Oxygen Therapy Flashcards
DO2=
CO x arterial O2 content
VO2 (oxygen use)
Co x O2a - O2v
Oxygen Extraction Ratio
normal 25% (art v venous O2 difference)
heart has very high demand
hypoxemia
deficiency of O2 in blood
hypoxia
O2 delivery to tissues not sufficient to meet metabolic demand
hypoxic hypoxia
shunting or pulmonary diffusion defects. drug OD, COPD, emphysema, atelectasis
circulatory hypoxia
decreased CO r/t CHF or MI
hemic hypoxia
decreased HGB content or function
demand hypoxia
inceased MVO2 like fever, seizure, MH
hystotoxic hypoxia
inability of cells to utilize O2 ex) cyanide toxicity
possible methods to improving oxygenation
increase VE increase CO increase O2 carrying capacity optimize V/Q decrease O2 consumption increase FiO2
nasal cannula
flow rates 1-6L/min
FiO2 increases about 4% per L/min
simple face masks
FiO2 40-60%
minimum 6L flow required to prevent rebreathing (minimum is pts MV)
face masks with reservoirs
FiO2 60-100%
venturi masks
more precise FiO2 24-50%
need set flow rate to actually deliver O2 (should say on mask)
what does high FiO2 over long periods do
decrease ciliary movement
alveolar epithelial damage
interstitial debris
absorption atelectasis
nitrogen is replaced by O2
under ventilated alveoli have decreased volume (due to greater uptake of O2)
increases pulmonary shunting (widens A-a gradient)
induced hypoventilation
chronic CO2 retainers rely on hypoxic drive ex) COPD
peripheral chemoreceptors are triggered by hypoxemia
increased O2 can lead to hypoventilation
retinopathy
O2 therapy in neonates can lead to vascular proliferation, fibrosis, retinal detachment, and blindness
<36 weeks gestational age, weight <1500gm, up to 44 weeks gestational age are considered high risk
sage O2 administration is PaO2 60-80mmHg
anemia, infection, and acidosis increase risk
causes of hypercapnea
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 postop period)
clinical manifestations of hypervapnea
vasodilation of peripheral vessels
indirectly increases HR after catechol release
produces effects due to an acidotic state
non specific signs influde HA, N/V, berating, flushing, shivering, restlessness
considerations for hypercapnia:
CNS
CV
pulmonary
CNS: regulation of ventilatory drive, CBF
CV: depression of smooth muscle and cardiac muscle
increased catecholamine release, will see initial vasodilation then SNS= vasoconstriction which always wins over
pulmonary: increased RR, PVR. can increase pulmonary artery pressures 60%, R shift of dissociation curve
hypocapnea clinical manifestations and tx
decrease in CBF, decrease in CO, coronary constriction, hypoxemia may result from hypoventilation
treatment: decrease MV
