RESPIRATORY FUNCTION DURING ANESTHESIA
Arterial oxygenation is impaired in most patients during anesthesia
with either spontaneous or controlled ventilation.[116]
[117]
[118]
[119]
[120]
[121]
In
otherwise
normal patients, it is generally accepted that the impairment in arterial oxygenation
during anesthesia is more severe in the elderly,[122]
[123]
the obese,[124]
and smokers.[125]
In various studies of healthy young to middle-aged patients under general anesthesia,
venous admixture (shunt) has been found to average 10%, and the scatter in V̇A/
ratios is small to moderate,[123]
[126]
whereas in patients with a more marked deterioration in preoperative pulmonary function,
general anesthesia causes considerable widening of the V̇A/
distribution and large increases in both low-V̇A/
(0.005 < V̇A/ < 0.1) (underventilated)
regions and shunting.[122]
[125]
[127]
The magnitude of shunting correlates closely
with the degree of atelectasis.[122]
[127]
In addition to the foregoing generalizations concerning respiratory
function during anesthesia, the effect of a given anesthetic on respiratory function
depends on the depth of general anesthesia, the patient's preoperative respiratory
condition, and the presence of special intraoperative anesthetic and surgical conditions.
Effect of Anesthetic Depth on Respiratory Pattern
The respiratory pattern is altered by the induction and deepening
of anesthesia. When the depth of anesthesia is inadequate (less than MAC), the respiratory
pattern may vary from excessive hyperventilation and vocalization to breath-holding.
As anesthetic depth approaches or equals MAC (light anesthesia), irregular respiration
progresses to a more regular pattern that is associated with a larger than normal
VT. However, during light but deepening anesthesia,
the approach to a more regular respiratory pattern may be interrupted by a pause
at the end of inspiration (a "hitch" in inspiration), followed by a relatively prolonged
and active expiration in which the patient seems to exhale forcefully rather than
passively. As anesthesia deepens to moderate levels, respiration becomes faster
and more regular, but shallower. The respiratory pattern is a sine wave losing the
inspiratory hitch and lengthened expiratory pause. There is little or no inspiratory
or expiratory pause, and the inspiratory and expiratory periods are equivalent.
Intercostal muscle activity is still present, and there is normal movement of the
thoracic cage with lifting of the chest during inspiration. The respiratory rate
is generally slower and the VT larger with nitrous
oxide-narcotic anesthesia than with anesthesia involving halogenated drugs. During
deep anesthesia with halogenated drugs, increasing respiratory depression is manifested
by increasingly rapid and shallow breathing (panting). On the other hand, with deep
nitrous oxide-narcotic anesthesia, respirations become slower but may remain deep.
In the case of very deep anesthesia with all inhaled drugs, respirations often become
jerky or gasping in character and irregular in pattern. This situation results from
loss of the active intercostal muscle contribution to inspiration. As a result,
a rocking boat movement occurs in which there is out-of-phase depression of the chest
wall during inspiration, flaring of the lower chest margins, and billowing of the
abdomen. The reason for this type of movement is that inspiration is dependent solely
on diaphragmatic effort. Independent of anesthetic depth, similar chest movements
may be simulated by upper and lower airway obstruction and by partial paralysis.
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