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PTHER 544 - Cardiorespiratory > 13. Oxygen Therapy, Delivery, and Common Drugs > Flashcards

13. Oxygen Therapy, Delivery, and Common Drugs Flashcards

1
Q

How does oxygenation occur?

A

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

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2
Q

Oxygen transport

  1. Two determinant of oxygen delivery?
  2. How does it occur?
A
  1. O2 content x cardiac output
    (How much and how easily it is transported)
  2. Convection/diffusion
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3
Q

Decreased Cardiac Output and 3 main changes in the body

A

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
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4
Q

Factors affecting oxygen utilization (O2 diffusion)

A
  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
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5
Q

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

A

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

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6
Q

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

A

SvO2 (saturation of venous blood):

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

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7
Q

Basic metabolic O2 needs

A

300ml/min/m2

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8
Q

Oxygen Therapy: When is it needed

A

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

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9
Q

Vitals indicating hypoxia

A

PaO2 < 80mmHg

SpO2 < 90%

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10
Q

Oxygen therapy: what does it intend to correct

A
  • Hyoxaemia (low oxygenation - PaO2)
  • Minimize WOB & stress on heart
  • Decrease symptoms of hypoxia
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11
Q

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

A

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

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12
Q

Oxygen delivery devices: variable rate devices

A
  • 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
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13
Q

Normal Respiratory flow rate

A

25-30L/min

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

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14
Q

Types of Variable Rate Devices

A
  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
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15
Q

Flow rates and FiO2

A 
Flow(L/min)-FiO2(%)
1-24
2-28
3-32
4-36
5-40
6-44
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16
Q

High Flow Devices

A
  • 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
17
Q

Why is O2 no longer humidified?

A
  • 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
18
Q

Implications for the absence of humidification? Alternative?

A
  • Dry air may dry out mucosa, thicken secretions, and make it difficult to cough secretions outs
  • Alternative: increase fluids (IV, oral fluids, nasal lubricants)
19
Q

Monitor oxygen content - 2 methods

A
  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)
20
Q

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

A

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)

21
Q

Why do we NOT administer oxygen in high concentrations

A

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
22
Q

Why is respiratory failure due to hypercapnia rare?

A
  • PT’s with COPD are accustomed to higher PaCO2

- relative rise in PaCO2 is small

23
Q

Oxygen prescription in COPD:

  1. Long-term
  2. Stable
  3. Ambulatory oxygen/Without chronic hypoxaemia
  4. Amount?
A
  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
24
Q

COPD: indications for ambulatory oxygen

A

Ambulatory oxygen:

  • improvement in 10% walking distance
  • dyspnea score
25
Q

COPD: desired SpO2 and O2

A

SpO2 88-90% (healthy is >92%)

- most will be on 1-4L/min O2

26
Q

Oxygen Toxicity: Breathing 100% oxygen (FiO2)

A 
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
27
Q

Oxygen Toxicity:

  • CXR
  • damage/structural changes
  • end stage toxicity
A
  • 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)
28
Q

How does Absorption Atelectasis occur?

A

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

29
Q

Aerosol Therapy: Nebuliser

A

Suspension of liquid/solid particles in gas

  • hydrates dried mucus
  • improves cough efficiency
  • restores/maintains function of mu conciliar year elevator
30
Q

Particle size —> delivery location

A
  • Large particles are deposited higher up
  • smaller particles are deposited deeper into lungs
  • 1-2um best for alveolar deposition
31
Q

Common Respiratory drugs

A
  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
32
Q

Puffer Types

A

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

PTHER 544 - Cardiorespiratory (12 decks)

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