Chapter 6, cont… (Page 3)

Is the patient adequately oxygenated?

FICK EQUATION

The Fick equation expresses the important relationship of tissue oxygen uptake (VO₂) to cardiac output (QT) and the arterial­venous oxygen content difference (CaO₂ ­ CvO₂):

(Eqn 6-3)

where CaO₂ is the arterial oxygen content, and CvO₂ is the mixed venous oxygen content.

This equation can be conceptually derived by thinking about oxygen delivery as follows: the amount of oxygen delivered to the tissues per minute equals the cardiac output (QT) times the arterial oxygen content (CaO₂) (see Fig. 6­1). The total amount of venous oxygen delivered to the right side of the heart is the cardiac output times the venous oxygen content, or QT x CvO₂. The total venous oxygen delivery must also equal the arterial oxygen delivery minus the amount of oxygen extracted by the tissues (VO₂).

Hence,

(Eqn 6-4)

Rearranging,

(Eqn 6-5)

(Eqn 6-3)

Average resting values for a normal subject are QT, 5000 ml/min; CaO₂, 20 ml/100 ml blood; CvO₂, 15 ml/100 ml blood; and VO₂, 250 ml/min.

Substituting these values into Equations 4 and 3:

750 ml O₂/min = 1000 ml O₂/min - (4)

250 ml O₂/min

and,

250 ml O₂/min =

(VO₂)

5000 ml blood/min x (3)

(Cardiac output)

5 ml O₂/100 ml blood

(CaO₂ ­ CvO₂)

MIXED VENOUS OXYGEN SATURATION

At the present time our ability to assess oxygenation is limited to the whole patient and does not extend to assessment of the individual organs. Specific organ hypoxia is usually recognized only after damage has occurred. This situation is unfortunate since some clinical conditions (e.g., septic shock) may cause selective organ hypoxia even though the global oxygen supply is adequate.

For patients with a normal mental status and a normal or near­normal cardiac output (determined by the history, physical examination, and chest x­ray), knowledge of their arterial oxygen content (CaO₂) is usually sufficient to assess the adequacy of oxygen delivery. This is often not true for patients with impaired cardiac output or hemodynamic instability (e.g., shock); in this group the single best measurement to assess oxygenation is usually the mixed venous oxygen saturation (SvO₂). Why is this so?

Equation 3 helps to explain the importance of SvO₂ in assessing oxygen adequacy. Arterial oxygen delivery is the product of cardiac output (QT) and arterial oxygen content (CaO₂); reduction in either QT or CaO₂ threatens the adequacy of oxygen delivery. In either case (reduced QT or reduced CaO₂), lactic acidosis and death will ensue if tissue oxygen uptake (VO₂) is not maintained by the product of QT times the (CaO₂ ­ CvO₂).

From Equation 3, the compensatory mechanisms for any decrease in oxygen delivery can be deduced; these mechanisms are outlined in Table 6­4 .

When cardiac output is decreased or when cardiac output cannot compensate for a decrease in CaO₂, the mixed venous oxygen content (and thus SvO₂ and PvO₂) will fall. Normally both the cardiac output and the (CaO₂ ­ CvO₂) can increase up to threefold as compensation: up to 15 L/min for QT and 15 ml O₂/100 ml for (CaO₂ ­ CvO₂). Increasing (CaO₂­CvO₂) is almost always at the expense of lowering CvO₂^*; thus SvO₂ is a barometer of the adequacy of oxygen delivery (QT x CaO₂) for the body's oxygen needs.

When the SvO₂ falls to 40% or less (roughly corresponding to a PvO₂ of 27 mm Hg at pH 7.36), the limits of compensation are such that any further fall will likely result in lactic acidosis. This condition should be considered preterminal unless reversal is fairly rapid.

The problems in using SvO₂ to assess global oxygenation are both technical and theoretical. Technical problems in obtaining a pulmonary artery sample are discussed in Chapter 8. Assuming that a proper sample is obtained and that the measurement is accurate, the following statement appears valid in patients at rest: a low SvO₂ indicates inadequate oxygen delivery for the body's needs; the lower the SvO₂, the more severe is the derangement.

Conversely, a normal SvO₂ does not assure that oxygenation is adequate; this is so for several reasons.

1. Regional hypoperfusion may be masked by an adequate blood flow to the rest of the body; thus one organ could be oxygen deficient, yet its oxygen­poor venous blood flow may not be enough to cause significant reduction in the mixed venous oxygen content.

2. Left­to­right systemic shunts may have the same effect as regional hypoperfusion. These shunts have been described in both septic and hemodynamic shock. If oxygenated blood is shunted from the arteries to the veins (thus bypassing capillaries), a normal (or even elevated) SvO₂ may result. This measurement could be falsely reassuring since selective tissues or organs may be critically hypoxic and on the verge of irreversible damage.

3. In some conditions, such as cyanide poisoning, oxygen delivery is adequate but the mitochondria are poisoned; thus oxygen transfer between systemic capillaries and the tissue cells does not take place. Again, SvO₂ may be normal or above normal.

In summary, SvO₂ is the best single measurement to use in assessing the adequacy of oxygenation in critically ill patients. If SvO₂ is reduced, the patient's ability to efficiently oxygenate the tissues is either impaired or severely strained. If SVO₂ is normal, oxygenation is probably adequate as long as there is no problem with regional hypoperfusion, left­to­right shunts, or mitochondrial oxygen uptake.

The PvO₂ measurement is an alternative to SvO₂ in assessing oxygenation. Both are obtained from mixed venous blood. Of the two, the SvO₂ should be more reliable since it is solely a function of arterial oxygen delivery and oxygen uptake. In contrast, PvO₂ depends on the SvO₂ and on the position of the oxygen dissociation curve. Venous blood is more acidotic than arterial blood; hence the venous oxygen dissociation curve is shifted to the right of the arterial curve. For a given SvO₂, the more the rightward shift of the curve, the higher the PvO₂. Other factors besides pH will also influence the curve, such as the concentration of 2,3­diphosphoglycerate; thus the exact relationship of SvO₂ to PvO₂ cannot be predicted in sick patients. If the PvO₂ is used to assess oxygenation, it must be measured and not simply estimated from the SvO₂. An SvO₂ measurement of 75% could represent a range of PvO₂ values depending on the position of the oxygen dissociation curve.

Fig. 6­5. Changes in SvO₂ when monitored continuously. A, Effect on SvO₂ of a, suctioning the patient's tracheal tube, b, bathing and weighing the patient, and c, turning the patient and changing his bed linen. Note the prolonged duration of the SvO₂ of less than 60%. B, Gradual decline in SvO₂ over the first 20 minutes heralded onset of cardiac arrest (arrow) for which resuscitation was successful. (From Baele, P.L., McMichan, J.C., Marsh, H.M., et al.: Anesth. Analg. 61:513517, 1982.)

Obviously, a mixed venous oxygen measurement is done only on very sick patients in whom there is reason to suspect inadequate oxygen delivery. There may also be technical problems in obtaining a proper sample­­it is not a simple test to be performed repeatedly (see Chapter 8). A fiberoptic sensor in some models of the Swan­Ganz catheter allows for continuous measurement of SvO₂. This modification greatly improves the monitoring of mixed venous oxygenation and also demonstrates how clinical changes can affect mixed venous oxygenation (Fig. 6­5). Fig. 6­5, A, demonstrates that routine nursing procedures (tracheal suctioning and weighing) can lower SvO₂. Fig. 6­5, B, shows the SvO₂ tracing from a patient who developed cardiac arrest. Before the arrest, the SvO₂ declined precipitously and, in fact, heralded the problem.^*

Mixed venous oxygen measurement represents a sophisticated attempt to answer the sometimes difficult question about the adequacy of overall oxygenation. However, for the vast majority of patients, measurement of arterial oxygen content will be sufficient to assess oxygenation.

SUMMARY

The second clinical question concerning oxygenation asks if oxygenation is adequate for the patient. This is sometimes a difficult question to answer. Unlike the first question posed in Chapter 5 (Are the lungs transferring oxygen properly'?), the answer to this question must always include information from the patient's history and physical examination. The most important laboratory measurement to help answer this question is the arterial oxygen content (CaO₂). CaO₂ is the amount of oxygen in the blood measured in ml O₂/100 ml blood and is determined by multiplying the hemoglobin oxygen saturation (SaO₂) times the hemoglobin content (in gm/100 ml blood) times 1.34 ml °2/ gm hemoglobin (hemoglobin's oxygen binding capacity).

Carbon monoxide affects oxygenation in two ways. First, it prevents oxygen from binding to hemoglobin, thus reducing the SaO₂; for every percent carboxyhemoglobin, SaO₂ is reduced 1%. Second, when carbon monoxide binds to hemoglobin, it causes a leftward shift of the oxygen dissociation curve, thus causing hemoglobin to hold onto oxygen more tightly than when carboxyhemoglobin is not present.

In critical illnesses such as shock or sepsis, the CaO₂ alone may be insufficient to determine the adequacy of oxygenation. In such situations, cardiac output, arterial oxygen transport, oxygen uptake, and mixed venous oxygen saturation may be measured. Unfortunately, such information can only be obtained with the aid of right heart catheterization, an invasive technique.

Mixed venous oxygen saturation (SvO₂) can be measured continuously by using a pulmonary artery catheter that is equipped with a special fiberoptic sensor. Continuous SvO₂ measurement has proved useful in monitoring the adequacy of oxygenation in critically ill patients. A low SvO₂ indicates inadequate oxygen delivery for the body's needs. If the SvO₂ is normal, overall oxygenation is probably adequate, provided that there is not significant regional hypoperfusion, left­to­right shunting, or interference with mitochondrial oxygen uptake.

REVIEW QUESTIONS

State whether each of the following is true or false.

1. Units for oxygen content are ml O₂/gm hemoglobin.

2. When PaO₂ is 100 mm Hg, SaO₂ is 98%, and hemoglobin content is 15 gm%, 86% of the available oxygen is carried on hemoglobin.

3. Mixed venous PO₂ increases one mm Hg with each mm Hg increase in PaO₂.

4. In a critically ill patient at rest, reduced SvO₂ indicates inadequate oxygen delivery to the tissues.

5. A P50 of 33 mm Hg indicates a reduced SaO₂ for a given PaO₂.

6. Arterial oxygen delivery is the product of cardiac output times arterial oxygen content.

7. Anemia can lower arterial PO₂ in the face of venous admixture.

8. To maintain oxygen uptake in the presence of a falling cardiac output, there must be a concomitant increase in the arterial­venous oxygen content difference.

9. Carbon monoxide shifts the oxygen dissociation curve to the left.

10. Methemoglobin shifts the oxygen dissociation curve to the right.

References

Baele, P.L., McMichan, J.C., Marsh, H.M., et al.: Continuous monitoring of mixed venous oxygen saturation in critically ill patients, Anesth. Analg. 61:513, 1982.

Comroe, J.H., Jr., and Botelho, S.: The unreliability of cyanosis in the recognition of arterial hypoxemia, Am. J. Med. Sci. 214:1, 1947.

Winter, P.M., and Miller, J.N.: Carbon monoxide poisoning, JAMA 236:1502, 1976.

Suggested readings

Filley, G., Beckwith, H., Reeves, J., et al.: Chronic obstructive pulmonary disease: oxygen transport in two clinical types, Am. J. Med. 44:26, 1968.

Kandel, G., and Aberman, A.: Mixed venous oxygen saturation: its role in the assessment of the critically ill patient, Arch. Intern. Med. 143:1400, 1983.

Kasnitz, P., Drurger, G.L., Yorra, F., et al.: Mixed venous oxygen tension and hyperlactatemia, JAMA 236:570, 1976.

Miller, M.J.: Tissue oxygenation in clinical medicine: an historical review, Anesth. Analg. 61:527, 1982.

Mithoefer, J., Holfand, F., and Keighley, J.: The effect of oxygen administration on mixed venous oxygenation in chronic obstructive pulmonary disease, Chest 66:122, 1974.

See also General References in Appendix G.

[Table of Contents][Previous Chapter][Chapter 6, Page 1][Chapter 6, Page 2][Next Chapter]