Chapter 6

Is the patient adequately oxygenated?

OUTLINE

• Clinical assessment
• Hypoxemia vs. hypoxia
• The oxygenation cycle
• SaO₂ and oxygen content
• Shifts of oxygen dissociation curve and P₅₀
• Carbon monoxide
• Effects of carbon monoxide exposure
• Methemoglobinemia and sulfhemoglobinemia
• Causes of reduced SaO₂
• Oxygen delivery
• Fick equation
• Mixed venous oxygen saturation
  

CLINICAL ASSESSMENT

Adequacy of oxygenation is deceptively difficult to assess in patients. Certainly if someone appears healthy, has no respiratory symptoms, and is being evaluated for a problem unrelated to the cardiopulmonary system (e.g., an orthopedic injury), there may be no concern about oxygenation.

In respiratory patients the situation is different. There is often a history of respiratory illness, or the patient may appear dyspneic or mentally confused or may manifest other signs suggesting a lack of oxygen. Given a clinical suspicion, there is no reliable way to assess adequacy of oxygenation without some measurement of blood oxygen. Mental status, pulse rate, breathing pattern, and a number of other clinical signs are unreliable guides to oxygenation. Physicians who practiced before the era of blood gas analysis had to make an educated guess about a patient's oxygenation status. Except for the most obvious case of cyanosis, this guess was as apt to be wrong as to be correct.

As was shown by Comroe many years ago (1947), even the assessment of cyanosis is unreliable. Too much depends on the patient's skin pigment, the available light, and interobserver variation. Also, since cyanosis does not occur until 5 gm of hemoglobin are desaturated in the skin capillaries, anemic patients may never appear cyanotic even when severely hypoxemic.

The history and physical examination are not to be slighted, however. How else would one know when to worry about a patient's level of oxygenation? Certainly if a healthy athlete breaks a toe, his or her oxygenation is not questioned. Conversely, oxygenation is an obvious concern in a patient suffering from pulmonary edema and shock. But what about the vast number of patients between these extremes ­­ the ones who initially have shortness of breath only on exertion, who are confused, or who have cardiomegaly of unknown cause? Many clinical signs and symptoms, shown in the following box, should make one question the patient's oxygenation status. In clinical practice, this questioning should lead to measurement of arterial partial pressure of oxygen (PaO₂) and/or percent saturation of hemoglobin with oxygen (SaO₂).

Blood gas machines provide measurement of both PaO₂ and SaO₂, but neither measurement tells how much oxygen is in the blood, a quantity that is provided by the oxygen content. Oxygen content takes into account the amount of hemoglobin available to carry the oxygen. Oxygen content is the minimal laboratory information needed to assess oxygenation. But even oxygen content may not be sufficient information in patients with compromised cardiac function.

HYPOXEMIA VS. HYPOXIA

Although the terms hypoxemia and hypoxia are often used interchangeably, they are not synonymous. Hypoxemia means low oxygen (hypox) in the blood (emia) and refers to either low arterial pressure of oxygen (PaO₂) or low arterial oxygen content (CaO₂). Patients can have low PaO₂ without much reduction in oxygen content (i.e., PaO₂ of 60 to 70 mm Hg), but such patients are still considered hypoxemic. Ideally the term should either be qualified or clearly understood in its context.

Hypoxemia is a more general term and signifies general lack of oxygen in the whole body. It thus includes hypoxemia (low oxygen in the blood), as well as those conditions in which the oxygen content is adequate but circulation is impaired, or in which insufficient oxygen is taken up by the tissues. The box below gives a general classification of hypoxia.

The whole process of oxygenation is, like all physiologic processes, dynamic; one thing affects another, and changes happen very quickly. Oxygen is a necessary element for life, and lack of it leads to death in a few minutes. The process of getting oxygen from the atmosphere into the blood and then to all the tissues involves not only the respiratory system, but also the heart and circulatory system. It will be helpful to review the entire cycle of human oxygenation and then discuss its components one at a time.

THE OXYGENATION CYCLE (Fig. 6­1)

Oxygen enters the blood by diffusion across the alveolar capillary membranes; the overall relationship of alveolar ventilation to capillary perfusion results in the arterial partial pressure of oxygen PaO₂ (see Chapter 5) and a percent saturation of the available hemoglobin SaO₂. (For a PaO₂ of 100 mm Hg, SaO₂ is approximately 97% at normal pH. SaO₂ for a given PaO₂ also depends on other factors, which are discussed in a later section.) The vast majority of oxygen molecules are carried by hemoglobin, with only a small amount dissolved in plasma. Thus arterial oxygen content (CaO₂) is largely determined by the SaO₂ and the hemoglobin content; when the latter is 15 gm%, CaO₂ is approximately 20 ml O₂/100 ml blood.

Fig. 6­1. The oxygenation cycle. Using representative normal values for barometric pressure, cardiac output, hemoglobin content, venous admixture, and oxygen uptake, the changes in oxygen pressure and oxygen content are shown from the arterial blood to the mixed venous blood. (PA, pulmonary arteries; PV, pulmonary veins; LA, left atrium; LV, left ventricle; RV, right ventricle; P(A­a)O₂, alveolar­arterial Po, difference; (CaO₂ ­ CvO₂), arterial­venous oxygen content difference; Hgb, hemoglobin; RA, right atrium; Trans, transport; PB, barometric pressure.)

Oxygen delivery to the tissues requires adequate cardiac output and arterial circulation. Cardiac output times the CaO₂ gives the amount of oxygen delivered to all tissues per minute; in an average person this amount is approximately 1000 ml °2/ min at rest. Normally, the body uses approximately one quarter of the oxygen that is delivered, or 250 ml O₂/min; this measurement is the metabolic oxygen consumption (VO₂). (At the same time, metabolism produces approximately 200 ml CO₂/ min.)

A disturbance in the oxygen cycle at any point up to and including oxygen consumption can result in hypoxemia or hypoxia, as shown in the box on p. 113.

Oxygen transport in the venous system is determined by the arterial oxygen delivery minus the oxygen uptake; using the values given previously, venous oxygen transport is 750 ml O₂/min. Venous oxygen contents in blood from the various organs and tissues vary widely, so venous oxygen levels are usually measured only in the pulmonary artery where the values are sure to represent mixed venous blood and thus the. body as a whole. Normal mixed venous oxygen content, percent saturation, and partial pressure are, respectively, 15 ml O₂/100 ml blood, 75% and 40 mm Hg.

Mixed venous blood, regardless of its partial pressure of oxygen, is fully oxygenated after passing through normal alveolar­capillary units. Mixed venous blood that does not pass through normal units, such as the small amount shunted past the lungs, mixes with oxygenated blood either in the pulmonary veins, the left atrium, or the left ventricle; this venous admixture results in some reduction of arterial oxygen content. Normal venous admixture accounts for the normal alveolar­arterial PO₂ difference (see Chapter 5).

SaO₂ AND OXYGEN CONTENT

Arterial partial pressure of oxygen PaO₂) determines the percent saturation of hemoglobin with oxygen SaO₂), which, along with available hemoglobin, largely determines the oxygen content. Fig. 6­2 shows PaO₂ vs. SaO₂ (the oxygen dissociation curve) and PaO₂ vs. oxygen content when the hemoglobin content is 10 gm% (anemia) and 15 gm% (normal).

Arterial oxygen content equals:

Amount of O₂ bound to hemoglobin + Amount of O₂ dissolved in plasma,

or (SaO₂ x Hgb x 1.34) + (0.003 x PaO₂) (Eqn 6-1)

where SaO₂ is the percent saturation of hemoglobin with oxygen, Hgb is the hemoglobin content in gm%, 1.34 is the oxygen binding capacity of hemoglobin (ml O₂/gm Hgb), and 0.003 is the milliliters of oxygen that dissolve in 100 ml plasma per mm Hg PaO₂. Normal arterial oxygen content is approximately 16 to 20 ml O₂/100 ml blood. Note that the amount of dissolved oxygen is not clinically significant at a normal PaO₂. Most of the oxygen is carried bound to hemoglobin, hence the importance of oxygen content, rather than just SaO₂ or PaO₂, as a gauge of oxygenation.

Note also that anemia does not affect SaO₂, only oxygen content. Thus the oxygen dissociation curve PaO₂ vs. SaO₂) is unaffected by hemoglobin content.

Fig. 6­2. PaO₂ vs. SaO₂ and oxygen content. The oxygen dissociation curve relates PaO₂ to SaO₂. The shape and the position of the curve are the same regardless of hemoglobin content. The right ordinate shows arterial oxygen contents for two different concentrations of hemoglobin: 15 gm% and 10 gm%. Normal P₅₀ is approximately 27 mm Hg. If this were the partial pressure of oxygen in arterial blood (a very sick patient), the oxygen content would be 10 ml O₂/100 ml blood for a hemoglobin content of 15 gm% and 6.7 ml O₂/100 ml blood for a hemoglobin content of 10 gm%. (The P50 is the PaO₂ at which hemoglobin is 50% saturated with oxygen.)

SHIFTS OF OXYGEN DISSOCIATION CURVE AND P₅₀

The partial pressure of oxygen is not affected by changes in hemoglobin or percent saturation. As discussed in Chapter 5, the arterial PO₂ is determined by the alveolar air­pulmonary capillary interface and is not affected by the chemical makeup of the blood. The solubility of oxygen in plasma is a physical constant and does not change with alterations of hemoglobin. However, the percent saturation of hemoglobin with oxygen SaO₂) for a given PaO₂ can change.

The oxygen dissociation curve shown in Fig. 6-2 is the standard curve for when the pH, arterial partial pressure of carbon dioxide (PaCO₂), body temperature, and concentration of 2,3­diphosphoglycerate (DPG) are normal. Alteration of these and other factors (e.g., the presence of carboxyhemoglobin) can shift the dissociation curve from its normal position (Fig. 6­3). Both the direction and the degree of shift are measured by the P50, which is the PaO₂ at which 50% of the hemoglobin is saturated with oxygen; it is normally approximately 27 mm Hg.

To determine P₅₀ a sample of blood (venous or arterial) is exposed to two different samples of air containing low concentrations of oxygen, usually 3% and 4%. (In effect, the blood is exposed to a fraction of inspired oxygen ( FIO₂) of 0.03 and 0.04; ambient air has 21% oxygen or an FIO₂ of 0.21.) This exposure will give two saturation points, one above and one below the usual range of P₅₀. A line is then drawn connecting the two saturations, and the 50% saturation point is identified. The PO₂ corresponding to this point is the P₅₀.

Fig. 6­3. Effects of pH, temperature, and 2,3­diphosphoglycerate (DPG) on the oxygen dissociation curve. A, Effect of pH on position of the curve. A high pH shifts the curve to the left, a low pH, to the right. B, Effect of temperature on position of the curve. A high temperature shifts the curve to the right, a low temperature to the left. C, Effect of 2,3­DPG on position of the curve. Increased 2,3­DPG shifts the curve to the right. (From Slonim, N.B., and Hamilton, L.H.: Respiratory physiology, ed. 4, St. Louis, 1981, The C.V. Mosby Co.)

A P50 higher than 27 mm Hg represents a rightward shift of the oxygen dissociation curve; less than 27 mm Hg represents a leftward shift. What happens when the curve is shifted? In a rightward shift, blood picks up less oxygen at the pulmonary capillary level but delivers relatively more oxygen at the tissue level (Fig. 6­3). A curve shifted to the right causes a reduction in SaO₂ for a given PaO₂ (see Table 6­3).

When the oxygen dissociation curve is shifted to the left, blood picks up more oxygen at the pulmonary capillary but delivers relatively less to the systemic capillary, where the PO₂ is normally very low. A curve shifted to the left causes an increase in SaO₂ for a given PaO₂.

In terms of oxygen delivery, a right shift is considered a helpful adaptation. Attempts have been made to artificially shift the curve and improve oxygen delivery, but such an attempt is generally not a useful therapeutic maneuver. Factors affecting the curve's position are complex, and altering one or two of them does not guarantee that the patient will benefit. Instead, an attempt should be made to maintain the patient's pH and body temperature within normal limits, and the exact position of the oxygen dissociation curve should not be a cause for concern.

CARBON MONOXIDE

Carbon monoxide (CO) combines avidly with hemoglobin, displacing oxygen and thereby lowering the percent saturation of hemoglobin with oxygen SaO₂). Small amounts of carbon monoxide are normally present in the blood (from the breakdown of hemoglobin), and less than 2% carboxyhemoglobin (HbCO) is generally acceptable. To the extent that the carboxyhemoglobin is increased, the percentage of oxyhemoglobin, and thus the oxygen content, is decreased. Carbon monoxide does not directly affect PaO₂, so the SaO₂ must be measured to appreciate a reduction in oxygen content.

Fig. 6­4 plots PaO₂ vs. oxygen content when no carbon monoxide is present and when the blood is 20%, 40%, and 60% saturated with carbon monoxide. For comparison a curve is also shown for an anemic patient (40% of normal hemoglobin). Note that the normal curve for PaO₂ vs. oxygen content has the same sigmoid shape as the curves of PaO₂ vs. SaO₂. This similarity exists because the only difference between SaO₂ and oxygen content for a given amount of hemoglobin is a constant (1.34 ml O₂/gm hemoglobin).

Most people who smoke cigarettes or cigars have an HbCO level between 5% and 10%. This amount is not usually clinically significant when cardiopulmonary function and the hemoglobin content are normal. However, small increases of HbCO can be harmful in the presence of angina, anemia, or pulmonary impairment.

Besides lowering the total oxygen content, carbon monoxide also shifts the oxygen dissociation curve to the left; this movement is best appreciated by comparing the oxygen dissociation curve in the presence of HbCO with the curve for anemia and identical arterial oxygen content (Fig. 6­4). At the capillary level, where the PO₂ is much lower than in the arteries, hemoglobin holds onto oxygen more strongly in the presence of carbon monoxide. This added effect (the first effect is reduction of arterial content) further aggravates the patient's hypoxia.

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