Oxygen Therapy

Question 1

DO2=

Answer 1

CO x arterial O2 content

Question 2

VO2 (oxygen use)

Answer 2

Co x O2a - O2v

Question 3

Oxygen Extraction Ratio

Answer 3

normal 25% (art v venous O2 difference)

heart has very high demand

Question 4

hypoxemia

Answer 4

deficiency of O2 in blood

Question 5

hypoxia

Answer 5

O2 delivery to tissues not sufficient to meet metabolic demand

Question 6

hypoxic hypoxia

Answer 6

shunting or pulmonary diffusion defects. drug OD, COPD, emphysema, atelectasis

Question 7

circulatory hypoxia

Answer 7

decreased CO r/t CHF or MI

Question 8

hemic hypoxia

Answer 8

decreased HGB content or function

Question 9

demand hypoxia

Answer 9

inceased MVO2 like fever, seizure, MH

Question 10

hystotoxic hypoxia

Answer 10

inability of cells to utilize O2 ex) cyanide toxicity

Question 11

possible methods to improving oxygenation

Answer 11

increase VE
increase CO
increase O2 carrying capacity
optimize V/Q
decrease O2 consumption
increase FiO2

Question 12

nasal cannula

Answer 12

flow rates 1-6L/min

FiO2 increases about 4% per L/min

Question 13

simple face masks

Answer 13

FiO2 40-60%

minimum 6L flow required to prevent rebreathing (minimum is pts MV)

Question 14

face masks with reservoirs

Answer 14

FiO2 60-100%

Question 15

venturi masks

Answer 15

more precise FiO2 24-50%

need set flow rate to actually deliver O2 (should say on mask)

Question 16

what does high FiO2 over long periods do

Answer 16

decrease ciliary movement
alveolar epithelial damage
interstitial debris

Question 17

absorption atelectasis

Answer 17

nitrogen is replaced by O2
under ventilated alveoli have decreased volume (due to greater uptake of O2)
increases pulmonary shunting (widens A-a gradient)

Question 18

induced hypoventilation

Answer 18

chronic CO2 retainers rely on hypoxic drive ex) COPD
peripheral chemoreceptors are triggered by hypoxemia
increased O2 can lead to hypoventilation

Question 19

retinopathy

Answer 19

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

Question 20

causes of hypercapnea

Answer 20

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)

Question 21

clinical manifestations of hypervapnea

Answer 21

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

Question 22

considerations for hypercapnia:
CNS
CV
pulmonary

Answer 22

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

Question 23

hypocapnea clinical manifestations and tx

Answer 23

decrease in CBF, decrease in CO, coronary constriction, hypoxemia may result from hypoventilation
treatment: decrease MV