almost always requires treatment with o2-> caused by severe hypoxemic hypoxia; occurs when there is 5 grams of reduced hemoglobin
When are the exceptions for giving o2 therapy for cyanosis
patients who are hypercarbic (high levels of CO2) or polycythemic (high levels of hb); premies
What is refractory Hypoxemia?
When Fi02 is increased and there is little to no increase in Pa02 (shunting= perfused, not ventilated)
What is the treatment for refractory hypoxemia?
Recruitment of more ACM (ventilator)
What are the hazards of o2?
Retinopathy of Prematurity
O2 induced hypoventilation
N2 Washout Atelectasis
What causes O2 toxicity?
High concentrations of O2 (FIO2) for prolonged periods of time (can lead to pulmonary 02 toxicity); Free Radical Theory
Free Radical Theory
When o2 concentration is greater than 50% there is not enough superoxide disumutase
What does o2 toxicity lead to?
ARDS, Bronciopulmonary dysplasia (neonates), Lung damage (often irreversible)
How fast does o2 toxicity take to occur?
At 100% O2= 1 day
At 50% O2= 3 days
Who can get oxygen toxicity?
How can you prevent oxygen toxicity?
Lowering dosage as fast as possible and want to improve O2 with as little FIO2 as possible
What are ways to increase Fi02?
recruitment of ACM (ventilator)
What is retinopathy of prematurity?
Permanent blindness or significantly impaired vision
What causes retinopathy of prematurity?
PaO2 greater than 80 torr that can cause retinal vasoconstriction- scarring of the retina and eventually pulling it out of position
Who can get retinopathy of prematurity?
Premature babies and low birth weights- the smaller a baby is at birth, the more likely that baby is to develop ROP; occurs with infants who have and haven't been on o2
What can RCS do to prevent retinopathy of prematurity?
Keep PaO2 60-80 torr for premies
Spo2 alarm 92-97%
premies on O2 need opthomology consult
Who gets O2 induced hypoventilation?
Occurs in chronic hypercarbic patients who are given o2
Who are chronic hyperbaric patients?
COPD, blue-bloaters, CF, Chronic Bronchitis- patients who have a long -term obstructive lung disease that decreases their ability to exhale CO2
What are the controls of ventilation?
Somatic drive, carbic drive, and hypoxic drive
What is the somatic drive?
Runs voluntary control of breathing
What controls the carbic drive?
Controlled by central chemoreceptors located in the medulla and indirectly detect CO2 levels through H. Practically instaneous feedback loop.
How does the carbic drive respond to high levels of PaCO2 (hypercarbic)
Increase frequency of breaths to blow off CO2
how does the carbic drive respond to low levels of PaCO2 (hypocarbic)
Decreases frequency of breaths to retain CO2
What kind of sensor is the carbic drive considered to be
extremely sensitive and adaptable to CO2 levels
What kind of sensor is the hypoxic drive considered to be?
A "fixed" sensor that doesn't adjust; stimulates breathing only when needed
What controls the hypoxic drive?
Peripheral chemoreceptors located in the carotid bodies and the aortic arch; turns on when PaO2 is less than 60 torr
What happens when the Pa02 is less than 60 torr
Overrides the carbic drive and Increases the frequency of breathing so that PaO2 increases
Is the hypoxic drive normally on?
No- it's not active under normal conditions
What happens in chronic hypercarbic patients (chronically high levels of CO2 and decreaed Pa02 and ph)when they are given O2 therapy?
O2 Induced Hypoventilation-> Decrease frequency of breathing and more shallow; chronic hypercarbic patients run on the hypoxic drive all the time because they have defects with their carbic drive; if increase PaO2 too much so above 60 torr hypoxic drive turns off and since carbic drive doesn't work they get no o2 and will pass out
How does N2 Washout Atelectasis occur?
Occurs when the nitrogen is all gone because of high O2 concentrations washing all out; shunting= collapsed lungs -> nitrogen keeps lungs inflated and without it will collapse
What are the two conditions that are required for N2 washout atelectasis?
High FiO2 (80-100)