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Physio > Pulm/Renal - Physiology - Pulmonary Gas Transport; Acid-Base Balance; Breathing Mechanics & Control; Respiratory Stress > Flashcards

Pulm/Renal - Physiology - Pulmonary Gas Transport; Acid-Base Balance; Breathing Mechanics & Control; Respiratory Stress Flashcards

1
Q

How much O2 is dissolved in a dL of blood?

A

0.003 mL for each mm of air pressure

(so, at 100 mmHg pO2, 0.3 mL)

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2
Q

At what partial pressure of oxygen (pO2) will the hemoglobin dissociation curve be at about the P50 (50% of Hgb bound)?

At what partial pressure of oxygen (pO2) will the hemoglobin dissociation curve be at about full saturation?

A

~27 mmHg

~55 mmHg

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3
Q
A

D.

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4
Q

What are some factors that might shift the oxygen dissociation curve to the right?

A

Increased temperature

Increased pCO2

Decreased pH

Increased 2,3-BPG

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5
Q

What are some factors that might shift the oxygen dissociation curve to the left?

A

Decreased temperature

Decreased pCO2

Increased pH

Decreased 2,3-BPG

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6
Q

What happens to ventilation at altitude?

A

It increases

(increased respiratory rate to blow off CO2)

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7
Q

How can high altitude directly affect the heart?

A

Right-sided hypertrophy due to pulmonary vasoconstriction

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8
Q

What effect do right-shifting factors have on the P50 for the oxyhemoglobin disassociation curve?

A

The P50 increases

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9
Q

If one gram of hemoglobin can carry 1.34 mL of O2, how much O2 can be carried in a dL?

A

20.1 mL

(1.34 mL/g * 15 g/dL)

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10
Q

What is the oxygen saturation of arterial blood at pO2 of 100 mmHg?

What is the oxygen saturation of mixed venous blood at pO2 ​of 40 mmHg?

A

97.5%

75%

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11
Q

What is an example condition where oxygen saturation might be low, but no cyanosis will be seen?

What is an example condition where oxygen saturation might be normal, but cyanosis can be seen?

A

Anemia

Polycythemia

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12
Q

Which is better at buffering H+, deoxyhemoglobin or oxyhemoglobin?

A

Deoxyhemoglobin

(this explains the Haldane effect –> blood is oxygenated at the lungs –> acidity increases –> more CO2 is formed from bicarbonate to be released)

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13
Q

Explain the Haldane effect.

A

Blood is oxygenated at the lungs –> *[H+] increases –> more CO2​ is formed from bicarbonate (LeChatlier)

*deoxyhemoglobin carries H+ better than oxyhemoglobin

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14
Q
A

D.

  • (C. is incorrect because H+ and HCO3- are produced in equal amounts.*
  • D. describes the Haldane effect.)*
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15
Q

When a patient is given O2, their CO2 levels will instantly rise. Why is this?

A

The Haldane effect

(deoxyhemoglobin carries H+ better than oxyhemoglobin)

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16
Q

What is the Henderson-Hasselbalch equation in terms of blood pH (give it without numbers)?

A

pH = a constant + log(kidneyFunction/LungFunction)

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17
Q

What is the Henderson-Hasselbalch equation in terms of blood pH (with numbers)?

Without numbers = pH = constant + kidney function / lung function

A

pH = 6.1 + log [HCO3-] / (0.03 * pCO2)

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18
Q

What would cause a person to move from point A to point B on the graph?

How will the body try to correct the pH if the problem is not fixed?

A

Respiratory acidosis (hypoventilation);

renal compensation (bicarbonate reabsorption)

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19
Q

What would cause a person to move from point A to point C on the graph?

How will the body try to correct the pH if the problem is not fixed?

A

Respiratory alkalosis (hyperventilation);

renal compensation (bicarbonate secretion)

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20
Q

What would cause a person to move from point A up the CO2 line (along the same line but further towards the top of the graph)?

How will the body try to correct the pH if the problem is not fixed?

A

Metabolic alkalosis;

respiratory compensation (hypoventilation)

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21
Q

What would cause a person to move from point A down the CO2 line (along the same line but further towards the bottom of the graph)?

How will the body try to correct the pH if the problem is not fixed?

A

Metabolic acidosis;

respiratory compensation (hyperventilation)

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22
Q

What will happen to bicarbonate levels in sustained respiratory acidosis?

A

They will increase (renal compensation)

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23
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.24

pCO2 60

pO2 50

HCO3- 26

A

Acute respiratory acidosis

(acidemia, elevated CO2, normal HCO3-)

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24
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.35

pCO2 60

pO2 50

HCO3- 32

A

Respiratory acidosis with partial metabolic compensation

(slight acidemia, elevated CO2, elevated HCO3-)

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25
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.6

pCO2 20

pO2 60

HCO3- 22

A

Acute respiratory alkalosis

(alkalemia, decreased CO2, normal HCO3-)

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26
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.1

pCO2 40

pO2 90

HCO3- 12

A

Acute metabolic acidosis

(alkalemia, normal CO2, decreased HCO3-)

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27
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.20

pCO2 20

pO2 90

HCO3- 8

A

Metabolic acidosis with partial respiratory compensation

(acidemia, decreased CO2, decreased HCO3-)

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28
Q

A patient presents with the following ABG.

What is your analysis?

pH 7.55

pCO2 46

pO2 88

HCO3- 36

A

Metabolic alkalosis with some respiratory compensation

(alkalemia, slightly increased CO2, increased HCO3-)

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29
Q

In general terms, describe the changes in pCO2 and HCO3- seen in respiratory acidosis.

A

pCO2 — Elevated (hypoventilation)

HCO3- — Elevated (compensation)

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30
Q

In general terms, describe the changes in pCO2 and HCO3- seen in metabolic acidosis.

A

HCO3- — Decreased

pCO2 — Decreased (compensation)

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31
Q

In general terms, describe the changes in pCO2 and HCO3- seen in respiratory alkalosis.

A

pCO2 — Decreased (hyperventilation)

HCO3- — Decreased (compensation)

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32
Q

In general terms, describe the changes in pCO2 and HCO3- seen in metabolic alkalosis.

A

HCO3- — Increased

pCO2 — Variable

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33
Q

What is a normal bicarbonate level?

A

24 mEq/L

(22 - 26)

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34
Q

Which diffuses faster, CO2 or O2?

A

CO2 (~20x faster)

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35
Q

Why is it important to check lactate levels in a patient with a severe infection?

A

To make sure the tissues are getting the oxygen they need

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36
Q

What are the four types of hypoxia?

A

Hypoxic

Anemic

Circulatory

Histotoxic

37
Q

Define each of the following types of hypoxia:

Hypoxic

Anemic

Circulatory

Histotoxic

A

Hypoxic - caused by pulmonary disease

Anemic - low oxygen-carrying capacity

Circulatory - poor blood flow

Histotoxic - inability to use oxygen (e.g. cyanide poisoning)

38
Q

Is supplemental oxygen ever not a useful treatment for hypoxia (Hypoxic, Anemic, Circulatory, Histotoxic)?

A

No. It can benefit all of these

39
Q

What does this equation describe?

PA = Pip + Pelastic

A

The alveolar pressure is equal to the intrapulmonary pressure plus the elastic

40
Q

What equation describes the mechanical pressures affecting alveolar pressure?

A

PA = Pip + Pelastic

(Note: Pip is often a negative value)

41
Q

How is compliance defined?

A

ΔV/ΔP

42
Q
A

E.

43
Q

How will a pneumothorax affect the chest wall - lung relationship?

A

The lung collapses inwards;

the chest flares out

44
Q

What effect does fibrosis have on lung compliance?

What effect does emphysema have on lung compliance?

A

It decreases;

it increases

45
Q

True/False.

When the lungs are contracting during exhalation, some small airways close early, trapping air in the alveoli.

A

True.

This is called air trapping and happens more as we age but may be present to a small degree in youth.

46
Q
A

D.

47
Q

Where is the functional residual capacity in this lung compliance graph?

A

The dashed line

48
Q

Where is the primary site of airway resistance in the respiratory system?

A

The medium-sized bronchi

49
Q
A

D.

50
Q

What is a normal FEV1/FVC?

A

80%

51
Q

What is the FEV1/FVC in a patient with restrictive lung disease?

What is the FEV1/FVC in a patient with obstructive lung disease?

A

Normal to elevated (both values decrease);

decreased

52
Q

Which disease category is categorized by air trapping, obstructive or restrictive lung disease?

A

Obstructive

53
Q
A

E.

54
Q

Can either H+ or HCO3- cross the blood-brain barrier?

What does this mean for respiratory control?

A

No;

central chemoreceptors respond to changes in CO2 only

55
Q

Describe the central chemoreceptors.

A

CO2-sensitive and pH-sensitive receptors on the ventral medulla that control minute-to-minute ventilation

56
Q

Which chemoreceptors are CO2-sensitive and pH-sensitive receptors on the ventral medulla that control minute-to-minute ventilation?

A

The central chemoreceptors

57
Q
A

D.

58
Q

Where are central chemoreceptors?

Where are peripheral chemoreceptors?

What does each sense?

A

The ventral medulla — CO2, pH

carotid and aortic bodies — O2, CO2, and pH

59
Q

Below what pO2 are peripheral chemoreceptors most active?

A

Below 50 mmHg

(only a slight response from 90 - 50 mmHg)

60
Q

Name some of the sensory receptors within the lungs.

A

Pulmonary stretch r.

irritant r.

Pulmonary J r.

Bronchial C r.

61
Q

Which is faster, peripheral or central chemoreceptor responses?

Which is stronger?

A

Peripheral;

central

62
Q

When is the activity of central and peripheral chemoreceptors magnified?

A

When paO2 is low

63
Q

Of the peripheral chemoreceptors, which is more important?

A

The carotid

(vs. the aortic)

64
Q

True/False.

Most of a patient’s respiratory rate is controlled by their FiO2.

A

False.

Most RR control comes from CO2 levels — O2 levels matter most once a patient drops below 100 mmHg paCO2

65
Q

Why should some patients with severe lung disease not be given supplemental O2?

A

They may be depending on hypoxic drive for their ventilation

(their CSF has normalized despite the chronically elevated CO2)

66
Q

Low blood pH is detected primarily by:

A

Peripheral chemoreceptors

67
Q

What is the typical resting minute ventilation?

What is the typical resting cardiac output?

A

5 - 6 L/min

5 L/min

68
Q

What type of abnormal breathing can be seen at high altitudes (especially during sleep) and also in CHF and brain damage?

A

Cheyne-Stokes respiration

(10-20 second periods of apnea and hyperventilation)

69
Q

Describe Cheyne-Stokes respiration.

A

10 - 20 second periods of apnea and hyperventilation

(can be seen in CHF, brain damage, at high altitudes, etc.)

70
Q
A

A.

71
Q

During exercise, CO can change from 5 L/min to 25 L/min.

How does oxygen consumption change during exercise?

A

From 300 mL/min to anywhere from 3,000 to 6,000 mL/min

72
Q

What happens to pulmonary capillaries when cardiac output increases?

A

Recruitment and distention

73
Q
A

C.

74
Q
A

A.

(Note: ‘capacity’ is a weird word here. The ‘capacity’ for oxygen-carrying hasn’t changed, even if the affinity has.)

75
Q

How does the body acclimitize to higher elevations?

A

Hyperventilation (immediate)

Erythrocytosis (takes 2 - 3 days)

Increased mitochondrial density

Increased 2,3-BPG

76
Q

Describe absorption atelectasis.

A

A small pulmonary duct gets blocked (e.g. by mucus) –> if the person has been receiving 100% supplemental oxygen, the gas keeps diffusing into the blood –> the alveoli collapse

(Note: this only happens with supplemental oxygen. Nitrogen partial pressures counteract the effects because the nitrogen won’t all diffuse through.)

77
Q

Describe ‘the bends’.

A

Deep diving puts the body under increased pressure

–> nitrogen is forced out into the tissues

–> while ascending, the nitrogen returns to the blood and forms expanding bubbles

78
Q

How extended are fetal lungs?

How is this changed at first breath?

A

40% of total lung capacity;

reversal of hypoxic vasoconstriction

79
Q

What is the oxygen content of the blood in a person with a 98% SpO2 and 15 g/dL hemoglobin?

A

(1.34 mL/g * 15 g/dL * 0.98 SpO2) + 0.003 (90 mmHg)

= 19.7 + 0.27

= ~20

80
Q

What is indicated by these results from patients B and C?

(Hint: Which parts of the graph are effort-dependent and which are effort-independent?)

A

They took sub-maximal measurements (potential malingering)

81
Q

True/False.

Forceful exhalation (as often seen in cases of COPD) can actually cause premature airway closure proximal to the air being expelled due to higher pressures within the thoracic cavity.

A

True.

(Think of emphysematous ‘pink puffers’ pursing their lips to increase intrapulmonary pressures.)

82
Q

True/False.

Positive pressure ventilation is the same method our bodies always use for respiration.

A

False.

Our bodies normally use negative pressure ventilation.

83
Q

Why is there typically a greater residual volume in patients with COPD?

A

Air trapping due to airway closure

84
Q

What is the diving reflex?

What cardiac presentation can it be used to disrupt?

A

When the face is immersed in cold water and the patient holds their breath, heart rate slows dramatically;

supraventricular tachycardia

85
Q

Which has better buffering capabilities, the blood or CSF?

A

Blood, due to presence of hemoglobin

(meaning CSF is more sensitive to changes in pH)

86
Q

True/False.

The ventilation response to changes in CO2 can differ dramatically from person to person based on age, fitness, race, personality, genetics, etc.

A

True.

87
Q

VO2 max is essentially a measurement of maximal:

A

Oxygen consumption

88
Q

Duing moderate exercise, describe what will happen to each of the following:

pAO2

paO2

paCO2

Arterial pH

A

No significant change

89
Q

During prolonged, strenuous exercise, describe what will happen to each of the following:

pAO2

paO2

paCO2

Arterial pH

A

pAO2 — increases

paO2 — decreases

paCO2 —decreases

Arterial pH — decreases (lactic acidosis)

Physio (12 decks)

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