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Lungs/Respiratory > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

What is the Inspiratory Reserve Volume (IRV)?

A

Air that can still be breathed in after normal inspiration

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2
Q

What is the Expiratory Reserve Volume (ERV)?

A

Air that can still be breathed out after normal inspiration

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3
Q

What is the Tidal Volume (TV)?

A

Air that moves into lung with each normal, quiet breath (typically 500 mL)

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4
Q

What is the Residual Volume (RV)?

A

Air in lung after maximal expiration; cannot be measured on spirometry

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5
Q

What is Inspiratory Capacity (IC)?

A

IC = IRV + TV

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6
Q

What is Functional Residual Capacity (FRC)?

A

FRC = ERV + RV

Volume of gas in the lungs after a normal expiration

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7
Q

What is the Vital Capacity (VC)?

A

TV + IRV + ERV

Maximum volume of gas that can be expired after maximum inspiration

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8
Q

What is the Total Lung Capacity (TLC)?

A

TV + IRV + ERV + RV

Volume of gas present in lungs after a maximal inspiration

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9
Q

What is the equation for determining physiologic dead space?

A

VD = VT x [(PaCO2 - PeCO2) / PaCO2]

VD = Physiologic Dead Space
VT = tidal volume
PaCO2 = arterial PCO2
PeCO2 = expired PCO2

TAco, PAco, PEco, PAco

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10
Q

What is the largest contributor to physiologic dead space in a healthy lung?

A

Apex of a healthy lung

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11
Q

What contributes to physiologic dead space?

A

anatomic dead space (fixed) and alveolar dead space (variable); it is the volume of inspired air that does not take part in gas exchange

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12
Q

What is minute ventilation (Ve) and what is the equation to calculate it?

A

Total volume of gas entering the lungs per minute

Ve = Vt x Respiratory Rate (RR)

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13
Q

What is alveolar ventilation (Va) and what is the equation to calculate it?

A

Volume of gas per unit time that reaches the alveoli (accounts for dead space)

Va = (Vt - Vd) x RR

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14
Q

What is elastic recoil?

A

Tendency for the lungs to COLLAPSE INWARD and the chest wall to SPRING OUTWARD

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15
Q

What is the significance of FRC on the pressure/volume curve?

A

At FRC, inward pull of lung is balanced by outward pull of chest and the system pressure is atmospheric

Airway and alveolar pressures are 0 and intrapleural pressure is negative (prevents pneumothorax)

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16
Q

What is compliance?

A

Change in lung volume for a given change in pressure (slope of pressure/volume curve)

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17
Q

When is compliance decreased?

A
  1. Pulmonary fibrosis
  2. Pneumonia
  3. Pulmonary Edema
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18
Q

When is compliance increased?

A
  1. emphysema

2. normal aging

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19
Q

What are the two forms of Hemoglobin (Hb)?

A

T (Taut; deoxygenated) form has low affinity for oxygen

R (Relaxed; oxygenated) form has a high affinity for oxygen

Taut in Tissues; Relaxed in Respiratory Tract

Binding of the first O2 molecule pushes Hb to relaxed state making it easier for O2 to bind to the other 3 heme groups

The only time Hb is in the taut shape is when NO oxygen molecules are bound

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20
Q

Why is the oxygen-hemoglobin dissociation curve sigmoidal?

A

Positive Cooperativity (the tetrameric Hb molecule can bind 4 oxygen molecules and has a higher affinity for each subsequent oxygen molecule bound)

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21
Q

Does 2,3 BPG stabilize or destabilize the taut form of Hb?

A

Stabilizes it, and thus, promotes O2 release

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22
Q

What are conditions that increase BPG?

A
  1. high altitude
  2. tissue hypoxia (COPD)
  3. CHF
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23
Q

Compared to adult Hb, does fetal Hb have a higher or lower affinity for BPG?

A

Lower affinity for BPG and thus a higher affinity for O2

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24
Q

What is methemoglobin?

A

Oxidized form of Hb (ferric, Fe3+) that does not bind 02 as readily, but has a higher affinity for cyanide

Iron in Hb is normally in a reduced state (Fe2+)

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25
Q

What is the classic presentation of methemoglobinemia?

A

Cyanosis, Chocolate Colored Blood and Pulse O2 = 85%

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26
Q

What drugs cause methemoglobinemia?

A

Nitrates, Benzocaine and Dapsone

Cause poisoning by oxidizing Fe2+ to Fe3+

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27
Q

How do you treat drug induced methemoglobinemia?

A

Methylene Blue

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28
Q

What mutation is associated with the inherited form of methemoglobinemia?

A

Cytochrome B5 reductase (enzyme that converts met Hg to Hg) is mutated in this autosomal recessive disease

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29
Q

When and how would you induce methemoglobinemia?

A

In cyanide poisoning, met Hg’s affinity for cyanide can be leveraged. You give nitrates followed by thiosulfate, which binds the methemoglobin + CN-, gets converted to thiocyanate and excreted by the kidney

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30
Q

What is carboxyhemoglobin?

A

Form of Hb bound to CO in place of O2

Causes decrease oxygen-binding capacity and a left shift in the oxygen-hemoglobin dissociation curve (decrease in O2 unloading to the tissues)

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31
Q

Which has a greater affinity for Hb, O2 for CO?

A

CO binds competitively to Hb with 200x greater affinity than O2

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32
Q

What is the classic presentation of carboxyhemoglobin?

A

Bright red blood, cherry red skin, recent onset headache (from CO exposure), Pulse O2 = 100% (machine can’t tell difference between O2 and CO)

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33
Q

How do you treat carboxyhemoglobinemia?

A

Treat with 100% O2 and hyperbaric O2

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34
Q

How does the myoglobin curve differ from hemoglobin curve?

A

Myoglobin is monomeric and thus does not show positive cooperativity; curve lacks sigmoidal appearance

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35
Q

What is the significance of a RIGHT SHIFT in the oxygen-hemoglobin dissociation curve?

A

DECREASED affinity of O2 (facilitates unloading of O2 to tissues)

36
Q

What is the significance of a LEFT SHIFT in the oxygen-hemoglobin dissociation curve?

A

INCREASE affinity of O2 (less O2 for tissues)

37
Q

An increase in what factors cause a right shift?

A

ACE BATs RIGHT Handed:

Acid (H+)
CO2
Exercise
2,3-BPG
Altitude
Temperature
38
Q

An increase in Fetal Hb causes what kind of shift?

A

LEFT SHIFT

Fetal Hb has a higher affinity for O2 because needs to steal O2 from mom

39
Q

An increase in carbon monoxide causes what kind of shift?

A

LEFT SHIFT

(CO binds Hb with higher affinity than O2, so there is low oxygen carried/provided to tissues, binding spots are occupied by CO)

40
Q

What is the equation for O2 content in the blood?

A

O2 content = (O2 binding capacity x % saturation) + dissolved O2

41
Q

How much can 1 g Hb bind?

A

1.34 mL of O2

42
Q

What is the normal amount of Hb in the blood?

A

15 g/dL

43
Q

What is the normal O2 binding capacity?

A

20.1 mL of O2/dL

44
Q

When there is a decrease in Hb, is there a decrease in O2 content in the blood, a decrease in O2 saturation, or a decrease in arterial PO2?

A

There is a decrease in O2 content, BUT NO CHANGE in O2 saturation and arterial PO2

45
Q

What is the equation for O2 delivery to the tissues?

A

CO x O2 content of blood

recall O2 content of blood = (O2 binding capacity x % saturation) + dissolved O2

46
Q

How does CO poisoning effect Hb concentration, %O2 sat of Hb, Dissolved O2 (PaO2), and total O2 content?

A

Hb concentration: Normal
%O2 sat of Hb: Decreased bc CO competes with O2)
Dissolved O2 (PaO2): Normal
Total O2 content: Decreased

47
Q

How does Anemia effect Hb concentration, %O2 sat of Hb, Dissolved O2 (PaO2), and total O2 content?

A

Hb concentration: Decreased
%O2 sat of Hb: Normal
Dissolved O2 (PaO2): Normal
Total O2 content: Decreased

48
Q

How does Polycythemia effect Hb concentration, %O2 sat of Hb, Dissolved O2 (PaO2), and total O2 content?

A

Hb concentration: Increased (excess RBCs)
%O2 sat of Hb: Normal
Dissolved O2 (PaO2): Normal
Total O2 content: Increased

49
Q

What are the consequences of pulmonary hypertension?

A

Cor pulmonale and subsequent right ventricular failure (jugular venous distention, edema, hepatomegaly)

50
Q

What is the equation for diffusion of gas in the alveoli?

A

Vgas = A/T x Dk (P1-P2)

where:
A = area
T = alveolar wall thickness
Dk (P1-P2) = difference in partial pressures

51
Q

In what disease is the area of alveoli decreased?

A

Emphysema

52
Q

In what disease is the thickness of alveolar wall increased?

A

Pulmonary Fibrosis

53
Q

What is meant by diffusion limited?

A

Gas does not equilibrate by the time the blood reaches the end of the capillary

54
Q

What is meant by perfusion limited?

A

Gas equilibrates early along the length of the capillary, diffusion can only be increased if blood flow increases

55
Q

What disease processes are diffusion limited?

A
  1. CO (blood is not in capillary long enough to reach EQ)
  2. Emphysema (smaller area to diffuse across)
  3. Pulmonary Fibrosis (thicker surface to diffuse across)
56
Q

What disease processes are profusion limited?

A
  1. O2 (normal healthy)
  2. CO2
  3. N2O
57
Q

What is the equation for pulmonary vascular resistance?

A

PVR = (Ppulm artery - Pleft atrium) / cardiac output

Ppulm artery = pressure in pulmonary artery
Pleft atrium = pulmonary wedge pressure

Remember ΔP = Q x R, so R = ΔP/Q (same as above)

R = 8ηl / πr4 (radius effects resistance the most bc its raised to the fourth power)

58
Q

What is the alveolar gas equation?

A

PAo2 = PIo2 - (PaCO2/R)

≈ 150 mmHg - (PaCO2/0.8)

normal PaCO2 = 40 mmHg, so PAo2 = 100 (healthy adult)

59
Q

How do you calculate the A-a gradient and what is the normal A-a value?

A

A-a gradient = PAO2 - PaO2 = 10-15 mmHg

60
Q

What are three common causes of increased A-a gradient (

A
  1. Right-to-left shunt
  2. V/Q mismatch
  3. Diffusion Limitation (e.g. fibrosis)
61
Q

What is the difference between Hypoxemia and Hypoxia?

A

Hypoxemia is a decrease in the partial pressure of arterial O2 (O2 content in the aorta is less than normal)

Hypoxia is decreased O2 delivery to the tissue

62
Q

What are examples/causes of Hypoxemia with a normal A-a gradient?

A
  1. High Altitude

2. Hypoventilation (eg. opioid use)

63
Q

What are examples/causes of Hypoxemia with an increased A-a gradient?

A
  1. V/Q mismatch
  2. Diffusion limited
  3. Right to left shunt
64
Q

What are examples/causes of Hypoxia?

A
  1. Decreased cardiac output
  2. Hypoxemia
  3. Amemia
  4. CO poisoning
  5. Methemaglobinemia
65
Q

What are examples/causes of Ischemia (loss of blood flow)?

A
  1. Impeded arterial flow

2. decreased venous drainage (if blood can’t exit, no blood can enter either)

66
Q

What is the ideal V/Q ratio?

A

V/Q = 1

for adequate gas exchange

67
Q

What is the V/Q ratio at the apex of the lung?

A

V/Q = 3

wasted ventilation

68
Q

What is the V/Q ratio at the base of the lung?

A

V/Q = 0.6

wasted perfusion

69
Q

Both ventilation and perfusion are greater or smaller at the base of the lung than the apex?

A

Greater

70
Q

What organisms thrive at the apex of the lungs?

A

Tuberculosis and other organisms that thrive in high O2

71
Q

What is the V/Q ratio in airway obstruction/shunt and does 100% oxygen improve PaO2?

A

V/Q = 0

In shunt, 100% O2 does NOT improve PaO2

72
Q

What is the V/Q ratio in blood flow obstruction and does 100% oxygen improve PaO2?

A

V/Q = infinity

100% O2 does improve PaO2

73
Q

What are the pressure changes in different zones of the lung?

A

Zone 1 (apex): PA > Pa > Pv

Zone 2 (middle): Pa > PA > Pv

Zone 3 (base): Pa > Pv > PA

74
Q

What are the 3 forms in which CO2 is transported from tissues to the lungs?

A
  1. HCO3- (90%)
  2. Carbaminohemoglobin or HbCO2 (5%); CO2 bound to Hb at N-terminus of globin not heme, CO2 binding favors the taut form (O2 unloaded)
  3. Dissolved CO2 (5%)
75
Q

What is the Haldane effect?

A

In the lungs, oxygenation of Hb promotes the dissociation of H+ from Hb, this shifts the equilibrium toward CO2 formation; therefore CO2 is released from RBCs

Bottom line: the greater amount of O2 in the lungs, causes more CO2 to be released

76
Q

What is the Bohr effect?

A

In peripheral tissue, increased H+ from tissue metabolism shifts the curve to the right, unloading O2

77
Q

Where is the majority of blood CO2 carried and in what form?

A

Majority of blood CO2 is carried as HCO3- in the plasma

78
Q

What happens to ventilation in high altitude?

A

Chronic INCREASE in ventilation bc…

Decrease in atmospheric oxygen (PO2) causes a decrease in PaO2, which increases ventilation and decreases PaCO2

79
Q

What kind of alkalosis or acidosis ensues due to high altitude?

A

Respiratory alkalosis (hyperventilation to blow off excess CO2)

Increase in renal excretion of HCO3- to compensate for respiratory alkalosis (can augment with acetazolamide)

80
Q

What changes in erythropoietin and 2,3 BPG result from high altitude?

A

INCREASE in epo, because the body will increase hematocrit and Hb in response to chronic hypoxia

INCREASE 2,3 BPG bc it binds to Hb so that Hb releases more O2

81
Q

What is the major sequelae from chronic hypoxic pulmonary vasoconstriction?

A

RVH

82
Q

What happens to the V/Q ratio during exercise?

A

V/Q ratio becomes more uniform from apex to base

exercise causes vasodilation of apical capillaries

83
Q

What happens to CO2 production, O2 consumption and ventilation during exercise?

A

CO2 production increases, O2 consumption increases and ventilation increases to meet O2 demand

84
Q

What happens to pulmonary blood flow during exercise?

A

Pulmonary blood flow increases due to increased CO

85
Q

What happens to the pH during strenuous exercise?

A

Decreases secondary to lactic acidosis

86
Q

What happens to PaO2 and PaCO2 during exercise?

A

NO CHANGE in PaO2 and PaCO2, but there is an increase in venous CO2 content and a decrease in venous O2 content (basically the body should compensate during exercise)

Lungs/Respiratory (4 decks)

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