3. Hyperbaric oxygen and oxygen toxicity Flashcards
Predicted PaO2 from FiO2
young adult in good health and breathing room air therefore
will have a PaO2 of 20.93 0.66 = 13.3 kPa (100 mmHg).
hyperventilation
can increase this to around 16 kPa (from the alveolar gas equation, the fall in PaCO2
allowing a rise in PaO2),
but further rises are possible only by enriching the inspired
oxygen concentration
Saturation, partial pressure and content:
13.3 kPa,
haemoglobin is almost 100% saturated. Further increases in inspired oxygen (FiO2)
can therefore increase the oxygen saturation (SpO2) only marginally, although the
PaO2 will rise substantially
the arterial oxygen content rises from
around 19 ml dl1 to only 21 ml d if breathinf 100% @ room air
Hyperbaric oxygenation
application of Henry’s Law, which
states that the number of molecules (in this case oxygen) which dissolve in the
solvent (plasma) is directly proportional to the partial pressure of the gas at the
surface of the liquid
very high arterial PaO2 values
(greater than 80 kPa) can be obtained. Thus, at 2 atmospheres the PaO2 will be 175
kPa. Even at these levels, however, the venous content will only be of the order of
18 ml dl1, and it is not until the blood is exposed to oxygen at 3 atmospheres of
pressure, at which the arterial content is 25.5 ml d
Content is
determined by the product of the [Hb] [% saturation] [1.31] (O2-carrying
capacity of Hb) plus dissolved oxygen. Dissolved oxygen (0.003 ml dl1 mmHg1) is
small and is usually ignored, except under these hyperbaric conditions when it
assumes great importance.
Decompression sickness
depth, the tissues become supersaturated with nitrogen. If the
diver ascends too rapidly, the partial pressure of nitrogen in tissues exceeds the
ambient pressure, and so the gas forms bubbles in the circulation and elsewhere
Hyperbaric treatment mimics controlled ascent from depth, and
this allows the nitrogen to wash out exponentially without causing symptoms.
Infection
Infection: the evidence supports the use of hyperbaric oxygen therapy as part of the
management of patients with bacterial infections. The main indications are for
anaerobic bacterial infections, particularly with clostridia, osteomyelitis and necrotizing
soft tissue infections. Oxygen-derived free radicals are bactericidal.
Carbon monoxide
Carbon monoxide (CO) poisoning: the half-life of CO while breathing 100%
oxygen is reduced to an hour. This is reduced further to about 20 minutes in a
hyperbaric chamber, but, unless the chamber is on site, the transfer time alone will
make this benefit negligible.
Delayed wound healing:
hyperbaric oxygen therapy may be of benefit to patients in
whom wound healing is delayed by ischaemia
Anaemic hypoxia:
Anaemic hypoxia: Jehovah’s witnesses who have lost blood but whose religious
beliefs prohibit transfusion, and others in whom very low haemoglobin concentrations
have compromised oxygen delivery to tissues, have been managed successfully
using hyperbaric oxygen.
Adverse Effects at Atmospheric Pre
Pulmonary pathology
pathological changes which begin with tracheobronchitis,
neutrophil recruitment and the release of inflammatory mediators.
Surfactant production is impaired, pulmonary interstitial oedema appears, followed,
after around 1 week of exposure, by the development of pulmonary fibrosis.
Mechanism of toxicity
: this is complex and not fully elucidated.
Although oxygen is a stable molecule,
it is readily transformed into substances that are potentially toxic.
In various normal metabolic pathways and enzymatic reactions, oxygen becomes
partially reduced to a superoxide anion (O2 –).
Both H2O2 and O2
– are potentially toxic and in higher concentrations
interact to produce highly reactive species of which the hydroxyl free radical is the
most dangerous
Oxygen toxicity
: the major problem is dose-related direct toxicity.
Dose–time curves have been constructed to allow the recommendation that
100% should be administered for no longer than 12 hours at atmospheric pressure,
80% for no longer than 24 hours
and 60% for no longer than 36 hours.
An FiO2 of 0.5 can be maintained indefinitely.
Defence mechanisms
: up to a partial pressure of oxygen of about 60 kPa, a number
of endogenous antioxidant enzymes are effective. These include catalase, superoxide
dismutase and glutathione peroxidase
Clinical features of oxygen toxicity
These are most marked in conscious patients who are breathing oxygen under
hyperbaric conditions.
include retrosternal discomfort, carinal irritation and coughing.
This becomes more severe with time, with a burning pain that is accompanied by the
urge to breathe deeply and to cough. As exposure continues, symptoms progress to
severe dyspnoea with paroxysmal coughing.
CNS symptoms may supervene, with nausea, facial twitching and numbness as
well as disturbances of taste and smell. Convulsions may occur, preceded by a
premonitory aura.
long-term ventilated patients in whom high inspired oxygen concentrations tend
to be the norm, the non-specific clinical signs will be those of progressively impaired
gas exchange with decreased pulmonary compliance
Obstetrics + Neonates
An FiO2 as high as 0.6 is associated with only a small increase in umbilical venous
oxygenation. However, what do rise are markers of oxygen free radical activity in
both mother and baby. These radicals deplete intrinsic antioxidant systems
Neonatal hyperoxia is
known, moreover, to mediate tissue damage in conditions as diverse as retinopathy
of prematurity, necrotizing enterocolitis, bronchopulmonary dysplasia and intracranial
haemorrhage.
Toxic Effects under Hyperbaric Conditions
This toxicity presents the major limitation of hyperbaric oxygen therapy. It is dose dependent and affects not only the lung but also the CNS, the visual system and
probably the myocardium, liver and renal tract.
Pulmonary toxicity: oxygen at 2 atmospheres produces symptoms in healthy volunteers
at 8–10 hours, together with a quantifiable decrease in vital capacity which
starts as early as 4 hours. This persists after exposure ceases.
CNS: oxygen at 2 atmospheres is associated with nausea, facial twitching and
numbness, olfactory and gustatory disturbance. Tonic–clonic seizures may then
supervene without any prodrome, although some subjects report a premonitory aura.
Eyes: hyperoxia may be associated in adults with narrowing of the visual fields and
myopia.
