Hypoxemia is the most harmful symptom occurring during respiratory failure and usually needs correction. However, there is not a fixed threshold of 'harmful' PaO2, as it depends on previous history, age, and hemodynamic conditions. What is most important is the global clinical assessment, i.e. the presence of signs suggesting inadequate oxygenation such as increased autonomic outflow, impairment of the central nervous system, etc. During acute respiratory acidosis, most of symptoms caused by inadequate oxygenation may also be due to hypercapnia and acidosis. However, hypoxemia must be corrected first.
Hypoxemia may occur in the presence of either low or high partial alveolar oxygen pressure PAO2. Low PAO2 is unavoidable during CO2 retention when the patient breathes room air since
where FAO2 is the alveolar fraction of oxygen, FiO2 is the inspired fraction of oxygen, and FACO2 is the alveolar fraction of CO2. This type of hypoxemia can easily be corrected by increasing FiO2. For example, when PACO2= 80 mmHg (10.66 kPa) (FACO2= 11.2), FAO2 can be restored to normal by increasing FiO 2 from 21 to 26.6 per cent.
Hypoxemia with high FAO2 is due to parenchymal disease, when part of the lung parenchyma is collapsed or consolidated, and represents true oxygenation impairment. Correction of this kind of hypoxemia (due to right to left shunt) is discussed elsewhere.
Various combinations of PO2 and PCO2 may occur, and their physiopathological meanings are listed in Table 1 (the conditions of high altitude or inhalation of hypoxic gas mixtures are excluded).
Table 1 Relationship between PO2 and PCO2
As with PO2, there is no threshold value of PCO2 or pH which is 'harmful' per se. Many factors may condition the response to increased CO2, such as the rate of increase in PCO2 (acute or chronic), age, and cardiovascular conditions. If associated with normoxia, near-normal pH, consciousness, and hemodynamic stability, a high PCO2 does not need any therapeutic intervention. The indications for mechanical assistance should be based on a global clinical assessment, considering the three main consequences of increased PCO2, i.e. tissue acidosis, impairment of the central nervous system, and the cardiovascular response ( Bidaniei a/ 1994).
The immediate buffering of PCO2 by fixed buffers (mainly hemoglobin) leads to an increase in HCO 3- of about 1 mmol/l for every increase of 10 mmHg (1.33 kPa) in
As molecular CO2 enters the cell membrane faster than HCO3-, it is generally believed that intracellular pH decreases more than extracellular pH. However, there is increasing evidence that the intracellular buffers limit tissue acidosis, and hypercapnia is well tolerated. There is no doubt that if cellular acidosis develops, cell function and viability are impaired.
Increasing PCO2 may have a severe effect on central nervous system activity. Experimentally, the brain excitability first decreases, then increases, with associated seizures, and finally decreases to anesthesia and coma. CO 2 is one of the major determinants of the cerebral vascular reactivity, both directly and indirectly (through pH changes), and acute hypercapnia may result in an increased cerebral blood flow and intracranial pressure.
The effect of hypercapnia on the cardiovascular system depends on the balance between the direct depressant effects of PCO2 on heart and peripheral vascular smooth muscles and the increased plasma levels of epinephrine (adrenaline) and norepinephrine (noradrenaline) due to activation of the sympathetic nervous system. In normal conditions, the net result is an increase in cardiac output and a slight decrease in peripheral resistance. The arterial pressure tends to rise and the pulmonary artery pressure may increase substantially. It is important to remember that these reactions are observed in intact subjects. In patients given b-blockers, for example, hypotension and decreased cardiac output may be observed.
It is evident that the indications for the mechanical treatment of respiratory acidosis are based on three symptoms: hypoxemia, hypercapnia, and acidosis. However, no threshold values can be established, and only the history (chronic or acute derangement), the trends (the rate and type of deterioration), and the clinical signs (hemodynamic instability and level of consciousness) should be used to determine whether mechanical treatment is appropriate.
However, other factors should be taken into consideration (i.e. the precipitating factors and the time required for correction of acidosis) before mechanical support is planned.
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