Assessment of Oxygenation- Not So Easy!

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 (eg, an orthopedic injury), there may be little or no concern about oxygenation.¹

In respiratory patients, the situation is different. There is often a previous 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.² 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 et al many years ago (1947), even the assessment of cyanosis is unreliable.³ 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.

In today’s critical care environment the assessment of oxygenation is crucial, especially for patients receiving mechanical ventilation. Despite advanced technology and a complex understanding of tissue oxygen delivery, it is often difficult to get a true assessment of the patient’s oxygenation status.⁴ In clinical practice, this should lead to measurement of arterial partial pressure of oxygen (Pao₂) and/or percent saturation of hemoglobin with oxygen (Sao₂). In an attempt to avoid the substantial risks of pulmonary injury associated with the utilization of high ventilator pressures and high Fio₂ delivery, clinicians often ask,”What is the optimal Pao₂?” and “What clinical intervention should be used to achieve the desired level of oxygenation?” Although the intent to minimize secondary, ventilator-induced lung injury should be lauded, any attempt to provide clinicians with a fixed numeric value to this question is misguided, not only because the oxygen requirements and clinical scenarios of our patients vary, but also because Pao₂ may be a poor indicator of these needs. A better question than “Is the Pao₂ acceptable?” is “Is the patient’s oxygenation adequate?” If we take oxygenation to mean the balance between the rate of oxygen delivery to the tissues and the rate of oxygen consumption, then Pao₂ as an indicator alone is limited. Over the past decades, several formulas have been developed in an attempt to assess the adequacy of oxygenation. Listed in the sidebar are some indicators of oxygenation that have been used to help the clinician assess the patient’s oxygenation status.

Clinicians today have an array of tools to help assess the patient’s oxygenation status, but the primary goal of improving oxygenation is to provide an increase in oxygen delivery without any harm to other organs. Recent studies have demonstrated that an improvement in Pao₂ alone is a good indicator of an increased oxygen delivery or improvement in respiratory pathophysiology. Studies of ARDSnet low-tidal volume, prone positioning, and the administration of inhaled nitric oxide are all examples of investigations^5-8 wherein either the treatment or control groups had a higher Pao₂, but this resulted in no improvement in mortality or ventilator duration. So despite the appearance of oxygenation improvement by Pao₂, exactly the opposite could have resulted.

In summary, assessing oxygenation is not as simple as performing an arterial blood gas analysis and evaluating the Pao₂. Oxygenation is a complex matrix of oxygen delivery and the cost of the interventions entailed in obtaining the desired Pao₂. There is a possibility that attempting to get normal oxygenation values in injured lungs might be more harmful than the disease pathophysiology that we are treating.⁹

---

Kenneth Miller, MEd, RRT-NPS, is clinical educator for respiratory care, Lehigh Valley Hospital, Allentown, Pa.

References

1. Casaburi R, Kukafka D, Cooper CB, Witek TJ Jr, Kesten S. Improvement in exercise tolerance with the combination of tiotropium and pulmonary rehabilitation in patients with COPD. Chest. 2005;127:809–17.
2. Goll V, Akca O, Greif R, et al. Ondansetron is no more effective than supplemental intraoperative oxygen for prevention of postoperative nausea and vomiting. Anesth Analg. 2001;92;112-73.
3. Vitale A, Dumke PR Jr, Comroe JH. Lack of correlation between rales and arterial oxygen saturation in patients with pulmonary congestion and pulmonary rdema. Circulation. 1954;10:81
4. Geelhoed GC, Landau LI, LeSouër PN. Evaluation of Sao2 as a predictor of outcome in 280 children presenting with acute asthma. Ann Emerg Med. 1994;23:1236-41.
5. Eisner M, Thompson BT, Schoenfeld D, Acute Respiratory Distress Syndrome Network. Airway pressures and early barotrauma in patients with acute lung injury and acute respiratory distress syndrome. Am J Respir Crit Care Med. 2002;165:978-82.
6. Gattinoni L, Tognoni G, Pesenti A, et al. Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med. 2001;345:568-73.
7. Marini J. Are recruiting maneuvers needed when ventilating acute respiratory distress syndrome? Crit Care Med. 2003;31:2701-3.
8. Brower BG, MacIntyre N, Mathay MA, et al. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratory distress syndrome ventilated with high positive end-expiratory pressure. Crit Care Med. 2003;31:2592-7.
9. Amato M, Barbas C, Medeiros D, et al. Beneficial effects of the “open lung approach” with low distending pressures in acute respiratory distress syndrome. Am J Respir Crit Care Med. 1995;152:1835-46.