Arterial Blood Gases

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Partial Pressure of Arterial Carbon Dioxide

ALVEOLAR VENTILATION Carbon dioxide diffuses so rapidly that the Paco2 usually provides an excellent index of the adequacy of ventilation. If the Pa co2 is greater than normal in a patient with a normal or low arterial pH, one can assume that V A is inadequate. The patient may have a low respiratory rate or tidal volume or may also have increased dead space due to emphysema, pulmonary emboli, or increased carbon dioxide production as in thyroid storm or sepsis. An elevated Pa co2 in the presence of metabolic alkalosis usually reflects compensatory effort to restore arterial pH to normal while an increased Pa co2 in a patient with metabolic acidosis generally indicates impending respiratory failure.

DEAD SPACE When the ventilation of an alveolar-capillary unit is normal but perfusion of the alveolar capillary is absent, the ventilation of these alveoli and their associated airways is referred to as dead space, or high ventilation-perfusion (V/Q) mismatching. V ds and the tidal volume (Vt) are often expressed as a ratio (Vds/Vt). This is determined in a pulmonary function laboratory (or a bedside metabolic cart) by measuring the Pa co2, measuring the average expired gas (PEco2) (not to be confused with ETco2), and using the Bohr equation:

The normal values are

When the physiologic dead space is increased, some of the work of ventilation is wasted because a greater fraction of ventilated air never reaches the functioning alveolar-capillary units. A patient with a dead space greater than 0.6 generally requires mechanical ventilation to maintain normal Pa co2.

TRANSPORT OF CARBON DIOXIDE IN THE BLOOD Under resting conditions, each 100 mL of blood transports an average of 4 mL of carbon dioxide from the tissues to the lungs. Transport of carbon dioxide is not as great a problem as is transport of oxygen because, even under the most abnormal conditions, carbon dioxide can usually be transported in far greater quantities than can oxygen. However, carbon dioxide in the blood does affect acid-base balance.

The carbon dioxide formed in cells diffuses out in the form of carbon dioxide rather than bicarbonate because the cell membrane is almost impermeable to bicarbonate ions. As the carbon dioxide enters the capillary, it initiates a number of almost instantaneous reactions essential for carbon dioxide transport.

First, a small portion of the carbon dioxide is transported to the lungs dissolved in plasma. The dissolved portion is approximately 0.36 mL of carbon dioxide in each 100 mL of blood. This is about 9% of all carbon dioxide transported.

Much of the dissolved carbon dioxide in the blood reacts with water to form carbonic acid; a reaction facilitated by carbonic anhydrase inside the red blood cells speeds up the reaction about 500-fold. The reaction occurs so rapidly that it reaches almost complete equilibrium within a fraction of a second. This allows tremendous amounts of carbon dioxide to react with red blood cell water even before the blood leaves the tissue capillaries.

In another fraction of a second, the carbonic acid formed in the red blood cells dissociates into hydrogen and bicarbonate ions. Most of the hydrogen ions then combine with the hemoglobin in the red blood cells because hemoglobin is a powerful acid-base buffer. At the same time, many of the bicarbonate ions diffuse into the plasma; to offset this ionic shift, chloride ions diffuse into the red blood cells. This diffusion is made possible by the presence of a special bicarbonate-chloride carrier protein in the red blood cell membrane that rapidly shuttles these two ions in opposite directions. Thus, the chloride content of venous red blood cells is greater than that of arterial red blood cells. This phenomenon is called the chloride shift.

The reversible combination of carbon dioxide with water in the red blood cells, under the influence of carbonic anhydrase, accounts for at least 60 to 70% of all the carbon dioxide transported from the tissues. Indeed, when a carbonic anhydrase inhibitor (acetazolamide) is administered to block the action of carbonic anhydrase in the red blood cells, carbon dioxide transport from the tissues becomes very poor and the tissue P co2 rises abruptly.

CARBAMINOHEMOGLOBIN AND CARBAMINOPROTEINS Carbon dioxide also reacts directly with hemoglobin to form carbaminohemoglobin (Hb-CO2). Since this reversible reaction occurs with a very loose bond, the carbon dioxide is easily released into the alveoli, where the P co2 is lower than that in the tissue capillaries. A small amount of carbon dioxide (usually equivalent to about 0.5 to 1.0 meq/L of bicarbonate) also reacts in this way with the plasma proteins, forming carbaminoproteins. This reaction is much less significant because the quantity of these proteins is only about one-fourth to one-half the quantity of hemoglobin.

The theoretical quantity of carbon dioxide that can be carried to the lungs in combination with hemoglobin and plasma proteins is approximately 20 to 30% of the total quantity transported—that is, about 1.5 mL of carbon dioxide in each 100 mL of blood. However, this reaction is much slower than the reaction of carbon dioxide with water, and it is doubtful that more than 15 to 25% of the total quantity of carbon dioxide is transported this way.

CARBON DIOXIDE DISSOCIATION CURVE Carbon dioxide can exist in the blood as free carbon dioxide and in chemical combinations with water, hemoglobin, and plasma proteins. The total quantity of carbon dioxide combined with the blood in all forms depends on the Pa co2.

The normal blood Paco2 averages about 40 mmHg in arterial blood and 46 mmHg in mixed venous blood. Although the normal total concentration of carbon dioxide in the blood is about 50 mL/dL (vol%), only 4 mL/dL of this is actually exchanged during normal transport of carbon dioxide. Thus, the concentration of carbon dioxide rises to about 52 mL/dL after the blood passes through the tissues and falls to about 48 mL/dL after the blood passes through the lungs.

EFFECT OF THE OXYGEN-HEMOGLOBIN REACTION ON CARBON DIOXIDE TRANSPORT: THE HALDANE EFFECT An increase in the carbon dioxide level in the blood causes oxygen to be displaced from the hemoglobin, and this promotes oxygen release to tissues at the capillary level. The reverse is also true; binding of oxygen with hemoglobin tends to displace carbon dioxide as blood moves through the pulmonary capillaries. Indeed, this so-called Haldane effect is quantitatively far more important in promoting carbon dioxide transport than the Bohr effect (see the section on "Oxyhemoglobin Saturation") is in promoting oxygen transport.

CHANGE IN BLOOD ACIDITY DURING CARBON DIOXIDE TRANSPORT The carbonic acid formed when carbon dioxide enters the blood in the tissue capillaries decreases the pH. However, the buffers of the blood prevent the hydrogen ion concentration from rising greatly. Ordinarily, arterial blood has a pH of approximately 7.40, and as the blood acquires carbon dioxide in the tissue capillaries, the pH falls to approximately 7.35. The reverse occurs when carbon dioxide is released from the blood in the lungs. Under conditions of high metabolic activity or when blood flow through the tissues is extremely sluggish, the decrease in pH in the blood as it leaves the tissues can be 0.50 or more.

CHANGES IN RESPIRATORY QUOTIENT As stated above, the RQ is the ratio of CO2 produced to O2 consumed. The RQ for the standard patient metabolizing a mixed diet of carbohydrates, fats, and protein is approximately 0.8. The RQs of the individual components are listed below:

Thus, the RQ can change in patients who eat (or are fed) diets containing predominantly fat or carbohydrates. Relying heavily on carbohydrates for a patient with little respiratory reserve can lead to respiratory acidosis due to an increase in required V M. However, the effect of diet on RQ is usually only an issue in the intensive care unit in a minority of patients with severe lung disease who are attempting to wean from mechanical ventilation.

MONITORING OXYGENATION AND VENTILATION A patient who is awake, alert, comfortable, and cooperative and has normal vital signs is generally oxygenating and ventilating adequately. However, if a patient is tachypneic and/or tachycardic and appears to be anxious and/or confused, hypercarbia or hypoxemia should be suspected. In comatose patients, it is sometimes very difficult to judge how well the patient is oxygenating or ventilating without serial blood gas determinations.

Cyanosis as a sign of inadequate oxygenation is almost worthless when the hemoglobin is less than 10 g/dL. Under such circumstances, the arterial oxygen saturation (Sao2) must be less than 65%, corresponding to a Pao2 of about 30 to 35 mmHg, before the patient looks cyanotic. It must be remembered that oxygenation and ventilation are two separate systems. A frequent clinical misconception is that a patient with an adequate Sa o2 must be ventilating adequately. This assumption is incorrect and dangerous, particularly with patients who are receiving supplemental oxygen. This is discussed below under "Noninvasive Monitoring, Pulse Oximetry."

Partial Pressure of Arterial Oxygen

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The Pao2 in normal, healthy young adults breathing room air at sea level is considered to be 90 to 100 mmHg. The Pa o2 is extremely important because it not only reflects the functional capabilities of the lungs but also determines the rate at which oxygen enters the tissue cells.

Factors that affect the Pao2 include the Va, the Fio2, the functional capabilities of the lungs, the mean airway pressure in mechanically ventilated patients, and the oxyhemoglobin dissociation curve.

ALVEOLAR VENTILATION If the patient hyperventilates, the Paco2 tends to fall and the Pao2 tends to rise. If the Paco2 falls by 1 mmHg, the Pao2 rises by about 1.0 to 1.2 mmHg; in accordance with the law of additive partial pressures. The lungs can make up for some pulmonary dysfunction by hyperventilating. This is seen in pregnant patients who have normal arterial blood gas values at term showing normal pH, a Pa co2 of 30 to 32, a Pao2 of 110 to 115, and a serum bicarbonate level of 20 to 22 meq/L. This is due to an increase in Vm (predominantly due to increased Vt), with resultant respiratory alkalosis with increased urinary excretion of bicarbonate to compensate.

FRACTION OF INSPIRED OXYGEN Unfortunately, the Fio2 is often not considered adequately in evaluating the Pa o2. If a patient is receiving oxygen by nasal cannula, the actual delivered Fi o2 is usually only 25 to 30 percent. With a properly fitting face mask, the inhaled Fi o2 is usually less than half that delivered to the mask. The approximate Pao2 values that might be expected in normal persons who are inhaling various concentrations of oxygen are listed in T.§bIe.,..2.2i-2.

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