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How will systemic oxygenation be monitored during single-lung ventilation? What is the mechanism of pulse oximetry?

Answer:

Pulse oximetry is still the hallmark for monitoring arterial oxygenation during lung resection, decreasing the need for repeated measurements of arterial blood gases. This technique uses spectrophotoelectric oximetric principles to determine oxygen saturation. Pulse oximeters are multiple-wavelength plethysmographs. The amplitude of the pulse is a function of arterial distention, hemoglobin oxygen saturation of the arterial blood inflow, and light wavelength. Hemoglobin saturation in the arterial blood is the result of the ratio between the pulse amplitude of red (660 nm = deoxyhemoglobin) and infrared (940 nm = oxyhemoglobin) light. Pulsatile waveform is a characteristic of arterial blood flow, so there is no interference from surrounding venous blood, skin, connective tissue, or bone. Arterial pulsations cause changes in light absorption, which are used to calculate oxygen saturation. Adequate finger pulsation generally is lost with hypothermia of a few degrees, hypotension (mean blood pressure less than 50 mmHg), and infusion of vasoconstrictive drugs. Accuracy of the measurement is also lost for values below 70% and can be affected by dyshemoglobinemias (such as carboxyhemoglobin, methemoglobin, and sulfhemoglobin) as well as intravenous dye injection. The use of arterial oxygen saturation to monitor organ perfusion has been recently questioned by data of cerebral desaturation in the absence of arterial desaturation.

Cerebral oximetry has recently become a popular monitor of brain perfusion during thoracic and cardiac anesthesia. The technique uses near-infrared spectroscopy (NIRS) to integrate venous and arterial hemoglobin oxygen saturation signals in a ratio of 3:1. The presence of autoregulatory mechanisms guarantee that the brain is perfused and oxygenated at the expenses of other organs. Therefore, when significant cerebral desaturation occurs (<65%), it is likely that other organs have already been exposed to the same insult, with a higher risk for damage. Specifically, brain hypoperfusion seems to correlate with renal ischemia and subsequent acute renal failure (ARF). The magnitude and the duration of mean arterial pressure values below autoregulation limits appear to correlate with the incidence of postoperative ARF after cardiac surgery. ARF is also a known complication after anatomical lung resection. At the present time, there are no studies correlating its incidence with cerebral desaturation. Postoperative changes in mental status have been reported for prolonged periods of cerebral desaturation after thoracic procedures. Proposed physiologic mechanisms include hypoxemia during single-lung ventilation and mediastinal shift with reduced cardiac output related to the lateral decubitus position.


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