13. Oxygen Therapy, Delivery, and Common Drugs

Question 1

How does oxygenation occur?

Answer 1

Oxygen diffuses from alveoli into capillaries at the lungs, transported to tissues, and must diffuse again from capillaries to cells of tissue

Question 2

Oxygen transport

1. Two determinant of oxygen delivery?
2. How does it occur?

Answer 2

1. O2 content x cardiac output
   (How much and how easily it is transported)
2. Convection/diffusion

Question 3

Decreased Cardiac Output and 3 main changes in the body

Answer 3

Lower O2 delivered to tissues but consumption is not altered (body still needs the same amount of O2), resulting in:

• increased extraction ratio (same amount of O2 taken out of Hb)
• SvO2 (saturation of venous blood): when O2 delivered to tissues, it’s only as much tissue requires

Question 4

Factors affecting oxygen utilization (O2 diffusion)

Answer 4

1. Quality and rate of blood flow (high CO, less time for diffusion because of high flow)
2. Pressure difference from capillary and tissue
3. Capillary surface area
4. Capillary permeability

Question 5

How does increased metabolic demand affect oxygen utilization (diffusion)?

Answer 5

Capillary dilation, increases SA, reduced resistance to flow, movement of oxygen into cell increased

Question 6

Why does the saturation of venous blood decrease with cardiac output?

Answer 6

SvO2 (saturation of venous blood):

- will be decreased (less than 60%, normal is 70%) due to increased extraction ratio

Question 7

Basic metabolic O2 needs

Answer 7

300ml/min/m2

Question 8

Oxygen Therapy: When is it needed

Answer 8

Instances that inhibit the transport of O2 from atmosphere to the tissues causing a patient to become hypoxic. Supplemental oxygen may be necessary to maintain adequate oxygenation

Question 9

Vitals indicating hypoxia

Answer 9

PaO2 < 80mmHg

SpO2 < 90%

Question 10

Oxygen therapy: what does it intend to correct

Answer 10

• Hyoxaemia (low oxygenation - PaO2)
• Minimize WOB & stress on heart
• Decrease symptoms of hypoxia

Question 11

Symptoms of Hypoxia (DD-TT-PP-HR)

Answer 11

Headache, restlessness
Tachycardia, Tachypnea
Dyspnea, Disorientation
Peripheral vasoconstriction, Paleness (cyanosis)

Question 12

Oxygen delivery devices: variable rate devices

Answer 12

• low flow rate
• provide oxygen at rate less than minute volume of patient
  (MV = TV x RR)
• caution: rates higher than 6L/min may cause mucosal irritation and drying, less effective if patient is a mouth breather

Question 13

Normal Respiratory flow rate

Answer 13

25-30L/min

- low flow is always below this level so that some room air is breathed in

Question 14

Types of Variable Rate Devices

Answer 14

1. Nasal prongs
   - cheap, patient compliant, enables pt to eat/drink, delivers 24-40% oxygen
2. Nasal prongs with reservoir
   - higher rates of O2 delivery
3. Non-rebreather mask (i.e. airplane mask)
   - Can deliver up to 100% oxygen as it contains reservoir bag
   - Has flaps and valves to prevent room air mixing with oxygen

Question 15

Flow rates and FiO2

Answer 15

Flow(L/min)-FiO2(%)
1-24
2-28
3-32
4-36
5-40
6-44

Question 16

High Flow Devices

Answer 16

• Delivers specific oxygen concentration regardless of patient’s ventilatory pattern, therefore everything that the patient breathes is from this device
• exceeds normal inspiratory flow rate (exceeds normal MV)
  E.g. Venturi mask - entertains room air and mixes it with fixed concentration with 100% oxygen

Question 17

Why is O2 no longer humidified?

Answer 17

• oxygen should be delivered warm and humidified, but instead is delivered dry from canister/large tank
• no longer humidified because of respiratory diseases (e.g. SARS) as it is believed water was a breeding ground for bacteria and viruses

Question 18

Implications for the absence of humidification? Alternative?

Answer 18

• Dry air may dry out mucosa, thicken secretions, and make it difficult to cough secretions outs
• Alternative: increase fluids (IV, oral fluids, nasal lubricants)

Question 19

Monitor oxygen content - 2 methods

Answer 19

1. ABG
2. Indirect SpO2 (pulse oximetry) — estimates arterial oxyhaemoglobin saturation using wavelength lights (does not work in: jaundice, dark nail polish, anaemia, poor perfusion, cold fingers)

Question 20

Hypercapnic Respiratory Failure: stimulus to breath in healthy vs. diseased

Answer 20

Healthy: triggered by increase in PaCO2 first, then drop in PaO2
- increase in CO2 to avoid acidosis

Diseased: mainly COPD, response to PaCO2 is blunted because they live with an increase in CO2.
- main stimulus: hypoxic drive (hypoxia in peripheral chemoreceptors)

Question 21

Why do we NOT administer oxygen in high concentrations

Answer 21

Administering O2 in high concentrations diminishes the drive to keep breathing

1. Decreased hypoxic drive:
   increased PaO2 will suppress the peripheral chemoreceptors
2. Further elevation of PaCO2
3. Respiratory failure

Question 22

Why is respiratory failure due to hypercapnia rare?

Answer 22

• PT’s with COPD are accustomed to higher PaCO2

- relative rise in PaCO2 is small

Question 23

Oxygen prescription in COPD:

1. Long-term
2. Stable
3. Ambulatory oxygen/Without chronic hypoxaemia
4. Amount?

Answer 23

1. Prescribed with PaO2<55mmHg or SpO2<88% on room air at rest. Long term oxygen therapy is >15hrs/day
2. Should be clinical stable (no exacerbation previous 4 weeks)
3. May be considered for ambulatory oxygen if they desaturated at least 4% to level below 90%
4. Oxygen is a drug - and the least amount prescribed for desired effect

Question 24

COPD: indications for ambulatory oxygen

Answer 24

Ambulatory oxygen:

• improvement in 10% walking distance
• dyspnea score

Question 25

COPD: desired SpO2 and O2

Answer 25

SpO2 88-90% (healthy is >92%) | - most will be on 1-4L/min O2

Question 26

Oxygen Toxicity: Breathing 100% oxygen (FiO2)

Answer 26

``` prolonged periods = lung damage Increase in cell metabolism, overproduction of free radicals by-products of cell metabolism 1. Kills/damage cells 2. Overwhelms antioxidant system 3. Lung damage mimics bronchopneumonia ```

Question 27

Oxygen Toxicity: - CXR - damage/structural changes - end stage toxicity

Answer 27

- patchy infiltrates, most notably lower lobes - damage to alveolar system; membranes leak; interstitial oedema; ARDS; worsens shunting - end stage: hyaline membrane formed (pulmonary fibrosis, hypertension)

Question 28

How does Absorption Atelectasis occur?

Answer 28

Breathing 100% oxygen, particularly if there is blockage/mucus plug in airway then all the O2 is absorbed from the alveolus and nothing is left to keep the alveoli open. No new incoming O2 due to blockage/mucus plug and alveolus collapses - worsens shunting

Question 29

Aerosol Therapy: Nebuliser

Answer 29

Suspension of liquid/solid particles in gas - hydrates dried mucus - improves cough efficiency - restores/maintains function of mu conciliar year elevator

Question 30

Particle size —> delivery location

Answer 30

- Large particles are deposited higher up - smaller particles are deposited deeper into lungs - 1-2um best for alveolar deposition

Question 31

Common Respiratory drugs

Answer 31

1. Mucolytics - breaks up mucus, e.g. cystic fibrosis - mistabron 2. Corticosteroids - prevents inflammation, e.g. asthma - Pulmicort 3. B-adrenergic agonists - stimulate SNS to cause bronchodilation - Ventolin 4. Anticholingeric - bronchodilation/blocks PSN to cause bronchoconstriction, e.g. COPD - Spiriva

Question 32

Puffer Types

Answer 32

RED: anti-inflammatory PURPLE: anti-inflammatory + bronchodilator GREEN: long lasting bronchodilator (maintenance throughout the entire day)