Clinical use

The most common indication for measuring SvO? is cardiovascular failure with hypotension or otherwise unexplained metabolic acidosis. The current philosophy of hemodynamic management of intensive care patients centers around the maintenance of an adequate cardiac output, although there is still considerable debate about what value should be sought and how it should be achieved. It is too often forgotten that measurement of cardiac output by thermodilution (taken as the clinical gold standard) is far from accurate. Under ideal circumstances thermodilution is accurate to within about 10 per cent, and most centers accept three readings within 10 per cent of each other for averaging. However, there are a number of potential sources of error, such as the presence of even minor tricuspid regurgitation which is common in ventilated intensive care patients (Jullien et,M 1995). Esophageal Doppler cardiac output monitoring appears to be as accurate as thermodilution, but it is user dependent to some extent and has its own sources of error.

The simple measurement of cardiac output, even leaving aside the accuracy of the available systems, only tells half the story, i.e. supply, and gives no indication of demand. This, in part, has led to the use of the derived variables oxygen delivery, oxygen consumption, and oxygen extraction ratio. When interpreting these variables it must be remembered that their calculation requires the measurement of a number of primary variables, each with a significant measurement error, creating a large potential error in the derived variable. The practice of indexing the values to body surface area serves to introduce further errors. In clinical practice, rather than in the laboratory, these derived variables add little to the simple measurement of SvO? which allows assessment of the adequacy of the cardiac output for the prevailing metabolic conditions.

If the microcirulation is intact and therefore responding appropriately to changes in local demand, a normal or high SvO? indicates that the oxygen delivery is adequate, or more than adequate, whereas a low SvO? suggests that oxygen delivery is too low. It can be argued that a high SvO? may be the result of shunting of blood away from nutrient capillaries and therefore may coexist with areas of hypoperfusion and cellular hypoxia. There is little evidence to support the concept of pathological microvascular shunting of blood in critical illness and no reason to believe that further increasing the cardiac output would improve this situation. Recent clinical studies in multiple organ failure have suggested that raising the cardiac output to supranormal levels increases mortality. The SvO? will also be raised if the tissues have stopped using oxygen, either because of metabolic poisoning or significant cell death. In neither of these situations will further increases in oxygen delivery be helpful.

Monitoring SvO2 in a patient with cardiovascular failure allows a rational approach to be made to managing the circulation without the use of any calculated or derived variables. The patient with a low SvO2 needs his or her cardiac output to be increased, first by intravascular volume optimization using the response of stroke volume and filling pressures to fluids or vasodilators or both. If SvO2 remains low once fluid status is optimized, the blood pressure will determine whether cardiac output is best improved by afterload reduction or inotropes. Similarly, the patient with a normal or high SvO2 who remains hypotensive after intravascular fluid optimization will require an increase in vascular resistance using vasopressors. It is unnecessary to calculate the error-prone systemic vascular resistance in order to make this decision, nor should the systemic vascular resistance itself be treated if the blood pressure and cardiac output are acceptable. It must also be remembered that fluid optimization and the state of the circulation need to be reviewed after each therapeutic maneuver.

Target SvO2 depends on the clinical situation faced. In high-output hypotensive states requiring vasopressors most would aim to keep SvO2 at or above normal (3 70 per cent), but in low-output states a target SvO2 of 60 per cent is usually accepted. These targets clearly need to be adjusted according to the clinical situation, response to treatment, underlying cardiac function, etc.

The other main indication for the measurement of SvO2 is severe respiratory failure, as a low SvO2 will exaggerate the effects of a pulmonary shunt. If some pulmonary blood flow has an oxygen content that is lower than normal, it will mix with the oxygenated blood in the left heart lowering the average arterial saturation proportionately. As the contribution of dissolved oxygen to total oxygen content is insignificant at atmospheric pressure it is not possible to make up for this deficiency by hyperoxygenating the blood flowing through the normal lung. To illustrate simply, a patient with a 25 per cent true shunt and otherwise perfect respiratory function will have an arterial saturation of 91 per cent if the SvO2 is 75 per cent. If the SvO2 falls to 40 per cent the arterial saturation will fall to 83 per cent with a consequent further lowering of SvO2, inducing a self-perpetuating downward spiral. Thus optimizing SvO2 is a valuable strategy in the support of severe respiratory failure.

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