Diffusion, Hypoxia, Hypercapnia Flashcards

1
Q

3 Conditions that Lower Diffusing Capacity

A

**Loss of interface

1- Emphysema

2- Interstitial lung disease

3- Pulmonary Vascular disease

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2
Q

4 Conditions that Inc Diffusing Capacity

A

1- Polycythemia - greater reservoir to bind CO

2- Early CHF - inc cap volume

3- Asthma - expand lung units

4- Alveolar hemorrhage - false; bleeding into lungs so binds w/ CO

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3
Q

4 Factors that Affect Rate of Diffusion

A
  • A- rate inc w/ in surface area
  • D - coefficient proportional to solubility of the gas and inversely proportional to molecular weight of gas
  • P1-P2 - partial pressure gradient; greater rate if greater difference
  • T - dec rate if thicker interface (diseases like interstitial edema or interstitial fibrosis)
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4
Q

What determines concentration / amount of gas dissolved?

A
  • C = solubility x partial pressure
    • Conc of O2 = .003 x PO2
    • Conc of CO2 = .067 x PCO2
  • So anything that inc partial pressure will inc the conc of that gas in plasma (more dissolved) and vice versa
  • Since CO2 and O2 have relatively low solubilities, partial pressure changes quickly during diffusion
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5
Q

How long does diffusion normally take? How is this affected by pathology?

A
  • Both CO2 and O2 equilibration takes about .25 seconds while RBC spends about .75 seconds at the interface at rest (done w/ plenty of time)
  • Even during exercise (inc perfusion rate so less time at interface) there is enough time for equilibration
  • BUT if diffusion impairment, it may take the entire .75 seconds so undetected at rest but “exercised induced de-saturation”

**More dramatic for O2 than CO2 b/c larger P gradient for O2

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6
Q

5 Causes of Hypoxia

A

NORMAL PA-aO2 (both dec)

  • 1- Hypoventilation
  • 2-High Altitude

INCREASED PA-aO2 (only PaO2 is dec)

  • 3- V/Q Mismatch
  • 4- Shunt
  • 5- Impaired Diffusion (thicker interface or dec SA of interface)
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7
Q

3 Causes of Hypercapnia

A
  • 1- Inc dead space w/o compensatory inc in minute ventilation
  • 2- Dec minute ventilation (can be CNS or muscle problem)
  • 3- Inc CO2 production w/o compensatory inc in minute ventilation
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8
Q

How does respiration change in pregnancy?

A
  • Anatomic changes - diaphragm elevates but lower ribs expand to comp - “barrel chest”
    • Dec residual volume, dec expiratory reserve
    • BUT inc tidal volume so minimal dec in TLC
  • Metabolic changes - inc metabolic rate so more CO2 production
  • Progesterone –> inc respiratory drive and inc sensitivity of respiratory centers to CO2 –> inc minute ventilation –> inc alveolar ventilation b/c dead space the same
  • Overall… inc minute vent/alveolar vent&raquo_space; inc CO2 prod –> overall respiratory alkalosis (pH7.4-7.47)
  • *Disproportional rise in minute ventilation**
  • If PACO2 is lower than PAO2 is reciprocally higher (so sats close to 100%)
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9
Q

Dyspnea in Pregnancy

A
  • Common; can start b/f major anatomic change
  • Likely due to progesterone-induce in alveolar vent
  • Also nasal congestion, inc blood flow, anemia, etc
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10
Q

Physiological Changes in Diving

A
  • Inc pressure surrounding chest wall (1 atm per 33 ft) –> dec lung volume (PV=nRT)
  • Inc partial pressures of ea gas b/c same gas composition … inc PO2 and inc PCO2 (which then means more dissolved b/c C = solubility x PartialP)
  • Mechanics affected b/c inc pressure on chest wall dec FRC and TLC (More pressure to overcome in inspiration AKA have to do more work to expand chest wall)
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11
Q

4 Steps of Breath Hold Diving

A
  • 1- Hyperventilate b/f diving to achieve low starting PCO2 (b/c PCO2 affects drive more) and high starting PO2
  • 2- Descent - lung volume dec while total pressure inc; both PO2 and PCO2 inc
  • 3-While under, CO2 produce/O2 consumed so inc PACO2 and dec PAO2
    • **Respiratory acidosis
    • **Stim chemoreceptors that inhibit further breath holding (drive to breath)
  • 4-Ascent - total pressure dec so partial pressures also dec; dec PACO2 and now even lower PAO2
    • **Can get hypoxic on ascent (may lose consciousness or die)
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12
Q

Barotrauma

A
  • if scuba diver holds breath on ascent then high starting pressure w/ inc volume while ascending can cause rupture of alveoli
  • Can lad to pneumothorax, alveolar hemorrhage, air embolism
  • 2nd most common cause of death in SCUBA divers
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13
Q

Decompression Illness

A
  • when diving there is inc dissolving of O2, CO2 and N2 then dec in amount dissolved during ascent (b/c dec partial pressure of gases) –> bubbles in tissues and blood vessels (goes from solution –> gas)
  • Block vessels, rupture tissues, activate clotting and inflammatory cascades, etc
  • Bends - bubbles in joints
  • Chokes - bubbles in pulmonary blood flow lead to chest pain, dyspnea and cough
  • Tx - immediate recompression (hyperbaric oxygen chamber) followed by slow decompression AND 100% oxygen to create nitrogen gradient to get it out of tissues
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14
Q

Nitrogen Narcosis

A
  • excess nitrogen dissolved in CNS –> alters neuronal cell membranes
  • Euphoria, amnesia, clumsiness, irrational behavior
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15
Q

Physio Changes at High Altitude

A
  • Drop in baro pressure –> inc volume w/ same air composition so partial pressure of O2 decreases proportionally
  • Dec PO2 –> chemoreceptor stimulation –> inc minure vent –> respiratory alkalosis
  • Inc 2,3-DPG so shift dissociation curve RIGHT
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16
Q

Acclimatization

A
  • Includes hyperventilation
  • physio changes to optimize O2 delivery and use in high altitude state; HIF-1-alpha (hypoxia inducible factor 1)
  • Happens w/in minutes to weeks and variable b/n people
17
Q

High Altitude Complications

A

BRAIN
-Acute mountain sickness - headache, dizziness, nausea, SOB, weak, difficulty sleeping

-High alt cerebral edema - - respond to hypoxia w/ cerebral vasodilation –> edema –> headache, loss of coordination, confusion, coma

LUNGS
-High alt pulmonary edema (MOST DEADLY) - elevated pulm artery pressures –> exaggerated vasoconstriction /dec NO/inc endothelin –> overperfusion –> pulmonary edema

18
Q

Treatment for High Altitude Complications

A
  • DESCEND
  • Portable hyperbaric chambers
  • For cerebral edema… can give dexamethasone temporarily (steroid that dec edema); acetazolamide (Na+ wasting to dec edema and improves the alkalemia by inc bicarb excretion)
  • For pulmonary edema… dec PA pressures w/ Ca-channel blocker, PDE inhibitors (inc NO), beta agonists