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CCN > Respiratory AP > Flashcards

Respiratory AP Flashcards

1
Q

What happens during inflammation?

A

Response to cellular injury, mediators (cytokines, etc) released. Area increased permeability, vasodilation. WBCs rush to area, clot and scar formation

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2
Q

What are the parts of the upper respiratory system?

A

Nose, nasal cavity, mucus membranes, sinuses, pharynx, larynx, cartilages (thyroid, cricoid, epiglottis)

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3
Q

What does the epiglottis do?

A

Closes the larynx during swallowing

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4
Q

What are the parts of the lower respiratory system?

A

Trachea, primary bronchus (L/R), tracheobronchial tree, terminal bronchioles, respiratory bronchioles, alveolar ducts, alveoli

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5
Q

Which cells produce mucus?

A

Goblet cells

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6
Q

When does the mucus membrane end?

A

Ends at terminal bronchioles. Respiratory bronchioles is the first place where gas exchange can happen

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7
Q

What is the carina?

A

Bifurcation to the L and R primary bronchus, landmark for ETT placement

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8
Q

What is the difference between the L and R bronchus?

A

R bronchus is wider and straighter

  1. Increased risk of aspiration into LRL
  2. Risk of intubation into R lung
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9
Q

What do the respiratory bronchioles do?

A

First site of gas exchange, 35% of gas exchange happens here

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10
Q

What are alveoli?

A

Site of gas exchange (65%), lined with epithelial cells in contact with capillaries

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11
Q

What are the Pores of Kohn?

A

Tiny openings allow air circulation, gas + pressure equalization, connecting alveoli in collateral ventilation

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12
Q

What is collateral ventilation in the alveoli?

A

Facilitated by Pores of Kohn, allows alveoli to still function as gas exchange unit even if some are collapsed or shunted

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13
Q

What are the types of alveolar cells?

A

Type 1: Gas exchange, diffusion
Type 2: Produce type 1 cells, surfactant. Highly metabolic and sensitive to decreased CO and perfusion
Type 3: Alveolar macrophages transport trapped particles into lymphatic vessels

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14
Q

What is surfactant?

A

Hydrophobic phospholipid molecule repels water and decreases surface tension in alveoli. Produced by type 2 cells, prevents fluid seeping in from capillaries

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15
Q

What is the half life of surfactant?

A

14 hrs, therefore body must keep producing

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16
Q

What is the hilius?

A

Area where tubular parts of the bronchus enters the lungs and visceral pleura folds over into parietal pleura

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17
Q

What is the pleural membrane consist of?

A

1 continuous membrane including visceral pleura and parietal pleura, folding over at the hilius

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18
Q

What is visceral lung pleura attached to?

A

Lung surface

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19
Q

What is parietal lung pleura attached to?

A

Thoracic wall, helps to ventilate and regulate pressure

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20
Q

What is the pleural cavity and what does it do

A

Space in between visceral and parietal pleura containing 30-50cc serous fluid. Functions to decrease friction and protect from thoracic infections

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21
Q

How are the lungs supplied with blood?

A
  1. Bronchial arteries carry oxygenated blood and nourish trachea to terminal bronchioles and lung tissues
  2. Pulmonary arteries carry deoxygenated blood but it’s enough to nourish alveolar ducts, alveoli, and respiratory bronchioles
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22
Q

What does lymphatic circulation do in the lungs?

A
  1. Remove foreign particles, cell debris
  2. Remove excess fluid to keep interstitial space dry

Nodes in the hilius

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23
Q

How does the diaphragm inhale/exhale?

A

Innervated by phrenic nerves C3-C5, moves down with inspiration and relaxes with expiration. Pressure changes create respiration

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24
Q

What are other muscles of respiration besides diaphragm?

A

External intercostals (inspiration, T2-T11), internal intercostals (expiration), abdominal wall muscles, accessory muscles

25
Q

How does the CNS control breathing?

A
  1. Nerve supply (Phrenic C3-C5)
  2. ANS
  3. Brain stem
  4. Central and peripheral chemoreceptors
26
Q

Which nerves control diaphragmic breathing?

A

Phrenic C3-C5

27
Q

Which cranial nerves control gag reflex?

A

CN IIIIV Glossal pharyngeal

CN X Vagal

28
Q

How does the ANS control respiration?

A

Bronchial muscles constrict (PNS) or dilate (SNS)

29
Q

How does the brain stem control respiration?

A
  1. Medulla and pons regulate rate / rhythm

2. Stretch receptors in airways stimulated by changes in lung volume and prevent over inflation (Herring Breuer reflex)

30
Q

What are the central chemoreceptors that control respiration?

A

Located in medulla, main chemoreceptor that responds to changes in PCO2. +++ sensitive to PCO2 and acidosis, increases RR to “blow off” CO2. Will respond to decreased PO2 also if resulting in lactic acidosis

31
Q

What are the peripheral chemoreceptors that control respiration?

A

Located in aorta and carotid body, respond to changes in PO2 and PCO2. Controls “hypoxic drive”, responds to very low levels of PO2 and drastic changes in PCO2

32
Q

What is hypoxic respiratory drive?

A

Peripheral chemoreceptors take over for pts with chronic CO2 retention, central chemoreceptors “go dormant”
e.g. COPD, emphysema

33
Q

What factors keep the lung interstitium dry?

A
  1. Hydrostatic pressure
  2. Colloidal oncotic pressure
  3. Capillary wall permeability
34
Q

What factors affect Vt? (Normal amount of air displaced during insp/exp)

A
  1. Compliance (ability to stretch)
  2. Elastance (ability to return to normal state)
  3. Resistance (amount of pressure needed to move air in/out)
35
Q

What factor influences lung compliance?

A

Surfactant (increase compliance)

Normal = 15-25 mm H2O

36
Q

As resistance increases compliance ?

A

Compliance decreases

37
Q

What is Poiseuille’s law regarding resistance?

A

As diameter increases, flow increases, resistance decreases

38
Q

What happens to the lung factors during emphysema?

A

Increase compliance (easy to breathe in), decrease elastance (hard to breathe out)

39
Q

What are the 2 ways ATP is produced?

A

Glucose undergoes glycolysis to form pyruvic acid which then:

  1. Aerobic respiration (krebs) uses O2 to create 38 ATP
  2. Anaerobic respiration creates 2 lactic acid and 2 ATP
40
Q

What does increased serum lactate levels indicate?

A

Decreased O2 perfusion leading to anaerobic metabolism. Will lead to lactic acidosis which will decrease muscle contractility and decrease CO

41
Q

How is oxygen transported in the body?

A

3% freely in plasma (PO2) and rest bound to hemoglobin (97%) (SaO2)

42
Q

How can oxygenation be measured?

A
  1. ABG measures SaO2 (partial pressure of O2 on PLASMA)

2. Pulse saturation measures SpO2 (% of O2 bound to hemoglobin per pulse)

43
Q

What does the oxy-hemoglobin curve indicate?

A

Increase in PO2 does not always result in increase SpO2.

44
Q

What things increase hemoglobin affinity?

A

Alkalemia

  1. Decreased temp
  2. Decreased PCO2
  3. Decreased 2,3 DPG
  4. Increased pH
45
Q

What things decrease hemoglobin affinity?

A

Acidemia

  1. Increased temp
  2. Increased PCO2
  3. Increased 2,3 DPG
  4. Decreased pH
46
Q

What is 2,3 DPG?

A

Molecule phosphate released from RBCs during hypoxia

47
Q

How is CO2 transported in the body in %?

A

CO2 is normally a volatile acid (gaseous).

5% is dissolved in plasma as PCO2.
25% bound to hemoglobin as carbamino-hemoglobin
70% bound to H2O as carbonic acid (H2CO3)

48
Q

What is carbonic acid?

A

CO2 binds H2O to partially dissolve into a more stable weak acid (H2CO3 Carbonic acid) which can travel and partially dissociate to H+ and bicarb HCO3-. Increased CO2 will lead to more H2CO3 being formed which increases H+ ions in the body leading to acidosis

49
Q

How does CO2 and elements travel up to the lungs for gas exchange?

A

H2CO3 travels on its own

Hemoglobin carries some CO2 to lungs

H+ binds to hemoglobin (carbamino-hemoglobin) as a “buffer” which makes H+ a weak acid and decreases acidotic potential

H2CO3 and H+ meet in lungs and break into CO2 + H2O

50
Q

Why does decreased CO result in pCO2 buildup?

A

Must be enough hemoglobin and CO to allow CO2 to travel in blood to be excreted

51
Q

What are the functions of pulmonary blood flow?

A
  1. Gas exchange
  2. Blood resevoir
  3. Filter small thrombi
52
Q

What is pulmonary deadspace? What types are there?

A

Ventilation is present but no contact with pulmonary blood flow

  1. Anatomical deadspace
  2. Alveolar deadspace
53
Q

What is anatomical deadspace?

A

Air from nose to terminal bronchioles not in direct contact with alveolar epithelium due to presence of cartilage and mucus membranes. Approx 30% of Vt

54
Q

What is alveolar deadspace?

A

Ventilation does not encounter sufficient blood flow at the alveolar level.
Caused by decreased CO, will cause increased WOB

55
Q

What is a pulmonary shunt? What types are there?

A

CO not contacting alveolar gas

  1. Anatomical / physiologic shunt
  2. Capillary shunt
  3. Shunt-like effect
  4. Silent unit
56
Q

What is an anatomical / physiologic shunt?

A

Some blood from bronchial, pleural, and some cardiac veins drain directly into L atrium instead of going through R atrium to get oxygenated (2-5% of CO)

57
Q

What is a capillary shunt?

A

Blood flows past unvented alveoli. Caused by decreased ventilation, alveolar collapse.

Increasing FiO2 will not increase PaO2 or SpO2

58
Q

What is a shunt like effect?

A

Diffusion defect in transport, gas exchange is impaired due to fluid in interstitial space. Ventilation and perfusion both OK

Increasing FiO2 will increase PaO2 and SpO2

59
Q

What is a silent unit?

A

Decreased ventilation and decreased perfusion

Resultant from prolonged decreased perfusion

CCN (27 decks)

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