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The metabolic effects of oxygen: The breathing of high partial pressures of oxygen (PO, > 0.6 Bars) causes predictable, but usually reversible, tissue damage. This primarily affects the lungs (Lorrain-Smith effect) and the brain (Paul Bert effect). Oxygen donates an electron to hydrogen ions (H*) to form water as the final phase of cellular metabolism (energy production). Oxygen is delivered to tissues via the blood, some in solution, but most bound to haemoglobin. Oxygen diffuses into cells along its diffusion gradient and in particular into the mitochondria of cells. Mitochondria contain numerous enzymes responsible for cellular metabolism and are profoundly “hypoxic” (PO, <5 mm Hg or 0.007 Bars). Various substrates, for example those produced by the breakdown of glucose, lose hydrogen (under the action of enzymes Called dehydrogenases) to a coenzyme acceptor (which is thus reduced). Oxygen is not necessary for this process, but is essential to regenerate the coenzyme acceptor as molecular oxygen is the final hydrogen acceptor. Oxygen radicals and oxygen toxicity. During these metabolic events, a superoxide (O;) and other free radicals such as hydrogen peroxide (H,O,) are produced in small amounts. A toxic accumulation is prevented by cellular enzymes such as superoxide dismutase (SOD) and catalase (which breaks down H,O,) and other antioxidants such as glutathione and vitamin E and C. These antioxidants scavenge oxygen radicals; reduced glutathione is the principal scavenging agent. An increase in the PO, in tissues induces the formation of increased levels of all ‘oxygen radicals and this in turn induces an increased formation of SOD and catalase. Only when the rate of formation of the radicals exceeds the rate of enzyme induction ‘oxygen radicals accumulate in the cells. The most vulnerable cellular components reactive substances such as O; and H,O, are the sulphydryl groups in proteins, acid and coenzyme A. Oxidation of these entities will inhibit key rogenases in glucose metabolism and will inhibit cell membrane transport 3, Different tissues vary in their vulnerability, and lung, brain ai ‘blood to be the most affected. In addition to this metabolic’ disruption in the 270 lungs and brain, the metabolicall i Progressive phase of collagen nea. Sieiaee im eae Oxygen toxicity of both the jun: in is it i 9 and brain is reversible in i system heen et ae man en to global convulsions relatively cayenne men : ee eb ne damage fare. In the lungs however, the path ical wr aeispaene oe reves bie when fibrosis occurs. The initial event in the ie ‘i iatarel Brut wed by a decrease in surfactant production and cant uidaake oh | losure and atelectasis (evidenced by a reduced vital sen avecisn eas oa ad te a change in alveolar cell morphology (ype | finally lung fibrosis with a loss of aaa. "pe ices), reduced lung compliance and Sources: Acott, C and Gorman, D Manual of Di " hens eee, iving and Hyperbaric Medicine 4" Ed Royal Adelaide Lobar, Tiller and Hensley Fluid, Electrol Interns. lyte and Acid-base Disturbances A Practical Guide for Pulmonary oxygen toxicity: In regard to the dose-time relationship of the inspired PO, and decrements of vital capacity, it would appear that a PO, < 0.6 Bar can be tolerated indefinitely. Individuals respond in a varied degree to elevated oxygen exposures, but a symptomless decrease in vital capacity is the usual first event, followed by retrosternal chest discomfort and pain, and eventually shortness of breath. These decrements in vital capacity reverse rapidly when the PO, is lowered below 0.6 Bars. A logarithmic dose calculation system exists to determine the likely decrease in vital capacity. This is called the “Units of Pulmonary Toxic Dose" (UPTD) and is based on 1 unit UPTD being the result of breathing 100% oxygen for one minute at one bar absolute pressure. This system i not as predictive as originally claimed. A UPTD of 615 ic equivalent to a 2% decrease in vital capacity and would be associated with mild symptoms of retrosternal discomfort or irritation. A UPTD score of 1425 is associated with a decrease in vital capacity of about 10%. Wright published a scale of percentage decrements of vital capacity and UPTD in 1972 —see Table 6. A decrease of 10% would be expected to recover completely, however, it may take a longer recovery time. Recoverytrom a decrease of VC of up to 45% has been recorded but it would be unwise to assume that all individuals would recover from this toxic decrease. Tabi p [UPTO units [Percentage decreaseinVC. ae nase — 2190 8. INTERPRETATION OF BLOOD GAS RESULTS NORMAL BLOOD GAS VALUES (breathing room ait which one is ae BE +e —renal compensation Pony 4 —tespiratory compensation AtEALosis BE -ve —renal compensation Fos, 4} —tespiratory compensation PITFALLS IN BLOOD GAS INTERPRETATION A ‘ie i rare spine? Blood gas results should be a reflection of the patient's Anxiety or pain associated with arterial puncture cf tinal conion. tthe results gem inconsistent wih cates the polent to the clinical picture, consider the following: a bood at picture of seute respiratory alkali, eg. 3 1, Was the sample arterial blood? Poo, At rest (patent not eyanoced, normal. Hb) pH 7.83 | BE 0 pies : | Which may complicate an already abnormal blood gas Peo, $-10 mm higher i picture, BE Variable reduction '. Isthere a laboratory error? I ee " acDitreees in BE and pH ate not predisable and tlt sgey ak Mek combed: et ‘on many variables: should be. i Temperature, metabolic rate, tissue perfusion, ‘ check that the actual pH corresponds approxi ‘oxygenation, haemoglobin, etc, ‘mately with your estimate. Question the person who drew the blood i if there is a gross discrepancy ring the laboratory and if une ' certain repeat the blood gases on a second sample. ino ni Rok: the, zeenl Tobe checked. Was there a delay in analysing the specimen? | COMMON CLINICAL CAUSES OF ABNORMAL Leukocytes (and to a lesser extent red cells) continue { BLOOD GAS PATTERNS active glycolysis at room temperature after blood is adidas drawa:'e. Metabolic ‘st WBC 7,00, room temperature: Aiba ttoniont pH falls 0.07 lactic acidosis BEfalls2 mmoles! | per hour | { Primary co, Hes S mm 5 ‘acetozolamide Seboens *Aminosol' infusions le at 37°C, fever or hypothermia in the ient may lead to serious errors in blood gas inter- Metabolic alkalosis mee. —vomiting ‘An abnormal should be recorded on the request form and the technician should be asked to —naso-gastric suction analyse the blood at the temperature of the patient. =a 48 = deel eee hans —Caihigt syndrome and hyperaldosteroniss rice and Bic eo Cael syndrome Respiratory acidosis Any cause of alveolar hypoventilation: Siren claves ng die eae ‘obstruction (e.g. blocked endo-tracheal osher causes of dsp coma —weakness or paralysis of respiratory muscles muscle dystrophy | ‘myasthaenia gravis Guillain-Barré syndrome ‘muscle relaxants severe asthma (clevated CO, is unusual in ‘asthma and is a dangerous sigh of exhaustion) Respiratory alkalosis ‘Any cause of alveolar hyperventilation: anxiety —acute ‘asthma (most acute asthmatics have a tow Peo) pulmonary oedema —pulmonary embolism pneumothorax Tite nee any cise alieylate toxiity (in dls) ‘Combined respiratory and metabolic avidosis —eardiac arrest severe respiratory failure drug overdose with respiratory and circulatory depression ‘Combined respiratory alkalosis and metabolic acidosis massive ‘embolism oer oot” acute haemorrhagic shock.