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Body in Balance Midterm #2 > Alveolar Gas Exchange > Flashcards

Alveolar Gas Exchange Flashcards

1
Q

Dalton’s Law

A

The partial pressure of a specific gas in a gas mixture is equal to the pressure the gas would exert if it occupied the total volume of the mixture without the other gases

The total pressure of the gas mixture is also the sum of the partial pressures of each gas in the mixture • PT = P1 + P2 + P3 + …

It is the law explaining the alveolar gas equation

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2
Q

Causes of CO2 Retention

A
  • High CO2 production and output of tissue beds
  • Low minute (alveolar) ventilation
    • High mechanical load
    • Weak or inefficient muscles
    • Insufficient drive
  • Ventilation-perfusion inequality
  • Abnormal breathing pattern (i.e. low Vt high f)
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3
Q

Blood-Gas Interface, Properties of the interface that affect diffusion in the lung and Properties of the gas

A

Blood-Gas Interface

  • Gas (molecule) movement is primarily by diffusion

Properties of the interface that affect diffusion in the lung

  • Large surface area of the membrane (50-100 m2)
  • Thin membrane (0.2-0.3 μm)
  • Physical properties of the membrane

Properties of the gas

  • Size of the molecule (molecular weight)
  • Partial pressure of the gas
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4
Q

Equation for Alveolar PCO2

A

PACO2 = VCO2 / VE (1-VD/VT)

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5
Q

assumptions made in the alveolar gas equation

A
  • No CO2 in inspired air
  • Inert gases are in equilibrium (nitrogen, etc)
  • Alveolar and arterial CO2 are in equilibrium
  • Ignore the change in volume between inspired and expired air
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6
Q

Other methods to measure the oxygenation function of the lung

A
  • PaO2/FI O2 or P/F ratio
  • Oxygenation index (OI) – useful when using positive pressure ventilation; takes into account oxygen being given on a ventilator
  • OI = (Mean airway pressure x FlO2 x 100) / PaO2
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7
Q

Increased PACO2 is caused by three things:

A
  • Increased CO2 production
  • Decreased minute ventilation
  • Increased dead space fraction
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8
Q

Increasing alveolar ventilation can be accomplished by:

A
  • Increasing (total) minute ventilation
    • Increasing tidal volume
    • Increasing respiratory rate
  • Decreasing dead space ventilation
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9
Q

Pulmonary Blood Flow

A
  • Pulmonary vasculature associated with airways and alveoli
  • Capillaries are small, just large enough for a red blood cell
    • Create a “sheet” of blood
  • Receives all of the right ventricular cardiac output
  • Pulmonary vascular system has a low resistance to flow
  • Red blood cells transit through the pulmonary capillary is short (0.75 s)
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10
Q

What Determines Alveolar PCO2?

A
  • CO2 is produced in the tissues (end-product of aerobic metabolism) and transported to the alveoli in blood (dissolved, bicarbonate, carbamino Hb)
    • VCO2 = CO2 production = Oxygen consumption x Respiratory Quotient
  • CO2 diffuses down a pressure gradient from blood to alveoli
  • CO2 is eliminated through ventilation of the alveoli
    • VA = VE (1 – VD/VT)
  • We also make several other assumptions:
    • No CO2 is inspired (PI CO2 can be assumed to be zero)
    • Inert gases are in equilibrium
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11
Q

The Alveolar PCO2

A
  • If we assume no CO2 is inspired then PI CO2 can be assumed to be zero
  • Carbon dioxide production directly influences alveolar PCO2
    • How much CO2 reaches the alveoli through delivery through blood
  • Alveolar ventilation directly affects PACO2 (increased ventilation equals decreaed alveolar PCO2)
  • Ignoring inert gases (assume they are in equilibrium) then:
  • PACO2 = CO2 production ÷ alveolar ventilation
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12
Q

Limitations of Gas Exchange

A

Oxygen and Carbon Dioxide diffuse across the normal alveolarcapillary membrane readily, and therefore the limitation of gas transfer is perfusion-limited under normal circumstances

In the following conditions the transfer of Oxygen and Carbon Dioxide at the alveolar-capillary membrane may become diffusion-limited:

  • Exercise (decreased transit time of blood)
  • Thickening of the alveolar-capillary membrane

Conditions Affecting Gas Diffusion

  • Changes in the surface area available for gas exchange
  • Ventilation-perfusion matching
  • Decrease in lung parenchyma

Thickening of the alveolar wall (interstitium)

  • Edema (likely minimal, if any, effect on diffusion of O2 and CO2)
  • Inflammation (inflammatory cells, lymphocytes, plasma cells)
  • Fibrosis (Diffuse Interstitial Pulmonary Fibrosis)
  • Sarcoidosis
  • Hypersensitivity pneumonitis
  • Radiation
  • Medications (Busulfan)
  • Collagen disorders

Smaller differences in partial pressure across the interface

  • Altitude
  • Gases added to inspired air (helium, nitrogen, anesthetics)

Changes in Perfusion (Perfusion limited gas transfer)

  • Fast pulmonary capillary transit times – gases don’t have the time to equilibrate
    • Exercise

Alterations in oxygen reaction with Hemoglobin (not a direct affect on diffusion)

  • Altered by other gases binding with Hb (CO)
  • Abnormal hemoglobin structure (Methemoglobin)
  • Oxygen reaction with hemoglobin is not linear
  • Changes in the oxygen dissociation curve
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13
Q

Tidal volume

A
  • the total amount of air entering and leaving the respiratory system with each breath (note that not all of this air will participate in gas exchange)

Tidal volume (TD) has two components: VT = VD + VA

  • VD = dead space volume
  • VA = alveolar volume
  • The alveolar portion of the tidal volume is the air leaving the alveoli with each breath (tidal volume - dead space volume); VA = VT - VD
  • Alveolar ventilation (VA) is the volume of air leaving alveoli each minute that has participated in gas exchange with blood (total ventilation - dead space ventilation) VA= VE - VD
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14
Q

Two Components of Dead Space

A
  • Anatomic dead space (conducting airways)
    • Can be measured using Fowler’s Method (100% oxygen breath)
  • Alveolar dead space (Air enters the alveoli but no blood flows past the alveoli to exchange gases)
    • Dead space = wasted ventilation
    • Relatively little excretion of CO2 occurs from high V/Q areas (dead space) of the lung
  • anatomic dead space is vertical rectangle and alveolar dead space is the horizontal rectangle on top
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15
Q

The Alveolar (PAO2) – arterial (PaO2) gradient (A-a gradient)

A
  • PAO2 calculated using the alveolar gas equation:
    • PAO2 = [(PB – PH2O) x FI O2] - (PaCO2 ÷ RQ)
  • PaO2 and PaCO2 are measured from arterial blood
  • A small A-a gradient is normal. In healthy persons:
    • About 50% is due to V/Q mismatch
    • About 50% is due to true shunts (Thebesian and Bronchial circulations)
    • Normal A-a gradient in ambient air is approximately (Age ÷ 4) + 4
  • A large A-a gradient is an indication of an abnormality in transporting oxygen from the alveoli to the systemic arterial blood
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16
Q

Physiologic Dead Space

A
  • Physiologic dead space = Anatomic Dead Space + Dead space-like effects of high V/Q areas
  • Includes the conducting airways and the alveoli that do not participate in gas exchange (eliminate CO2)
  • The Bohr Equation can be used to calculate the fraction of physiologic dead space: see picture
  • Normal physiologic dead space fraction is 0.2 - 0.3
  • Can use modified Bohr Equation
    • Example: • Arterial CO2 measured in an arterial blood gas equals 40 mm Hg • End-tidal CO2 measured in exhaled breath equals 32 mm Hg • Then VD/VT = (40 – 32) / 40 = 0.2
17
Q

Fick’s Law (Gas Diffusion)

A
  • Diffusion proportional to:
    • Area of the membrane
    • Difference in partial pressures of gases
    • Diffusion constant
      • Properties of the membrane
      • Properties of the gas
        • Molecular weight
        • Solubility
  • Inversely proportional to: Membrane thickness
18
Q

Tidal volume

A

the volume of air moving in and out of the lungs with normal breathing

19
Q

Limitations of Oxygen Diffusion (Across the alveolar-capillary membrane)

A
  • Time blood spends in the pulmonary capillary bed (transit time)
  • Normally not a limiting factor but may be limited in:
    • Disease states that thicken or change the membrane property
    • Low inspired PO2 (decreases the pressure gradient)
    • Exercise (decreases the transit time)
20
Q

Hypoxemia with a normal A-a gradient

A
  • Decreased inspired oxygen (PI O2)
  • Alveolar hypoventilation (increased PACO2)
21
Q

Oxygen movement at the interface (layers/components it moves through)

A
  • Alveoli (PAO2)
  • Epithelium
  • Interstitial space and basement membrane
  • Endothelium Plasma (PaO2)
  • Erythrocyte membrane
  • RBC Cytoplasm
  • Hemoglobin (SO2)
22
Q

Carbon Dioxide Transport in Blood

A

CO2 is transported in the blood in three forms:

  1. Dissolved: CO2 is 24 times more soluble than O2 (0.067 mL/dL/mm Hg)
  2. In the form of bicarbonate: CO2 + H2O H2CO3 H+ + HCO3 - (The first reaction occurs quickly in the RBC due to carbonic anhydrase)
  3. In the form of carbaminohemoglobin:
  • Deoxygenated Hb binds H+ (see #2) to form HHb
  • CO2 combines with HHb in the RBC to form carbaminohemogobin
  • The affinity for deoxygenated blood for CO2 is called the Haldane effect
23
Q

What causes a low PaO2? (Etiologies of Hypoxemia)

A
  • Decreased inspired oxygen tension
  • Alveolar hypoventilation
  • Diffusion impairment
  • Ventilation
  • Perfusion mismatch
  • Anatomic (or True) shunt
24
Q

What happens to the PaCO2 in Lung Disease?

A
  • The most common arterial blood gas pattern in patients with mild or moderate lung disease is hypoxemia and low CO2
  • High arterial CO2 is more likely to be seen in severe lung disease
25
Q

Changes in Ventilation effects on alveolar PCO2 and PO2

A

Increasing alveolar ventilation

  • Decreases alveolar PCO2 (direct effect)
  • Increases alveolar PO2 (by decreasing PCO2)

Decreasing alveolar ventilation

  • Increases alveolar PCO2 (direct effect)
  • Decreases alveolar PO2 (by increasing PCO2)
26
Q

Limitations of Using the A-a Gradient

A
  • Normal in some causes of hypoxemia
  • Not constant at different inspired oxygen concentrations
    • A-a increases as inspired (alveolar) PO2 increases, the relationship is nonlinear and complex
  • Therapeutic interventions can alter A-a gradient
    • Recruiting alveoli (improving V/Q matching) with positive pressure ventilation can improve A-a gradient independent of inspired oxygen
27
Q

Hypoxemia with increased A-a gradient

A
  • Diffusion abnormality
  • V/Q mismatch
  • Anatomic (True) shunt
28
Q

Write the equations to determine PA CO2 and PAO2.

A

Alveolar Gas Equation

PAO2 = [(PB – PH2O) x FIO2] - (PaCO2 ÷ RQ)

The alveolar gas equation can be used to estimate PAO2; and explains how changes in barometric pressure, inspired oxygen concentration, and alveolar CO2 can affect PAO2 • PACO2 is determined by CO2 production and alveolar ventilation

PB = atmospheric pressurre

PH20= the saturated vapour pressure of water at body temperature and the prevailing atmospheric pressure

FIO2 = The fraction of inspired gas that is oxygen (expressed as a decimal)

PaCO2 = The arterial partial pressure of carbon dioxide (pCO2)

RQ = resipiratory exchange ratio (?)

29
Q

Minute (total) ventilation

A
  • the volume of air leaving the lung each minute
  • VE = fB x VT
    • VE = minute ventilation (mL/min.)
    • fB = respiratory rate (breaths/min)
    • VT = tidal volume (mL/breath)
30
Q

CO2 Diffusion Across the Alveolar Membrane

A
  • The characteristics of CO2 diffusion are similar to O2 diffusion despite CO2 higher solubility
    • CO2 diffuses 20 times more rapidly than oxygen
  • This is because the difference in partial pressure is small (driving pressure)
  • Again, the partial pressures may not equilibrate in disease states that affect membrane properties or blood transit time

Body in Balance Midterm #2 (26 decks)

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