In ii ip m w a MMjf if I rfl j totkb ami tf HV

TABLE 22-7 Po2 Levels at Various Temperatures

Exercise During strenuous exercise, several factors can shift the oxyhemoglobin dissociation curve to the right. Exercising muscles release large quantities of carbon dioxide and other acids, increasing the hydrogen ion concentration in muscle capillary blood. In addition, the temperature of the muscle often rises as much as 3 to 4°C, and phosphate compounds are also released. All these factors acting together shift the oxyhemoglobin dissociation curve of the blood in the muscle capillaries considerably to the right. This allows oxygen to be released to the muscle at a P o2 as high as 40 mmHg even though as much as 75% of the oxygen has been removed from the hemoglobin. In the lungs, the shift occurs in the opposite direction, allowing pickup of extra amounts of oxygen from the alveoli.

2,3-Diphosphoglycerate Except for hemoglobin, the compound present in greatest quantity in red blood cells is 2,3-DPG. A normal concentration of 2,3-DPG in a red blood cell keeps the oxyhemoglobin dissociation curve shifted slightly to the right all the time. In addition, under hypoxic conditions lasting longer than a few hours, the quantity of 2,3-DPG increases considerably, shifting the oxyhemoglobin dissociation curve even farther to the right. This can cause the P o2 in the plasma to be as much as 10 mmHg higher than it would have been otherwise. However, the presence of increased 2,3-DPG makes it more difficult for the hemoglobin to combine with oxygen in the lungs.

If the concentration of 2,3-DPG falls, as it does in stored blood or during sepsis, the hemoglobin holds on to its oxygen more tightly and the Pa o2 tends to fall. This is an important consideration during large-volume resuscitations with banked blood.

Other Methods of Evaluating Oxygenation

Pao2/Fio2 RATIO A quick way to estimate the impairment of oxygenation is to calculate the Pa o2/Fio2 ratio. Normally, the ratio is about 500 to 600, which usually correlates to a pulmonary shunt (QS/QT) of about 3 to 5%. However, if a patient has a Pa o2 of 80 mmHg on 40% oxygen, the Pao2/Fio2 ratio is 80/0.4, or 200. A Pao2/Fio2 ratio of less than 200 corresponds with a QS/QT of about 20%. The usual relationship between Pa o2/Fio2 ratios and the QS/QT in patients with a normal cardiac output is shown in Table.., .22,-8,. Pao2/Fio2 ratios are also used as criteria for the diagnosis of ARDS/acute lung injury (ALI). In a patient with alveolar infiltrates in at least 3 of 4 quadrants on chest x-ray, a normal pulmonary capillary wedge pressure, and a mechanism known to cause ARDS/ALI, a Pa o2/Fio2 of less than 300 indicates ALI, while a ratio less than 200 indicates ARDS. However, some researchers no longer distinguish between ARDS and ALI and classify all patients with a Pao2/Fio2 ratio less than 300 as having ARDS.





















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TABLE 22-8 Interpretation of Pao2/Fio2 Ratio

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TABLE 22-8 Interpretation of Pao2/Fio2 Ratio

Physiologic Shunting in the Lung (Venous-Arterial Admixture)

Although abnormal gas diffusion or distribution in the lungs can cause abnormal blood gas values, the most important cause is usually V/Q mismatching. When considering ventilation and perfusion, there can be four types of alveolar capillary units: (1) if ventilation and perfusion are normal, the unit is normal; (2) if there is ventilation without perfusion, the unit is considered to be dead space (or high V/Q); (3) if there is perfusion without ventilation, the unit is considered to be a (right-to-left) shunt (or low V/Q); and (4) if there is neither ventilation nor perfusion, the unit is silent.

The amount of physiologic shunting in the lung, or venous-arterial admixture (QS/QT), is probably the most sensitive guide to the onset and progression of acute respiratory failure. The shunt is that fraction of blood passing through the lungs without being oxygenated. Normally, the amount for venous-arterial admixture is about 3 to 5 percent of the cardiac output. This small amount of shunting is largely due to the drainage of deoxygenated blood in bronchial veins into oxygenated blood in pulmonary veins.

Physiologic shunting is harder to determine than alveolar-arterial oxygen differences because it requires drawing both arterial and mixed venous (pulmonary artery) blood samples and determining their oxygen contents. Mixed venous samples from the pulmonary artery are preferable to those obtained from central venous pressure catheters. However, central venous blood does give a reasonable estimate of the amount of shunting present if cardiac output is relatively normal.

Although an Fio2 of 1.0 was generally used in the past to determine the amount of physiologic shunting in the lung, the high Fi o2 in itself may cause increased shunting. Now the shunt with an Fio2 of 0.4 is considered to be a better indicator of lung function.

The QS/QT can be calculated from a modification of Berggren's formula:

QS Ceo; - CaOj QT CcO] - Cvoj where Cco2 is the pulmonary capillary oxygen content, Cao2 is the arterial content, and Svo2 is the mixed venous oxygen content. Thus, if Cco2 is 20 mL/dL, Cao2 is 19 mL/dL, and Svo2 is 14 mL/dL, the shunt is

The amount of shunting in the lung can also be estimated from arterial blood alone, using an assumption that the arteriovenous oxygen difference is approximately 5

In general, if cardiac output doubles, the amount of shunt associated with a particular P(A - a) o2 increases by about 50 percent (T§Mej22.-9.). This is partly related to the fact that, if only a small amount of blood is going through the lung, the blood flow tends to go to well-ventilated alveoli. If cardiac output increases, there is increasing likelihood that some of the blood will go through less well-ventilated tissue.

TABLE 22-9 Relation Between the Physiologic Shunt in the Lung (Qs/Qt) and P(A - a)o2 while Breathing 100% o2

Thus, if cardiac output is high, relatively mild hypoxemia can result from a high shunt. For example, at a Pa o2 of 300 mmHg, if the cardiac output is 2.5 L/min, the shunt might be 11 percent, but at a cardiac output of 10.0 L/min, the shunt would be 32 percent. To factor in the changes due to an increased or decreased cardiac output, one uses the shunt index (SI). The SI is the percent shunt divided by the cardiac index. For example, at a normal cardiac index of 3.5 (L/min)/m 2 and a shunt of 5.0 percent, the SI is 5.0/3.5 = 1.4. If a patient has a shunt of 20 percent with a cardiac index of 2.5 (L/min)/m 2, the SI is 8.0. Patients with an SI above 5.0 usually require oxygenation support.

If the cardiac index is not known, the critical QS/QT is about 20 to 25 percent. Above these values, the patient usually has enough of a V/Q abnormality to warrant oxygenation support and positive end-expiratory pressure (PEEP).

Oxygen Availability

Oxygen availability is determined by the amount of oxygen brought to the capillaries, or oxygen delivery (D o2), and the dissociation of oxygen from hemoglobin at the tissues. To a certain extent, a good heart, which can increase cardiac output appropriately, can make up for bad lungs and a low hemoglobin level. The reverse is also true. However, a combination of poor oxygenation, low hemoglobin level, and low cardiac output may be rapidly fatal.

OXYGEN CONTENT The oxygen content of blood is determined primarily by the hemoglobin level and the oxyhemoglobin saturation. When fully saturated, each gram of hemoglobin measured clinically can carry 1.34 mL of oxygen. Thus, a patient with a hemoglobin concentration of 15.0 g/dL can carry about 20.1 mL of oxygen per 100 mL in the red blood cells when the hemoglobin is fully saturated. Although the Pa o2 determines the rate at which oxygen enters the tissues, it contributes very little to the total oxygen content of blood. Each millimeter of mercury of Pa o2 represents only 0.0031 mL of oxygen in 100 mL of blood. Thus, a patient with a normal Pao2 of 100 mmHg has only 0.31 mL of oxygen dissolved in the plasma.

The oxygen content of arterial blood (Cao2) can be calculated from the following formula:

Thus, in a patient with a hemoglobin concentration of 15.0 g/dL, an Sa o2 of 98%, and a Pao2 of 100 mmHg,

= 20.0 mL per deciliter of blood

If the hemoglobin concentration falls to 10.0 g/dL, even if Sa o2 and Pao2 remain the same, Cao2 falls by about a third. For example,

= I -MinLOi ptrdetililerof blood

Even with only 10 g of hemoglobin, the red blood cells are carrying over 40 times as much oxygen as is the plasma.

CARDIAC OUTPUT Oxygen content (in milliliters per liter of blood) multiplied by cardiac output (in liters per minute) is equal to D o2. Thus, the Do2 in a patient with 15.0 g of 98% saturated hemoglobin, a Pao2 of 100 mmHg, and a cardiac output of 5 L/min is

Do; = (Cap! pCTdLX I OXconiiac output) = {[hemoglobin]* 3 .34XSehV 3 00)

+ [Paoj)(0-003)}<! GKcardiac output) = [(15)(lJ4X9S/100)+{J 00)(0.003)]( 10X5)

The factor 10 is used to convert oxygen content from milliliters per 100 mL of blood to milliliters per liter of blood.

Since the normal oxygen consumption of an average resting adult male is about 250 to 300 mL/min [approximately 3 (mL/kg)/min], the tissue on average takes up about 25% of the oxygen brought to it, although the percent oxygen extraction varies by organ. Thus, the Sa o2 falls from about 98% in arterial blood to about 73% in mixed venous blood. If there is no change in oxygen consumption but cardiac output doubles to 10 L/min, the amount of oxygen removed from each liter of blood is halved, and the venous oxyhemoglobin saturation will be about 85%. On the other hand, if cardiac output falls to 2.5 L/min, venous oxyhemoglobin saturation will fall to about 48 percent.

OXYGEN DISSOCIATION IN THE TISSUES The ability of blood to give up more oxygen (increasing the arteriovenous oxygen difference) as cardiac output falls and thus maintain oxygen delivery is an important defense mechanism sometimes referred to as oxygen reserve. Unfortunately, there is a limit to this so-called oxygen reserve because the Po2 in most tissues seldom falls below 26 mmHg, which is the P5C for hemoglobin (Po2 at which hemoglobin is 50% saturated).

The lowest value to which the Po2 in capillaries can fall is about 18 to 20 mmHg because this is the usual capillary-mitochondrial gradient for oxygen. The saturation at a Po2 of 20 mmHg is referred to as the S20, and this is normally about 33%. The only places where the P o2 in venous blood is normally as low as 20 mmHg are the coronary sinus, renal medulla, and perhaps the jugular venous bulb at the base of the brain. A relatively mild degree of alkalosis can raise the S 20 by 4 to 5%, thereby greatly reducing oxygen availability to the myocardium. Thus, alkalosis (e.g., when metabolic acidosis is treated with bicarbonate) in low-flow states can be deleterious.

COMBINATION OF HEMOGLOBIN WITH CARBON MONOXIDE Carbon monoxide combines with hemoglobin at the same point on the hemoglobin molecule that oxygen does. Furthermore, it binds about 230 times more strongly than oxygen does. Therefore, an alveolar carbon monoxide level of 0.4 mmHg, which is 77 that of the PaO2, allows the carbon monoxide to compete equally with oxygen for combination with hemoglobin, causing half the hemoglobin in the blood to bind with carbon monoxide instead of oxygen. An alveolar carbon monoxide level of 0.7 mmHg (about 0.1% in air) can be lethal. Oxygen at high alveolar pressures displaces carbon monoxide from hemoglobin much more rapidly than atmospheric oxygen does. Patients with carbon monoxide poisoning can also benefit from simultaneous administration of 4 to 5% carbon dioxide, which strongly stimulates the respiratory center, increasing V A, reducing the alveolar carbon monoxide concentration and allowing increased carbon monoxide to be released from the blood. A 96% oxygen and 4% carbon dioxide therapy removes carbon monoxide from the blood 10 to 20 times more rapidly than would be removed by breathing room air. The half-life of Hb—CO in a patient breathing room air is 2 to 3 h; if the patient is breathing 100% O2, the half-life is about 20 to 30 min. The most effective way to clear Hb—CO is by increasing the Pa o2 above that attainable by breathing 100% oxygen—that is, in a hyperbaric oxygen chamber.

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