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Physiology > Pulm Deck 2 > Flashcards

Pulm Deck 2 Flashcards

1
Q

where are alveolar (A) PO2 & PCO2 set?

where are arterial (a) PO2 & PCO2 set before they enter the alveoi?

A 
PAO2= 100 mmHg
PACO2= 40 mmHg
PaO2= 40 mmHg
PaCO2= 46 mmHg
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2
Q

what happens in shunt alveoli? what happens in dead space alveoli?

A

shunt- perfused but not ventilated (PaO2= 40, PaCO2= 45); V/Q= 0

dead space- ventilated but not perfused- PaO2= 150, PaCo2= 0); V/Q= infinity

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3
Q

what happens to the V/Q ratio in the bottom of the lung?

A
  • have more blood flow than ventilation; V/Q ratio is very low
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4
Q

what does a high V/Q ratio represent?

A
  • high alveolar ventilation; low alveolar perfusion
  • like dead space alveolus
  • ventilation exceeds perfusion
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5
Q

what happens to the V/Q ratio at the top of the lungs?

A
  • have more ventilation than blood flow (but still less ventilation than the bottom of the lung)
  • however, the relative ratio causes a high V/Q ratio
  • get over-ventilation & dead space
    (alveolar PaO2 is higher and CO2 lower)
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6
Q

The majority of oxygenated blood leaving the lung comes from the _____, this causes the arterial PO2 to be ______ than atmospheric pressure

A

base, lower

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7
Q

what is the AaDO2 and what is normal?

A
  • alveolar-arterial PO2 difference; - - normal is less than 15
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8
Q

what are the two reasons for AaDO2?

A

1) V-Q inequality

2) Anatomic shunt- veins that go directly into LV

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9
Q

how do you calculate AaDO2?

A

alveolar PO2 (gas equation= 100 mmHg) - arterial PO2 (blood draw)

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10
Q

what is hypoxemia?

A

when arterial blood oxygen (PaO2) is below 80 mmHg

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11
Q

what are the four causes of hypoxemia?

A
  1. hypoventilation
  2. diffusion limitation
  3. shut (anatomic or physiologic)
  4. V/Q mismatch
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12
Q

what 2 things happen during hypoventilation? What happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is hypoventilation caused by?

A
  1. alveolar PO2 decreases
  2. alveolar CO2 increases
    - AaDO2 is normal (gas exchange is normal)
    - arterial PO2 increases with 100% O2
    - caused by drugs that depress central drive to breathe
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13
Q

With diffusion limitation, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what is diffusion limitation caused by?

A
  • AaDO2 increases (have more alveolar, less arterial)
  • arterial PO2 increases with 100% O2
  • caused by lung edema, fibrosis, capillary block
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14
Q

With an anatomic/physiological shunt, what happens to AaDO2? What is the arterial PO2 response to 100% oxygen? what happens to arterial PCO2?

A
  • AaDO2 increases (have more alveolar, less arterial)
  • additional O2 will not increase arterial PO2 b/c shunted blood isn’t exposed to enriched O2 (a physiological shunt will decrease O2 on 100% O2)
  • PCO2 does not change b/c chemoreceptors which increase ventilation
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15
Q

what is the main cause of hypoxemia in patients with respiratory disorders?

A

V/Q inequality with LOW V/Q ratio

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16
Q

In V/Q inequality, what happens to AaDO2? Does 100% O2 help?

A
  • AaDO2 is increased (high alveolar, low arterial)

- 100% O2 helps

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17
Q

2 ways O2 is transported in blood, and which does blood gas analysis measure?

A
  1. dissolved (= blood gas, PaO2)

2. bound to hemoglobin

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18
Q

what is Henry’s law?

A

the concentration of a solute gas in a solution is directly proportional to the partial pressure of that gas above the solution (C=khP)

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19
Q

dissolved PaO2 measured as mL/min

A

3mL O2 dissolves/ 1L blood X 5 L/min= 15 mL O2/min

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20
Q

At partial pressures

< 60 mmHg: small changes in pressure lead to _______

A

release of large amounts of O2

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21
Q

what is the normal P50 for O2? what happens if it’s higher?

A

27 mmHg

- if higher, have right shift of the curve, less affinity for O2, and lower saturation

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22
Q

what is the Bohr effect?

A

decreased P50= increased affinity and a left shift is caused by

  • decreased temp
  • decreased PCO2
  • decreased DPG
  • increased pH
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23
Q

what is CO’s affinity for hemoglobin like?

A
  • affinity of CO for Hb is 200 times greater; all binding sites are occupied at 1 mmHg CO
  • affinity for O2 is also enhanced and unloading prevented
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24
Q

what is SO2? what is is normally and what is the PaO2 at 90%?

A 
oxygen saturation- the amount of O2 combined with hemoglobin/capacity
OR O2 binding sites occupied 
normal- 97.5
hyoxemia (80mm Hg PO2)- 94.5
90%= 60 mmHg= danger
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25
Q

what is the concentration of O2 when SO2= 100%?

A

1 g hb= 1.34 mL O2

15 g hb= 20.1 mL O2/ 100 mL blood

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26
Q

what is the SO2 in tissue? how much O2 is extracted from the blood?

A

SO2= 75% (15.1 mL O2/100)

= 19.5-15.1= 4.4 mLO2/100 mL blood (or 220mL O2/min)

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27
Q

how is CO2 transported in the blood?

A
  1. dissolved (10%)
  2. ** as bicarb (HCO3-) (60-70%)
  3. as carbamino compounds with proteins (carbaminohemoglobin) (20-30%)
28
Q

dissolved Co2 per 1 mmHg of PCO2

A

0.067 mL Co2/100mL of blood (20x more than O2)

29
Q

equation for bicarbonate

A

Co2+H20 H2CO3 H+ + HCO3-

30
Q

what is the haldane effect?

A
  • free Hb can bind more CO2 than HbO2

- SO lower O2 saturation, larger CO2 concentration

31
Q

what’s the chloride shift caused by?

A

an increase in H+ or HCO3- causes HCO3- to diffuse out and Cl- to move in to maintain electrical neutrality

32
Q

what happens when you get a decrease in pH?

A

H+ shifts equation left, increase CO2, causes right shift of O2 dissociation curve (higher P50), facilitates offloading, Hb carries more CO2

33
Q

what are the 4 major types of tissue hypoxia?

A
  1. hypoxic hypoxia (cyanosis from decreased PaO2)
  2. circulatory hypoxia (reduced blood flow to tissues)
  3. anemic hypoxia (blood can’t carry O2)
  4. histotoxic hypoxia (cell can use O2 due to poison)
34
Q

T/F- CO2 dissociation curve is directly proportional to PCO2

A

T

35
Q

what is tissue hypoxia?

A

insufficient O2 is available to maintain adequate aerobic metabolism

36
Q

2 factors determining O2 delivery to the tissues?

A

O2 content

blood flow

37
Q

where are the respiratory centers responsible for generating and controlling the rhythmic pattern located?

A

generating- medulla (automatic)

controlling- pons

38
Q

major sites of respiratory control for autonomic respiration

A
  1. control center- brainstem
  2. central chemoreceptors
  3. peripheral chemoreceptors
  4. pulmonary mechanoreceptors/sensory nerves
39
Q

major sites of respiratory control for voluntary respiration

A
  1. motor cortex (hyper/hypoventilation)

2. output to CST

40
Q

two groups of cells in the medulla that generate breathing pattern

A

dorsal respiratory group- inspiration

ventral respiratory group- expiration (and a little inspiration)

41
Q

two groups of cells in the pontine respiratory group

A
  • apneustic center- lower pons- excitatory effect on DRG (stimulates inspiration)
  • pneumotaxic center- higher pons- inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing
42
Q

where are the central chemoreceptors located? what are they sensitive to?

A
  • ventrolateral surface of the medulla oblongata;
  • sensitive to changes in pH in CSF (PCO2)
  • responsible for most of min-by-min control (60-70% of response)
  • H+ can cross BBB at low pH
43
Q

2 sites of peripheral chemoreceptors? what do they respond to?

A
  • carotid body*** (CN9) & aortic arch (vagus)
  • respond to decreases in PO2**, decreases in pH (carotid only), increases is PCO2
  • carotid body has robust firing when PaO2 < 70 mmHg; not important during normal conditions; has fast response
  • CB responds to arterial PO2
44
Q

what is the Hering-Breur inflation and deflation reflex? what receptors does it involve?

A
  • inflation of the lung inhibits inspiratory muscle activity (CN10)
  • deflation initiates inspiratory activity
  • pulmonary stretch receptors
45
Q

what are irritant receptors?

A
  • rapidly adapting stretch receptors
  • respond to irritants- smoke, dust, cold air
  • cause bronchoconstriction
  • asthma?
46
Q

what are J receptors and bronchial C fibers?

A
  • juxtacapillary receptors- endings are in capillary walls- inject something into pulmonary circulation, get rapid response
  • cause rapid shallow breathing (e.g. pulmonary edema)
  • bronchial C- supplied by bronchial circulation
47
Q

other receptors

A
  • nose/upper airway receptors
  • joint/muscle pain
  • pain/temperature
  • arterial baroreceptors
48
Q

what happens to the ventilatory response to CO2 (slope of response curve) when you lower PaO2? what are some things that lower the ventilatory response?

A
  • ventilation at a given PaCO2 is higher
  • ventilatory response to CO2 become steeper than 2-3 mL/min
  • lowered by sleep, aging, drugs, COPD (increased work of breathing)
49
Q

what happens to ventilation at a fixed high PCO2 when O2 is decreased? what is this called? when does it become important?

A
  • as PO2 drops, ventilation increases rapidly - (occurs when PaO2 is below 100 mmHg, versus 50-70 mmHg normally)
  • called hypoxic stimulation; is important in patients with chronic CO2 retention
50
Q

what happens to PaO2, PCO2, and pH during moderate exercise? severe exercise?

A

moderate exercise- gases don’t change but ventilation is still increased
severe exercise- cross anaerobic threshold, lactic acid released, pH decreased, ventilation increases

51
Q

what is the difference between obstructive sleep apnea and central sleep apnea?

A
  • with both, see depressed airflow for a period of time
  • with central sleep apnea, also see decreases in pleural pressure, signifying that the diaphragm is not receiving signals to contract
52
Q

what does Kussmaul breathing look like and what is it a sign of?

A
  • deep breathing with reduced frequency

- typical in metabolic acidosis

53
Q

what does apneustic respiration look like?

A
  • sustained periods of inspiration followed by brief expiration
  • losing input from vagal nerve/pneumotaxic center (inhibits DRG (inhibits inspiration)- associated with fine control of the frequency of breathing)
54
Q

what are two examples of end of the line, shakey breathing? what are they mostly due to?

A

cheyne-stokes (rapid bouts of hyperventilation), biots (slow bouts of hyperventilation)
- brain injury, neuronal damage

55
Q

what happens to barometric pressure and inspired PO2 with higher altitude?

A

both decrease

- low PO2 is the most important problem at high altitude

56
Q

how does acclimatization occur when climbing mt everest?

A
  • hyperventilation, reducing the PaCO2 via hypoxic stimulation of peripheral chemoreceptors
57
Q

what allows the PO2 of mixed venous blood at higher altitudes to be only 7mmHg lower?

A
  • polycythemia- increase in red blood cell concentration over time
  • erythropoietin from kidney increases Hb/O2 carrying capacity
58
Q

parts of the physiological response to high altitude

A
  • hyperventilation
  • polycythemia
  • shift of binding curve due to changes in 2,3 DPG
  • maximal breathing capacity increases with less dense air
  • alveolar hypoxia results in pulmonary vasoconstriction, right heart hypertrophy and pulmonary edema
59
Q

what is the diving response?

A
  • peripheral vasoconstriction due to sympathetic activity induced by apnea and enhanced by cold water on face
  • results in initial hypertension (sympathetics)
  • then vagally induced bradycardia
  • lower HR gives a higher O2 saturation
60
Q

when does hypoxic loss of conciousness occur?

A

PO2: 20-25 mmHg

61
Q

3 preventable pathophysiological mechanisms that lead to death in divers

A

1) hyperventilation- reduces CO2 drive to breath, hypoxic signal is voluntarily overridden
2) ascent blackout- PO2 in lungs decreases as you ascend, exacerbated b/c less O2 left
3) carbohydrate depletion- less CO2 production reduces hypoxic drive to breathe

62
Q

what happens to the lungs as you descend?

A
  • when mechanical compression of the wall has occurred, maintenance of pressure equilibrium is achieved by redistribution of blood volume from extra-throacic to intra-thoracic
  • leads to edema and capillary rupture
63
Q

when does decompression sickness occur?

A
  • decreased breathing over-saturates tissues with nitrogen
  • decreased pressure causes it to leak out too quickly
  • N2 can form bubbles which cause pain in joints
64
Q

what is inert gas narcosis?

A
  • increased N2 causes euphoria/loss of coordination, coma
65
Q

what are the effects of high O2 for prolonged periods of time?

A
  • in CNS- vomiting/dizzy/vision/hearing impairment (confusion/seizures/coma @ 4ATM)
  • in Lung- lower tolerance- high O2 can cause damage of endothelial cells/pulmonary capillaries/ substernal pain, impaired gas exchange, etc.
66
Q

what can hyperbaric O2 therapy be used for?

A
  • CO poisoning
  • anemic crisis
  • gas gangrene
  • impaired bone/wound healing

Physiology (22 decks)

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