Oxygen Therapy Flashcards

1
Q

oxygen delivery

A

-DO2 = CO x arterial oxygen content (CaO2)

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2
Q

failure of oxygen delivery leads to

A
  • hypotension
  • acidosis
  • coagulopathy
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3
Q

oxygen use

A

VO2 = CO x (PaO2 - PvO2)

  • oxygen extraction ratio; normal is about 25%
  • heart has very high demand
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4
Q

why is oxygen therapy important in surgical patients?

A

they are at increased risk for hypoxia and hypoxemia

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5
Q

hypoxemia

A

deficiency of oxygen in the blood

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6
Q

hypoxia

A

oxygen delivery to the tissues is not sufficient to meet the metabolic demand

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7
Q

anesthesia goal

A

maintain oxygenation and ventilation that is sufficient to meet the metabolic demand

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8
Q

oxygen therapy goal

A

prevent and correct hypoxemia and tissue hypoxia

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9
Q

hypoxic hypoxia

A

shunting or pulmonary diffusion defect; can be caused by a drug OD, COPD exacerbation, asthma, atelectasis, or emphysema

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10
Q

circulatory hypoxia

A

decrease in CO to the point where oxygen delivery to the tissues is inadequate; common causes are CHF or MI

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11
Q

hemic hypoxica

A

a decreased Hgb content (such as anemia) and/or decreased function of Hgb; anemia, carboxy-hemoglobinemia, methemoglobinemia

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12
Q

demand hypoxia

A

an increase in the metabolic rate or oxygen demands of the body such that insufficient oxygen is delivered to the body; fever, seizure, MH

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13
Q

histotoxic hypoxia

A

inability of the cells themselves to use oxygen such as in cyanide poisoning

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14
Q

hypoxia S/S

A
  • vasodilation
  • tachycardia
  • tachypnea
  • cyanosis
  • confusion
  • lactic acidosis
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15
Q

improving oxygenation in mechanically ventilated patients

A
  • treatment tailored to cause
  • increase VE
  • increase CO
  • increase O2 carrying capacity
  • optimize V/Q relationship
  • decrease O2 consumption
  • increase FiO2
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16
Q

nasal cannula

A
  • flow rates 1-6 L/min

- FiO2 increases about 4% per L/min

17
Q

simple face mask

A
  • FiO2 40-60%
  • min 6L flow required to prevent rebreathing; min is essentially whatever the patient’s minute ventilation is to prevent rebreathing of CO2
18
Q

face masks with reservoirs

A

-FiO2 60-100%

19
Q

Venturi Masks

A
  • more precise FiO2 24-50%

- Bernoulli’s Principle

20
Q

oxygen toxicity

A
  • high FiO2 over long period of time can be harmful to lung tissue
  • decrease ciliary movement, so lungs can’t get rid of mucous or debris as easily
  • alveolar epithelial damage
  • interstitial fibrosis
  • dependent upon - FiO2, duration, and patient susceptibility
21
Q

what is generally considered a “safe” amount of oxygen?

A

100% for up to 10-20 hours

22
Q

what has been shown to have oxygen toxicity?

A

50-60% for more than 24-72 hours

23
Q

high risk populations for oxygen toxicity?

A
  • older than 70 years
  • history of radiation to the lungs/chest
  • bleomycin (used to treat various types of cancer)
24
Q

s/s of oxygen toxicity

A
  • cough
  • dyspnea
  • rales
  • hypoxemia
  • increased A:a (alveolar to arterial) gradient
  • decreased diffusion diffusion capacity
25
Q

absorption atelectasis

A
  • nitrogen (insoluble so normally stays in lungs to keep them open) replaced by oxygen
  • under-ventilated alveoli have decreased volume, due to a greater uptake of oxygen
  • increases pulmonary shunting; widen A-a gradient
26
Q

induced hypoventilation

A
  • chronic CO2 retainers rely on hypoxic drive
  • peripheral chemoreceptors are triggered by hypoxemia
  • increased O2 can lead to hypoventilation
27
Q

fire hazard

A
  • oxygen supports combustion

- use extreme caution with head and neck cases

28
Q

retinopathy

A
  • oxygen therapy in neonates can lead to vascular proliferation, fibrosis, retinal detachment, and blindness
  • safe O2 administration –> PaO2 60-80 mmHg
29
Q

population at risk for oxygen induced retinopathy

A
  • <36 weeks gestational age; but actually can happen up to 44 weeks gestational age
  • weight <1500 gm
  • up to 44 weeks gestational age are considered high risk
30
Q

hypercapnia

A
  • increased PaCO2 > 45 mmHg

- causes –> increased CO2 concentration, increased CO2 production

31
Q

causes of hypercapnia

A
  • increased alveolar dead space –> decreased alveolar perfusion, interruptions in pulmonary circulation, pulmonary disease
  • decreased alveolar ventilation –> can be central or peripheral, resp depression most common cause in immediate postoperative period
32
Q

clinical manifestations of hypercapnia

A
  • directly produces vasodilation of peripheral vessels
  • indirectly increases HR after catecholamine release
  • produces effects due to an acidotic state
  • non-specific signs –> HA, N/V, sweating, flushing, shivering, restlessness
33
Q

CNS considerations with hypercapnia

A
  • regulation of ventilatory drive –> increased CO2 makes you want to breath more
  • cerebral blood flow –> increases 1-2 mL/100g/min for every 1 mmHg increase in PaCO2
34
Q

CV considerations with hypercapnia

A
  • depression of smooth muscle and cardiac muscle
  • increased catecholamine release
  • vasodilation versus vasoconstriction - because of the increased catecholamine release; might see initial vasodilation then vasoconstriction from SNS activation; HOWEVER if SNS blockade, vasodilation will prevail
35
Q

pulmonary considerations with hypercapnia

A
  • increased RR
  • increased PVR (b/c CO2 increases vasoconstriction of pulmonary vessels)
  • R shift of oxy-Hgb dissociation curve
36
Q

treatment for hypercapnia

A
  • adjust treatment to cause

- increase Ve

37
Q

hypocapnia

A
  • CO2 < 35 mmHg

- cause usually iatrogenic

38
Q

clinical manifestations of hypocapnia

A
  • decreased CBF, decreased ICP
  • decreased CO, coronary constriction
  • hypoxemia may result from hypoventilation
39
Q

hypocapnia treatment

A

-decrease minute ventilation