IN 1874, Jacob Heiberg wrote that during chloroform anesthesia, noisy, obstructed breathing, particularly during inspiration, could be prevented by pulling the jaw forward. He was not sure how this worked and proposed freezing a corpse to find out. 1Unfortunately, I have not been able to find any report of this proposed study, which was conceived without the advantage of modern imaging methods. Even earlier, writers had suggested that obstruction of the airway in unconscious subjects often could be overcome by pulling the tongue forward, and they suggested that the “inelastic ligaments” between the tongue and epiglottis would act on the epiglottis, which was considered to be the cause of the problem. If this method failed, then intubation of the trachea was advocated, 2which could explain why we are perhaps more skilled in using instruments to keep the airway patent than we are informed about how the body does it. Indeed, tracheal intubation has been with us for a millennium. 2It is only now, with modern methods of investigation and imaging, that we are unraveling the complexities of how the airway is controlled. Thus, in an early study, Boidin 3used a fiberscope to show how head position affected the epiglottis, and Nandi et al. 4showed how the epiglottis moved with head extension. This issue of Anesthesiology contains two studies of the airway during anesthesia. 5,6Such investigations are important for several reasons, despite the increasing variety of apparatuses being marketed to hold the upper airway open. First, all of the devices that we could choose have disadvantages, from minor morbidity caused by an apparatus in the airway, 7to the dangers associated with misplacement and blockage, to the apparent risk of transmission of serious disease, 8of which, in Europe, variant Creutzfeldt–Jakob disease is the latest worry. Simple, safe methods of airway management with minimal intrusion could have many advantages. Second, after anesthesia, the control of the airway has to be relinquished to the patient, and in many other circumstances, patients’ control systems may be impaired, either by disease or deliberately during sedation. In some cases, the consequences of poor airway control are striking and disastrous, but in others, the consequences of inadequate airway control are not clear. In patients with overt, sleep-disordered breathing, a study conducted over 4 yr showed a “dose” relationship with hypertension. 9Perhaps airway obstruction is a cardiovascular stress that plays a part in complications such as postoperative myocardial ischemia and infarction.
Anesthesiologists are ideally positioned to study and understand these phenomena. We spend our career maintaining the airway, often with our own hands. We attempt to predict, maybe optimistically, 10when we may encounter difficulties with the airway; we address the consequences of returning control of the airway to the patient after anesthesia;11and we are aware that sedation may lead to adverse events. 12
An early study of the upper airway muscles concluded, “The simultaneous contraction of opposing muscles maintains airway patency.”13The reality is more complex: the activity of the pharyngeal muscles is not simple, and there are clear differences between the different muscles. In conscious subjects, muscle activation is affected by factors such as breathing route, posture, and blood pressure. The control of pharyngeal muscle activity has both central and reflex components. 14Anesthesia of the airway reduces airway muscle activity in patients with sleep-disordered breathing and can induce airway obstruction during sleep in normal subjects. 15General anesthetics reduce the central component of this control. 16The coordination of the respiratory muscles is complex, particularly the interaction of some of the less accessible muscles of the velopharynx, 17but the muscles in this region are vital in the interaction between the jaw, the pharynx, and airway resistance. 18,19
Studies of anesthetic actions in this field have been few. In the past, the pharynx has been a “border post” between specialties, and studies of the respiratory system were usually conducted after the upper airway had been bypassed and “secured.” When obstructive sleep apnea became recognized as an important cause of morbidity, research on airway control impairment in this condition accelerated, and we gained knowledge of how the normal airway is controlled. However, there are important differences between the normal airway and the airway in sleep apnea and associated conditions such as obesity. One striking difference is in the shape of the pharyngeal airway, which is narrowed from the side in obesity. 20In obese subjects, the circumference of the neck is an independent predictor of sleep apnea. 21Although we know that sedative and anesthetic agents disturb airway control, 22,23and there can be clear differences between different types of sedatives, 24the precise effects of depressant drugs have not been investigated. Since partial neuromuscular block has little effect on airway patency, 25and local anesthesia of the airway can cause obstruction, 15I suspect that the afferent and central parts of the system are those mainly affected. The Starling resistor model of airway collapse predicts that resistance upstream of the point of collapse is important, since that resistance regulates the pressure at the point of airway collapse. There may be simple clinical steps we can take to reduce the likelihood of collapse by optimizing this part of the airway.
Airway obstruction in sleep apnea syndrome can also cause transient lung abnormalities and perhaps may worsen gas exchange. 26Episodic hypoxemia in patients after surgery has been linked to airway obstruction and is considered by some to be analogous to sleep apnea syndrome. Breathing problems after surgery are certainly common in patients who already have impaired airway control. 27Although episodic postoperative hypoxemia has been associated with morbidity, such as cardiac ischemia 28and delirium, 29these are merely observational links, and it is not clear if hypoxemia, in general, impairs outcome from surgery. Oxygen therapy is widely used to prevent hypoxemia, but it does not affect the number or severity of the episodes of obstruction. Nasal continuous positive airway pressure can overcome airway obstruction in sedation and anesthesia, 30but this treatment is ineffective after surgery. 31
In the studies in this issue of Anesthesiology, airway muscle activity was either very small or deliberately abolished. 6Consequently, these studies tell us about the physical properties of the passive upper airway, which is affected by internal pressure, flow, and gravity when it is not affected by important muscle activity. Eastwood et al. 5showed that when the depth of anesthesia was reduced, the pharynx became less collapsible. Similar findings have been reported in sedation with midazolam. 32It is not yet clear how much small or residual quantities of anesthetic and sedative agents disturb the control of the airway. This topic is difficult to study because of the sleep state of the patient. When aroused, airway control may be satisfactory, but when left alone, the same patient may have persistent airway obstruction or may show repeated cycles of obstruction and recovery. 33I find that a useful feature of impending airway difficulty is the “poof” sign that comes from expiration through a lax mouth, indicating diversion from the nasopharyngeal route, which is normal in conscious subjects.
What can we learn from these studies? Perhaps we should measure neck circumference rather than thyromental distance! We should certainly consider nasal obstruction as a potential cause of airway difficulty. We should think more about the efficacy of the maneuvers we apply, 19,34not just in terms of the measures used in the present studies, but in terms of how we can judge how well the airway is maintained (a magnetic resonance imaging scan is not often at hand) and in terms of important clinical outcomes that could be related to how well we can maintain the airway.