Is the patient adequately oxygenated?
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).
|CLUES TO SUGGEST INADEQUATE OXYGENATION
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.
|CAUSES OF HYPOXIA A GENERAL CLASSIFICATION
1. Hypoxemia (reduced arterial oxygen content)
2. Reduced oxygen delivery
3. Decreased tissue oxygen uptake
*See Table 51
**See Table 63
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
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
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)
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.
|Clinical Problem 1|
|What is the arterial oxygen content if PaO2 is 92 mm Hg, SaO2 is 98%, and hemoglobin is 15 gm%?|
|Clinical Problem 2|
|Which patient is more hypoxemic, A or B?
Test Patient A Patient B
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
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 (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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