Week 10: Hunyady's Respiratory Physio 3 (Ben) Flashcards

1
Q

Where is most of the resistance in the bronchial tree?

A

Within the 1st eight airway generations

  • Larger airways are more resistant

(opposite of blood circulation)

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2
Q

What are 3 bronchodilators which decrease airway resistance via bronchial smooth muscle relaxation?

A
  1. Epinephrine - via B2 adrenergic receptors
  2. NO
  3. VIP
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3
Q

What are 3 bronchoconstrictors which increase resistance via bronchial smooth muscle contraction?

A
  1. Acetylcholine - M1 Receptor —> Ca++
  2. Histamine - H1 Receptor —> Ca++
  3. Environmental Factors - dust, smoke, cold air
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4
Q

What is the relationship between lung volume and airway resistance?

Why?

A

it is an inverse relationship

(when lung volume is high, resistance is low)

because when the lung expands, airways also expand

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5
Q

What is the effect of inspired gas density on airway resistance?

A
  • larger gas molecules (N2 compared to He) have higher density and thus higher viscosity
  • as the Hagen-Poiseuille Law states, this leads to higher resistance

(N2 can be replaced with He for patients with airway resistance issues)

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6
Q

How does air flow affect airway resistance?

A

When air flow increases enough, it will become turbulent causing an increase in resistance

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7
Q

What two pressures are summed to get alveolar pressure?

A

Pelastic - retraction tendency pressure

Ppleural - pressure in the pleural space (often negative, but made positive during exhalation)

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8
Q

What is the Equal Pressure Point?

A

in forced exhalation, the point along the airway at which intrapleural and alveolar pressures are equal

  • just proximal to this point, the alveolar pressure is lower than intrapleural (since Palv decreases towards the mouth)
  • if this point is within non-cartilaginous airways, the pressure difference can constrict the airway
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9
Q

How does emphysema affect compliance?

And what does this mean for expiration?

A

it increases compliance

  • this decreases Pelastic (retraction tendency) and thus decreases Palv (b/c Palv = Pel + Ppl)
  • when Palv is less, expiratory force decreases
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10
Q

How does emphysema affect the equal pressure point?

A

it moves deeper into the lung

  • this means it is potentially in non-cartilaginous airways and thus can result in airway constriction
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11
Q

What is Henry’s Law in relation to respiratory gas tensions?

A

the amount of dissolved gas is proportional to its partial pressure in the gas phase

(in other words, the higher the partial pressure of a gas in the lung, the more of it will diffuse into the blood)

[gas]dissolved = α x Pgas

(α is a solubility coefficient for the gas)

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12
Q

What is the “dead space” volume and alveolar volume for the usual tidal volume of 500 ml?

A

dead space - 150 ml

alveolar - 350 ml

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13
Q

What is the anatomical dead space?

A

the volume within the conducting airways that do not participate in gas exchange

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14
Q

How can the anatomical dead space be measured via O2 inhalation?

A
  1. pt inhales pure O2
  2. as pt exhales, gas concentrations of exhaled air are continuosly measured
  3. the initial volume containing very little N2 gas represents the volume held in the dead space
  4. when the N2 concentration rises, this marks the beginning of exhalation of the alveolar volume (where N2 gas from previous non pure O2 breaths diffused into the air from the blood)
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15
Q

What is the equation for estimating the physiological dead space using collected expired tidal volume?

Explain how its parameters are measured.

A

VD = VT x (PACO2 - PECO2)/PACO2

  1. an expired tidal volume (VT) sample can be taken and its CO2 concentration (PECO2) measured
  2. the partial pressure of CO2 in the alveoli (PACO2) can be estimated by measuring the concentration of CO2 continuously as another tidal volume is exhaled and omitting the initial volume low in CO2 (which comes from the dead space)
  3. using these measured parameters dead space (VD) can be determined
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16
Q

What is the alveolar ventilation rate (considering normal, average conditions)?

A

4.9 L/min

(VA = 350 ml and breathing rate = 14/min)

17
Q

What is the equation for alveolar PCO2 (PACO2)?

A

PACO2 = 863 · (VCO2/VA)

  • where the V expressions should have a circle over them indicating a rate (ml/min), not just a volume
  • VCO2 is the rate of CO2 production
  • VA is alveolar ventilation rate
18
Q

How are hyper- and hypoventilation defined in terms of PACO2?

A

PACO2 > 40 mmHg = hypoventilation

PACO2 < 40 mmHg = hyperventilation

19
Q

Why is PO2 slightly lower in arteries than in alveoli?

(Even though the two equilibrate during respiration.)

(2 reasons)

A
  1. Bronchial Venous Blood - mixes with oxygenated blood from alveolar capillaries going back to heart via pulmonary veins
  2. Ventilation-Perfusion Mismatching - normal alveolar ventilation = 4.0 L/min, pulmonary blood flow = 5.0 L/min
20
Q

How does ventilation-perfusion ratio (V/Q) compare in different parts of the lung?

(think apex to base)

A

Apex - ventilation is greater than perfusion (V/Q > 1)

Base - ventilation is less than perfusion (V/Q < 1)

21
Q
A