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Anesthesiology > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

1
Q

How does oxygen consumption and CO2 production change with GA?

A

Decreases both by ~15%

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2
Q

What is the RQ for carbohydrates? Proteins? Lipids?

A

Carbs: 1
Proteins: 0.8
Lipids: 0.7

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3
Q

How would a hemi-diaphragmatic paralysis decrease pulmonary function?

A

~25% (diaphragm accounts for 75% of chest volume change)

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4
Q

What is the end-expiration intrapleural pressure in a healthy patient?

A

-5 cm H2O (while alveolar pressure is 0 since there is no air flow): this keeps the alveoli open

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5
Q

What is Laplace’s law?

A

Alveolar pressure = 2 * (surface tension / radius)

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6
Q

How does surfactant affect smaller alveoli compared to larger ones?

A

Surfactant is more concentrated in smaller alveoli so it decreases surface tension to a greater extent than in large radii alveoli

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7
Q

What makes up FRC?

A

Expiratory reserve volume + residual volume

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8
Q

Factors that decrease FRC?

A

Restrictive lung disease, obesity, pregnancy, posture (standing>sitting>supine>prone), height (taller people have more FRC), gender (men have more FRC than women)

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9
Q

What patient postures have the most reduced FRC?

A

Supine > prone > sitting > standing (least reduction in FRC)

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10
Q

What is closing capacity?

A

Volume at which small airways begin to close; Residual volume + closing volume

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11
Q

How does closing capacity change with obesity?

A

It does not change; however, ERV decreases and so FRC decreases causing tidal volumes to shift towards residual volume; since closing volume has not changed, the tidal volumes are not less than closing capacity

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12
Q

How does closing capacity change with age?

A

Increases with age (or any disease states within the lungh like COPD, etc that increase airway obstruction)

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13
Q

How does closing capacity change with GA?

A

Decreases under general anesthesia (bronchodilation of volatile anesthetics so you decrease airway obstruction leading to decreased closing capacity)

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14
Q

What is the formula for airway resistance for laminar flow?

A

Resistance = (8 * length * viscosity) / (pi * radius^4)

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15
Q

What is the major determinant for turbulent flow?

A

Density

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16
Q

Formula for Reynold’s number

A

R = (velocity * diameter * density) / viscosity

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17
Q

What Reynold’s number indicates turbulent flow?

A

> 2000

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18
Q

What happens to FRC under GA?

A

Decreases (ribcage moves inward in supine position + abdominal contents fall into thorax)

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19
Q

Would positive-pressure ventilation increase or decrease dead-space?

A

Increase by ~50%; higher alveolar pressure = West zones moved downward: alveoli at apex that were barely being perfused due to low arteriolar pressures will be totally occluded = ventilation without perfusion (dead space)

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20
Q

In a normal, sitting patient, where is ventilation and perfusion at its maximum?

A

Both are maximal near the base

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21
Q

Non-cardiac causes of acute pulmonary HTN?

A

Hypoxia, hypercarbia, acidosis, autonomic system

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22
Q

What does hypocarbia do to pulmonary vasculature?

A

Pulmonary vasodilator and causes bronchoconstriction

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23
Q

How does the effects of hypoxia, acidosis, and hypercarbia differ between pulmonary and systemic vasculature?

A

Pulmonary: vasoconstriction
Systemic: vasodilation

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24
Q

What anesthetic inhibits hypoxic pulmonary vasoconstriction?

A

N2O and volatile agents (2 MAC), inhaled nitric oxide, nitrates

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25
Q

What is the alveolar gas equation?

A

PAO2 = FiO2 ( Pbarometric - PH2O) - PaCO2/RQ

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26
Q

How does an increase in cardiac output change the A-a gradient?

A
  1. increased CO = increased mixed venous PO2, and more left over oxygen
  2. Intrapulmonary shunting decreases
    You get a decrease in the A-a gradient
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27
Q

What is responsible for the ventilatory response to hypercarbia?

A

Chemoreceptors in contact with the 4th ventricular CSF on the anterolateral surface of the medulla; BBB permeable to CO2 which reacts with H20 forming H+ ions = lowering pH = stimulates chemoreceptor

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28
Q

What region of the brain coordinates inspiration?

A

Dorsal & ventral medullary center

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29
Q

What region of the brain coordinates expiration?

A

Ventral medullary center

30
Q

What does the carotid and aortic bodies respond to?

A

Primary responsible for increasing ventilation in response to HYPOXIA

31
Q

Why do you not give severe COPDer’s too much supplemental oxygen?

A

High O2 levels interrupt needed hypoxic pulmonary vasoconstriction (since these patients have severe V/Q mismatch)

32
Q

After a carotid endarterectomy, how long does it take for the carotid bodies to become functional again?

A

Up to a year

33
Q

Why wait to do a contralateral carotid endarterectomy if one side was recently done?

A

The patient will not be able to respond with their peripheral O2 chemoreceptors (takes up to a year)

34
Q

What would blood in the ventricles due to respirations?

A

H+ ions in blood will decrease pH, stimulating the chemoreceptors on the anterolateral surface of the medulla exposed to the 4th ventricle = increased minute ventilation

35
Q

If an asthmatic becomes bronchospastic after intubation, what is the underlying cause?

A

Activation of vagal stimulation

36
Q

Treatment for profound bronchospasm after intubation?

A

Epinephrine IV 20 mcg (albuterol can only be used if there is air movement)

37
Q

Chronic bronchitis or emphysema: risk of right heart failure?

A

Chronic bronchitis

38
Q

What is bronchiectasis?

A

Permanent dilation of bronchi from destructive inflammatory changes usually secondary to recurrent infections

39
Q

What do you suspect with an increased end tidal nitrogen?

A

Venous air embolism

40
Q

What would the flow volume loop look like for a variable intrathoracic lesion?

A

Obstruction on expiration

41
Q

What would the flow volume loop look like for a variable extrathoracic lesion?

A

Obstruction on inspiration

42
Q

What portion of the brain controls rate and pattern of breathing?

A

Pneumotaxic center

43
Q

What is the role of the apneustic center?

A

Antagonizes the effects of the pneumotaxic center

44
Q

What is the Hering-Breuer Reflex?

A

Overinflation of lung -> stimulation of lung stretch receptors -> activates apneustic center -> inhibits inspiratory center -> inspiration stops

45
Q

Where are the peripheral chemoreceptors located and what cranial nerves are they associated with?

A

Carotid bodies (CN IX), aortic bodies (CN X)

46
Q

At what PaO2 do the peripheral chemoreceptors activate?

A

< 60mmHg

47
Q

How are peripheral chemoreceptors affected by volatile anesthetics?

A

Response to hypoxia is eliminated by as little as 0.1 MAC

48
Q

How is CO2 transported in the vasculature?

A

85% in bicarbonate, 10% bound to amino acids, 5% dissolved

49
Q

How does an increase in PaCO2 affect cerebral blood flow?

A

Increased CO2 increases CBF through NO and PGI2-mediated vasodilation

50
Q

How does hypercarbia affect the cardiovascular system?

A

CO2 is a direct cardiac depressant balanced by increases in SNS activity (causing elevated MAP and CO)

51
Q

What should you worry about with Halothane and hypercarbia?

A

Halothane sensitizes the myocardium to epinephrine so you increase the risk of arrhythmias from the SNS activation of hypercarbia

52
Q

How does hypocarbia affect the CV system?

A

Decreases cardiac output

53
Q

What does hypercarbia do to the GI system?

A

Increases hepatic and portal venous blood flow (while the SNS activation will cause constriction)

54
Q

What lung cells make surfactant?

A

Type II pneumocytes

55
Q

What increases the P50 (PO2 at which Hgb is 50% saturated)?

A

Right shift in the oxyhemoglobin dissociation curve (hyperthermia, acidosis, pregnancy, increased 2,3 DPG, volatile anesthetics, sickled hemoglobin)

56
Q

What decreases the P50 (Po2 at which Hgb is 50% saturated)?

A

Left shift in oxyhemoglobin dissociation curve (hypothermia, alkalosis, fetal hemoglobin, hethemoglobin, carboxyhemoglobin, decreased 2,3 DPG)

57
Q

What muscles are involved in inspiration? Expiration?

A

Inspiration: diaphragm, scalenes, SCM, external intercostals, large back muscles (big breathe)
Expiration: passive process, internal intercostals (forced), abdominal muscles

58
Q

What makes up the majority of airway resistance: conducting airways, transitional airways, respiratory airways?

A

Conducting airways (90%) which include larger airway to the terminal bronchioles

59
Q

What kind of flow (laminar or turbulent) is seen in the conducting (larger) airways? In the terminal bronchioles?

A

Larger: turbulent flow

Terminal bronchioles: laminar flow

60
Q

How does PaO2, PaCO2 and CSF fluid change with increased elevation?

A

PaO2 decreases (since atmospheric pressure decreases), this causes increased ventilation which leads to a decreased PaCO2 -> alkalosis -> H+ moves out of CSF to the plasma to correct the alkalosis -> increased CSF pH

61
Q

How do volatile anesthetics affect CO2 responsiveness?

A
  1. Increases PaCO2 before normal ventilation

2. Decreased responsiveness in ventilation per PaCO2

62
Q

What is dead space ventilation? What is a shunt?

A

Dead space: ventilation without perfusion

Shunt: Perfusion without ventilation

63
Q

What is the P/F ratio and what is a normal ratio?

A

PaO2/FiO2, normal is greater than 300

64
Q

What does the flow loop look like for a patient with obstructive lung disease?

A

Near normal inspiratory loop (lower) with a scooped expiratory curve (overcoming the lesion)

65
Q

What is FEF25-75?

A

Forced expiratory flow between 25% of FVC and 75% of FVC

Generally effort independent (unlike FVC or FEV1) and an early indicator of obstructive disease

66
Q

When is FRC the lowest in the post-operative period?

A

12 hour post op

67
Q

Following cessation of smoking, how long does it take for ciliary function to return to normal? Normal carboxyhemoglobin levels? Maximal benefits?

A

Ciliary function: 2-4 weeks
Carboxyhemoglobin levels: 24 hours
Maximal benefits: 8+ weeks

68
Q

What ECG findings do you expect to see in a patient with COPD?

A

Right-heart strain (i.e. poor R-wave progression, enlarged P-waves, R>S in V1, RBBB, RAD)

69
Q

How would an upper abdominal surgery affect PFTs?

A

Decreases FRC (decreased lung compliance and increases shunting and hypoxia) secondary to a ~25% decrease in ERV and increase in RV by ~10%

70
Q

Which is the best anatomic estimate for the level of the carina: 3rd thoracic vertebrae, sternal angle, nipple line, one finger breadth below the sternal notch

A

Sternal angle

71
Q

What pressure is the best marker for dynamic compliance? Static compliance?

A

Dynamic: Peak pressure
Static: Plateau pressure

72
Q

What is RSBI, how is it calculated, and what value indicates possible extubation?

A

Rapid Shallow Breathing Index = RSBI = RR/Vt (in liters)

If RSBI

Anesthesiology (21 decks)

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