Tests Of Respiratory Control Rationale and Scientific Basis

The respiratory control system may be considered to have three functional components: (1) sensory receptors that provide information about the status of the respiratory system (only chemoreceptors that measure arterial Pco2, Po2, and pH are usually considered or tested, but there are many other sensory inputs of importance); (2) the central integrating circuits; and (3) the motor output to the respiratory muscles. The tests available are stimulus response tests, in which a receptor is stimulated and the motor output or a downstream mechanical effect of motor output, is measured. It is important to recognize that these tests are generally unable to separate the three functional components of the control system.

Minute ventilation and arterial Pco2 are maintained at normal levels even with quite marked weakness of the respiratory muscles, implying that the control system compensates for the weakness by driving the respiratory muscles harder than normal. The mechanism by which the control system identifies muscle weakness and adjusts its motor output is unknown. The increased motor output is difficult to appreciate because it succeeds in generating only normal pressures, volumes, and flows. It is most readily apparent when accessory muscles or abdominal muscles are more active than normal during quiet breathing.

If phasic contraction of scalenes, sternocleidomastoids, pectoral muscles, or abdominal muscles can be palpated, it is safe to conclude that respiratory motor output is above normal.

When respiratory muscles are chronically severely weak and arterial Pco2 begins to rise, two explanations are possible. The muscles may be so weak that they cannot continually generate sufficient alveolar ventilation. Otherwise, an abnormality of the ventilatory control system may be allowing the Pco2 to rise even though the muscles themselves are quite capable of keeping it normal. A gradual shift in the Pco2 "set point" of the controller does seem to occur in some patients with muscle disease, as it does in some cases of sleep apnea and chronic obstructive pulmonary disease.

Laboratory tests of overall respiration that have been used to try to assess the control system include inhalation of hyper-capnic or hypoxic gas mixtures to stimulate chemoreceptors, with measurements of ventilation or occlusion pressure to assess motor output, and sleep studies to monitor behavior of the control system during sleep.

In patients with weak muscles, interpretation of slopes of conventional ventilatory curves is clouded for several reasons.

• The output of the controller is abnormally high when ventilation is normal. The controller may therefore be on the nonlinear part of its normal response curve.

• The high motor neuron output cannot be measured directly and its mechanical effect (e.g., ventilation) is reduced in the presence of weakness.

• The response will become flat if ventilation nears the limit of respiratory muscle endurance and that limit may be only a short distance above resting ventilation.

Abnormal central control of respiration is well documented in bulbar poliomyelitis and other conditions affecting the central nervous system, presumably because of direct involvement of medullary respiratory centers. It has been suggested that certain muscle diseases are also associated with primary abnormalities of central respiratory control; these conditions include myotonic dystrophy, acid maltase deficiency, and other congenital myopathies. Impaired ventilatory responses to CO2 and/or hypoxia have frequently been described, but in many cases, respiratory muscle function was assessed inadequately. In myotonic dystrophy it has been shown that the relations between hypercapnia and both maximum respiratory pressures and VC are similar to those in nonmyotonic diseases (30).

Occlusion pressure is the pressure generated in the airway (and by inference the pressure generated in the pleural space) by contraction of inspiratory muscles when the airway has been occluded at end expiration. It was introduced to separate hypoventilation due to high pulmonary resistance or elastance from hypoventilation due to a failure of the respiratory pump apparatus (i.e., the muscles, passive components of the chest wall, and the control system) (31, 32). Occlusion pressure amplitude does not directly assess either the degree of muscle weakness or the degree of neuronal adjustment to the weakness. P01 is the pressure generated in the first 100 milliseconds of inspiration against an occluded airway. Its timing is such that it is not influenced by the conscious response to occlusion and as an index of ventilatory drive it has the advantage over ventilation of being independent of the mechanical properties of the lung (31). It is, however, dependent on the contractile state and function of the respiratory muscles and consequently on the lung volume at which it is measured. For example, because of the length-tension relationship of the muscles, a reduced value for a given neural output would be expected with pulmonary hyperinflation and an elevated FRC. On the other

Figure 9. Relation of sleep hypoxemia to daytime blood gases and VC in 20 patients with chronic myopathy (regression line [solid line] ± 95% confidence limits [dashed lines]). The abscissa in each panel shows the nadir SaO2 in REM sleep. More severe REM desaturation occurs with lower awake PaO2 (top panel), higher awake PaCO2 (middle panel), and lower VC (lowerpanel). Reprinted by permission from Reference 23.

Figure 9. Relation of sleep hypoxemia to daytime blood gases and VC in 20 patients with chronic myopathy (regression line [solid line] ± 95% confidence limits [dashed lines]). The abscissa in each panel shows the nadir SaO2 in REM sleep. More severe REM desaturation occurs with lower awake PaO2 (top panel), higher awake PaCO2 (middle panel), and lower VC (lowerpanel). Reprinted by permission from Reference 23.

hand, if inspiration starts below equilibrium lung volume the value of P01 recorded depends on relaxation of the expiratory muscles.

Values of P01 are around 1 cm H2O in normal subjects at rest, around 3 cm H2O in patients with stable chronic obstructive pulmonary disease, and may be 10 cm H2O or more in acute respiratory failure due to chronic obstructive pulmonary disease or acute respiratory distress syndrome. Such values reflect a high ventilatory drive consequent on a greatly increased mechanical load. Some, although not all, studies have suggested that in patients with chronic obstructive pulmonary disease receiving ventilatory support values greater than 4-6 cm H2O are associated with failure to wean (33).

In patients with weak muscles, resting P01 tends to be normal or slightly increased (34). In the model of acute respiratory muscle weakness provided by partial curarization of healthy subjects, the slope of P01 response to CO2 is increased even though the ventilatory response is reduced (35). However, in patients with chronic weakness the ventilatory and P0.1 slopes are both diminished (even though resting P0.1 is normal or increased). Hence, a reduced response in such individuals does not necessarily imply impaired ventilatory drive (30).

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