Critical Care

Monitoring of oxygenation with oximetry

Seppo Ranta MD and Ilkka Kalli MD
Department of Anesthesiology and Intensive Care Medicine
Helsinki University Central Hospital, Finland

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One of the most important recent advancements in monitoring critically ill or anesthetized patients has been the advent of pulse oximetry. Its portability, noninvasiveness, and reasonably high accuracy probably make it the single most useful physiologic monitor available. However, the ubiquitous use of pulse oximetry by individuals with limited knowledge of physiology and pathophysiology seems to have spread the perceived utility of arterial blood oxyhemoglobin saturation monitoring to areas where factors other than mere adequacy/inadequacy of oxygen saturation must enter into the interpretation of oximetry results. The misinterpretation of oximetry takes the form of two erroneous assumptions. 1) If the pulse oximeter displays 90%, then the patient is in an acceptable state, at least from the standpoint of pulmonary function. 2) A low or decreasing oximeter reading is caused by a pulmonary problem. Leaving aside conditions in which pulse oximetry is inaccurate, e.g. methemoglobinemia and carboxyhemoglobinemia, common clinical scenarios relevant to monitoring oxygenation with oximetry are briefly discussed below.

Ventilation, oximetry, and oxygen therapy

Properly functioning pulse oximeter should reliably reflect arterial blood oxyhemoglobin saturation. However, whether or not an SpO2 of 90% indicates that the patient has adequate pulmonary function in terms of ventilation depends, among other things, on the inspired oxygen concentration.

Assuming a normal position of the oxyhemoglobin dissociation curve, an arterial blood oxyhemoglobin saturation of 90% would require an arterial blood oxygen tension of 60 mmHg. To achieve this with an alveolar-arterial oxygen tension gradient in the normal range (e.g. 15 mmHg), the alveolar oxygen tension would have to average 75 mmHg. If normal values are given to the barometric pressure (O2 = 760 mmHg) and the water vapor pressure (PH2O = 47 mmHg), the alveolar air equation allows examination of the relationship between alveolar carbon dioxide tension (PACO2), alveolar oxygen tension and inspired oxygen concentration (FiO2), as shown in equations 1 -2:

(1) PAO2 = (O2 – PH2O) · FiO2 – 1.25 · PACO2
(2) PAO2 = (760 – 47) · FiO2 – 1.25 · PACO2

Solving for PACO2 and assuming PAO2 = 75:
(3) PACO2= (713 · FiO2 – 75) / 1.25

Hence, if the patient is breathing room air (FiO2 = 0.21), and the PAO2 falls because of hypoventilation, the PAO2 of 75 mmHg and SpO2 of 90% will be reached at a PACO2 of about 60 mmHg. Since the arterial blood carbon dioxide tension is usually close to the PACO2, we can say that even mild hypoventilation will effect a drop in SpO2 to the ‘magic’ 90% if no supplemental oxygen is given. In reality, the PaCO2 will likely be slightly lower than 60 mmHg, if respiratory acidosis shifts the oxyhemoglobin dissociation curve to the right. In the presence of abnormally high alveolar-arterial oxygen tension gradient, the PAO2 required for a PaO2 of 60 mmHg will be higher than in the current example, and a SpO2 of 90% will be reached at even lower PaCO2. Therefore, in the great majority of cases, an SpO2 of 90% or more in a patient breathing room air means that the PaCO2 is no more than 60 mmHg, and no severe alveolar hypoventilation is present. In these relatively narrow clinical circumstances, the pulse oximeter can be used to monitor adequacy of ventilation.

Figure 1. Interdependence of FiO2 and PaCO2 when PAO2 is fixed to 75 mmHg. Assuming a normal position of the oxyhemoglobin dissociation curve, a P(A-a)O2 of 15 mmHg, and PACO2 » PaCO2, the line defines a boundary between the combination of FiO2 and PaCO2 that results in SpO2 greater or less than 90 %.

Unfortunately, administration of supplemental oxygen is common, even routine, despite the availability of pulse oximetry and regardless of whether or not the patient has a condition that should or could be alleviated with oxygen therapy. Recent studies suggesting a beneficial effect from oxygen on the frequency of postoperative infections is likely to increase the pressure for oxygen administration in the recovery room even further 1. Even though the true FiO2 achieved with various oxygen devices is difficult to as certain and likely varies from patient to patient, few patients receive supplemental oxygen at an FiO2 less than 0.35. If we recalculate the PaCO2 needed to drop PAO2 to 75 mmHg, PaO2 to 60 mmHg and SpO2 to 90 % at an FiO2 of 0.35, the result will be 140 mmHg! Since a patient breathing only 25 % oxygen can hypoventilate to a PaCO2 of 83 mmHg and still maintain a SpO2 of 90 %, it is safe to say that any amount of supplemental oxygen will completely invalidate the use of the pulse oximeter as a monitor of ventilation (2). The relationship between FiO2 and PaCO2, under the assumptions described above, is linear as shown in Figure 1 and equation (3).

Pulmonary causes of arterial blood desaturation

For the patient to receive appropriate care, detection of hypoxemia must lead to etiological workup and therapy. Since severe hypoxemia is life threatening, therapy with oxygen needs to be instituted before the cause is established. While oxygen therapy is almost always effective in increasing PaO2, it rarely corrects the underlying problem. Besides hypoventilation, there are five other direct lung-related causes for hypoxemia when it is defined as lower than expected PaO2 (Table 1). Of these a low inspired oxygen concentration is the only condition in which oxygen supplementation, by definition, is the therapy of choice. A number of incidents have been described where equipment failure or contamination of the oxygen supply with another gas results in widespread reduction in FiO2 in operating suites and intensive care units.

Impaired diffusion is a feature in many chronic pulmonary parenchymal diseases, but also in acute conditions resulting in accumulation of fluid or debris in the alveoli. The degree of diffusion impairment is rarely measured outside the pulmonary function laboratory, and the desaturation from impaired diffusion usually cannot differentiated from other causes of venous admixture, intrapulmonary shunt and low ventilation/perfusion ratio. The significance and therapeutic aspects of impaired diffusion in acute lung injury remain poorly defined.

Intrapulmonary shunt and areas of low but finite ventilation/perfusion ratio usually coexist in acute lung injury. Their combined effect on oxygenation is estimated in the calculation of venous admixture, but they need separate consideration for diagnostic and therapeutic purposes. By definition, low ventilation/perfusion areas still receive ventilation, albeit in reduced quantities. Hence, an increase in inspired oxygen concentration still reaches these alveoli, and the hypoxemia caused by them can be alleviated with oxygen therapy. In contrast, an intrapulmonary shunt is caused by perfusion of alveoli with no ventilation, which makes the ensuing hypoxemia unresponsive to oxygen supplementation. Of all the direct pulmonary causes of low PaO2, intrapulmonary shunting is the only one that does not respond to oxygen therapy. This makes increased FiO2 a very effective emergency measure for increasing PaO2. In fact, if PaO2 does not respond to oxygen as expected, one must assume that significant shunting is present.

An obvious, but often forgotten reason for hypoxemia is low barometric pressure. A rarely advertised fact of commercial airline travel is that the passenger cabin is not pressurized to sea level at cruising altitude, but has a pressure equivalent to 5000 to 6000 feet above sea level. Since the barometric pressure decreases roughly one inch of mercury per every 1000 feet of altitude, a cabin pressure altitude of 5000 feet reduces barometric pressure from 760 to 633 mmHg. It is evident from the equation (1) that a decrease in PAO2, and PaO2 are inevitable consequences of such a decrease in barometric pressure. Unless compensated for by an increase in FiO2 or hyperventilation, and that symptomatic hypoxemia may occur during air travel in passengers whose oxygenation is borderline at sea level3.

As the fundamental etiology of hypoxemia is revealed and specific therapy directed to it, the FiO2 can and should be reduced. The use of high inspired oxygen concentrations tends to mask hypoxemia because it renders even a poorly ventilated alveolus capable of fully oxygenating capillary blood. A patient breathing 35 % oxygen with a P(A-a)O2 of 15 mmHg will have a PaO2 of 185 mmHg and a SpO2 of 100 %. It will take a 5.6-fold increase in P(A-a)O2 from 15 to 85 mmHg to reduce PaO2 to 115 mmHg, and cause a detectable fall in SpO2 from 100% to 99 %. Deterioration of gas exchange would be detected much sooner if the patient initially were breathing room air with a PaO2 of 85 mmHg, because SpO2 would be sensitive to much smaller changes in oxygen tension. Since even severe gas exchange abnormalities can be covered up by pushing SpO2 to the flat part of the oxyhemoglobin dissociation curve and uncovered by sudden withdrawal of supplemental oxygen, it is important to assure uninterrupted oxygen therapy to those patients who have been found to need it.

If hypoxemia is defined on the basis of oxyhemoglobin saturation, one must further consider situations in which the oxyhemoglobin dissociation curve is right-shifted and saturation is low with respect to oxygen tension. In clinical practice, the most common reason for a major discrepancy of this kind is profound acidemia. The relationship between PaO2 and saturation return back to normal when acidosis is corrected.

Extrapulmonary causes of arterial blood desaturation

Since the lungs provide carbon dioxide removal and oxygen uptake, derangements from normoxia and eucapnia rightfully direct attention first to the respiratory system. However, changes in oxygenation may be of extrapulmonary origin. In adult patients, whose likelihood of developing right-to-left shunting of blood is low, the most common non-pulmonary condition impairing oxygenation of arterial blood is low tissue oxygen supply/demand ratio. While this may be caused by increased oxygen uptake in hypermetabolic states, by far the most common reason is inadequate oxygen supply from reduced blood flow, anemia, or both. When oxygen extraction increases in the face of inadequate oxygen flow to the tissues, the oxygen content of the venous effluent falls in a proportional manner.

The hypoxemia-producing effect of intrapulmonary shunt regions in the lungs depends on the oxygen saturation of the blood that bypasses patent alveoli through these routes. . Thus, the arterial blood oxygenation may vary with the tissue oxygen supply/demand relationships even though the gas exchange capacity of the lungs remains unchanged. Therapy directed to the lungs may not be effective in correcting hypoxemia and may in fact make it worse if the attempted therapy, such as application of positive end-expiratory pressure, further reduces blood flow. Consideration of the entire cardiopulmonary system is necessary to establish and correct the relative contributions of pulmonary and extrapulmonary factors on gas exchange. If a central line is in place, monitoring of mixed or central venous oxygen saturation and estimation of peripheral oxygen extraction ratio ([SaO2-SvO2]/SaO2) is a simple and effective tool in detecting changes in oxygen supply/demand conditions in most cases.

Advances in monitoring technology have greatly facilitated the diagnosis and monitoring of acute cardiopulmonary conditions by making them more timely and precise. However, the information provided by these devices must be interpreted with sound consideration of the physiologic and pathophysiologic processes in operation, to avoid over-reliance on equipment and misdirected or delayed therapy.

Table 1. Pulmonary causes of hypoxemia

References

1. Ayas N. Bergstrom LR. Schwab TR. Narr BJ. Unrecognized severe postoperative hypercapnia: a case of apneic oxygenation. Mayo Clinic Proceedings. 73(1):51-4, 1998
2. Denault A. Frechette D. Skrobik Y. Best evidence in anesthetic practice. Prevention: supplemental oxygen reduces the incidence of surgical-wound infection. Canadian Journal of Anaesthesia. 48(9):844-6, 2001
3. Lawless N. Tobias S. Mayorga MA. FiO2 and positive end-expiratory pressure as compensation for altitude-induced hypoxemia in an acute respiratory distress syndrome model: implications for air transportation of critically ill patients. Critical Care Medicine. 29(11):2149-55, 2001

Last updated: 1 April 2002Created
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