As mentioned earlier, it is best to think of blood gases as participating in two separate systems: oxygenation and ventilation. When interpreting blood gas values, the clinician can evaluate the oxygenation system with the Pao2 and the ventilation system with the Paco2 and pH. The therapies can also be separated into oxygenation and ventilation.
There are generally five causes of hypoxemia (low Pao2 in the blood). They include hypoventilation, low Fi o2, V/Q mismatch, shunt, and diffusion.
HYPOVENTILATION As seen from the alveolar air equation, hypoventilation causes hypoxemia by having a high carbon dioxide. This is usually corrected with increased Va, which reduces the Pco2. If a patient is on supplemental oxygen, hypoventilation is rarely a cause of hypoxemia, since the Fi o2 would be significantly elevated.
LOW INSPIRED OXYGEN This causes hypoxemia in two clinical situations. The first is at altitudes where the atmospheric pressure is reduced and thus Pi o2 is reduced. The second, more common cause is inadvertent administration of hypoxic gases to a patient. This most commonly occurs when an E cylinder (green oxygen canister) becomes empty. A full E cylinder contains 2200 lb/in2 of pressure and 660 L of oxygen. Since oxygen is stored as a gas, the amount of oxygen in an E cylinder is directly proportional to the pressure. Thus, a canister with 1100 lb/in 2 contains approximately 330 L of oxygen. If one knows how much oxygen, in liters, is contained in an E cylinder and the flow rate of oxygen, one can determine when the E cylinder will become empty. This calculation should be performed for all patients receiving supplemental oxygen from an E cylinder.
VENTILATION-PERFUSION MISMATCH V/Q mismatch is the most common cause of hypoxemia. Atelectasis, pneumonia, congestive heart failure, pulmonary embolus, and ARDS all cause V/Q mismatch. V/Q mismatch causes hypoxemia because areas of low V/Q ratios (low ventilation and high perfusion) act like a shunt. However, these disorders respond to supplemental oxygen.
SHUNT Shunt occurs when areas of the lung are perfused but not ventilated. Hypoxemia due to shunt does not respond to supplemental oxygen. Severe ARDS and cardiac anomalies, such as tetralogy of Fallot, are examples of shunt.
DIFFUSION As discussed previously, oxygen diffuses rapidly across the alveolus. This factor does not generally cause hypoxemia at rest. Rather, it usually causes hypoxemia during exercise.
Treatment for hypoxemia is supplemental oxygen. There are three levels of therapy for hypoxemia: (1) supplemental oxygen via nasal canula or face mask; (2) noninvasive ventilation, such as a continuous positive airway pressure (CPAP) or bilevel positive pressure ventilation (BipAP) mask, in which a patient is given positive-pressure ventilation via a face mask; and (3) mechanical ventilation via an endotrachial tube. Due to entrainment of air around a face mask, the maximum amount of supplemental oxygen that can be administered is 60% but varies with the tightness of the seal. If a patient is still hypoxemic, the clinician needs to administer one of the positive-pressure modes of ventilation. For invasive and noninvasive mechanical ventilation, it is helpful to think of oxygenation separately from ventilation. Specifically, Fio2 and PEEP or CPAP should be used to control oxygenation. Both Fio2 and PEEP or CPAP should be titrated upward until hypoxemia is resolved.
Ventilatory failure is often diagnosed by a P co2 that is greater than expected for a given bicarboninate level. However, the diagnosis can also be made clinically with a high sensitivity by evaluating the respiratory rate, (f), the use of accessory muscles, and the degree of distress. Ventilatory failure can be broken into two broad categories: (1) neuromuscular disorders, including stroke, Guillain-Barre syndrome, and drugs, such as narcotics, that alter the drive to breath; and (2) increased work of breathing, which can be due to asthma, chronic obstructive pulmonary disease, ARDS, and sepsis, which increase C o2 production.
Ventilatory failure is usually treated with mechanical ventilation either invasively or noninvasively. Like oxygenation, ventilation can be thought of as a separate system and is controlled by f and Vt, the components of Vm (Table,i22-10). When the Pco2 is elevated, f and Vt can be changed to increase the Vm and reduce the Pco2.
TABLE 22-10 An Approach to the Ventilator Management of Hypoxic and Hypercarbic Patients*
AutoPEEP When placing patients who may have obstructive airway disease on mechanical ventilation, it is important to evaluate for autoPEEP. AutoPEEP, or dynamic hyperinflation, occurs when a patient receives a breath from the ventilator prior to fully exhaling the previous breath. Dynamic hyperinflation is usually caused by a limitation to airflow, such as asthma. Such limitation results in a buildup of intrathoracic pressure and has the same physiologic consequences as does PEEP: decreased right heart preload, increased right heart afterload, and decreased left heart afterload). Indeed, autoPEEP is an unfortunate cause of pulseless electrical activity in ventilated patients, and the physiologic characteristics are similar to those of a tension pneumothorax and result in decreased preload. While one may suspect a diagnosis of autoPEEP in a wheezing patient with increased airway pressures, autoPEEP can be directly measured from the ventilator by blocking the exhalation port (usually found under the ventilator) just prior to inhalation (end exhalation). The pressure that the manometer reads is the measure of autoPEEP. Like regular PEEP, autoPEEP of 5 mmHg or greater can decrease preload.
If autoPEEP is detected, the treatment is to change the ventilator settings to allow a longer time for exhalation or to have a smaller breath to exhale. This is best accomplished by decreasing f, decreasing Vt, and increasing the inspiratory-to-expiratory ratio. In patients with obstructive airway disease and elevated P co2, one must be cautious about attempting to normalize the Pco2, since this may result in significant autoPEEP. Rather, an elevated P co2 may have to be accepted until the obstructive airway disease is reversed.
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