-output pressure)/TPR

Same as Q=ΔP/R

CO=VR

CO=Q (flow)

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96
Q

How can veins move blood to arteries in order to raise arterial pressure?

A

Smooth muscle contraction

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97
Q

What’s the equation for Starling’s pressures?

A

Jv=Kf[(Pc-Pi)-(πc-πi)]

Jv = Fluid movement
Kf= fluid movement
Pc = capillary hydrostatic pressure
Pi = intersitial hydrostatic pressure
πc = capillary oncotic pressure
πi = interstitial oncotic pressure
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98
Q

How do you calculate Mean Arterial Pressure if given blood pressure?

A

MAP=⅔ diastolic + ⅓ systolic

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99
Q

How does aortic stenosis change pulse pressure? Is this good for the heart?

A

pulse pressure is decreased

No, because the heart still has to work way harder.

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100
Q

What consequence happens during reactive hyperemia?

A

It forms reactive oxygen species.

An ischemic tissue gets a ton of oxygen and makes that stuff.

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101
Q

What is associated with Cushing Reflex?

A

Short version:
↑ Intracranial pressure results in ↑ BP, irregular breathing, and reduced HR
Long version:
↑ intracranial pressure (due to trauma) → constricts arterioles → cerebral ischemia → ↑PaCO2 (decrease pH) → central reflex sympathetic tone → vasoconstriction (↑ BP) → ↑ stretch on baroreceptors (vagus stimulation) → peripheral baroreceptor induced bradycardia

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102
Q 
What is the average pressure of 
aorta?
large arteries?
arterioles?
capillaries?
Vena Cava?
Right atrium?
A 
Aorta: 100
large arteries: 100
arterioles: 50
capillaries: 20
Vena Cava: 4
Right atrium: 0-2
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103
Q 
What are the average PULMONARY pressures of: 
Pulmonary artery
pulmonary capillaries
pulmonary vein 
Left atrium
A

Pulmonary artery: 15
pulmonary capillaries: 10
pulmonary vein: 8
Left atrium: 2-5

104
Q

In the Starling equation, what is meant by filtration?

absorption?

A

Filtration : movement out of capillary

Absorption: movement into capillary

105
Q

What type of molecules diffuse easily across? Give 2 examples

A

Lipid soluble.
Oxygen,
CO2

106
Q

What type of molecules do not diffuse easily across? Give examples

A

Water, ions, glucose, amino acids,

must go AROUND endothelial cells instead of through them.

107
Q

How do proteins get across the capillaries?

A

Through fenestrated caps only.

108
Q

What 4 factors allow for quick diffusion through capillaries

A

Smaller molecules
higher pressure
Larger surface area
Thin wall

109
Q

Jv=Kf[(Pc-Pi)-(πc-πi)]

How does an increase in protein concentration affect the Starling equation?

A

↑ Protein = ↑ Capillary oncotic pressure.

110
Q

Jv=Kf[(Pc-Pi)-(πc-πi)]

How would toxin that gets into the capillaries affect the Starling equation?

A

Toxin would poke holes in the capillaries, allowing faster water diffusion.
Kf would increase.

111
Q

Jv=Kf[(Pc-Pi)-(πc-πi)]

How would the Starling equation differ if seen from the venous side of the capillary bed rather than the arterial side of the capillary bed?

A

Capillary hydrostatic pressure is higher on the arterial end

112
Q

Which Starling forces OPPOSE filtration?

Favor Filtration?

A

Oppose:
Interstitial Hydrostatic
Capillary oncotic pressure

Favor:
Cap Hydrostatic pressure
Interstitial oncotic pressure

113
Q

What is the definition of edema?

When, then, does edema form?

A

the volume of interstitial fluid exceeds the ability of the lymphatics to return it to the circulation.
Edema forms in increased filtration, or lymph drain is impaired.

114
Q

How does histamine affect permeability?

How does albumin affect permeability?

A

Increases permeability. Fluid from cap –> Interstitial space. Causes edema.

Albumin = protein.
More protein = increased cap oncotic pressure
If less albumin - there’s cap oncotic pressure, so less flows into the cap = stays in interstitial. = edema

115
Q

What is the function of the flaps on lymphatic vessels?

Where does lymph fluid go?

A

Proteins and water can enter lymph- but they cannot backtrack.
Into the thoracic duct

116
Q

What 5 things can cause capillary hydrostatic pressure to increase?

A

Arteriole dilation
Venous Constriction
Increased Venous Pressure
Heart Failure

117
Q

What 4 things can decreases capillary ONCOTIC pressure?

A

Decreased plasma protein concentration
Severe liver failure
Protein malnutrition
Nephrotic syndrome (Loss of protein in urine)

118
Q

What 3 things can impair lymphatic drainage?

A
  • Standing (not compressing lymphatics)
  • Lymph node removal
  • Parasites in lymphs
119
Q

What is lymph’s role in transportation of protein, hormones and fats? (big compounds)

A

Blood vessels are tighter htan lymph and harder to get into. So big ol’ deals like chylomicrons, proteins and hormones have to get around the body via the lymph system.

120
Q

Fat cannot easily diffuse into the bloodstream. How does it get around the body?

A

Fat is put into a chylomicron, which are huge. So the chylomicron must go into lymph

121
Q

A patient with moderate edema arrives to the office, after further testing you diagnose a DVT. What is the relationship between the DVT and the edema?

A

The venous obstruction caused an increase in capillary hydrostatic pressure, causing fluid to rush from cap to interstitial.

122
Q

A patient with moderate edema arrives to the office, after further testing you diagnose heart failure. What is the relationship between the CHF and the edema?

A

There’s fluid build up on the venous side (remember that venous changes affect capillaries the most)
causing increase in capillary hydrostatic pressure.

123
Q

You’re in a third world country and a patient comes into the shack clinic that you’ve built with your own bare hands out of driftwood. Under your severely callused hands you palpate boggy tissue in the feet and shins of your 13 year old patient - EDEMA! You are certain the mechanism of this edema was caused by: ?

A

Malnutrition. Decreases plasma proteins decreases capillary oncotic pressure, so more fluid is left in the tissue.

124
Q

You’re a cruise ship doctor for Holland Cruise. You have another 70 year old woman whom, while playing the penny slot at the casino, got angry at the machine and slammed her head into it. She presents with irregular breathing and a reduced heart rate. Her blood gases reveal increased CO2. What is happening?

A

Cushing Reflex
The trauma from hitting her head caused an
↑ intracranial pressure → constricts arterioles → cerebral ischemia → ↑PaCO2 (decrease pH) → central reflex sympathetic tone → vasoconstriction (↑ BP) → ↑ stretch on baroreceptors (vagus stimulation) → peripheral baroreceptor induced bradycardia

125
Q

Define autoregulation?

A

You need autoregulation to maintain constant blood flow to certain organs even when arterial pressure changes

126
Q

What organs need constant flow of blood at all times?

A

Kidney, brain, heart, skeletal muscle

127
Q

What is active hyperemia?

A

Blood flow to an organ is proportional to its metabolic activity.
The metabolic activity can change.

128
Q

What is reactive hyperemia

A

Increase in blood flow in RESPONSE to a pathology. Such as: Thrombus! Obstruction of arteries is removed and oxygen is restored!

129
Q

What is the Myogenic hypothesis? When is this applied?

A

Vascular muscle contracts when stretched.
Applies when arterial pressure stretches the arterioles, so the artrioles contract.
Why?
You need to keep the blood flow the same in spite of the pressure increase. So you increase resistance through constriction.

130
Q

How does Starling’s Law apply to Myogenic hypothesis and high blood pressure?

A

If you have a high blood pressure, the arteries will constrict in order to reduce blood flow, to make up for the increased blood pressure caused by the constriction, veins dilate.
Dilation causes decreased restriction so higher blood flow.

131
Q

What is metabolic hypothesis?

A

Tissues let the heart know that they need blood when they create vasodilator metabolites (CO2, H+, K+, lactate, adenosine = CHALK)

132
Q

How does metabolic hypothesis account for vasoconstriction of organs that have low metabolic activity?

A

The spontaneous increase in blood flow washes out the vasodilator metabolites.

133
Q

In coronary circulation, what is the most important vaso control? What are the vasoactive metabolites?

A

Local metabolic control.

Hypoxia→ adenosine→ vasodilation

134
Q

In cerebral circulation, what is the most important vaso control? What are the vasoactive metabolites?

A 
Local metabolic control
Increase CO2(decrease in pH)→ vasodilation to wash CO2 out
135
Q

There are 6 circulatory systems. Which has the highest density of sympathetic innervation?
Does it produce vasoconstriction or dilation?

A

Skin - vasoconstriction via a1

Skeletal muscle - vasoconstriction via a1 or vasodilation via b2

136
Q 
Are the following vasodilators or vasoconstrictors?
Histamine
Bradykinin
Serotonin
Prostaglandin E
Prostaglanding F
Thromboxane
ANF
A 
Histamine - vasodilatoin
Bradykinin - Vasodilation
Serotonin - vasoconstriction (during blood vessel damage) 
Prostaglandin E - Vasodilator
Prostablandin F- Vasoconstrict
Thromboxane - vasoconstrictor
ANF: Vasodilator
137
Q

What causes hypoxia in coronary circulation?

A

Increase demand for systemic O2, so heart muscles pump harder and use up more O2.

138
Q

In pulmonary circulation, what is the most important vaso control? What are the vasoactive metabolites?

A

Local

Hypoxia→ vasoconstriction (get the blood away from crappy spots)

139
Q

What regulates blood flow to skeletal muscle at rest?

during exercise?

A

Rest: Sympathetic innervation via a1 - vasoconstrict and B2 - vasodilate.
Exercise: Local metabolites. CHALK Lactate, adenosine, K+

140
Q

In which tissues is mechanical compression important?

A

Skeletal muscle and coronary

141
Q

How does sympathetic response work in skin?

A

As body temp increases, sympathetic a1 receptors are inhibited = vasodilation occurs to dissipate off heat.

142
Q

In cutaneous blood flow, what is the local effect? Neural?

A

Local: Trauma releases histamine resulting in redness, and a wheal
Neural: Sympathetic a1 receptors cause vasoconstriction.
(Inhibit sympathetic a1 to increase flow)

143
Q

What receptors do somatic nerves use? What do they innervate? What ligands do they use?

A

Nicotinic receptors
Skeletal muscle
ACh

144
Q

What receptors do parasympathetic nerves use?

A

nicotinic ACh at presynapse and muscarinic ACh at post synapse

145
Q

What receptors do sympathetic nerves use?

A

alpha, beta, dopamine, nicotinic, muscarinic

146
Q

What tissue uses sympathetic nerves on a muscarinic receptor?

A

Sweat glands

147
Q

How does an agonist work?

Antagonists?

A
  • Activate a receptor as a direct result of binding.

- binds to receptor but does not generate signal. Interferes with agonists

148
Q

What does it mean to be cholinergic?
Where are these located?
If you inhibited cholinergic receptors, what could be the result?

A

To use Acetylcholine.
Located on all preganglionic autonomic fibers, all post ganglion parasympathetic and sweat glands.

If you inhibit cholinergic receptors, this would inhibit ALL autonomic responses and somatic responses

149
Q

Where is epinephrine synthesized?

A

adrenal medulla

150
Q

How are catecholamines synthesized?

A

Tyrosine –> DOPA –>Dopamine –> norepihephrine –> Epinephrine

Tyrosine to dopamine occurs in the cytoplasm.
Dopamine to NE occurs in the vesicle, and NE to epi occurs in medulla

151
Q

How is acetylcholine synthesized and released?

What are the 3 fates of ACh?

A
  • Ac CoA + choline inside the cell. enzyme: ChAT
  • ACh goes into a vesicle via VAT
  • ACh released due
    to Ca++ influx
    Fates:
    1) be a positive stimulus on mAChR or nAChR on another cell
    2) Degrade into choline and acetate
    3) attach onto self cell M or N receptors
152
Q

If hemicholinium enters the system, what is the consequence?
Vesamicol?
Botulinium toxin?

A

Stops the intake of choline into the cell
Vesamicol: ACh cannot go into vesicle
Bot Tox: Cannot be released from the cell

153
Q

How is NE syntheiszed and released?

What are the 3 fates of NE?

A
  • Tyrosine goes into cell via NA dependant tyrosine
  • Tyrosine turns into DOPA, turns into DOPAMINE.
  • Dopamine goes into a vesicle via VMAT and turns into NE
  • Transported via NET NE released due to Ca influx
    Fates:
    1) Self receptor b2 positive stimulus
  • Self receptor a1 negative stimulus
    2) Self reentry into cell for recycle
    3) alpha beta receptor on separate cell.
154
Q

What happens to the system if Reserpine enters?

Cocaine?

A

Reserpine: cannot put dopamine and NE into vesicle
Cocaine: NE can’t be recycled

155
Q

Adrenal medulla creates what ligands? In what fraction?

A

80%Epi

20% NE

156
Q

What does it mean to be adrenergic?

A

Relates to epinephrine and NE

157
Q

WHat receptors are found on smooth muscle of blood vessels? How does a blood vessel relax?

A

ONLY alpha beta.

Parsymapthetic still release ACh, but it’s through the endothelium not the smooth muscle.

158
Q

What happens in the termination of catecholamines?

A

Reuptake into NET and DET (NE transport and dopamine Transport)
Then stored in vesicles by VMAT

Metabolism of Catechols - via MAO (Monoamine oxidase) and COMT (Catecho=O-methyltrasnferase)

159
Q 
Where are alpha 1 receptors located?
alpha 2
Beta 1?
Beta2?
What do they do?
A

Alpha1: peripheral arteries –> Vasoconstrict
alpha2: inhibits NE, ACh, and insulin release
B1: Located in heart –> increase HR
B2: Lungs and artery walls –> Bronchodilation

160
Q

What is renin? and what does it do?!

A

Renin is associated with the juxtaglomerular appratus of the kidney, Beta 1 receptor –> it increases angtiotensin (I–>II), which vasoconstricts.

161
Q

Where are M1 receptors?
M2?
M3?

A 
1: Autonomic ganglia
gastric glands
brain
2: Heart
3: Pupils
Glands 
Blood vesells
162
Q

What are ionotriopc receptors?

A

super fast, change conformation to allow ions through

163
Q

What are metabotropic receptors?

A

Slow. Use Gproteins as secondary messegners

164
Q

What is the MOA of Reserpine? Receptor system?

MAO inhibitrs?

A

INhibit NT storage. Adrenergic

NT inactivation or degredation, adrenergic

165
Q

What is the MOA of Bot Tox? Receptor system?

ACE inhibitors?

A

Inhibt NT release, cholinergic

NT inactivate or degrade, cholinergic

166
Q

What is the MOA of Nicotine? Receptor system?

Cocaine?

A

Mimic or block NT at receptor. Cholinergic

Inhibit NT reuptake, adrenergic

167
Q

What does blocking of a neuronal nicotinic receptor cause?

A

Blocks literally everything bc nicotinic is for ACh which is all preganglionic.

168
Q

What does blocking of a acetylcholinesterase cause?

monoamine oxidase?

A

Inhibition of ACh breakdown

MOA: Catecholamine accumulation in terminal

169
Q

What does blocking of a muscarinic receptor cause?

Agonist and antagonist

A

Agonist: parasympathetic tone dominates

Antagonist: sympathetic tone dominates

170
Q

What does blocking beta 1 adrenergic receptors do?

A

antagonist b1 blocker is an antagonist that inhibits sympathetic activation of heart. = low HR and contractility

171
Q

You lose 30% of your blood volume - what happens to the:
Cardiac output?
Central Venous pressure?
Arterial pressure?

A

↓ CO
↓ preload, SV, venous return,
↓ Central venous pressure
↓ arterial pressure

172
Q

What can case you to lose 30% of your blood?

A

Hemorrhage

dehydration, loss of fluids

173
Q

What is the baroreceptor Reflex to loss of blood volume?

A

↓ stretch in baroreceptors → decreased afferent baroreceptor firing → ↑ efferent sympathetic firing → ↓ efferent parasympathetic firing → vasoconstriction, ↑ HR, contractility, BP

174
Q

What is the renin- angiotension -adlosterone reflex to loss of blood volume?

A

Hypotension → ↓ arterial pressure → secretion of renin → renin converts angiotensinogen to angiotensin I → ACE converts angiotensin I to angiotensin II → angiotensin II → ↑ aldosterone → ↑ Na reabsorption → ↑ BP

175
Q

What is the capillary response to loss of blood volume?

A

Hypotension → ↓ capillary hydrostatic pressure → ↑ fluid absorption → ↑ blood volume

176
Q

If you think about exercise, it counts as a workout. Why?

A

Primes your system.

The muscles that are predicted to become active will vasodilate, causing a drop of TPR.

177
Q

When you exercise, what happens to peripheral resistance?
cardiac output?
A-V oxygen difference?
Arterial pressure?

A

Peripheral Resistance? increases (in muscles that are not going to be used)
Decreases in muscles that are going to be used
Cardiac output? increases
A-V O2 difference: increases
Arterial pressure: increases

178
Q

If you don’t prime your body for exercise prior to exercise, what could happen to the muscle’s BP and TPR?
What’s the equation?

A

Large reduction in TPR and BP
There is a decreased firing of baroreceptors

BP = CO* TPR

179
Q

What is the function of central command?

A

Directs the autnomic nervous system. Increases Sympathetic, decreases parasympathetic.
Generall increases cardiac output

180
Q

When sympathetic control is turned on by the Central command, what happens to splanchinic arterioles?
Renal arterioles?
Veins?

A

Constrict all.

181
Q

What is the function of local command?

A

Increases vasodilator metabolites (CHALK: lactate CO2)
Dilates skeletal muscle
Decreases TPR

182
Q

How is local control different in rest vs exercise?

A

Exercisey skeletal muscle is abundant in vasodilator metabolites.
in rest those vasodilators are washed away via spontaneous increased Pa

183
Q

What regulates blood during posture changes?

What happens when a person stands up?

A

The baroreceptors reflex.

Muscle pumps in veins push blood up to the head.

184
Q

When Eric stands up too fast and gets light headed, this is called what?
If this is pathological, what’s wrong?

A

orthostatic hypotension

The muscle pumps in the veins aren’t good, so blood pools in the lower extremity. = Edema and hypotension.

185
Q

When discussing metabolic demand of tissue, what are 2 goals that must be met?

A
  1. Arterial beds have constant (high input) pressure

2. To change flow, alter resistance of individual vascular beds

186
Q

A patient has been in a car accident and is hemorrhaging. It’s obvious his body has not recruited any compensatory changes to help him. He’s seconds from death when your attending asks you, “what reflex receptor is not working here?”

A

Baroreceptor.

187
Q

Hemorrhage will cause what effect on Cardiac Output?

EDV (Right atrial pressure)?

A

Decrease CO

Decrease EDV

188
Q

Heart failure will cause what effect on Cardiac Output?

EDV (Right atrial pressure)?

A

Decrease CO

Increase EDV

189
Q

The Baroreceptor uses the classical reflex path. What is this path?

A 
Detection
Afferent
Coordinator center
Efferent
Effector
190
Q

What do mechanoreceptors respond to ?

A

Arterial pressure changes

191
Q

What do chemoreceptors respond to?

A

PO2, PCO2, pH

192
Q

Where is the carotid sinus located? What is it?

A

Baroreceptor efferent nerve. Branch off:
Glossopharyngeal –> Sinus nerve of Hering –> Carotid sinus
Where the common carotid branches off

193
Q

Where is the Aortic sinus located? What is it?

A

Baroreceptor efferent nerve branching off Vagus nerve.

Located along ductus arteriosus.

194
Q

What do the carotid sinus and aortic sinus feed into?

A

Nucleus tractus solitarius

195
Q

Where is the Neural tractus solitarius located?
Vasomotor area?
Rostral Ventrolateral medulla?
Dorsal motor nucleus (of vagus and nucleus ambiguous)

A

Dorsal Medulla

Ventral medulla

Rostral ventrolateral is located in the vasomotor area (ventral)

Dorsal part of medulla.

196
Q

If the rostral ventrolateral medulla is stimulated, what is affected?
If the dorsal motor nucleus is stimulated, what is effected?

A

Vasculature response

Cardiac Response

197
Q

The baroreceptors signal the medulla and afferent neurons being firing like crazy! What must be happening?

A

Increase in blood pressure

198
Q

Where do the baroreceptors send their signals?

A

Medulla

199
Q

What center controls the set point?

A

Nucleus tractus solitarius.

200
Q

If the Mean Arterial Blood pressure deviates from the set point, what is the sequence of events?

A

The baroreceptors are stimulated and send a signal to the NTS in the medulla. The NTS stimulates the SNS and PNS, which changes the MABP.

201
Q

How does stimulating the SNS change blood pressure?

PNS?

A

SNS is a cardiac accelerator and vasoconstrictor. So increases BP
PNS is a cardiac decelerator via the sinuatrial node.

202
Q

What is the equation fr BP?

A 
BP = CO * TPR
CO = SV * HR

BP = SV * HR * TPR

203
Q

BP = SV* HR * TPR

What is TPR dependent on?

What is SV dependent on?

HR?

A

TPR: Sympathetic stimulation of arterioles

SV: Sympathetic stimulation of heart.
Increased Preload

HR: SNS and PNS Stimulation

204
Q

What is the mechanism of chronic hypertension?

A

Your blood pressure slowly kept increasing the Set point. So your baroreceptors adapted to that set point.

205
Q

What is the sequence of events in acute hypertension?

A

Hypertension → ↑ arterial pressure → decrease stretch in baroreceptors → decrease afferent nerve firing → ↑ efferent parasympathetic (vagus), ↓ efferent sympathetic → ↓ HR at SA node

206
Q

What are the sympathetic effects on the heart during acute hypotension?

Vessels?

Kidney?

A

Incresae HR and contractility via the SA node directly.

Constrict arterioles and veins to increase TPR & Decrease venous capacitance

Fluid retention

207
Q

What are the parasympathetic effects on the heart?

A

Vagus nerve decrease SA node rate.

208
Q

What hormones are associated with the RAAS response?

A

Renin,
Angiotensin II
Aldosterone
Vasopressin

209
Q

What is renin’s role in RAAS?
Angiotensin II?
Aldosterone?
Vasopressin?

A

Renin: Converts angiotensinogen to angiotensin I.

Angiotensin II: Vasoconstricts
Increases secretion of Vasopressin and Aldosterone
Increases thirst

Adlosterone: Increase Sodium reabsorption = water retention

Vasopressin: antidiuretic hormone increases renal fluid reabsorption (

210
Q

What 3 hormones are produced in response to high TPR?

A

ANF: INhibits renin

Bradykinin: Vasodilate (broken down by angiotensin II)

Nitric Oxide: Vasodilate

211
Q

What and when is renin secreted by?

A

The best cells. JG cells.

Justaglomerular cells in response to low BP.

212
Q

Why is angiotensin II a pharm target?

What is used?

A

crazy powerful vasoconstrictor

ACE inhibitors for AC enzyme
ARBs - block receptor

213
Q

When is vasopressin secreted

A

When angiotensin II is.

214
Q

What protects the heart from overdilation?

This is secreted by excessive preload. What causes excessive prelaod?

A

Natriueretic peptide

arteriole dilation (decrease TPR)
Increase fluid loss
Ihibition of renin (decreases TPR and preload)

215
Q

When you exercise, what part of the cerebral cortex is stimulated?
What does this cause? Name receptors as well.

A

Central command

Increase in sympathetic output. B1 and A1
Decrease in PNS.

Vasodilation in periphery from vasodilator metabolites.

216
Q

In what systems are the PNS and SNS cooperative? Are they ever complemetnary?

A

Sex and urination

yes, I guess so.

217
Q

If TSH is absent in a patient, and there are hyperdynamic heart sounds, what could be going on?

A

hyperthyroidism.

218
Q

How does the thyroid impact the compensatory mechanism for arterial pressure?

A

T3 stimulates RAAS

219
Q

T3’s affect on the heart is similar to what other system?

A

Beta adrenergic sympathetic stimulation

220
Q

Hyperthyroidism does what to the

HR?
Pa?
TPR?
Ejection fraction?
Myocard O2 consumption
What are other related symptoms?
A 
Hr: Increase
Pa:Increase
TPR: Decease
Ejectino fraction: Increase
Myocard O2: Increase

Angina

221
Q

A pt comes in with a TSH is at 101. what is normal?

A

Less than 5

222
Q 
Hypothyroidism does what to the
HR?
Pa? 
TPR
Ejectino fraction?
Myocard O2 consumption?

Other symptoms?

A 
HR: decrease or normal
Pa: decrease or normal
TPR: increased
EJection fraction: decrease
myocard O2: decrease

Ventricular arrhtymia

223
Q

A patient presents with SOB.She has noticed htat she can no longer walk up stairs without resting. She frequently wakes up in the middle of the night with angina. Diagnoiss?

A

Heart failure

224
Q

What is the body’s response to heart failure?

A

Because of the reduced CO and SV,
SYmpathetic activity increases
Promotes renal salt and water retention to incrrease bood volume to raise end diastolic pressure and volume.
LV hypertrophy.

Obviously this wears outs and you die. (unless you’re Shelby Kite and get an LVAD to pump your heart outside your body)

225
Q

How does a multiunit smooth muscle fiber work?

What are examples?

A

Each individual fiber is innervated by separate nerve

Examples: ciliary muscles of eye, iris, piloerector muscles

226
Q

How does a single unit smooth muscle fiber work?

What are examples?

A

Bunch of fibers innervated by one nerve - have gap jxns to help signal through
Examples: GI, Bile duct, uterus

227
Q

Which smooth muscle fiber, multiunit or subunit has a regular action potential?

A

SIngle unit

228
Q

what hormones can stimluate the Ca influx of smooth muscle?

What environental factors can cause Ca influx?

A

ACh
NE
Nitric oxide

Environment: Hypoxia,
Excess Co2
Increase H+

229
Q

What are 2 types of action potentials in smooth muscle?

A

Spike potential

Plateau

230
Q

What are 3 ways Calcium influx can occur?

A
  • Spontaneous depolarization
  • Environmental factor
  • hormones or neurotransmitters can cause this via GPCR –> PLC → IP3
231
Q

In smooth muscle contraction, What happens after Calcium influx?

A

Calcium binds to Calmodulin Which binds to myosin light chain kinase

232
Q

What does binding of MLCK cause

A

Phosphorylateion of mysoin which increases ATPase activity.

233
Q

Smooth muscle contraction can be inhibited by what 5 things

A 
Calponin 
Caldesmon
Low intracellular Ca
cAMP
IP3
234
Q

What is the main point of the latch mechanism?

A

Decreases energy demands

235
Q

What is the length tension curve of smooth muscle

A

Bell curve. As length increases, tension does until optimal, then goes back down.

236
Q

A patient comes in with edema in the legs. As an osteopathic physician, you know that you can decreases lymphatic obstruction through the thoracic inlet followed by doming and rigorous pedal pump. What is the relationship between edema and lymphatic obstruction?

A
  • Increase in intersitial fluid oncotic pressure

- increase lymphatic hydrostatic pressure

237
Q

What are the 4 myocardial O2 demand increasers?

A 
myoCARDial O2
Cardiac Output
Afterload
Rate
Diameter of ventricle
238
Q

What are the 4 myocardial O2 demand increasers?

A 
myoCARDial O2
Cardiac Output
Afterload
Rate
Diameter of ventricle
239
Q

How does innervation differ between skeletal and smooth muscle?

A

Skeletal: only alpha motor neurons
Smooth:
Intrinsic & Extrinsic

240
Q

What does intrinsic innervation of smooth muscle consist of?

A

Nerve plexus within organ. Myogenic and metabolites.

241
Q

What does extrinsic innervation of smooth muscle consist of?

A

Autonomic NS.

242
Q

What are the neurotransmitters for skeletal muscle?

Smooth muscle?

A

Skeletal: ACh

Smooth: 
ACh - 
Epi - 
NO - 
Prostacyclin
EDHF
Adenosine
Endothelins
243
Q 
What is the effect of the following neurotransmitters on Smooth muscle?
ACh - 
Epi - 
NO - 
Prostacyclin
EDHF
Adenosine
Endothelins
A

ACh - Contract Gi.
Epi - Contract vascular smooth
NO - Relax GI

(CV system:)
Prostacyclin -Relax Smooth via increase Ca ATPase
EDHF - Relax (opens K+, hyperpolarize, prevents contraction)
Adenosine - Relaxation
Endothelins - Contract via Intracellular Ca+ increase

244
Q

How does the nerve and muscle contact each other in skeletal muscle?
Smooth muscle?

A

Skeletal: neuromuscular junction

Smooth: Has varicosities that release neurotransmitter.

245
Q

How are receptors distributed on skeletal muscle?

Smooth muscle?

A

Skeletal: Nicotinic ACh receptors at motor end plate

Smooth:
- 3 receptors for different NTs. Appear all over the cell

246
Q

What are the 5 ways smooth muscles can be stimulated to contract?

A
  • Hormones
  • NTs
  • Stretch
  • Pacemaker cells
  • Environment
247
Q

What neurotransmitters affect smooth muscle?

A

R: cholinergic
R: Adrenergic
R: Adenosine

NO (no receptor)

248
Q

What is the mechanism of Nitric Oxide?

A

High flow rate → more shear stress on vessel → activates stretch receptors → increase intracellular calcium → activates NO synthase in BC endothelium → NO produced → diffuses through endothelial cell into smooth muscle → increase cGMP → relaxes/vasodilates

249
Q

What environmental factors cal stimulate smooth muscle?

A

Hypoxia
Excess CO2
Increase H+
CHALK Metabolites

250
Q

What is the resting membrane potential in skeletal muscle?

Smooth muscle?

A

Skeletal -90

Smooth - 60

251
Q

How does Smooth muscle use less ATP?

A
  • Slower cycling
  • Less Cross bridges
  • Myosin Isoform must be less ATP using
252
Q

How does the latch mechanism work?

A

Maintains contraction, slower cycling

253
Q

What is plasticity, and what is it’s role in smooth muscle?

A

Plasticity: having active tension at short muscle fiber lengths.
Hollow organs can stretch to incredible amounts without damage and still do good work.

254
Q

How does plasticity work?

A

Thick filaments are randomly arranged.

  • Initial stretch of actin and myosin: creates passive tension
  • Actin separates and binds to new myosin around them.
255
Q

What is the speed of action potential between these 3?

AV node
His bundles/Purkinje
Myocytes

A

His/Purkinje > Myocytes > AV node

Fast to slow

256
Q

The SA node is the pacemaker in a normal heart. Why?
What takes over if the SA node is compromised?
And then?
What are the bpm of these dudes?

A

It’s fastest conduction velocity at 70-80 bpm
AV node: 40-60 bpm
Purkinje: 20-35 bpm

257
Q

If you block a Calcium channel, what happens to the action potential?

A

decrease ionotropy and chronotropy

CardioPulm2 (3 decks)

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