13. Oxygen Therapy, Delivery, and Common Drugs Flashcards
How does oxygenation occur?
Oxygen diffuses from alveoli into capillaries at the lungs, transported to tissues, and must diffuse again from capillaries to cells of tissue
Oxygen transport
- Two determinant of oxygen delivery?
- How does it occur?
- O2 content x cardiac output
(How much and how easily it is transported) - Convection/diffusion
Decreased Cardiac Output and 3 main changes in the body
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
Factors affecting oxygen utilization (O2 diffusion)
- Quality and rate of blood flow (high CO, less time for diffusion because of high flow)
- Pressure difference from capillary and tissue
- Capillary surface area
- Capillary permeability
How does increased metabolic demand affect oxygen utilization (diffusion)?
Capillary dilation, increases SA, reduced resistance to flow, movement of oxygen into cell increased
Why does the saturation of venous blood decrease with cardiac output?
SvO2 (saturation of venous blood):
- will be decreased (less than 60%, normal is 70%) due to increased extraction ratio
Basic metabolic O2 needs
300ml/min/m2
Oxygen Therapy: When is it needed
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
Vitals indicating hypoxia
PaO2 < 80mmHg
SpO2 < 90%
Oxygen therapy: what does it intend to correct
- Hyoxaemia (low oxygenation - PaO2)
- Minimize WOB & stress on heart
- Decrease symptoms of hypoxia
Symptoms of Hypoxia (DD-TT-PP-HR)
Headache, restlessness
Tachycardia, Tachypnea
Dyspnea, Disorientation
Peripheral vasoconstriction, Paleness (cyanosis)
Oxygen delivery devices: variable rate devices
- 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
Normal Respiratory flow rate
25-30L/min
- low flow is always below this level so that some room air is breathed in
Types of Variable Rate Devices
- Nasal prongs
- cheap, patient compliant, enables pt to eat/drink, delivers 24-40% oxygen - Nasal prongs with reservoir
- higher rates of O2 delivery - 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
Flow rates and FiO2
Flow(L/min)-FiO2(%) 1-24 2-28 3-32 4-36 5-40 6-44
High Flow Devices
- 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
Why is O2 no longer humidified?
- 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
Implications for the absence of humidification? Alternative?
- Dry air may dry out mucosa, thicken secretions, and make it difficult to cough secretions outs
- Alternative: increase fluids (IV, oral fluids, nasal lubricants)
Monitor oxygen content - 2 methods
- ABG
- Indirect SpO2 (pulse oximetry) — estimates arterial oxyhaemoglobin saturation using wavelength lights (does not work in: jaundice, dark nail polish, anaemia, poor perfusion, cold fingers)
Hypercapnic Respiratory Failure: stimulus to breath in healthy vs. diseased
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)
Why do we NOT administer oxygen in high concentrations
Administering O2 in high concentrations diminishes the drive to keep breathing
- Decreased hypoxic drive:
increased PaO2 will suppress the peripheral chemoreceptors - Further elevation of PaCO2
- Respiratory failure
Why is respiratory failure due to hypercapnia rare?
- PT’s with COPD are accustomed to higher PaCO2
- relative rise in PaCO2 is small
Oxygen prescription in COPD:
- Long-term
- Stable
- Ambulatory oxygen/Without chronic hypoxaemia
- Amount?
- Prescribed with PaO2<55mmHg or SpO2<88% on room air at rest. Long term oxygen therapy is >15hrs/day
- Should be clinical stable (no exacerbation previous 4 weeks)
- May be considered for ambulatory oxygen if they desaturated at least 4% to level below 90%
- Oxygen is a drug - and the least amount prescribed for desired effect
COPD: indications for ambulatory oxygen
Ambulatory oxygen:
- improvement in 10% walking distance
- dyspnea score
COPD: desired SpO2 and O2
SpO2 88-90% (healthy is >92%)
- most will be on 1-4L/min O2
Oxygen Toxicity: Breathing 100% oxygen (FiO2)
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
Oxygen Toxicity:
- CXR
- damage/structural changes
- end stage toxicity
- 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)
How does Absorption Atelectasis occur?
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
Aerosol Therapy: Nebuliser
Suspension of liquid/solid particles in gas
- hydrates dried mucus
- improves cough efficiency
- restores/maintains function of mu conciliar year elevator
Particle size —> delivery location
- Large particles are deposited higher up
- smaller particles are deposited deeper into lungs
- 1-2um best for alveolar deposition
Common Respiratory drugs
- Mucolytics
- breaks up mucus, e.g. cystic fibrosis
- mistabron - Corticosteroids
- prevents inflammation, e.g. asthma
- Pulmicort - B-adrenergic agonists
- stimulate SNS to cause bronchodilation
- Ventolin - Anticholingeric
- bronchodilation/blocks PSN to cause bronchoconstriction, e.g. COPD
- Spiriva
Puffer Types
RED: anti-inflammatory
PURPLE: anti-inflammatory + bronchodilator
GREEN: long lasting bronchodilator (maintenance throughout the entire day)
