Equations Flashcards

1
Q

What is Dalton’s law

A

Dalton’s law states that in a mixture of non-reacting gases, the total pressure exerted is equal to the sum of the partial pressures of the individual gases.

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2
Q

Boyle’s law

A

Boyle’s law states that at constant temperature for a fixed mass, the absolute pressure and the volume of a gas are inversely proportional.

  • an increase in volume decreases the pressure of a gas
  • a decrease in volume increases the pressure of a gas
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3
Q

Henry’s law

A

At a constant temperature, the amount of a given gas that dissolves in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid.

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4
Q

Alveolar gas equation

A

PAO2 = PiO2 - PaCO2/R

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5
Q

Laplace’s law

A

Laplace’s equation describes the relationship between P pressure inside alveoli, surface tension (T) and radius (r)
P = 2T / r
As the radius decreases, the pressure increases

  • surfactant stabilises alveoli of different sizes by altering surface tension depending of SA of alveolus
  • pressure needs to be equal so that alveoli do not collapse
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6
Q

What produces surfactant

A

Produced by type II pneumocytes from 34 weeks gestation, large increase in the 2 weeks before birth

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7
Q

What is surfactant?

A

Surface active phospholipid

  • phosphatidyl choline
  • phosphatidyl glycerol
  • phosphatidyl inositol
  • surfactant proteins A, B, C, D
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8
Q

What does surfactant do?

A

Virtual abolition of surface tension
Allows homogenous aeration
Allows maintenance of functional residual capacity

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9
Q

What does the volume of the lung depend on (and therefore pressure as Boyle’s law)

A
  1. Transpulmonary pressure - the difference in pressure between inside and outside of the lung
  2. How stretchable the lungs are -determines how much they will stretch for any given change in transpulmonary pressure
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10
Q

Transpulmonary pressure

A

Transpulmonary pressure is the transmural (across a wall) pressure that governs static properties of the lungs
Palv - Pip = Transpulmonary pressure
pressure inside alveoli - pressure of intrapleural fluid = Transpulmonary pressure

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11
Q

What is respiratory distress syndrome?

A
  • Not enough surfacant to reduce surface tension, the infant can only inspire by strenous effects, can lead to exuastion, inability to breathe and lung collapse
  • Leading death in premature babies, surfactant-synthesizing cells may be too immature to function properly
  • Production occurs in last gestation stimulated by cortisol secretion

treatment assisted breathing, administration of natural or synthetic surfactant through trachea

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12
Q

Airway resistance

A

Airway resistance is inversely proportional to the fourth power of the airway radii
smaller radius = greater resistance

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13
Q

What holds airways open? -Physical factors (2)

A
  1. Cartilage - in bronchi (2)
  2. Elastic connective tissue, these fibres are pulled upon as the lungs expand during inspiration, this helps pull the airways open further between breaths - this is LATERAL TRACTION
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14
Q

What holds airways open? -Neural factors/Chemical factors

A

Neuroendocrine and paracrine factors and influence smooth muscle and thereby airway resistance.
eg, epinephrine relaxes smooth airways by effecting beta-adrenergic receptors
eg. leukotrienes (produced during inflammation) contract the muscle

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15
Q

What factors does the partial pressure of a gas depend on?

A
  1. heat = speed of particles

2. concentration of the gas

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16
Q

What factors determine the value of P O2 of the alveolar air?

A
  1. PO2 of atomspheric air
  2. rate of aveolar ventilation
  3. the rate of total-body oxygen consumption

Typical alveolar pressure
P O2 = 105mmHg
P CO2 = 40mmHg

air breathed
P O2 = 160mmHg
P CO2 = 0.3mmHg (treated as 0)
The alveolar O2 is lower because some of the oxygen in the alveolar leaves to enter the pulmonary capillaries

17
Q

What happens to alveolar PO2 and alveolar PCO2 when the air breathing has a low PO2 (eg high altitude)

A
  • alveolar P O2 decreases

- NO change to CO2

18
Q

What happens to alveolar PO2 and alveolar PCO2 when there increased metabolism (eg during exercise)

A
  • alveolar P O2 decreases (as more o2 is used in the cells there is a high conc grad so more o2 moves from the alveoli into the pulmonary capillaries)
  • increased P CO2 (more co2 diffuses out of cells into capillaries and then into alveoli)
19
Q

What happens to alveolar PO2 and alveolar PCO2 when there is increased ventilation

A
  • Alveolar PO2 increases

- Alveolar PCO2 decreases

20
Q

What happens to alveolar PO2 and alveolar PCO2 when there increased ventilation and increased metabolism (during exercise with increased breathing)

A

-Opposing effects cancel each other out so alveolar O2 does not change

21
Q

Hyperventilation (increased ventilation relative to metabolism)

A

When there is a decrease in the ratio of Co2 production to alveolar ventilation

  • too much ventilation for the amount of Co2 produced
  • reduced PCO2 value
22
Q

Hypoventilation (decreased ventilation relative to metabolism)

A

When there is an increase in the ratio of Co2 production to alveolar ventilation

  • reduced ventilation
  • cannot keep up with Co2 production
  • increased PCo2 value
23
Q

How does diffusion between pulmonary capillaries and alveoli achieve complete diffusion?

A
  • Conc grad
  • Slow flow of blood in capillaries
  • Short distance
24
Q

What occurs during exercise to increase gaseous exchange?

A
  • During exercise increased CO increases pulmonary pressures

- This opens capilaries at the apex of each lung, enhancing gaseous exchange

25
Q

What occurs in pulmonary edema?

A

Some of the alveoli are filled with fluid, this increases the diffusion barrier for gases

26
Q

What occurs in diffuse interstitial fibrosis?

A

Alveolar walls become severely thickened with connective tissue (fibrotic)
-fibrosis may occur from infection, autoimmune disease, hypersensitivity to inspired substances, exposure to toxic airborne channels and other causes
symptoms shortness of breath, poor oxygenation of blood
diffusion problems are often restricted to O2 as Co2 diffuses more rapidly

27
Q

What is ventilation-perfusion inequality?

A

This is when there is mismatching between air supply (ventilation) and blood supply (perfusion) in each individual alveoli

  • The major effect of ventilation-perfusion inequality is to decrease P O2 of systemic arterial blood
  • upright position increases filling of blood vessels at the bottom of the lung due to gravity, this contributes to the difference in blood-flow distribution
28
Q

What can cause marked increases in ventilation-perfusion inequalities?

A
  • In diseases states, lung compliance, airway resistance and vascular resistance can cause marked increases in ventilation-perfusion inequalities
    1. ventilated alveoli with no blood supply at all (dead space or wasted ventilation)
    2. blood flowing through areas of the lung with no ventilation (shunt) eg due to collapsed alveoli
29
Q

Why do ventilation-perfusion inequalities affect CO2 elimination less?

A
  • small increases in alveoli PCO2 leads to increases alveoli ventilation
  • this usually prevents further increases in arterial PCO2
  • severe diseased states can lead to increased arterial PCO2
30
Q

What mechanisms reduce ventilation-perfusion inequalities to maintain effective gaseous exchange?

A
  • decrease in ventilation in alveolar O2 (eg due to mucous plug) leads to a decrease in alveolar PO2 and the area around it
  • This leads to vasoconstriction and blood is diverted away from the poorly ventilated area
  • This ensures that blood flows to the healthy parts of the lung rather than the diseased areas
  • If there is decrease in blood flow (eg due to a blood clot), there is reduced PCO2 to area of the lung
  • this causes local bronchoconstriction which diverts airflow to areas of the lung with better perfusion
31
Q

What is Poiseulle’s law?

A

-relatively small changes in the radius of the airways causes large changes in airway resistance.

R= 8π X L / X R^4

  • An individual small airway has much greater resistance than a large airway, however there are many more small airways than large ones.
  • Therefore, resistance is greatest at the bronchi of intermediate size, in between the fourth and eighth bifurcation.[1]