Chapter 4, cont… (Page 2)

PCO₂ and alveolar ventilation

CLINICAL IMPORTANCE OF THE PCO₂ EQUATION

The simple relationships expressed by the PaCO₂ equation (Equation 8) are key to understanding patients with respiratory problems.

By defining PaCO₂, Equation 8 demonstrates both what determines PaCO₂ and what does not. PaCO₂ equals the level of carbon dioxide production over alveolar ventilation (times a constant), and nothing more. PaCO₂ is not equated to such clinically apparent factors as rate and depth of breathing, level of anxiety, mental status, or sensation of dyspnea.

True, VA = VE ­ VD, and VE is the breathing frequency times the tidal volume, but these variables do not define PaCO₂. One cannot infer the PaCO₂ from the VE alone since VE gives no information on either VA or VCO₂. In addition, since neither VA nor VCO2 can be determined clinically, one cannot reliably determine PaCO₂ on clinical grounds alone. If one is concerned about the status of a patient's VA, there is no clinical substitute for measuring PaCO₂.

The importance of this observation in patient care cannot be overstated. For years, before arterial blood gas analysis became widely available, many physicians thought that the level of VA (and hence PaCO₂) could be reliably estimated at the bedside. With the advent of blood gas analysis, clinical assessment has been shown unreliable both by formal study (Mithoefer, Bossman, Thibeault, et al., 1968) and by everyday experience. The physiologic reason is apparent -- one cannot estimate VA reliably nor know a given patient's VCO2.

PCO₂ IN THE CLINICAL SETTING

Knowing the PaCO₂ is not enough, of course, to fully evaluate alveolar ventilation. PaCO₂ must be explained and understood in light of the full clinical picture.

For example, a patient with asthma, who is using his accessory muscles during an acute bronchospasm attack, is trying to hyperventilate and thus blow off carbon dioxide (the respiratory stimulus is not hypoxemia but an irritation of lung receptors in the narrowed bronchi). If such a patient has a "normal" PaCO₂, e.g., 40 mm Hg, then VA is adequate for carbon dioxide production (by definition). However, PaCO₂ in the "normal" range during an acute asthma attack is indicative of a very severe airways obstruction and an inability to hyperventilate despite the respiratory effort. It may signify impending respiratory failure and an imminent need for intubation and artificial ventilation. In this setting, PaCO₂ of 40 mm Hg is not "normal", and is certainly not reassuring.

As another example, a patient with diabetic ketoacidosis should hyperventilate in response to the acidemia. A PaCO₂ of 40 mm Hg, pH of 7.25, in a patient with acidosis suggests an additional primary respiratory problem is inhibiting the ventilatory response to acidemia. Although the patient's PaCO₂ is adequate for carbon dioxide production, it is far from optimal considering the metabolic acidosis.

Interpreting PaCO₂ in light of the clinical picture (and not just as a number) is essential for good patient management whenever a blood gas analysis is obtained. Such assessment will often determine major management decisions, such as the use of intubation and artificial ventilation.

PHYSIOLOGIC BASIS FOR HYPERCAPNIA

Failure to bring in enough fresh air to adequately eliminate carbon dioxide is one type of respiratory failure and is called ventilatory failure (see Chapter 11). Thus the hallmark of ventilatory failure is hypercapnia Ä elevated PaCO2.

It can now be appreciated that there is only one fundamental reason for hypercapnia in clinical medicine: decreased alveolar ventilation (VA) relative to carbon dioxide production. This can be viewed as the physiologic basis for all carbon dioxide retention. Under this broad physiologic umbrella can be classified every clinical case of hypercapnia (see box on page 81). This categorization derives directly from the physiologic relationships expressed in Equations 2 and 8.

Decreased alveolar ventilation caused by decreased or inadequate minute ventilation

Decreased VA may occur from anything that decreases VE, e.g., respiratory center depression (drug overdose) or chest wall dysfunction (paralysis from neuromuscular disease). Whatever the actual clinical cause, VE is reduced enough to lower VA and raise arterial carbon dioxide pressure (PaCO₂). The decrease in VE may be manifested by an alteration in tidal volume and/or breathing frequency (Equation 1).

VA can also be decreased (relative to carbon dioxide production) because of inadequate VE; in such cases VE does not actually decrease from the patient's normal resting value, but instead it does not increase appropriately. For example, if, during exercise, carbon dioxide production (VCO₂) increases but VE does not, PaCO₂ will increase. This occurrence is sometimes seen in patients with severe emphysema who simply cannot augment VE above their resting level. In such cases the fundamental cause is still inadequate VA for the level of VCO₂. In the most extreme cases of increased carbon dioxide production (during very heavy exercise), healthy people increase their VE and VA appropriately and PaCO₂ does not increase.

Decreased alveolar ventilation caused by increased dead space ventilation

Increased physiologic dead space is a more common cause of hypercapnia than decreased minute ventilation. In fact, increased dead space ventilation (VD) is an underlying mechanism in virtually all cases of obstructive and restrictive lung disease that lead to carbon dioxide retention. Increased VD may occur in two ways. The most common way is from an imbalance in ventilation/perfusion (V/Q) relationships; this is the same V/Q imbalance responsible for most clinical hypoxemia (discussed in Chapter 5).

The V/Q imbalance may so alter the architecture of the lungs that there is more dead space and less alveolar (gas­exchanging) space than normal. For such a patient to have sufficient alveolar ventilation, he must either take deeper breaths or breathe more frequently to compensate for the increased dead space and to deliver enough air to the gas exchanging alveoli; although many patients are able to do this, some are not, either because of fatigue, muscle weakness, or a decreased "drive,, to breathe (see Chapter 5 for further discussion).

The second way increased VD can occur is occasionally seen in patients with severe restrictive lung disease; these patients breathe shallowly and rapidly. With their small tidal volume, the dead space volume is proportionately higher even though the anatomic dead space may be unchanged. Since anatomic dead space comes before alveolar space, VA Will be lower.

Note that in both of these examples (severe obstructive disease and severe restrictive disease), the VE may be normal or even above normal, but the distribution of VE is abnormal. In other words, the ratio of dead space to tidal volume (VD/VT) is abnormally high and is the reason for hypercapnia.

Decreased alveolar ventilation from combined causes

Finally, patients may have a combination of both processes: diminished VE and increased VD. This may occur, for example, in patients with severe lung disease who become "tired out" and cannot maintain VE because of muscle fatigue or chest bellows impairment.

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