Author: David R. Hillman, M.D., FANZCA
ASA Monitor 07 2017, Vol.81, 20-22.
David R. Hillman, M.D., FANZCA, Centre for Sleep Science, University of Western Australia Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital Nedlands, Western Australia.
Anesthesia and sleep have much in common, particularly where breathing is concerned. This relationship is based on the similarities in physiological changes that occur with transition from consciousness to unconsciousness in each state. Wakefulness stimulates breathing through non-specific excitatory activity mediated through the ascending arousal system.1 Recent evidence suggests that the parabrachial complex, a component of this system, has key roles in both the generation of wakefulness and in the patterning of breathing during it.2 This activity diminishes with loss of consciousness, whether at induction of anesthesia or at sleep onset.
Shared Physiological Changes of Sleep and Anesthesia
The neurophysiological pathways involved in transition from wakefulness to sleep are activated by anesthetic drugs and so are deeply implicated in the mechanisms of anesthesia.3 Given this, it is perhaps not surprising that similar physiological changes occur with loss of consciousness in both states. Volition is lost and there is a decrease in ventilatory drive,4,5 skeletal muscle activation,6 –8 reflex gain7,9 and end-expiratory lung volume.10,11 Both the upper-airway (UAW) and respiratory muscles are affected. Decreased activation of the UAW muscles results in narrowing and increased collapsibility of the pharynx. Decreased activation of the respiratory muscles results in reduced ventilatory effort. Furthermore, loss of activation of muscles of the chest wall is associated with a decrease in end-expiratory lung volume. This has its own destabilizing effect on the UAW, as it is associated with loss of longitudinal traction on it with a resulting increase in its collapsibility.12
Neither anesthesia nor sleep are homogenous states and so the magnitude of these changes can vary within them. While the changes are abrupt at loss of consciousness in either state, the changes increase with increasing depth of anaesthesia and, in the case of sleep, with transitions from non-rapid eye movement (NREM) to rapid eye movement (REM) sleep.1,6,13,14
“Sleep and anesthesia are closely allied states and it is incumbent on anesthesiologists to understand the nature of these inter-relationships and their implications for perioperative care.”
Changes Are More Profound During Anesthesia
While the nature of these physiological changes is similar in either state, they are more profound during anesthesia. Anesthesia can be deepened to a point where breathing efforts cease, whereas the capacity to breathe is preserved during normal sleep, although it can be grossly diminished in individuals with weak or excessively loaded respiratory muscles. Furthermore, while the capacity to arouse is preserved during sleep – providing protection against prolonged episodes of UAW obstruction or hypoventilation – abolition of arousal responses is a basic objective of general anesthesia.
Implications of These Physiological Changes
These changes have a relatively minor effect on breathing of healthy individuals overnight, with an increase in PCO2 levels of the order of 2 to 6 mmHg during sleep, reflecting the diminution in ventilatory drive.15 Given the more profound effects of anesthesia, the increases in PCO2 levels are considerably greater when spontaneously breathing under general anesthesia. While UAW patency is reasonably well maintained during sleep in most healthy individuals, the tendency for UAW obstruction is greater during general anesthesia.16
However, if the UAW is narrow or excessively floppy, these changes are accompanied by UAW obstruction, particularly during REM sleep, where ventilatory drive and muscle activation are at their nadir and, when supine, where the influence of gravity on the tongue and soft palate act to further restrict the UAW. Similarly, if the inspiratory pump muscles (diaphragm, rib cage and accessory muscles) are weak (as with respiratory neuromuscular diseases) or excessively loaded (as with morbid obesity or respiratory conditions associated with large elastic or resistive loads) then sleep-related reductions in ventilatory drive can result in substantial sleep hypoventilation.17 Again, these changes tend to be particularly apparent during REM sleep given that ventilatory drive is at its nadir during this sleep stage.1
These sleep-related influences on breathing have their parallels during anesthesia where those with narrow or excessively collapsible UAWs are prone to obstruct and those with weak or excessively loaded inspiratory muscles are prone to excessive hypoventilation.16,18
Breathing Behavior in One State Provides Insights Into Likely Behavior in the Other
Given the similarities in the physiological changes affecting breathing in either state, it is not surprising that predisposition to UAW obstruction or significant hypoventilation in one state provides useful guidance regarding likely behavior in the other. Patients with difficult, obstruction-prone airways during sleep often have difficult, obstruction-prone airways during anesthesia and recovery from it.4 Patients with a tendency to hypoventilate during sleep are prone to excessive hypoventilation during anesthesia and sedation and to postoperative respiratory failure.18 This makes understanding of and inquiry about sleep-disordered breathing a valuable component of preoperative assessment of patients presenting for general anesthesia. The converse is also true: breathing behavior during anesthesia and recovery from it provides a useful guide to likely breathing behavior during sleep.
Identifying Those at Greatest Perioperative Risk: Importance of Arousal Thresholds
While UAW obstruction and hypoventilation are readily managed in the O.R. and post-anesthesia care unit (PACU), a particular clinical problem is how to identify those at risk of recurrence of these problems beyond PACU if capacity to arouse from such events is compromised, for example by opioids or sedatives. Severity of sleep-disordered breathing provides some guidance here. The most commonly used severity metric is apnea hypopnea index (AHI), the number of apneas (obstructions) and hypopneas (partial obstructions) per hour of sleep. However, this metric does not reflect propensity to arouse from an obstructive event, and it is arousal failure that allows such an event to persist to a life-threatening extent.
Notably, there is a substantial inherent variability between individuals in their arousal thresholds to breathing disturbances during sleep that is readily evident on study of breathing during sleep. Some respond briskly to relatively minor degrees of UAW obstruction or hypoventilation, while others with high arousal thresholds may endure relatively prolonged episodes of disordered breathing before arousal eventually occurs. This different behavior is a well-recognized example of the phenotypic variability that exists between individuals in the characteristics that determine their breathing behavior during sleep.19 While low arousal thresholds during sleep may lead to exaggerated sleep disruption in response to relatively minor breathing events in individuals with this predisposition, it is those with high arousal thresholds to disordered breathing during sleep that may be particularly vulnerable to prolonged, potentially dangerous episodes of hypoventilation or obstruction when under the influence of sedatives or opioids perioperatively.20,21
This provides an example of the way in which knowledge of adverse breathing behavior during sleep may have predictive value for adverse breathing behavior perioperatively, allowing those at particular risk of UAW obstruction or hypoventilation to be more readily identified so that appropriate strategies can be adopted to circumvent the problem or detect it early.
Anesthesiologists have an ever-expanding role in perioperative management, encapsulated in the term “perioperative physician.” This provides additional impetus for understanding breathing disorders of sleep. To recognize these problems in patients preoperatively is to be forewarned of potential breathing problems during anesthesia – difficult airways, hypoventilation; and beyond it, UAW obstruction with risk of asphyxia and postoperative respiratory failure. Sleep and anesthesia are closely allied states and it is incumbent on anesthesiologists to understand the nature of these interrelationships and their implications for perioperative care.
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