The Physiology of Respiratory Sensations

Respiratory Sensations and Ventilatory Control

Acute hypoxemia and acute hypercapnia stimulate the chemoreceptors and lead to an increase in ventilation. These changes in PaO2 and PaCO2 also lead to a sensation most commonly described as "air hunger, urge to breathe, or need to breathe"3,4,5. Because the intensity of the sensations seemed to increase in concert with the change in ventilation, physiologists initially thought the sensation was the consequence of the physical activity of the breathing. More recent studies, however, have demonstrated that these alterations in blood gases can cause air hunger in spinal cord-injured patients maintained on mechanical ventilators4 as well as in experimental subjects whose ventilation is fixed because of the administration of a paralytic agent5. In addition, if you ask a person to voluntarily constrain her breathing while you increase her PaCO2 level by administering a mixture of inhaled gases that contains elevated levels of carbon dioxide, the intensity of the discomfort is heightened (In this example, the subject is asked to maintain a constant level of ventilation despite the increased output from the controller associated with acute hypercapnia; in this sense, the ventilation is constrained6). The sensation of air hunger, therefore, appears to arise directly from information projected from the chemoreceptors to the sensory cortex because the activity of the ventilatory muscles is unchanged but the intensity of the discomfort is increasing. We will see shortly, however, that the amount of breathing the individual is doing for any given level of hypoxemia or hypercapnia can affect the intensity of the sensation.

As discussed in Chapter 6, other factors may also stimulate the controller. Acute acidemia activates the chemoreceptors and produces a sensation of air hunger even in the absence of changes in blood gases. Pathologic conditions such as pulmonary embolism (blood clots to the lungs), asthma, and heart failure (with increases in pulmonary vascular pressures and leakage of fluid from pulmonary capillaries) also cause an increase in ventilation, probably from stimulation of pulmonary receptors. Although these conditions may be associated with multiple respiratory sensations, patients with these problems may describe a sensation of air hunger, even in the absence of alterations in PaO2 or PaCO2.

The increase in ventilation associated with exercise is attributable to a number of factors that stimulate the controller in different ways (see Chapters 6 and 9). The breathing sensation associated with exercise, however, is somewhat different than the air hunger noted above. In studies of the respiratory sensations associated with exercise, a sensation of heavy breathing or breathing more appears to be most characteristic7. We believe this sensation is an indicator of cardiovascular fitness (more on this in Chapter 9).

Elevated ventilation implies that ventilatory muscle activity has increased. In many cases, this heightened activity is perceived as a sensation of increased work or effort of breathing. The sense of effort is thought to result from a neural message that is sent from the motor cortex to the sensory cortex at the same time as the signal is sent to the muscles to contract. This “copy” of the motor message has been given the name corollary discharge and is thought to be a mechanism by which the sensory cortex is able to monitor the activity of the motor cortex (Fig. 8-1).

In the example of a person with a normal ventilatory pump, we are not usually aware of a sense of effort to breathe, much as it does not require significant effort to raise your arm or to walk down the street, activities that require the activation of a number of skeletal muscles. However, if you are asked to lift a 50-lb weight or to walk down the street with legs weakened by polio, the output of the motor cortex and the sense of effort will increase substantially. In most clinical sensations, the work or effort of breathing becomes prominent when there is a problem with the ventilatory pump, such as increased airflow obstruction, a stiff chest wall, or a weakened diaphragm.