11 OXYGEN MONITORING AND ASSESSMENT
James B. Haenel R.R.T., Jeffrey L. Johnson M.D.

1. How does a pulse oximeter work?

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Light-absorption characteristics differ for the four most common circulating species of hemoglobin in adults:

1. Reduced hemoglobin (RHb)
2. Oxygenated hemoglobin (O2Hb)
3. Methemoglobin (Met Hb)
4. Carboxyhemoglobin (CO Hb)

Current pulse oximeters transmit two wavelengths of light, red (680 nm) and infrared (940 nm), and these differentiate O2Hb from RHb. Using optical plethysmography, the pulse oximeter measures hemoglobin saturation only during arterial pulsation.

2. How accurate is pulse oximetry?

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The device is highly accurate at saturations > 80%. This results in an overall accuracy of ± 5%.

3. Are clinicians accurate in determining arterial desaturation by “visual oximetry” (how red is the blood)?

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No. Pulse oximetry should be regarded as the fifth vital sign.

4. How does the pulse oximeter respond to an abnormal species of hemoglobin?

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In carbon monoxide or cyanide poisoning, the oximeter interprets an abnormal hemoglobin as a combination of O2Hb and RHb, which results in an erroneously high saturation. Based on the light absorption of Met Hb, the pulse oximeter may display a saturation of 85%.

5. Can any other environmental or clinical conditions result in inaccurate pulse oximetry values?

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Reliability depends on a strong arterial pulse plus good light transmission. Inaccuracy results with hypotension (mean arterial pressure < 50 mmHg), hypothermia (< 35°C), vascular disease (poor peripheral perfusion), and vasopressor therapy (vasoconstriction). Bright lights, intravenous dyes, nail polish, and excessive motion each may produce bad information.

6. What is the relationship between oxyhemoglobin saturation (Sao2) and partial pressure of oxygen (Pao2)?

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Proper interpretation of pulse oximetry requires recall of the oxyhemoglobin dissociation curve. A rightward shift (decreased hemoglobin affinity for oxygen) facilitates oxygen unloading at the tissue level. Increasing temperature, increasing Paco2, increasing 2,3-diphosphoglycerate, and increasing hydrogen ion concentration-all “increases”-shift the curve to the right. When the Pao2 is > 100 mmHg, however, the curve is virtually flat. Consequently a large drop in Pao2 (e.g., from 200 to 100 mmHg) may occur with no discernible change in Sao2. (See Figure 11-1.)

7. What are the indications for continuous pulse oximetry?

Figure 11-1 Oxyhemoglobin dissociation curve.
Any patient who either is or might get sick. Pulse oximetry should be considered standard monitoring in critical care units. Pulse oximetry is uniquely valuable during patient transport, when weaning from the ventilator, and after major ventilator changes. Critically ill patients who are outside the intensive care unit (ICU) (emergency department or radiology suite) also should be monitored by pulse oximetry.

8. How does a continuous mixed venous oximeter work?

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Mixed venous oximetry uses reflective spectrophotometry. Narrow wavebands of light are transmitted via a fiberoptic bundle to the blood flowing past the tip of the catheter and are reflected by a separate fiberoptic bundle to a photodetector that determines relative absorption of the specific wavelength. A microprocessor calculates mixed venous hemoglobin saturation (Svo2).

9. What is the normal value for mixed venous oxygen saturation?

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The normal oxygen tension in mixed venous blood (Pvo2) is 40 mmHg. Under physiologic conditions, this is equivalent to an Svo2 of 75%, which is on the steep portion of the oxyhemoglobin dissociation curve. Three fourths of the oxygen (see Chapters 4, 5, and 6) delivered out of the aorta (Do2) returns to the right heart unused.

10. Using a pulmonary artery catheter, how can oxygen delivery and consumption be determined?

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The Fick equation shows the relationship between systemic oxygen delivery (Do2) and oxygen consumption (Vo2):

VO2 = CO x (CaO2 – CVO2)

where Cao2 is arterial oxygen content, Cvo2 is mixed venous oxygen content, and CO is cardiac output. Oxygen delivery is determined by the following equation:

DO2 = CaO2 x CO

where Cao2 is (1.36 × [hemoglobin concentration] × [arterial oxygen saturation] + Pao2 × 0.003) and Cvo2 is (1.36 × [hemoglobin concentration] × [venous oxygen saturation] + Pao2 × 0.003).

11. Describe the four primary causes of a sudden fall in Svo2.

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A stable, normal Svo2 ensures a balance of Do2 and Vo2, whereas a sudden fall in Svo2 provides an early warning of (1) low CO, (2) arterial oxygen desaturation, (3) drop in hemoglobin, or (4) increased Vo2.

12. Why does Svo2 rise during general anesthesia?

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General anesthesia suppresses metabolic demands; vo2 decreases (extracting less oxygen peripherally), and Svo2 rises.

13. Why does Svo2 rise with septic shock?

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During sepsis, large peripheral shunts, high cardiac output, and poor oxygen extraction contribute to an elevated Svo2.

14. State the advantages of continuous monitoring of Svo2.

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Svo2 provides prompt feedback about therapeutic interventions and disease progression. Svo2 trends are more important, however, than absolute values. With time, the catheter tip gets progressively gummed up with tissue proteins; the catheter should be recalibrated every 12-24 hours.

15. Are there any disadvantages to computer-generated hemodynamic profiling?

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Yes-even when it is wrong, we tend to believe it. Comprehensive hemodynamic profiling includes a constellation of parameters: cardiac output, Pao2, Svo2, urine output, serum lactate level, and great-toe temperature.

16. What is dual oximetry?

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Dual oximetry consists of simultaneous monitoring of arterial (Sao2) and mixed venous (Svo2) hemoglobin saturation to provide real-time, continuous information about pulmonary function, oxygen transport, and oxygen extraction ratio. Dual oximetry is particularly useful for real-time assessment during a best trial of positive end-expiratory pressure.

17. What is transcutaneous oxygen monitoring (TCM)?

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TCM is a method of continuously recording skin Po2 (Ptco2), which is not equal to arterial Po2. In 1975, Van Duzee observed that the lipid component of the stratum corneum melts as skin temperature increases, and gas diffusion can increase by 1000-fold. The Ptco2 electrode is designed to heat the skin to 44°C. The elevated temperature also increases dermal blood flow and “arterializes” the capillary blood. The interpretation of pulse oximetry and TCM are the same, however.

18. If the skin beneath the sensor is arterialized, why is the Ptco2 not equal to the Pao2?

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Four factors contribute to the difference between Ptco2 and Pao2:

1. The rightward shift of the oxygen-hemoglobin dissociation curve with heating
2. Variations in the skin oxygen permeability
3. Metabolic consumption of oxygen by the dermal tissue
4. Cutaneous blood flow

Because factors 1 and 3 tend to cancel each other, the relationship between Ptco2 and Pao2 is effectively linear and depends only on oxygen permeability and skin blood flow.

19. What is an oxygen debt?

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An oxygen debt is the net cumulative difference between oxygen consumption measured at baseline and during any pathologic state. It is the amount of oxygen needed by the cells to compensate for the mismatch between oxygen delivery and oxygen demand.

20. Name the five physiologic mechanisms responsible for causing hypoxemia. Do they all result in a widened alveolar-arterial gradient (A-a gradient)?

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1. Low inspired oxygen fraction (e.g., high altitude)
2. Alveolar hypoventilation (physiologic dead space)
3. Diffusion limitation
4. Ventilation/perfusion mismatch (most common cause for hypoxemia-this really includes both mechanism 2 and 5)
5. Shunt (adult respiratory distress syndrome, severe pneumonia)

Alveolar hypoventilation and a low FiO2 may result in hypoxemia with a normal A-a gradient.

KEY POINTS: PHYSIOLOGIC CAUSES OF HYPOXEMIA

1. Low FiO2: normal A-a gradient
2. Alveolar hypoventilation or dead space: normal A-a gradient
3. Diffusion defect: abnormal A-a gradient
4. Ventilation/perfusion mismatch: most important cause with abnormal gradient
5. Shunt: abnormal A-a gradient; does not correct with oxygen therapy alone

21. How should a hypoxic event be managed?

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Before you even start trying to make the diagnosis, give oxygen. The first maneuver for intubated patients is to hand-ventilate with an ambu-bag. A ruptured endotracheal tube cuff is self-evident, whereas difficult bagging implies airway obstruction, bronchospasm, or tension pneumothorax. Inability to pass a suction catheter confirms endotracheal tube obstruction. If the obstruction is not reversible by changing head position or by cuff deflation, the endotracheal tube must be replaced immediately. If there is difficulty with bagging and no evidence of airway obstruction, listen to the chest for breath sounds to exclude a tension pneumothorax. The mechanical ventilator and breathing circuit must be examined for malfunction. Send arterial blood gases to confirm hypoxia (low Po2) and rule out hypoventilation (high Pco2).
Next, get a chest x-ray (to rule out a pneumothorax and to confirm the correct position of the endotracheal tube) and review recent medications, interventions (e.g., suctioning, position changes, nursing care), and changes in clinical status. Most acute hypoxic events in the ICU are due to easily identified and reversible mechanical problems, such as disconnects from oxygen delivery systems or mucus plugging that requires suctioning. (See Figure 11-2).