Hazards Of Oxygen Therapy

Front 1

Hazards of High PaO2

Back 1

Oxygen Induced Hypoventilation

Retinopathy of Prematurity

Front 2

Hazards of High FIO2

Back 2

Absorption Atelectasis

Oxygen Toxicity

Front 3

Who is at risk for Oxygen Induced Hypoventilation?

Back 3

Unstable Chronic PCO2 Retainers with PaO2's above 60 mm Hg

Front 4

Hazards of Oxygen Induced Hypoventilation

Back 4

Elevation of PCO2

Decrease in pH (Acidosis)

Acute superimposed on Chronic CO2 retention

Front 5

What is the Mechanism for Oxygen Induced Hypoventilation?

Back 5

Under debate

Possibly Bohr/Haldane Effect

Front 6

Strategy to minimize and avoid Oxygen Induced Hypoventilation

Back 6

Identify pt early

Treat conservatively with supplemental O2

Establish specific outcome targets
-PaO2 50-60 mm Hg
-Monitor vent. and acid/base balance
-SpO2 monitoring is inadequate to capture the hazard

Use non-variable oxygen device if pt is still unstable

Front 7

ROP Def.

Back 7

A disorder of retinal blood vessel development in the premature infant

Front 8

What can ROP cause?

Back 8

Retinal vascular proliferation

Scarring

Retinal Detachment

Blindness

Front 9

What is the cause of ROP?

Back 9

Prematurity

Front 10

Qualifications of a premature infant

Back 10

All babies less than 1500g birth weight

Younger than 32 weeks (28 weeks) gestation

Front 11

What types of premature infants are at risk for ROP?

Back 11

PaO2 > 80 mm Hg

Low birth weights
-<1kg 20-25% incidence
-1-1.5 kg 2% incidence

Patent ductus arteriosus

Front 12

Patent Ductus Arteriosus

Back 12

Duct between the aorta and pulm artery stays open after birth

Front 13

What is the mechanism for ROP?

Back 13

Hyperoxia causes severe vasoconstriction of retinal blood vessels THEN vessels will grow too rapidly once they develop

Front 14

4 Factors that must coincide for ROP

Back 14

Avascular retina at birth

Development of immature retinal vessels

High and/or fluctuating tissue O2

Abnormal chemical/hormonal signals

Front 15

How to minimize/avoid ROP
NPR=Neonatal Resuscitation Protocol

Back 15

Identify pt at risk early

Treat conservatively with O2

Establish Outcome targets
-PaO2 50-70 mm Hg
-SpO2 84-94%

Hazard not specific to O2 therapy

Front 16

Who is at risk for absorption Atelectasis?

Back 16

Chronic CO2 retainers (severe COPD) and pt with Neuromuscular Disease

Pt on FIO2 > 0.5

Hazard increases as FIO2 increases 1.0

Risk is aggravated by
-shunt like effect
-partial airway obstruction
-small tidal vol.
(absorption will occur quicker)

Front 17

What will absorption atelectasis cause?

Back 17

Alv. collapse due to absorption of oxygen

Atelectasis reduces FRC

Reduced FRC
-worsens hypoxemia
-increases work of breathing

Front 18

What is the mechanism for absorption atelectasis?

Back 18

Nitrogen makes up 78% of alv. gas on room air

Nitrogen is a alv stabilizing gas

Increased FIO2's replace Nitrogen with O2

Decreased V/Q results in oxygen absorption faster than oxygen replacement in alv.

Absorption can lead to alv. instability = collapse

Front 19

Strategy to minimize/avoid hazards of Absorption Atelectasis

Back 19

FIO2 < or equal to 0.5 appear safe

Consider PEEP if PaO2 is unacceptable on FIO2 of 0.5

Re-evaluate target PaO2 if FIO2 > 0.5 is needed

Front 20

Who is at risk for Oxygen Toxicity?

Back 20

Pt on FIO2> 0.5

Hazards increases as FIO2 increase toward 1.0

Risk is aggravated by
-time of exposure to increased FIO2 (short term nto at risk)

Front 21

Risk of Oxygen Toxicity is lessened by

Back 21

Previous oxygen use

Previous development of severe acute pulm. disease

Front 22

Hazards of Oxygen Toxicity?

Back 22

Series of potentially revesible pathophysiological inflammatory changes in lung tissue

Pulmonary edema NOT caused by LSHF

Front 23

Three phases of Oxygen Toxicity

Back 23

Exudative Phase = damage phase

Proliferative phase = repair phase

Recovery Phase = Lung remodeling

Front 24

Phase 1 of ARDS/Oxygen Toxicity

Back 24

Exudative Phase

Acute Damage Phase

Capillary Endothelium Leaks

Alv. Type I cells
-decreased oxygen diffusion = decreased P/F ratio

Alv. Type II cells
-collapsed alv due to lack of surfactant = decreased FRC

Front 25

Phase 2 of ARDS/Oxygen Toxicity

Back 25

Fibroliferative Phase

Early Repair Phase

Lungs cont. to fill with fluid and scar tissue begins to form

This phase can begin as early as 5-7 days after initial onset and has an increased risk of death

Front 26

Phase 3 of ARDS/Oxygen Toxicity

Back 26

Recovery Phase

Longterm Outcome

Fluid begins to drain and the lungs begin to heal

Many ARDS survivors will return to normal lung function within 6-12 months

Some survivors will have lasting effects due to scarring and damage

Front 27

Mechanism for Oxygen Toxicity

Back 27

Free radicals in lung tissue increase with increased PAO2

PAO2 increases in direct proportion to FIO2

Free Radical cause cellular damage

Anti-oxidants protect cells from free radicals

Front 28

Oxygen Free Radicals

Back 28

Hydrogen Peroxide

Super Oxide Radicals

Singlet Excited

Hydroxyl Radical

Front 29

Intracellular Defense Anti- Oxidants

Back 29

Superoxide Dismutase

Catalase

Glutathione Peroxide

Glutathione

Vit E

Vit C

Front 30

Clinical Manifestations of Oxygen Toxicity

Back 30

Tracheobrochitis

Cough

Substernal Pain

Nausea

Vomiting

Anorexia

Parathesia

Refractory Hypoxemia

Diffuse bilateral infiltrates on CXR

Atelectasis

Decreased Comp.

Increased WOB

Mortality > 50%

Front 31

Strategy to minimize/avoid Oxygen Toxicity

Back 31

FIO's <0.5 appear to be safe

Consider PEEP therapy if PaO2 is unacceptable on FIO2 of 0.5

Re-evaulate target PaO2 if FIO2 > 0.5 is needed