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VTS(ECC) Study > West Respiratory Phys > Flashcards

West Respiratory Phys Flashcards

1
Q

List other functions of the lung besides gas exchange

A

Metabolizes some compounds, filters unwanted materials from the circulation, acts as a reservoir for blood

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2
Q

Fick’s law of diffusion?

A

The amount of gas that moves across a sheet of tissue is proportional to the area of the sheet but inversely proportional to its thickness

V = A/T x D x (P1-P2) where A = area, T = thickness, D - diffusion constant, P1, P2 = partial pressure of gas on either side of sheet

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3
Q

How thick is the blood-gas barrier?

A

3 micrometers

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4
Q

About how many alveoli in the human lung? How thick are they?

A

About 500 million; each is 1/3 mm diameter

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5
Q

Describe the airways in terms of large structures–>smaller structures using the terms trachea, alveoli, etc

A

Trachea–>R&L mainstem bronchi–>lobar bronchi–>segmental bronchi–>terminal bronchioles–>respiratory bronchioles–>alveolar ducts–>alveolar sacs

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6
Q

What components of the airway are part of the conducting zone? Transitional and respiratory zones?

A

Conducting- trachea, bronchi, bronchioles, terminal bronchiolesTransitional/respiratory- respiratory bronchioles, alveolar ducts, alveolar sacs

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7
Q

Describe the diffusion path from alveolar gas to the interior of the erythrocyte

A

See pg 3Layer of surfactant–>alveolar epithelium–>interstitium–>capillary endothelium–>plasma

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8
Q

What is the function of the conducting airways?

A

Lead inspired air to the gas-exchanging regions of the lung (example is bronchi)They make up the anatomic dead space b/c they don’t participate in gas exchange

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9
Q

What helps increase the volume in the thoracic cavity during inspiration?

A

Contraction of diaphragm, intercostal muscles raising the ribs

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10
Q

Why does inhaled dust frequently settle in the terminal bronchioles?

A

Because the velocity of gas falls rapidly in the region of the terminal bronchioles

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11
Q

A normal breath of 500 ml requires how much distending pressure for the lung?

A

<3 cm h2o

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12
Q

T/F- Initially the pulmonary arteries, veins, and bronchi are far apart but become closer together towards the periphery of the lung?

A

False- they become further apart towards the periphery

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13
Q

What is the diameter of a capillary segment in the lung?

A

about 7-10 micrometers, just big enough for a RBC

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14
Q

What are some reasons why the capillaries in the lung can be easily damaged?

A

Extremely thin, inflation of the lung can raise the wall stresses of the capillaries and cause structural changes– this can cause leakage of plasma and even RBC into alveolar spaces

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15
Q

What is the function of surfactant?

A

Dramatically lowers the surface tension of the alveolar lining layer- increases stability of alveoli, although collapse of small airways is still possible

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16
Q

Mechanism of filtering out particles in the different areas of the airways?

A

Nose- filters out large particlesConducting airways- filters small particles via mucociliary ladder into epiglottis, where they are swallowedAlveoli- no mucociliary ladder; macrophages engulf the particles and they are removed via lymphatics or blood flow

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17
Q

What is functional residual capacity?

A

Volume of gas in the lung after normal expiration

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18
Q

Definition of total ventilation?

A

Total volume of air leaving the lung each minute (volume of each breath x RR in bpm)

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19
Q

What does Boyle’s law state?

A

Pressure x volume is constant at constant temperature (P1 x V1) = (P2 x V2)

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20
Q

Describe the alveolar ventilation equation

A

Va=[Vco2/Pco2] x K
The partial pressure of CO2 is proportional to the fractional concentration of the gas in the alveoli, or PCO2=FCO2 x K, where K is a constant

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21
Q

How do you measure dead space ? (what equation/method?)

A

Bohr’s method
[VD/VT] = [PACO2-PECO2] / PACO2
*E=mixed expired, A=alveolar

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22
Q

T/F: Ventilation per unit volume is greater near the bottom of the lung as opposed to the top of the lung?

A

True

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23
Q

T/F: In the lateral position, the dependent lung is best ventilated?

A

True

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24
Q

[Mult Choice]
Concerning the blood-gas barrier of the human lung:
A. The thinnest part of the blood-gas barrier is about 3 micrometers thick
B. The total area of the blood-gas barrier is about 1 square meter
C. About 10% of the area of the alveolar wall is occupied by capillaries
D. If the pressure in the capillaries rises to unphysiologically high levels, the blood-gas barrier can be damaged
E. O2 crosses the blood-gas barrier by active transport

A

D

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25
Q

How much more rapidly does CO2 diffuse through lung tissue (as compared to O2) and why?

A

It diffuses about 20 times more rapidly than O2 because it has a higher solubility but not a very different molecular weight. The rate of transfer of a gas is proportional to a diffusion constant, which depends on the properties of the tissue and the particular gas. The constant is proportional to the solubility of the gas and inversely proportional to the square root of the molecular weight.

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26
Q

What type of gas is diffusion limited and what does this mean?

A

Carbon monoxide- the amount of carbon monoxide that gets into the blood is limited by the diffusion properties of the blood-gas barrier and not by the amount of blood available; a large amount of this gas can be taken up by the cell without a resultant increase in partial pressure in the blood (because of the tight bond that forms between it and hemoglobin)

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27
Q

What type of gas is perfusion limited and what does this mean?

A

Nitrous oxide- partial pressure of nitrous oxide rises rapidly when it moves into the blood because it does not combine with hemoglobin; the amount of nitrous oxide in the blood has reached that of alveolar gas by the time the rbc is only 1/10 of the way through the capillary, then no more nitrous oxide is transferred

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28
Q

Is oxygen diffusion or perfusion limited in normal health?

A

Normally, it is perfusion limited like nitric oxide; the pO2 virtually reaches that of alveolar gas when the RBC is about 1/3 the way along the capillary

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29
Q

In what situation would O2 be diffusion limited?

A

When the diffusion properties of the lungs are impaired (thickening of blood-gas barrier). Blood PO2 does not reach the alveolar value by the end of the capillary

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30
Q

What are the two stages of uptake of O2 (or CO) to the RBC?

A
  1. Diffusion through the blood-gas barrier (including the plasma and RBC interior)
  2. Reaction with hemoglobin
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31
Q

What are the normal main pulmonary artery pressures?

A

Systolic- 25 mm Hg
Mean- 15 mm Hg
Diastolic- 8 mm Hg

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32
Q

What are the normal pressures in the LA/LV/RA/RV/aorta?

A 
LA- 5 mm Hg
LV- 120
RA- 2
RV- 25
Aorta- 100
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33
Q

T/F: The walls of the pulmonary artery and its branches are thick with a large amount of smooth muscle?

A

False-Thin walls because the pressures in these vessels is very low; no smooth muscle needed because the blood is staying in the lungs and does not need to be pumped to organs that are far above the level of the heart

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34
Q

Define transmural pressure

A

The pressure difference between the inside and outside of the capillaries

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35
Q

What happens to the large vessels (MPA, for example) as the lung expands?

A

They are pulled open by the radial traction of the elastic lung parenchyma that surrounds them. This leads to low pressure around them (even lower than intrapleural pressure)

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36
Q

T/F: The behavior of the capillaries and the larger blood vessels in the thorax are similar?

A

False- they are so different they are often referred to as alveolar & extra-alveolar vessels

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37
Q

What is the difference between alveolar and extra-alveolar vessels in terms of pressure and give an example of each?

A

Alveolar: capillaries and slightly larger vessels in the corners of the alveolar walls

  • Their caliber is determined by relationship between alveolar pressure and pressure within them
  • Can be compressed with increased alveolar pressure

Extra-alveolar: arteries and veins that run through the lung parenchyma

  • Their caliber is determined by lung volume b/c this determines the expanding pull on their walls
  • Not affected by increased alveolar pressure
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38
Q

Write the equation for vascular resistance

A

Vascular resistance= (input pressure-output pressure) / blood flow

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39
Q

What is a normal pulmonary vascular resistance?

A

1.7 mm Hg/liter/min

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40
Q

What two mechanisms are responsible for the decreased pulmonary vascular resistance when increased arterial or venous pressure?

A
  1. Recruitment

2. Distension

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41
Q

Describe recruitment & distension of pulmonary vessels

A
  1. Recruitment: As pulmonary pressure rises, capillaries that are normally closed open; this is the chief mechanism for lowering pulm vascular resistance
  2. Distension: Widening of individual capillary segments; occurs at higher vascular pressures
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42
Q

What is the critical opening pressure?

A

Describes the pressure at which pulmonary artery pressure must be raised above downstream pressure before any flow occurs through the extra-alveolar vessels; this is because the extra alveolar vessels have smooth muscle and elastic tissue that resist distension and reduce the caliber of the vessels when lung volume is low
P 42

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43
Q

Name some drugs that increase pulmonary vascular resistance

A

Histamine, serotonin, norepi

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44
Q

Name drugs that can relax smothuc pulmonary ciculation

A

Acetylcholine, isoproteronol

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45
Q

T/F: The lung has equal amounts of blood flow to all the parts of the pulmonary circulation

A

False- Blood flow decreases almost linearly from bottom to top in upright human lung; reaches very low values at the apex- it is affected by posture and exercise

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46
Q

What type of pressure influences the uneven distribution of blood flow in the lung?

A

Hydrostatic pressure- the difference in pressure between top and bottom of lung is ~23 mm Hg, which is a large pressure difference for such a low pressure system

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47
Q

Describe “zone 1” of the lung aka anatomic dead space

A

Does not occur under normal conditions because pulmonary arterial pressure is just sufficient to raise blood to the top of the lung. If arterial pressure is reduced or alveolar pressure is raised, zone 1 may occur. In this zone, pulmonary artery pressure falls below alveolar pressure and squishes the capillaries, occluding blood flow

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48
Q

Describe “zone 2” of the lung

A

In this zone pulmonary arterial pressure increases b/c the hydrostatic effect and now exceeds alveolar pressure. Venous pressure is still less than alveolar pressure which leads to pressure-flow characteristics.

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49
Q

Describe “zone 3” of the lung

A

Venous pressure>alveolar pressure; flow is determined by arterial-venous pressure difference. There is increased blood flow down this region of the lung caused by distension of the capillaries

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50
Q

True or False: Expiration is a passive process during rest

A

True. The lung and chest wall are elastic and tend to return to their equilibrium positions after being expanded during inspiration

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51
Q

What is hysteresis?

A

This is the phenomenon of a difference in the pressure-volume curve on inspiration v. expiration. The lung volume at any given pressure during deflation is larger than during inflation.

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52
Q

The slope of the pressure-volume curve is also known as….

A

Compliance = Change in Volume / Change in Pressure

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53
Q

A reduced lung compliance can be seen in what conditions?

A

Increase of fibrous tissue in the lungs, pulmonary edema, atelectasis, and with high pulmonary venous pressure

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54
Q

An increased lung compliance can be seen in what conditions?

A

Pulmonary emphysema, and in the normal aging lung due to changes in the elastic tissue of the lung

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55
Q

What cells make surfactant and what is DPPC?

A

Surfactant is made by type II pneumocytes. Surfactant is a phospholipid of which dipalmitoyl phosphatidylcholine (DPPC) is an important constituent. DPPC is synthesized in the lung from fatty acids.

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56
Q

How does surfactant reduce surface tension?

A

The molecules of DPPC are hydrophobic at one end and hydrophilic at the other. When they align themselves, the intermolecular repulsive forces oppose the normal attractive forces between the liquid molecules normally responsible for surface tension.

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57
Q

Name 3 physiological advantages of surfactant

A
  1. A low surface tension in the alveoli increase the compliance of the lung and reduces the work of expanding it with each breath.
  2. They promote stability of the alveoli by reducing the tendency of small alveoli to empty into large alveoli.
  3. They help to keep the alveoli dry by reducing the hydrostatic pressure in the tissue outside the capillaries.
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58
Q

What is Poiseuille’s law for laminar flow?

A

Volume flow rate = (Driving pressure * Pi * radius^4)/ (8 *viscosity * length)

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59
Q

What is Reynold’s number and what is the equation for it?

A

Reynold’s number determines whether flow will be laminar or turbulent. A value greater than 2000 is most consistent with turbulent flow.

Re = 2rvd / n
where r is radius, v is average velocity, d is density, and n is viscosity.

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60
Q

What is the major site of resistance in the bronchial tree?

A

The medium-size bronchi contribute the most to airway resistance.

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61
Q

What % of oxygen consumption is done during quiet breathing?

A

Less than 5%

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62
Q

What is Laplace’s law?

A

Pressure = (2 x surface tension) / radius

Pressure is inversely proportional to the radius for the same surface tension

Is 4 x surface tension / radius if the sphere is a bubble

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63
Q

What is Cheyne-Stokes respiration?

A

Periods of apnea of 10-20 seconds, followed by equal periods of hyperventilation when the tidal volume gradually waxes and then wanes. This is seen in patients at high altitude (especially during sleep), it is also seen in patients with severe heart disease or brain disease.

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64
Q

Describe hypoxic pulmonary vasoconstriction

A

When the PO2 of alveolar gas is reduced, there is contraction of smooth muscle in the walls of small arterioles in the hypoxic region.

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65
Q

What is the mechanism of hypoxic pulmonary vasoconstriction?

A

Unknown; possibly inhibition of voltage gated K channels and membrane depolarization, leading to increased Ca ion concentration in the cytoplasm. Increased cytoplasmic Ca ion concentration is the major trigger for smooth muscle contraction
Nitric oxide may also be inhibited

66
Q

At what alveolar PO2 does hypoxic pulmonary vasoconstriction occur?

A

<70 mm Hg; at lower values the local blood flow may even be almost abolished

67
Q

How does NO play a role in hypoxic pulmonary vasoconstriction (HPVC)?

A

It’s an endothelium-derived relaxing factor for blood vessels. Formed from L-arginine via catalysis by endothelial NO synthase. Activates guanylate cyclase and increases synthesis of cyclic GMP, which leads to smooth muscle relaxation. Inhibitors of NO synthase augment hypoxic pulmonary vasoconstriction

68
Q

What role do pulmonary vascular endothelial cells play in pulmonary vasculature?

A

They release potent vasoconstrictors such as endothelin-1 and thromboxane A2.

69
Q

Why is HPVC important ?

A

Helps direct blood flow away from hypoxic areas of lung, making deleterious effects on gas exchange less severe. Also occurs during fetal life

70
Q

Concerning the ventilatory response to carbon dioxide:
A. It is increased if the alveolar PO2 is raised.
B. It depends only on the central chemoreceptors.
C. It is increased during sleep.
D. It is increased if the work of breathing is raised.
E. It is a major factor controlling the normal level of ventilation.

A

E is correct. The normal level of ventilation is controlled by the ventilatory response to CO2.

The ventilatory response to CO2 is increased if the alveolar PO2 is reduced, the ventilatory response depends on the peripheral chemoreceptors in addition to the central chemoreceptors, and the ventilatory response is reduces during sleep and if the work of breathing is increased.

71
Q

Concerning the ventilatory response to hypoxia:
A. It is the major stimulus to ventilation at high altitude.
B. It is primarily brought about by the central chemoreceptors.
C. It is reduced if the PCO2 is raised
D. It rarely stimulates ventilation in patients with chronic lung disease.
E. It is important in mild carbon monoxide poisoning.

A

A is correct. Ventilation increases greatly at high altitude in response to hypoxic stimulation of chemoreceptors.

It’s the peripheral chemoreceptors, not the central, that are responsible for the response. The response is increased if the PCO2 is also raised. Hypoxic stimulation is often important in patients with longstanding severe lung disease who have nearly normal values for the pH of the CSF and blood. Mild carbon monoxide poisoning is associated with a normal arterial PO2, and therefore, there is no stimulation of the peripheral chemoreceptors.

72
Q 
The most important stimulus controlling the level of resting ventilation is:
A. PO2 on peripheral chemoreceptors.
B. PCO2 on peripheral chemoreceptors.
C. pH on peripheral chemoreceptors.
D. pH of CSF on central chemoreceptors.
E. PO2 on central chemoreceptors
A

D. is correct. The most important stimulus comes from the pH of the CSF on the central receptors.

The effect of PO2 on the peripheral chemoreceptors under normoxic conditions is very small. Changes in PCO2 do affect the peripheral chemoreceptors but the magnitude is less than that for the central chemoreceptors. The effect of changes in pH on peripheral chemoreceptors under normal conditions is small, and changes in PO2 don’t affect the central chemoreceptors.

73
Q

What is the Henderson-Hasselbach equation

A

pH = 6.1 + log [ (HCO3) / (0.03 x PCO2) ]

74
Q

How does NO play a role in hypoxic pulmonary vasoconstriction?

A

It’s an endothelium-derived relaxing factor for blood vessels. Formed from L-arginine via catalysis by endothelial NO synthase. Activates guanylate cyclase and increases synthesis of guanosine

75
Q

hello

A

test

76
Q

What is Starling’s Law?

A

Net flow out = K (Pc - Pi) - δ (πc - πi)

K = filtration coefficient, δ = reflection coefficient, P = hydrostatic pressure, π = colloid osmotic pressure

77
Q

Why is HPVC important ?

A

Helps direct blood flow away from hypoxic areas of lung, making deleterious effects on gas exchange less severe. Also occurs during fetal life

78
Q

Net fluid equation for the lungs?

A 
K[(Pc-Pi)-(omega)(IIc-IIi)]
K-constant (filtration coefficient)
P-hydrostatic pressure
omega-reflection coefficient
II- pi, osmotic pressure
79
Q

What is the approximate COP within a capillary?

A

25-28 mm Hg

80
Q

What is the approximate COP of interstitial fluid in lung?

A

20 mm Hg

81
Q

Where does fluid go when it leaves the pulmonary capillaries (when it leaks out into interstitium)

A

Is removed via lymphatics in perivascular space and is drained by hilar LN

82
Q

Where does pulmonary edema accumulate in the lung in early vs late stages?

A

Early- interstitial edema, peribronchial and perivascular spaces
Late- Fluid crosses alveolar epithelium into alveolar spaces

83
Q

How is fluid pumped out of epithelial cells in alveolar space?

A

Na/K ATPase

84
Q

T/F: The lung filters blood and removes small blood thrombi before reaching the brain or other vital organs. It also traps WBC to later release them

A

True

85
Q

What is the only known example of biological activation by passage thru the pulmonary circulation?

A

Angiotensin I–>angiotensin II via ACE in surface of capillary endothelial cells

86
Q

Name some vasoactive substances that are completely or partially inactivated during passage thru the lung?

A

serotonin, norepinephrine, prostaglandins E2 & F2alpha, leukotrienes

87
Q

Name some vasoactive materials that pass through the lung w/out significant gain or loss of activity

A

Epinephrine, prostaglandin A1 & A2, angiotensin II, vasopressin

88
Q

How is the lung involved in clotting mechanisms?

A

There are a large # of mast cells containing heparin in the interstitium

89
Q

What are the 4 causes of hypoxemia?

A
  1. Shunt
  2. Diffusion impairment
  3. V/Q mismatch
  4. Hypoventilation
90
Q

Name some causes of hypoventilation

A

Drugs- morphine, barbituates
Damage to chest wall
Paralysis of respiratory muscles
High resistance to breathing

91
Q

Which equation describes the relationship between the fall in PO2 and the rise in PCO2 that occurs in hypoventilation

A

Alveolar gas equation

P 59

92
Q

T/F: Hypoventilation always reduces the alveolar and arterial PO2 except when the subject breathes an enriched O2 mixture?

A

True

93
Q

Examples of diffusion impairment?

A

Exercise, blood-gas barrier thickened, low O2 mixture inhaled

94
Q

Describe shunting of blood and how it causes hypoxemia

A

Refers to blood that enters the arterial system without going thru ventilated areas of the lung

95
Q

At sea level and body temperature, what is the PO2 in the inspired air? in the lungs? in the mitochondria?

A

150 mmHg
100 mmHg
30 mmHg

96
Q

What is the fluctuation in alveolar Po2 with each breath?

A

The fluctuation in alveolar Po2 with each breath is only about 3 mm Hg, because the tidal volume is small compared with the volume of gas in the lung

97
Q

What is a normal alveolar PCO2?

A

40 mmHg

98
Q

T/F: PO2 in the tissue/mitochondria is about 30 mmHg and identical throughout the body

A

The “tissue” PO2 probably

differs considerably throughout the body, and in some cells at least, the PO2 is as low as 1 mm Hg. However,

99
Q

What are possible causes for hypoventilation?

A

Drugs as morphine and barbiturates that depress the central drive to the respiratory muscles, damage to the chest wall or paralysis of the respiratory muscles, and a high resistance to breathing (for example, very dense gas at great depth underwa- ter)

100
Q

What is the relationship between alveolar ventilation and PCO2, derived from the alveolar ventilation equation?

A

PCO2 =

[(CO2 production) / (alveolar ventilation)] x K (constant)

101
Q

What is the respiratory exchange ratio?

A

The respiratory exchange ratio is given by the CO2

production/O2 consumption and has a normal value of 0.8

102
Q

Give the simplified form of the alveolar gas equation

A

Alveolar PO2 (PAO2) is the PO2 from the inspired gas (PIO2) minus the PO2 consumed (using respiratory exchange ratio):

PAO2 = PIO2 - [PACO2/R] + F

Where: R is the respiratory exchange ratio and F is a small correction factor

103
Q

If alveolar ventilation is suddenly increased after an episode of hypoventilation, which one comes to equilibrium first: alveolar PO2 or alveolar PCO2

A

The alveolar PCO2
takes longer to come to equilibrium due to the
large amount of CO2
in the form of bicarbonate in the blood and interstitial fluid

104
Q

Give 2 reasons for the fact that PO2 of arterial blood does not reach PO2 of alveolar gas

A
  • Incomplete O2 diffusion
  • Shunt (blood enters the arterial system without going through ventilated areas of the lung, ex. arteries perfusing bronchi or coronary venous blood that drains directly into the left ventricle)
105
Q

How many mLs of O2 is dissolved in 100 mLs of blood for each mmhg of PO2?

A

0.3 ml O2/100 mL of blood for each mmhg of PO2

106
Q

Which form of hemoglobin binds oxygen? Ferrous or ferric

A

Ferrous hemoglobin.

Ferric hemoglobin (methemoglobin) cannot bind oxygen.
Ferrous ion is oxidized to the ferric form by various drugs and chemicals, including nitrites, sulfonamides, and acetanilid.
107
Q

Above what PO2 does the Hb-O2 dissociation curve becomes flatter?

A

PO2 50 mmhg

108
Q

Give the definition of O2 capacity

A

O2 capacity is the maximum amount of O2 that can be combined with Hb.

109
Q

How many mls of O2 is combined in 1 gram of pure Hb?

A

1.39 mLs of O2.

Some measurements give 1.34 or 1.36 ml. The reason is that under the normal conditions of the body, some of the hemoglobin is in forms such as methemoglobin that cannot combine with O2.

110
Q

What is the definition of O2 saturation?

A

The O2 saturation of Hb is the percentage of the available binding sites of hemoglobin that have O2 attached and is given by:
[(O2 combined with Hb) / (O2 ×capacity)] x 100

111
Q

What is the O2 saturation of arterial blood with a PO2

of 100 mmHg? 40 mmHg?

A

The O2 saturation of arterial blood with PO2 of 100 mm Hg is about 97.5%, whereas that of mixed venous blood with a PO2 of 40 mm Hg is about 75%

112
Q

What form of hemoglobin is the R (relaxed) state/ the T (tense) state?

A

The oxygenated form is the R (relaxed) state, whereas the deoxy form is the T (tense) state.

113
Q

What is the formula for the total O2 concentration in blood?

A

[O2] = [1.39 x Hb x %Sat] + 0.003 x PO2

114
Q

What is the effect of anemia on the concentration of oxygen in blood? Effect of polycythemia? effect of carbon monoxide?

A

For an equal %HbO2 saturation:

  • Anemia and carbon monoxide –> lowers the concentration
  • Polycythemia –> increases the concentration
115
Q

What is the effect of carbon monoxide on the O2 dissociation curve?

A

Shift to the left (more tight to Hb)

116
Q

What color is Hb?

A

Purple

117
Q

Which patient is more likely to appear clinically cyanotic? the anemic or polycythemic patient?

A

Polycythemic patient

118
Q

What is the consequence of a shift of the O2 dissociation curve to the right?

A

The O2 affinity of Hb is reduced –> more unloading of O2 at a given PO2 in a tissue capillary

119
Q

What are the factors leading to a shift of the O2 dissociation curve to the right?

A

Increase in H+ concentration, PCO2, temperature, and the concentration of 2,3-diphosphoglycerate in the red cells (binds to Hb at high concentrations)

(=what would happen in an exercising muscle)

120
Q

What are conditions that affect 2,3-DPG within the red blood cell?

A

Remember 2,3-diphosphoglycerate (2,3-DPG) is a special intermediate of glycolysis in erythrocytes which is rapidly consumed under conditions of normal oxygen tension. However, when hypoxia is encountered in peripheral tissues, the concentration of 2,3-DPG can accumulate to significant levels within hours

Increase: chronic hypoxia (for example at high altitude or in the presence of chronic lung disease), Erythropoietin treatment

Decrease: hypophosphatemia, stored red blood cells (blood bank), high pyruvate kinase activity

121
Q

What is the affinity of CO for Hb compared to O2?

A

CO has about 240 times the affinity of O2 for Hb.

For example, at a PCO of 0.16 mm Hg, about 75% of the Hb is combined with CO as COHb

122
Q

What is the solubility of CO2 compared to O2?

A

CO2 is about 20 times more soluble than O2

123
Q

What are the 3 forms of CO2 carried in the blood in?

A

CO2 is carried in the blood in three forms: dissolved, as bicarbonate, and in combination with proteins as carbamino compounds.

124
Q

What is the percentage of CO2 that evolves from the blood into the lung, in the dissolved form?

A

About 10% of the CO2 that is evolved into the lung from the blood is in the dissolved form

125
Q

Differentials for respiratory alkalosis

A

decreased CO2, hypoventilation, high altitude, anxiety attack, pain, fear, hypotension, pulmonary disease, neurological disorders

126
Q

Differentials for respiratory acidosis

A

hypoventilation (head trauma, neuromuscular disease, airway obstruction, pleural disease), rebreathing or excess dead space, malignant hyperthermia

127
Q

What receptors are responsible for raising ventilation in response to metabolic acidosis.

A

peripheral chemoreceptors in response to H+ ions

128
Q

T/F: respiratory compensation in response to metabolic alkalosis occurs most of the time.

A

False: respiratory compensation sometimes occurs by a reduction in alveolar minute ventilation that raises the pCO2. However, compensation is often small and may be absent.

129
Q

What is the mechanism of respiratory compensation in response to metabolic alkalosis?

A

Reduction in alveolar minute ventilation that raises pCO2.

130
Q

T/F: CO2 diffuses about 20 times faster than O2 through tissue

A

True

131
Q

Define hypoxia versus hypoxemia

A

Hypoxia
Hypoxia[1] is a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level.

Hypoxemia
Hypoxemia is an abnormally low level of oxygen in the blood.[1][2] More specifically, it is an oxygen deficiency in arterial blood.[3] Hypoxemia has many causes, often respiratory disorders, and can cause tissue hypoxia as the blood is not supplying enough oxygen to the body.

132
Q

Discuss the causes of tissue hypoxia

A
  1. hypoxic hypoxia (low PO2 in arterial blood), by pulmonary disease
  2. reduced ability of blood to carry oxygen, as in anemia or carbon monoxide
  3. reduction in tissue blood flow (shock, local obstruction)
  4. toxic substance that interferes with the ability of the tissues to utilize available O2 (histotoxic hypoxia): cyanide
133
Q

What nerves supply the diaphragm and which cervical segments do they come from?

A

The diaphragm is supplied by the phrenic nerves from cervical segments 3, 4, and 5

134
Q

When the diaphragm is paralyzed, does the diaphragm move up or down during inspiration?

A

When the diaphragm is paralyzed, it moves up rather than down with inspiration because the intrathoracic pressure falls.

135
Q

T/F: During quiet breathing, expiration is active

A

F

136
Q

What are the most important muscles for active expiration?

A

The most important muscles of expiration are those of the abdominal wall, including the rectus abdominis, internal and external oblique muscles, and transversus abdominis.

137
Q

Which muscles assist active expiration? internal intercostal muscles OR external intercostal muscles?

A

The internal intercostal muscles assist active expiration by pulling the ribs downward and inward (opposite to the action of the external intercostal muscles assisting inspiration)

138
Q

Define hysteresis

A

The lung pressure-volume curves during inflation and
deflation are different. This behavior is known as hysteresis.
The lung volume at any given pressure during deflation is larger than during inflation.

139
Q

What does the slope of the pressure-volume curve represent?

A

Compliance

140
Q

What are the reasons for increased or decreased compliance?

A
  • Increased compliance: pulmonary emphysema, normal aging lung
  • Decreased compliance: increase of fibrous tissue in the lungs, alveolar edema, atelectasis, increased pulmonary venous pressure
141
Q

What is Laplace’s law?

A

Laplace’s law: pressure = (4 × surface tension)/radius.

142
Q

Define surface tension

A

Surface tension is the force (in dynes, for example) acting across an imaginary line 1 cm long in the surface of the liquid

143
Q

What are the physiological advantages of surfactant?

A

First, a low surface tension in the alveoli increases the compliance of the lung and reduces the work of expanding it with each breath. Next, stability of the alveoli is promoted. A third role of surfactant is to help to keep the alveoli dry.

144
Q

Where is the peripheral chemoreceptor located?

A
  1. carotid bodies at the bifurcation of the common carotid arteries
  2. in the aortic bodies above and below the aortic arch
145
Q

True/false: peripheral chemoreceptor’s response is to the concentration of oxygen in arterial rather than to venous.

A

False: response to the pO2 of artery rather than venous pO2

146
Q

True/false: peripheral chemoreceptors are responsible for all the increase of ventilation that occurs in human in response to arterial hypoxemia

A

True

147
Q

Where is pulmonary stretch receptors located?

A

Airway smooth muscle

148
Q

What’s the main reflex of pulmonary stretch receptors? And what’s the name of the reflex?

A

Hering-Breuer inflation reflex: Slowing or RR due to an increase in expiratory time

149
Q

Location of irritant receptors? What’s the reflex effect of the irritant receptor?

A

lie between airway epithelial cells, reflex effects include bronchoconstriction and hyperpnea

150
Q

J receptors: where are they located, what’s the reflex effect of J receptors?

A

in the alveolar walls, close to the capillaries (Juxtacapillary)
result in rapid, shallow breathing, although intense stimulation causes apnea

151
Q

What are the activators of J receptors?

A
  1. engorgement of pulmonary capillaries

2. increase in the interstitial fluid volume of the alveolar wall

152
Q

In what condition (disease) J receptors play a role in the rapid, shallow breathing and dyspnea?

A

Left heart failure, interstitial lung disease

153
Q

T/F: arterial baroreceptors

  1. increase in arterial blood pressure can cause reflex hypoventilation or apnea through stimulation of aortic and carotid sinus baroreceptors
  2. Decrease in blood pressure may result in hyperventilation
A

True

154
Q

True/False: lowering the PO2 may result in higher ventilation for a given PCO2

A

True

155
Q

What causes the rightward shift of the O2 dissociation curve at moderate altitude?

A

Increase in concentration of 2-3-DPG, which develops primarily because of respiratory alkalosis

156
Q

At higher altitude, which direction does the O2 dissociation curve shift?

A

Leftward shift due to respiratory alkalosis

157
Q

What’s the mechanism of the development of pulmonary edema from pulmonary hypertension?

A

arteriolar vasoconstriction is not even, and leakage occurs in unprotected, damaged capillaries. The edema fluid has high protein concentration, indicating that the permeability of the capillaries is increased.

158
Q

Where do the first pathological changes associated with oxygen toxicity occur?

A

endothelial cells of the pulmonary capillary impair gas exchange

159
Q

T/F: Collapse is particularly likely to occur at the bottom of the lung, where the parenchyma is least well expanded or the small airways are actually closed

A

True

160
Q

What causes decompression sickness?

A

Formation of nitrogen bubbles during ascent from a deep dive due to high solubility.

161
Q

What are the premonitory symptoms of convulsion from oxygen toxicity?

A

nausea, ringing in the ears, twitching of the face

162
Q

True/False: the likelihood of convulsions depends on the inspired PO2 and the duration of exposure.

A

True

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