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The two major functions of the lungs are to supply oxygen to blood for delivery to tissues and to clear blood of carbon dioxide produced during tissue metabolism. When the lungs fail to provide adequate oxygenation of blood, Type I respiratory failure, also known as hypoxemic respiratory failure, is present. Hypoxemic respiratory failure occurs only when a significant amount of intrapulmonary shunt is present. When the lungs fail to provide an adequate clearance of carbon dioxide, Type II respiratory failure, also known as ventilatory failure, is present. Some patients suffer from both ventilatory failure and hypoxemic respiratory failure, for example, a patient intubated for severe emphysema with bilateral pneumonia. However, most patients with respiratory failure will display predominant features of only one of these mechanisms. This chapter will discuss ventilatory failure.


It is important to understand that ventilatory failure can occur even with a normal arterial partial pressure of carbon dioxide (Paco2); ventilatory failure is not synonymous with elevated Paco2. For instance, a patient may have status asthmaticus with severe bronchospasm and impending respiratory arrest, yet have a normal Paco2. Likewise, a patient with a high bicarbonate level of 35 mEq/L due to diuretic therapy will usually have a compensatory elevation in Paco2 to buffer pH, but ventilatory failure is not present. Ventilatory failure is not synonymous with a requirement for mechanical ventilation either, as many patients with ventilatory failure are effectively managed without mechanical ventilatory support. Ventilatory failure can be acute, chronic, or acute superimposed on chronic.


The balance of tissue CO2 production and its subsequent excretion through the lungs determines the arterial carbon dioxide level (Paco2). Paco2 is thus dependent on the production of carbon dioxide (V̇co2), minute ventilation (V̇e), and the fraction of tidal volume (Vt) that encounters unperfused alveoli, known as dead space (Vd):


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where k is a constant of 0.863 if V̇co2 is in milliliters per minute.


As carbon dioxide is transferred from blood across alveolar membranes, the airways and unperfused alveoli are useless in removing carbon dioxide. Dead space has a fixed component that is “anatomic” due to the conducting airways (trachea and airways proximal to respiratory bronchioles) and a variable “physiological” component due to the fraction of alveoli that are ventilated but unperfused. In reality, increased dead space is often due to areas of lung that receive minimal perfusion (as opposed to none) but have normal or near normal ventilation. This creates high ventilation-to-perfusion ratio alveolar units, or V̇/Q mismatching. It is crucial to note that hypoventilation in a normoxic environment must lead to a higher Paco2 (hypercarbia) and a lower arterial Pao2 (hypoxemia), yet the alveolar to arterial difference of the partial pressure of oxygen (a–aDo2, or ...

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