Oxygen Therapy Flashcards
oxygen delivery
-DO2 = CO x arterial oxygen content (CaO2)
failure of oxygen delivery leads to
- hypotension
- acidosis
- coagulopathy
oxygen use
VO2 = CO x (PaO2 - PvO2)
- oxygen extraction ratio; normal is about 25%
- heart has very high demand
why is oxygen therapy important in surgical patients?
they are at increased risk for hypoxia and hypoxemia
hypoxemia
deficiency of oxygen in the blood
hypoxia
oxygen delivery to the tissues is not sufficient to meet the metabolic demand
anesthesia goal
maintain oxygenation and ventilation that is sufficient to meet the metabolic demand
oxygen therapy goal
prevent and correct hypoxemia and tissue hypoxia
hypoxic hypoxia
shunting or pulmonary diffusion defect; can be caused by a drug OD, COPD exacerbation, asthma, atelectasis, or emphysema
circulatory hypoxia
decrease in CO to the point where oxygen delivery to the tissues is inadequate; common causes are CHF or MI
hemic hypoxica
a decreased Hgb content (such as anemia) and/or decreased function of Hgb; anemia, carboxy-hemoglobinemia, methemoglobinemia
demand hypoxia
an increase in the metabolic rate or oxygen demands of the body such that insufficient oxygen is delivered to the body; fever, seizure, MH
histotoxic hypoxia
inability of the cells themselves to use oxygen such as in cyanide poisoning
hypoxia S/S
- vasodilation
- tachycardia
- tachypnea
- cyanosis
- confusion
- lactic acidosis
improving oxygenation in mechanically ventilated patients
- treatment tailored to cause
- increase VE
- increase CO
- increase O2 carrying capacity
- optimize V/Q relationship
- decrease O2 consumption
- increase FiO2
nasal cannula
- flow rates 1-6 L/min
- FiO2 increases about 4% per L/min
simple face mask
- 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
face masks with reservoirs
-FiO2 60-100%
Venturi Masks
- more precise FiO2 24-50%
- Bernoulli’s Principle
oxygen toxicity
- 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
what is generally considered a “safe” amount of oxygen?
100% for up to 10-20 hours
what has been shown to have oxygen toxicity?
50-60% for more than 24-72 hours
high risk populations for oxygen toxicity?
- older than 70 years
- history of radiation to the lungs/chest
- bleomycin (used to treat various types of cancer)
s/s of oxygen toxicity
- cough
- dyspnea
- rales
- hypoxemia
- increased A:a (alveolar to arterial) gradient
- decreased diffusion diffusion capacity
absorption atelectasis
- 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
induced hypoventilation
- chronic CO2 retainers rely on hypoxic drive
- peripheral chemoreceptors are triggered by hypoxemia
- increased O2 can lead to hypoventilation
fire hazard
- oxygen supports combustion
- use extreme caution with head and neck cases
retinopathy
- oxygen therapy in neonates can lead to vascular proliferation, fibrosis, retinal detachment, and blindness
- safe O2 administration –> PaO2 60-80 mmHg
population at risk for oxygen induced retinopathy
- <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
hypercapnia
- increased PaCO2 > 45 mmHg
- causes –> increased CO2 concentration, increased CO2 production
causes of hypercapnia
- 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
clinical manifestations of hypercapnia
- 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
CNS considerations with hypercapnia
- 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
CV considerations with hypercapnia
- 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
pulmonary considerations with hypercapnia
- increased RR
- increased PVR (b/c CO2 increases vasoconstriction of pulmonary vessels)
- R shift of oxy-Hgb dissociation curve
treatment for hypercapnia
- adjust treatment to cause
- increase Ve
hypocapnia
- CO2 < 35 mmHg
- cause usually iatrogenic
clinical manifestations of hypocapnia
- decreased CBF, decreased ICP
- decreased CO, coronary constriction
- hypoxemia may result from hypoventilation
hypocapnia treatment
-decrease minute ventilation
