PaCO 2 must fall into one of three categories:
1. below 35 mmHg (4.6 kPa) is defined as respiratory alkalosis (alveolar hyperventilation);
2. between 35 and 45 mmHg (between 4.6 and 6 kPa) is defined as normal alveolar ventilation;
3. above 45 mmHg (6 kPa) is defined as respiratory acidosis (ventilatory failure).
Classification of the arterial pH relative to the PaCO2 allows the clinician to determine whether the primary abnormality is ventilatory (respiratory acid-base imbalance) or metabolic acid-base imbalance.
Acute respiratory alkalosis (alveolar hyperventilation)
In this condition PaCO2 < 35 mmHg (4.6 kPa), pH > 7.45, base deficit is less than 3 mmol/l, and bicarbonate is less than 22 mmol/l.
Significant renal compensation has not been elicited. The alveolar hyperventilation is assumed to be recent and probably secondary to either hypoxemia or respiratory center stimulation (pain, fright, anxiety, etc.).
Chronic respiratory alkalosis (alveolar hyperventilation)
In this condition PaCO2 < 35 mmHg (4.6 kPa) and pH is between 7.40 and 7.45.
This most probably represents a long-standing hyperventilation (at least 24 h) with renal compensation for the respiratory alkalosis. Subacute or partly compensated respiratory alkalosis (alveolar hyperventilation)
In this condition PaCO2 < 35 mmHg (4.6 kPa), pH is between 7.46 and 7.50, base deficit is greater than 3 mmol/l, and bicarbonate is less than 22 mmol/l.
The renal system seldom compensates for an alkalotic pH below 7.45; with long-standing alveolar hyperventilation this is more common. Completely compensated metabolic acidosis
In this condition PaCO2 < 35 mmHg (4.6 kPa), pH is between 7.35 and 7.40, base deficit is greater than 3 mmol/l, and bicarbonate is less than 22 mmol/l. Alveolar hyperventilation in the presence of a pH between 7.35 and 7.40 reflects a primary metabolic acidosis in which the ventilatory system has normalized the pH.
This rarely represents a primary alveolar hyperventilation because it is very unusual for either the renal or the pulmonary system to overcompensate. Further, the renal system seldom compensates for a respiratory alkalosis below pH 7.45.
Partly compensated metabolic acidosis
In this condition PaCO2 < 35 mmHg (4.6 kPa), pH < 7.35, base deficit is greater than 5 mmol/l, and bicarbonate is less than 18 mmol/l.
This most probably represents a primary metabolic acidosis to which the ventilatory system has responded with hyperventilation. The ventilatory system is incapable of providing the work of breathing necessary to compensate completely for the metabolic acidosis.
In this condition PaCO2 is between 35 and 45 mmHg (4.6 and 6 kPa), pH > 7.45, base excess is greater than 3 mmol/l, and bicarbonate is greater than 26 mmol/l.
This represents a primary metabolic alkalosis to which the ventilatory system has not responded. This interpretation may change when accompanied by hypoxemia since that could represent a chronic CO2 retainer that is relatively hyperventilating in response to an acute arterial oxygenation deficit.
In this condition PaCO2 is between 35 and 45 mmHg (4.6 and 6 kPa), pH < 7.35, base deficit is greater than 3 mmol/l, and bicarbonate is less than 22 mmol/l.
This represents a metabolic acidosis to which the ventilatory system has not responded. It is reasonable to expect some alveolar hyperventilation when pH < 7.30 unless the patient is unable to increase alveolar ventilation.
Partly compensated metabolic alkalosis
In this condition PaCO2 > 45 mmHg (6 kPa), pH > 7.45, base excess is greater than 3 mmol/l, and bicarbonate is greater than 26 mmol/l.
This usually represents a primary metabolic alkalosis for which the ventilatory system has partly compensated. It may represent acute alveolar hyperventilation (respiratory alkalosis) superimposed on chronic ventilatory failure. It is rare to see this phenomenon with pH < 7.50 because a conscious person will seldom significantly hypoventilate to compensate for a metabolic alkalosis. It is unusual to see a PaCO2 rise higher than 60 mmHg (8 kPa) in a conscious person, but an obtunded or unconscious patient can manifest higher PaCO2 levels in response to a severe metabolic alkalosis.
Chronic ventilatory failure (respiratory acidosis)
In this condition PaCO2 > 45 mmHg (6 kPa), pH is between 7.35 and 7.45, base excess is greater than 3 mmol/l, and bicarbonate is greater than 26 mmol/l.
This is an exception to the overcompensation rule in that it is common for the chronic hypercapnic patient to have pH > 7.40. This chronic hypercapnia probably reflects an altered intracellular CO 2 concentration because CO2 excretion has been less than CO2 production for a considerable period of time. The elevated peripheral (intracellular) CO 2 stores create an increase in intracellular H + concentration that is relatively independent of the blood pH. Progressive intracellular adaptation to the elevated PaCO2 and H+ occurs so that essential mitochondrial functions can be maintained.
Acute ventilatory failure (respiratory acidosis)
In this condition PaCO2 > 45 mmHg (6 kPa), pH < 7.35, base excess is less than 3 mmol/l, and bicarbonate is greater than 22 mmol/l. This represents an acute decompensation or failure of the ventilatory mechanism. This is often a life-threatening process and requires appropriate and rapid attention. Step 2: assessment of arterial oxygenation
Following classification of the PaCO2 and pH values (Table,...!), complete assessment of the arterial oxygenation status requires measurement of PaO2, oxyhemoglobin saturation SaO2 (per cent), and hemoglobin content (g/dl).
Table 4 Seven primary blood gas classifications
Although normal hemoglobin content in adults is greater than 12 g/dl, it is reasonable to assume that a content above 8 g/dl provides an adequate oxygen-carrying capacity for patients with adequate myocardial function; patients with heart disease probably require at least 10 g/dl. In the following discussion a hemoglobin content of 10 g/dl is assumed.
This measurement provides the best single indication of oxygen content because almost all the oxygen in the blood exists as oxyhemoglobin. As shown in Fig 1,
SaO2 has a predictable relationship with PaO2 under normal circumstances. Any departure from that relationship implies an alteration in the affinity of hemoglobin for oxygen. Essentially, a shift to the right (decreased affinity) is present when the SaO2 is less than predicted for the PaO2, and vice versa. When the affinity is decreased, it is prudent to base clinical judgments on SaO2 rather than PaO2.
Fig. 1 The hemoglobin dissociation curve for oxygen. The vertical axis represents the portion of the potential oxygen-carrying hemoglobin sites that are chemically combined with oxygen (percentage saturation). The horizontal axis represents the partial pressure of oxygen in the plasma in mmHg (kPa = mmHg * 0.133). The non-linear relationship between percentage saturation and PO2 accounts for the vast majority of oxygen reserves in the blood. Normally, hemoglobin is 50 per cent saturated with oxygen at a plasma PO2 of 27 mmHg (3.6 kPa); this is designated P50. Normal mixed venous (pulmonary arterial) blood is 75 per cent saturated with oxygen at a plasma PO2 of 40 mmHg (5.3 kPa). Arterial blood with a plasma PO2 of 60 mmHg (8.0 kPa) is normally 90 per cent saturated with oxygen, arterial blood with a plasma PO2 of 80 mmHg (10.7 kPa) is normally 95 per cent saturated with oxygen, and arterial blood with a plasma PO2 of 97 mmHg (12.9 kPa) is normally 97 per cent saturated with oxygen. (Reproduced with permission from Shapiroefa/ (19,9,4,),.)
This is the traditional measurement upon which the clinical assessment of arterial oxygenation is based. Arterial hypoxemia in adults is defined as PaO2 < 80 mmHg (10.7 kPa) while breathing room air. Since there is no clinically significant improvement in the oxygen delivery capabilities of blood with 90 per cent SaO2 compared with 95 per cent SaO2, most practitioners of critical care medicine and respiratory care consider clinically significant hypoxemia to be present at PaO2 < 60 mmHg (8 kPa).
The maintenance of adequate tissue oxygenation with moderate hypoxemia (PaO2 between 40 and 60 mmHg (5.3 and 8 kPa)) primarily depends upon cardiovascular function and oxygen consumption. However, severe hypoxemia (PaO2 < 40 mmHg (5.3 kPa)) must be considered a direct threat to tissue oxygenation because there is a diminished oxygen 'driving force' in the systemic capillaries and the oxyhemoglobin saturation is less than 75 per cent, which increases the affinity of hemoglobin for oxygen because oxygen does not occupy the fourth heme site. This combination of increased affinity and decreased driving force significantly diminishes the movement of oxygen molecules from the systemic capillaries to the extracellular fluid compartment.
Since many patients are already receiving oxygen therapy when blood gas values are obtained, it is essential that the probable hypoxemic state be assessed so that the oxygen therapy is not removed unnecessarily. Apart from special circumstances, oxygen therapy should not be removed to assess hypoxemia.
In this condition PaO2 remains below 60 mmHg (8 kPa) despite increased inspired oxygen concentration. Corrected hypoxemia
On oxygen therapy, PaO2 is between 60 mmHg (8 kPa) and 100 mmHg (13.3 kPa). Hypoxemia is assumed to exist on room air because PaO2 is less than the predicted normal level for that oxygen therapy.
PaO2 is less than the minimal predicted normal at room air for that oxygen therapy but greater than 100 mmHg (13.3 kPa). It is assumed that hypoxemia exists on room air so that oxygen therapy is required, but it can be decreased.
When the actual PaO2 is greater than the theoretically minimal PaO2 for that FiO2, the patient may not be hypoxemic on room air. However, it is recommended that the patient is re-evaluated at a significantly lower FiO 2 before discontinuing oxygen therapy completely.
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