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Pulmonary - Physiology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What is the formula for flow?

• formula for resistance?

A

F = ∆P/R
R = 8nl/r^4
• ∆P = difference in pressure
• R = resistance

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2
Q

What can be said about the rate of oxygen uptake and oxygen consumption and CO2 production and excretion during steady state?

A

O2 uptake = O2 consumption

CO2 production = CO2 excretion

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3
Q

What is tidal volume (TV)?
• Functional Residual Capacity (FRC)?
• Residual Volume (RV)?

A

Tidal volume ~500 mL = volume of a normal breathe

Functional Residual Capcacity (FRC) = volume of air leftover in lungs after a normal breath

Residual Volume (RV) = amount of air left in the lungs after maximum exhalation

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4
Q

What volumes compose:
• Inspiratory Capacity?
• Functional Residual Capacity?

A

Inspiratory Capacity:
• Tidal Volume + Inspiratory Reserve Volume (the extra air you could inhale above and beyond tidal volume)

Functional Residual Capacity:
• Residual Volume + Expiratory Reserve Volume (the air you could exhale if you pushed as hard has you could)

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5
Q

What volumes compose:
• Vital Capacity?
• Total Lung Capacity?

A

Vital Capacity:
• Tidal Volume + Inspiratory Reserve Volume + Expiratory Reserve Volume

Total Lung Capacity:
•Inspiratory Reserve Volume + Tidal Volume + Expiratory reserve volume + Residual Volume

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6
Q

T or F: Residual Volume can’t be measured with a spirometer

A

True

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7
Q

What is the normal FEV1/FVC ratio?

A

80% which means you exhale most of your breathe in the 1st second

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8
Q

Someone has a FEV1/FVC ratio that is less than 0.7, name 4 diseases they might have?

A

COPD:

1) Emphysema
2) Chronic Bronchitis
3) Bronchietasis
4) Asthma

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9
Q

Someone has an FEV1/FVC that is greater than 0.8, what are some possible pathologies that could cause this?

A

Mechanical Breathing Disorders:
• Weakness, Neuromuscular

Interstitial Diseases:
• Pulmonary Fibrosis
• ARDS
• Sarcoidosis 
• Hypersensitivity Pneumonitis
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10
Q

How can the physiological dead space be measured?

A

End tidal Pco2 / arterial Pco2

• Less CO2

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11
Q

How would a pulmonary embolus affect alveolar dead space?

A

It would increase because no blood is supplying that lung tissue

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12
Q

What is the formula for Minute Ventilation?

• Alveolar ventilation?

A

MINUTE VENTILATION:
Vmv = TV x f

  • TV = tidal volume
  • f = respiratory rate

ALVEOLAR VENTILATION:
Valv = (TV - dead space)*Respiratory Rate

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13
Q

T or F: if you want to take up a greater amount of O2 increasing breathing rate is the most important factor.

A

False, Depth of breathing is a more important factor in increasing Alveolar Ventilation

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14
Q

What is the transmural pressure between breaths if the elastic recoil of the lungs is X.

A

X - the transmural exactly opposes the elastic recoil of the lungs, this keeps the lungs from collapsing

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15
Q

How many cm H2O is equivalent to 760 mmHg?

A

1033 cmH2O = 760 mmHg

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16
Q

What is the primary driving force of airflow into and out of the lung?

A

• Pressure Difference between the mouth and Alveoli

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17
Q

What is the formula to calculate Transplural pressure?

A

Ptp = Palv - Pip

Intrapleural Pressure = Pressure outside the lungs
Alveolar Pressure = Pressure Inside the lungs

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18
Q

What is Ptp (transpleural pressure) between breaths?

A

Ptp = 0

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19
Q

Name the nerve and muscles responsible for inspiration?

A

Scalene
Sternocleidomastoids
EXTERNAL INTERCOSTAL MM.

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20
Q

Name the muscles responsible for expiration?

A

NONE - at rest

During Ex.:
• INTERNAL INTERCOSTALS
• External Obliques
• Transverse abdominus

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21
Q

When is the maximal magnitude of Alveolar pressure achieved in inspiration?
•When is elastic recoil of the lung maxed out?

A

Palv = most negative 1/2 through inspiration

Elastic Recoil = Maximal at the end of inspiration

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22
Q

What is the difference in response of a compliant lung compared to a non-compliant lung with the same Transpleural pressure?

A

Compliant Lung will inflate more with the same applied pressure

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23
Q

What is hysteresis?

• explain why we see it?

A

Hysteresis:
• Asymmetry of pressure-volume curves for inspiration and expiration

• Caused by surface tension that is higher in the closed lung which reduces its compliance

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24
Q 
Explain what happens to the following in restrictive disease. 
• FVC
• TLC
• RV 
• FRC
A

They have difficulty getting air in so all these values are decreased.

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25
Q 
Explain what happens to the following in obstructive disease. 
• FVC
• TLC
• RV 
• FRC
A

FRC- increased (more air is just hanging out in the lungs)

TLC - Increase (barrel chested)

RV - Increased (b/c its just more empty space)

FVC - Decreased b/c FEC is decreased

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26
Q

Why do people with emphysema purse their lips?

A
  • To prevent airway collapse of LARGER AIRWAYS during FORCED expiration
  • AIRWAY COLLAPSE happens because there is not enough pressure generated in the airway to push out on the walls and prevent collapse
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27
Q

Differentiate the 4 types of COPD based on their effect on flow.

A

FLOW = Q = Patm - Palv / R

∆P - decreased in emphysema
R - increased in asthma and bronchitis

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28
Q

What two factors determine lung compliance?

A
  • Tissue Properties: connective tissue and interdependence by shared walls of the alveoli
  • Surface Properties: surface tension determines this
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29
Q

What happens to alveoli that are not coated by surfactant?

A

Atelectasis

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30
Q

What is the formula for collapsing pressure?

A

P = 2T/r

  • T = surface tension
  • r = radius of the sphere
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31
Q

What airway has the highest resistance to fluid flow?

A

Medium Bronchi

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32
Q

What is the normal respiratory quotient (RQ)?

• what is this determined by?

A

normal RQ = 0.8

Determined by what we eat.
• RQ carbs = 1
• RQ fat = 0.7
• RQ protein = 0.8

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33
Q

What is the normal partial pressure of oxygen in air?

• how do we come up with this number?

A

159 mmHg = 760 mmHg x 0.21

or for inhaled air:

150 mmHg = (760 mmHg - 47 mmHg) x 0.21

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34
Q

T or F: at the same partial pressure there is the same amount of dissolved CO2 in water as there is O2.

A

False, solubility depends on a constant - remember Henry’s law Cx = alphaPx

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35
Q

What is Fick’s law?

A

gas flow (vol/time) = (A/z) x D x (P1 - P2)

  • A = Area available for diffusion
  • z = thickness of barrier
  • D = diffusion constant
  • P = partial pressure
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36
Q

What is the diffusion quotient in Fick’s law dependent on?

A
  • Solubility of the Gas

* Size of the gas

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37
Q

Which diffuses faster into blood or tissue CO2 or O2?

A

CO2, it dissolves about 20x faster

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38
Q 
What is the partial pressure of O2 and CO2 in:
• Air
• Alveoli 
•Pulmonary Veins/Systemic Arteries
• Pulmonary Arteries/ Systemic Veins
A

Air:
• PO2 = 160 mmHg
• PCO2 = 0.3 mmHg

Alveoli:
• PO2 = 105 mmHg
• PCO2 = 40 mmHg

Pulmonary Veins/ Systemic Arteries:
• PO2 = 100 mmHg
• PCO2 = 40 mmHg

Pulmonary Arteries / Systemic Veins:
• PO2 = 40 mmHg
• PCO2 = 46 mmHg

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39
Q

What determines the alveolar partial pressure of CO2 (PACO2)?

A

• The amount produced in the body and alveolar ventilation

PACO2 ~ Vco2 (rate of CO2 production) / Valv (rate of alveolar ventilation)

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40
Q

What happens to PACO2 as alveolar ventilation increases?

A

PACO2 is reduced by increased alveolar ventilation because you get more CO2 out and more oxygen in

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41
Q

What is the driving stimulus for respiration?

A

PCO2

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42
Q

Define Hyperventilation and Hypoventilation?

A

Hypoventilation:
• alveolar ventilation is to low for CO2 production

Hyperventilation
• Alveolar ventilation is excessive for CO2 production

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43
Q

What 3 factors determine the alveolar partial pressure of oxygen (PAO2)?
•What is the formula?

A

PO2 of inspired air

Alveolar Ventilation - more ventilation = greater PO2

Cellular O2 consumption - increased then PAO2 will decrease because more gets sucked into the blood

Formula:
• PAO2 = PIO2 - PACO2/R

  • PIO2 = inspired O2
  • PACO2 = alveolar CO2
  • R = CO2 production/O2 consumption (typically 0.8)
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44
Q

Hypoxemia is defined as what arterial O2 sat. and below?

• causes?

A

100 mmHg and below is hypoxemia.

  • High Altitude - low PIO2
  • Alveolar Ventilation Poor - hypoventilation
  • Diffusion Defect - fibrosis
  • Right to Left Shunt
45
Q

What is the A-a gradient?

A
  • Difference between PAO2 and PaO2

* if oxygen is having trouble diffusing or if there is a R to L shunt you’ll see this

46
Q

What formula is used to measure the severity of acute lung injury?

A

PaO2/FiO2
• FiO2 = fraction of O2 in inspired air

• e.g. 100mmHg/0.21 = 476 mmHg is normal

47
Q

What is Hypercapnia?

A

Hypercapnia = higher than normal PCO2

48
Q

T or F: even during the hardest exercise, there is still time for the O2 in blood to equilibriate with blood in the alveolar capillaries.

A

True

49
Q

Differentiate perfusion limited and diffusion limited gas transfer.

A

Perfusion Limited:
• Limited by the amount of blood coming in
• THIS IS THE TYPICAL CASE for blood OXYGENATION because there is plenty of time for equilbration, the limiting factor is more blood coming in

Diffusion Limited:
• Limited by how fast the gas can get across the barrier

50
Q

What are some examples where gas transfer in the lung is diffusion limited?

A
  • High Altitude
  • Fibrosis
  • Emphysema
51
Q

What is bronchial circulation?

A

Systemic circulation from the ascending aorta that supplies LARGE extrapulmonary conducting airways

52
Q

Why is pulmonary tissue rarely infarcted?

A

Dual Blood Supply prevents infarction

53
Q

How do pulmonary vascular pressures compare to systemic pressures?
• what happens if this low pressure is not maintained?

A

Pulmonary Vascular Pressures:
• Typically are 10mmHg to 14 mmHg

If not maintained you get FLUID LEAK into the interstitial space leading to SYMPTOMS of HEART FAILURE

54
Q

How is pulmonary vascular resistance (PVR) calculated?

A

PVR = (Ppa - Pla)/Cardiac Output

Ppa = pulmonary artery pressure
Pla = Left atrial Pressure (pulmonary wedge pressure)
55
Q

What value of pulmonary vascular pressure defines pulmonary HTN?
• what is a PRIMARY cause of this disease?

A

greater than 25 mmHg defines pulmonary HTN

PRIMARY CAUSE:
• Inactivating mutation of the BMPR2 gene that normally functions to down regulate smooth muscle proliferation

56
Q

What are 5 causes of secondary pulmonary HTN?

A
  • COPD
  • Mitral Stenosis
  • Recurrent Thromboemboli
  • Auto-immune Disease
  • Left-to-Right Shunt
57
Q

NOTE: Pulmonary endothelial cells convert angiotensin I to angiotensin II, inactivate bradykinin, and remove PGs and LTs.

A

NOTE: Pulmonary endothelial cells convert angiotensin I to angiotensin II, inactivate bradykinin, and remove PGs and LTs.

58
Q

What is the MOST IMPORTANT regulatory factor of PULMONARY blood flow?

A

HYPOXIA-INDUCED PULMONARY VASOCONSTRICTION => involves the opening of Ca2+ channels causing Ca2+ release leading to smooth muscle contraction

note: this is the opposite effect that we see in the systemic circulation

59
Q

T or F: the protective mechanism of Hypoxia-Induced Pulmonary Vasoconstriction may fail if lung disease is widespread.

A

True

60
Q

What part of the lung is most perfused?

• what risk is there if arterial pressure drops below alveolar pressure?

A

Apex - Zone 1

At APEX there is a risk that arteriole pressure may drop below venous pressure leading to INCREASED RISK OF COLLAPSE

61
Q

Differentiate the relative PA, Pa, and Pv in the 3 zones of the lung.
• What drives blood flow in Zones 1 and 2?

A 
Zone 1 (apex): 
• PA > Pa > Pv

Zone 2 (middle):
• Pa > PA > Pv
• Blood flow driven by difference in arteriolar and alveolar pressures

Zone 3 (lower):
• Pa > Pv > PA
• Blood flow driven by difference in arterial and venous pressure

62
Q

Explain why ventilation is higher for basal alveoli?

A

APICAL alveoli are distended because the APICAL plural pressure is more subatomospheric

  • More distention = less compliance so there is LESS VENTILATION in the APEX of the lung
  • The opposite is true at the base of the lung
63
Q

Which part of the lung is overinflated and which is overperfused?
• How does this affect the ventilation and perfusion ratios in these two areas?
• what is the normal V/Q?

A

APEX - overinflated
• Too much ventilation (despite it being low) compared to perfusion (which is even lower than vent.) => INCREASED V/Q ratio

BASE - underperfused
• LOW V/Q ratio

Normal V/Q = 0.8

64
Q 
What situations would lead to the following V/Q ratios? 
• V/Q = infinity 
• V/Q = 1.5 
• V/Q = 0.5 
• V/Q = 0
A

V/Q = infinity => Pulmonary Embolus - there is no perfusion

V/Q = 1.5 => decreased perfusion and/or increased ventilation

V/Q = 0.5 => increased perfusion and/or decreased ventilation

V/Q = 0 => Choking - there is no ventilation

65
Q

Why does TB flourish in the lung APEX?

A

because it is a highly oxygenated environment

66
Q

What is the A - a gradient?

A

Difference in alveolar and arteriolar O2 partial pressure

= PAO2 - PaO2 ; should be CLOSE TO ZERO

67
Q

How would you expect the A - a gradient to be affected in barbituate or opiate overdose?
• what would be the primary problem?

A

A - a gradient should be normal

HYPOVENTILATION (mechanical) is the main problem leading to Respiratory Acidosis

68
Q

What are the 2 broad issues that can cause diffusion defects?
• how is the A - a gradient affected?

A
  1. LOW PO2 (high altitude) - A-a gradient is NORMAL
  2. Problems with membranes - reduction in area, increase in thickness - A-a gradient INCREASED

think about Fick’s law DA∆P/z; area and thickness are related to membrane while ∆P is controlled by the partial pressure of O2

69
Q

T or F: diffusion defects seen in emphysema can be corrected by use of supplemetal O2.

A

True, Oxygen will fix diffusion defects but WILL NOT FIX SHUNTS

70
Q

A 12 year old with trisomy 21 an O2 saturation of 89%, when given supplemental O2 this saturation stays at 89%. What is happening?

A

Cardiac Shunting:
• Kid probably has a VSD or ASD that has progressed from a L to R shunt to a R to L shunt (Eisenmenger’s)

SHUNT DOES NOT CORRECT BECAUSE BLOOD THAT IS MAKING IT TO THE LUNGS IS GETTING FULLY OXYGENATED, HOWEVER SYSTEMIC VENOUS BLOOD CONTINUES TO MIX AND DILUTE THIS BLOOD DUE TO SHUNTING

71
Q

What is the most common cause of hypoxemia?
• does this occur in COPD?
• can it be corrected?

A
  • Ventilation - Perfusion Mismatching
  • YES this occurs in COPD
  • Corrected with 100% Oxygen
72
Q

Explain how edema fluid is cleared from the lungs.

A
  1. ENaC channel is expressed on type I and II pneumocytes
  2. H2O following into pneumocyte
  3. Na+/K+ ATPase moves Na+ into blood and H2O follows
73
Q

T or F: the partial pressure of O2 in the blood is a measure of both dissolved and bound oxygen.

A

FALSE, PO2 is a measure of DISSOLVED oxygen only, oxygen that is bound to Hbg does not contribute

74
Q

What term refers to both dissolved oxygen and oxygen bound to Hgb?
• how is this calculated

A

Oxygen content = PO2 and HbgO2 or:

= O2binding capcity x %saturation + dissolved O2

75
Q

What drives diffusion of oxygen out of the alveolus and into the blood: O2 content or dissolved oxygen?

A

DISSOLVED OXYGEN is the only oxygen that contributes to diffusion b/c it is the only oxygen generating a partial pressure

• Hbg acts as an oxygen sink to keep PO2 dissolved in blood low to facilitate binding

76
Q

T or F: there is a large reserve for oxygen as activity increases?

A

True, Hb is still 75% saturated as blood leaves the tissue capillaries

***This decreases during exercise

77
Q

Does a higher P50 indicated an increased or decreased affinity for Oxygen?

A

Higher P50 leads to a DECREASED affinity for Oxygen

This is known as the RIGHT shift

78
Q

What some things that cause a right shift of the Hbg binding curve?

A

TAP
• Temperature - conformational change of Hbg
• Acidosis - Bohr Effect
• Phosphoglycerate - binds Hbg

79
Q

What is the Bohr Effect?

A

Both H+ and CO2 can bind to Hbg and decrease Hbg affinity for O2

80
Q

Explain the differences of CO poisoning and anemia on their effect of the O2 binding curve.

A

CO Poisoning:
• LOCKS hgb in high affinity conformation and RUINS the sigmoid binding curve

Anemia:
• Just lowers the amount of Oxygen Content in the blood

81
Q

What are the 3 mechanisms of CO2 transport in the blood?

A
  1. Dissolved CO2 (5-10%)
  2. Hbg/Protein binding (10 - 20%)
  3. Bicarbonate Formation (80-90%)
82
Q

What enzyme is responsible for the following rxn:

H2O + CO2 H2CO3 HCO3- + H+

A

Carbonic Anhydrase

83
Q

Explain the following Steps in CO2 transport via Bicarbonate:
• Rate limiting step in bicarb. formation
• Where this occurs?
• How HCO3- leaves cells?

A

Rate Limiting Step:
CO2 + H2O —> H2CO3

Where:
• Occurs INSIDE OF CELLS ONLY because CARBONIC ANHYDRASE only exists in cells

CO2 most often just diffuses back out of cells when the equilibrium favors conversion of HCO3- to CO2 (aka low CO2 tension) HCO3- Can also leave the cell via the BAND 3 PROTEIN (HCO3-/Cl-) exchanger

84
Q

What is Hamburger’s Phenomenon?
• when does it occur?
• How does this pertain to the Bohr effect?

A

HCO3- exits cells and Cl- enters, this causes cellular swelling

Exchange happens via Band 3 Protein

*Contributes to Bohr Effect b/c the H+ left behind then binds to Hbg to decrease Hbg affinity for O2

85
Q

Differentiate the Shape of the O2 and CO2 binding curve.

• Consequences of this on PO2 and PCO2?

A

O2 curve:
•Sigmoidal so stays steady/ Maxes out at high pressures

CO2:
• Linear means that changes over broad range will have a great effect on CO2 content

86
Q

What is the Haldane effect?

A
  • Deoxygenation of blood improves its ability to carry CO2
  • Low O2 saturation causes left shift of Hbg binding curve
  • H+ binding is increased by the reduction in O2 binding
  • Increased H+ binding increases CO2 removal by blood
  • Oxygenated blood has a reduced affinity for CO2
87
Q

What is the the ratio of HCO3 excretion in kidney vs. CO2 excretion in the lung?

A

HCO3 excretion in Kidney = 100 mEq/day

CO2 excretion in lung = 10,000 mEq/day

88
Q

What has the greatest control over acid-base balance in the blood?

A

Alveolar Ventilation b/c it controls the rate of CO2 elimination

89
Q

What is the compensatory mechanism for respiratory acidosis?

A

HCO3- retention in the kidney

90
Q

What are some lung disease that result in respiratory acidosis?

A

ARDS
COPD
PULMONARY EDEMA
PNEUMONIA

91
Q

What are some lung diseases that result in respiratory alkylosis?
• Compensation?

A 
Hyperventilation:
• Neurological 
• High Altitude 
• Pneumonia 
• Pulmonary Embolism 
• Severe Anemia

Kidney compensates by increasing HCO3- excretion

92
Q

What are some causes of Non-anion gap metabolic acidosis?

A

Chronic Diarrhea
Renal Failure

Results in compensatory hyperventilation

93
Q

What are the central respiratory centers?

• what role do they play?

A

Medulla Oblongata:
• DRG (dorsal respiratory group) = fire during inspiration
• VRG (ventral respiratory group) = rhythm generating neurons that get activated by large increases ventilation

Pons:
• Apneurtic center - terminates a breath, fine tunes breathing
• Pneumotaxic center - modifies activity of apneurtic center.

CORTEX CAN TAKE OVER WHEN WE DECIDE TO

94
Q

What is the most important 1) factor in normal breathing rate 2) stimulus controlling normal breathing

A
  1. PCO2 = most important factor controlling normal breathing because it can cross the BBB and get converted to H+ and HCO3- in the CSF
  2. H+ is the actual stimulus that triggers an increase in breathing when PCO2 is high

Note: HCO3- in blood and CO2 bound to Hbg are NOT important because they can’t cross the BBB

95
Q

What indicators of Hypoxia do the carotid bodies respond to?
• When does this response become activated?
• How rapid is this response once the threshold for response is reached?

A

Decreased PO2 > Increased PCO2 > Decreased pH

Response becomes activated:
• PO2 below 60mmHg (More important in EXERCISE)

• Response is VERY RAPID once threshold for response is reached

96
Q

What response do the aortic bodies have to decrease PO2, Increased PCO2 and Decreased pH?

A

Decreased PO2 and PCO2 increase respiration but pH HAS NO EFFECT ON AORTIC BODIES

97
Q

Why does taking a deep breath slow down breathing?

• what is this called?

A

Hering-Breuer reflex = slowed frequency of breathing due to increased stretch in the lungs

98
Q

T or F: irritants can increases respiration rate.

A

True, irritant receptors in the lungs increase RR

99
Q

What is the role of Juxtapulmonary Receptors (J receptors) and when are they activated?

A

J Receptors:
• Activated when there is a lot of INTERSTITIAL FLUID

What Happens:
• SHALLOW RAPID BREATHING

100
Q

Would you expect anemia to have an effect on breathing via peripheral receptors?

A

NO - receptors respond to PO2 not bound O2, PO2 is not affected in anemia

101
Q

What is more tightly controlled PO2 or PCO2?

A

PCO2 - controlled by detection in central neural center

102
Q

What is the problem with giving a person with severe COPD 100% O2?

A
  • These people may have CO2 detectors that have RESET to respond only to very high PCO2
  • THEY RELY on PERIPHERAL receptors then to detect PO2 to tell them to breath
  • If we make PO2 too high then they may stop breathing

This could cause sudden death

103
Q

***Why do sick people hyperventilate?

A

Fever increases PCO2 stimulating Breathing

104
Q

***How might you change someone’s diet to raise their RQ?

A

More carbs = higher RQ

Recall RQ = O2 utilization / CO2 production

105
Q

***Respiratory rate rises when you begin to exercise, what is the most immediate reason for this?

A

JOINT RECEPTORS DETECT MOVEMENT

106
Q

***T or F: Levels of O2 can be detected centrally and peripherally, while levels of CO2 can only be detected peripherally.

A

FALSE, the opposite is true

107
Q

***T or F: Some with an O2 sat. of 89-90% at sea level will need supplemental O2 before getting on a plane.

A

True

108
Q

What are the effects of exercise Systemic Arterial and Venous PCO2?
• PO2?

A

Systemic Arterial PCO2 - decreases due to hyperventilation

Systemic Venous PCO2 - Increase due to increased cellular respiration

Arterial PO2 is constant

109
Q

What is the adaptive response to high altitude?

A

Hyperventilation:
•Decrease in PCO2 and increase in pH cause respiratory alkylosis but decrease ventilation

Renal Compensation:
• Respiratory alkylosis compensated by renal excretion of HCO3-

EPO Sythesis:
• Stimulated in response to hypoxia

Increased 2,3 DPG production by Red Cell = RIGHT SHIFT

Pulmonary - Physiology (4 decks)

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