Oxygen Therapy Basics

Question 1

What flow should be selected for: Nasal Prongs?

Answer 1

1-6 lpm

Question 2

What flow should be selected for: simple mask?

Answer 2

6-10lpm

• but if it goes over 8, just switch to NRB or escalate further if indicated

Question 3

What flow should be selected for: NRB Mask?

Answer 3

6lpm to whatever keeps the reservoir inflated

Question 4

What flow should be selected for: Large Volume Neb?

Answer 4

Flush

• For it to be a fixed performance device, the total flow must be greater than 60lpm

Question 5

How to calculate total flow

Answer 5

1. magic box to find air/o2 ratio
2. Add the ratio parts togehter and multiply by flow (i.e 40% (3+1) = 48)

Question 6

Tank calculations: H tank conversion factor?

Answer 6

• H: 3.14
• M: 1.57
• E: 0.28
• D: 0.16

Question 7

Tank calculations: M tank conversion factor?

Answer 7

• H: 3.14
• M: 1.57
• E: 0.28
• D: 0.16

Question 8

Tank calculations: E tank conversion factor?

Answer 8

• H: 3.14
• M: 1.57
• E: 0.28
• D: 0.16

Question 9

Tank calculations: D tank conversion factor?

Answer 9

• H: 3.14
• M: 1.57
• E: 0.28
• D: 0.16

Question 10

Indications for O2 therapy

Answer 10

1. Hypoxemia
2. Labored breathing/dyspnea
3. Increased myocardial work

Question 11

Signs and symptoms of hypoxemia

Answer 11

1. Tachycardia
2. Dyspnea
3. Cyanosis (unless anemia is present)
4. Impairment of special senses
5. Headache
6. Slight hyperventilation and mental disturbances

Question 12

Why are high O2 concentrations at risk of causing atelectasis?

Answer 12

High O2 concentrations can washout nitrogen in the lungs and reduce production of surfactant.

• Collapse occurs bc less gas remains in the alveoli when O2 is diffused into the blood leading to collapse
• loss of nitrogen reduces the alveolar volume and can increase the physiological shunt, potentially causing hypoxemia

Question 13

Why is hypoxemia a consequence of untreated anemia?

Answer 13

Anemia reduces the carrying capacity of blood meaning tissue may be deprived of O2

• Hb can be increased via pack RBC

Question 14

What is O2 toxicity?

Answer 14

High O2 concentrations lead to the production of free radicals which are hazardous to tissue.

• Important with ARDS when lung tissue is already inflamed
• Free radicals can contribute to the inflammation and damage to blood vessels in the lungs caused by endotoxins
• Free radicals can damage the delicate air sacs in the lungs, contributing to the breakdown of lung tissue characteristic of emphysema.

Question 15

What O2 target can you safely assume to prevent ROP in infants?

Answer 15

Maintain PaO2 below 80 mmHg

• normal Pao2 in infants is 50-70mmHg

Question 16

Normal hemoglobin level (Hb)

Answer 16

12-16 g/DL or 120-160 g/L

g/dL = g/100ml = g% = vol%

Question 17

Why are simple O2 therapies like NRB effective for CO poisoning?

Answer 17

CO affinity for Hb is faster than O2 but also gets released more readily when PaO2 is high

• hyperbarics can further increase dissociation of hb from CO

Question 18

What are diffusion defects and what is the key issue?

Answer 18

Problems with gas crossing the ac membrane. Examples would be:

• pulmonary fibrosis (thickened ac membrane)
• Pulmonary edema (fluid in alveoli)
• pneumonitis
• remember, Oxygen moves by diffusion from alveoli to blood, down a partial pressure gradient.

Question 19

Why are increased O2 concentration therapies (like NRB) effective for diffusion defects?

Answer 19

Giving high FiO2 increases increase alveolar PO2 (PaO2)) which:

• increases the gradient for diffusion
• helps O2 cross the barrier
• tldr; even though membrane is thicker or flooded, enough pressure = enough push.

Question 20

Why are high O2 concentration therapies alone not affective in managing hypoxemia due to anatomic right to left shunts (or CHDs, AV malformations, severe atelectasis, ARDS etc.)

Answer 20

Blood passes via areas where there’s no gas exchange at all. increases FiO2 isn’t effective bc blood never sees alveolar O2 causing refractory hypoxemia

• TLDR; no gas contact and no alveolar ventilation = total arterial PO2 doesn’t rise

Question 21

What is core problem with alveolar hypoventilation?

Answer 21

Inadequate ventilation to clear CO2 leading to:

• Hypercapnia
• Resp acidosis
• Often associated with neuromuscular disorders, obesity hypoventilation, COPD exacerbations, or CNS depression

Question 22

What therapy should you choose for alveolar hypoventilation?

Answer 22

PAP (BiPAP or CPAP)

• optiflow is supportive, not corrective in this case. It is good as a bridge or temporary step in treatment in this case.

Question 23

When should you use aerosols vs PAP in clinical therapies?

• don’t fixate too hard on this

Answer 23

Question 24

What is the core issue with stagnant (circulatory/ischemic) hypoxia?

Answer 24

O2 content and carrying capacity are normal, but capillary persuion is diminished as a result of:

• Decreased HR
• Decreased CO
• shock
• embolism

Question 25

Why is EtOH poisoning (alcohol) relevant when a patient is hypoxic?

Answer 25

Cyanide and EtOH poisoning impair oxidative enzymes resulting in hypoxia. **its rare** but good to consider. - Is accompanied by increased venous PO2 levels

Question 26

When should you consider using a low flow device ?

Answer 26

1. Regular and consistent vent pattern 2. RR less than 25 b/min 3. consistent Vt of 300-700 (not fluctuating but within that range at a consistent tightish range)

Question 27

How do you calculate inspiratory flow

Answer 27

Inspiratory flow = Vt (L)/Inspiratory time (s) - Flow will be in L/s so mulitply by 60 to change to L/min - Note, don't forget to convert mL to L as Vt is often in mL