Local anesthetic agents inhibit the excitation-conduction process in peripheral nerves. In sufficient tissue concentra- tion, they may affect the heart and smooth muscles of blood vessels, resulting in hemodynamic depression.
A. Direct Effects—All local anesthetics produce a dose- related decrease in velocity of atrial conduction, atrioventric- ular conduction, and ventricular conduction. Lidocaine decreases the maximum rate of depolarization, action poten- tial duration, and effective refractory period. Bupivacaine, etidocaine, and tetracaine, which are highly potent local anesthetics, tend to decrease conduction velocity through various parts of the heart at relatively low concentrations. An extremely high concentration of local anesthetics will depress spontaneous pacemaker activity in the sinus node, resulting in sinus bradycardia and sinus arrest.
All local anesthetics essentially exert a dose-dependent negative inotropic action. High doses of bupivacaine are car- diotoxic. A biphasic peripheral vascular effect of local anes- thetic agents may be observed, with vasoconstriction followed by vasodilation in high concentration.
B. Indirect Effects—Spinal or epidural anesthesia is asso- ciated with sympathetic blockade that may result in pro- found hypotension owing to peripheral vasodilation. The higher the spinal level of the blockade, the lower is the blood pressure.
Below the T5 dermatomal level, epidural anesthesia is not usually associated with significant cardiovascular changes. From T5 to T1, it produces about a 20% decrease in blood pressure. At T1 or above, bradycardia and a fall in cardiac output may develop as a result of blockade of cardiac sympa- thetic accelerator nerves. In addition to peripheral vasodila- tion, myocardial contractility is depressed. Hypovolemic patients are more susceptible to sympathetic blockade; pro- found hypotension may occur when the preload is too low. High epidural anesthesia may decrease coronary and hepatic blood flow and may alter normal autoregulation of cerebral and renal blood flow as well.
Anesthesia & the Respiratory System
Inhalation Anesthesia
A. Control of Ventilation—In general, all volatile anesthet- ics decrease ventilation in a dose-related manner. When the patient is allowed to breathe spontaneously, the decrease in tidal volume reflects the depth of anesthesia. Although
anesthesia reduces metabolism and thus CO2production, it also increases dead space. Postoperative hypoventilation may occur under the residual effect of anesthesia on the respira- tory center with resulting hypercapnia and hypoxemia.
With the exception of ether, all inhalation anesthetics cause not only a rise in resting PaCO2but also a diminished responsiveness of ventilation to added CO2. This shifts the CO2 response curve downward and to the right, causing hypoventilation in the immediate postanesthesia period. Doxapram, which produces respiratory stimulation via peripheral carotid chemoreceptors, may be useful, but mechanical ventilation until the residual anesthesia effect completely wears off is the best treatment.
In general, inhalation anesthetics depress the hyperventi- lation response to hypoxemia by acting directly on the carotid body. This hypoxic ventilatory response is impaired in a dose-related manner; however, the dose required is much smaller than that required for depressing the hyper- capnic ventilatory response. In the immediate postoperative period, the patient may fail to respond to hypoxemia by increasing ventilation because of impairment of this defense mechanism by residual anesthetic agent.
1. Response to loading and stimulations—In a con- scious person, inspiratory effort increases when external resistance is imposed. This response is markedly depressed by anesthesia. Under the influence of anesthetics, patients with chronic obstructive pulmonary disease in particular may fail to increase ventilation when airway resistance is increased.
Ventilation increases with surgical stimulation during anesthesia. When all stimulation ceases at the conclusion of the procedure, spontaneous breathing may diminish or stop. 2. Apnea threshold—The apnea threshold is the PaCO2
level at which spontaneous ventilatory effort ceases. The dif- ference between the PaCO2 during spontaneous breathing
and during apnea is generally a constant value of 5–9 mm Hg, independent of anesthetic depth. When PaCO2is too low as a result of prolonged hyperventilation during anesthesia, postoperative hypoventilation or apnea can occur and lead to hypoxemia.
3. Posthyperventilation hypoxemia—Following pro- longed anesthesia with hyperventilation, the body stores of CO2are depleted. Refilling CO2stores leads to low PaCO2and hypoventilation. Hypoxemia may occur if supplemental oxy- gen is not provided.
B. Mechanics of Respiration—General anesthesia and muscle paralysis have a significant impact on respiratory mechanics that may lead to impaired gas exchange.
1. Functional residual capacity—With induction of gen- eral anesthesia, functional residual capacity is reduced by about 500 mL within 30 seconds. The mechanisms of this effect remain unclear. Increased elastic recoil of the lung, decreased outward recoil of the chest wall, and peripheral alveolar atelectasis owing to absorption or hypoventilation
in the dependent portions of the lung are the most likely underlying mechanisms. Other possibilities include trapping of gas distal to the closed airways, increased activity of expira- tory or decreased activity of inspiratory muscles, and increased thoracic or abdominal blood volume, alone or in combination. Twenty-four hours after recovery from anesthesia— particularly following upper abdominal surgery—functional residual capacity continues to fall to the lowest value (70–80% of the preoperative level). It takes about 7–10 days to return to the preoperative volume. When closing capac- ity exceeds functional residual capacity, regions with a low ventilation-perfusion (V/. Q) ratio develop, leading to atelec-. tasis, shunting, and impaired gas exchange. Widening of the alveolar-arterial PO2gradient and some degree of hypox- emia are not uncommon in the immediate postoperative period.
2. Compliance of the lung and chest wall—The com- pliance of the total respiratory system and lungs is reduced. The pressure-volume curve shifts rightward, following induction of general anesthesia. This may be due to a decrease in functional residual capacity, an increase in recoil of the lung, and paralysis of the diaphragm. The reduction in total compliance results in a need for greater airway pressures to inflate the lungs to a given volume under anesthetic influ- ence. A restrictive ventilatory pattern with impaired gas exchange may occur during the recovery period.
3. Airway resistance—Following induction of general anesthesia and endotracheal intubation, pulmonary resist- ance may be doubled. The size of the airway may be altered by the decrease of lung recoil, and bronchial smooth muscle tone may be diminished by some anesthetics. The pressure- flow relationship is affected, and dynamic compliance is also decreased.
4. Intrapulmonary gas distribution—Changes in the vertical pleural pressure gradient secondary to alterations in the shape or pattern of chest wall motion during anesthesia may influence the intrapulmonary distribution of inspired gas. In contrast to the awake state, preferential ventilation of the nondependent lung occurs in patients under general anesthesia. This redistribution does not depend on the use of muscle paralytic agents. Abnormal gas distribution and V/. Q. mismatching may exist when there is a residual effect of anesthetics or muscle relaxant.
5. Postoperative vital capacity—The characteristic pul- monary function profile following abdominal or thoracic surgery is a restrictive pattern with markedly reduced inspiratory capacity and vital capacity. Patients usually breathe with a shallow volume at a higher rate and cough ineffectively. The vital capacity is reduced by 50–70% of preoperative values immediately after upper abdominal sur- gery and remains depressed for 7–10 days. Only moderate or minimal reduction in vital capacity is observed following extremity surgery. If not improved, this defect of pul- monary mechanics may lead to atelectasis and pneumonia
during the postoperative period. Although residual effects of anesthetics and muscle relaxants may have some contribu- tion during the immediate postoperative period, the reduc- tion of vital capacity appears to be more related to surgical pain and the noxious reflex, which limit excursion of the diaphragm more than the anesthesia itself.
6. Diaphragmatic function—Normally, the muscles of the chest wall, the diaphragm, and the abdominal muscles have important roles in the regional distribution of inhaled gases. Anesthesia and muscle paralysis have a significant impact on the mechanics of the chest wall, particularly the diaphragm, causing irregularities of gas distribution and exchange. Both anesthesia and muscle paralysis move the diaphragm cephalad in the recumbent and decubitus posi- tions at the end of expiration. This is of greatest significance for the dependent parts of the diaphragm, for which abdom- inal pressure has the greatest influence. While displacement of the diaphragm during spontaneous inspiration is maxi- mal in dependent regions and minimal in nondependent regions, the relationship is reversed during paralysis with mechanical ventilation. Regional gas volume and distribu- tion are in proportion to diaphragmatic movement. In states of anesthesia and paralysis, the anteroposterior diameters of both the rib cage and the abdomen decrease while the trans- verse diameters increase. Compliance of the rigid thoracic compartment increases, and that of the abdomen and diaphragm decrease. The persistent tonic activity of the diaphragm throughout expiration is also abolished, and the motion of the diaphragm becomes passive. In contrast to active breathing, displacement of the diaphragm and the associated gas distribution will be different. Mismatch of ventilation and perfusion may be exaggerated.
C. Pulmonary Gas Exchange—Under general anesthesia, oxygen consumption normally decreases by approximately 10%. This may decline to 25% of normal depending on the fall in body temperature. It is raised substantially if shivering occurs. The production of CO2fluctuates with oxygen con- sumption. While it is not uncommon to mechanically hyper- ventilate a paralyzed patient, hypoventilation usually occurs during anesthesia with spontaneous breathing. Diffusing capacity for carbon monoxide remains unaltered, indicating that transfer across the alveolar-capillary membrane is not affected. Studies on gas exchange indicate the occurrence of ventilation-perfusion mismatching during anesthesia. The increase in P(A–a)O2gradient may be due to increased perfu-
sion of regions with low V/. Q ratio or increased shunt (or. both). The increase in alveolar dead space appears to be a result of the relative maldistribution of ventilation. D. Pulmonary Circulation—Normally, hypoxic pulmonary vasoconstriction is a powerful physiologic response. The mechanism is triggered by regional alveolar hypoxia (low PAO2 or low P–vO2), which causes precapillary pulmonary arterial constriction. The increase of vascular tone in the hypoxic area diverts blood flow to areas of higher oxygen
tension. This optimizes ventilation-perfusion matching in the lung and thus reduces venous admixture and maintains better gas exchange. All three currently used inhalation anes- thetics inhibit hypoxic pulmonary vasoconstriction in a dose-dependent manner. This special effect of volatile agents may contribute to the inefficiency of oxygen exchange during anesthesia.
E. Diffusion Hypoxemia and Absorption Atelectasis—At the conclusion of inhalation anesthesia, when the patient starts to breathe spontaneously, diffusion hypoxemia may occur. Since nitrous oxide is 30 times more soluble than nitrogen, it will rapidly diffuse from the pulmonary capillary blood and dilute the inspired alveolar air. This causes a reduction in PaO2that can be corrected with supplemental
oxygen.
When high concentrations of oxygen are used during anesthesia, the lung units with low ventilation-perfusion ratios may become unstable and collapse. This absorption atelectasis may widen the PAO2–PaO2 gradient, particularly
when ventilation is shallow and inadequate.
Narcotic Anesthesia
All opioid agonists produce a dose-dependent depression of ventilation by acting on the central respiratory center. The ventilatory effects of opioids include a decreased respiratory rate, decreased minute ventilation, increased arterial CO2ten- sion, and decreased ventilatory response to CO2. Although equianalgesic doses of opioids are likely to produce equivalent depression of ventilation, the peak effects and durations are determined by the pharmacokinetics of each drug. Depression of ventilation is augmented and prolonged in eld- erly and debilitated patients and in the presence of other CNS depressants. Airway reflexes are blunted, as is the hypoxic ven- tilatory response. Additionally, fentanyl may cause chest wall rigidity and compromise ventilatory function.
Regional Anesthesia
Diaphragmatic function is usually preserved even with high spinal anesthesia as long as the cervical portion of the spinal cord is not involved. With paralysis of the thoracic cage, the patient may appear to experience an incoordinate breathing pattern with paradoxical abdominal respiration even though ventilatory function is well maintained at the 75–85% level. The blockade of intercostal nerves leads to abdominal mus- cle paralysis that may limit the ability to cough and clear secretions. When anesthetics reach the cervical region or fourth ventricle, total apnea develops.
Anesthesia & Body Temperature
Hypothermia may occur with general anesthesia. Not only are the thermoregulatory centers depressed by anesthetic agents, but the interior and exterior of the body are also exposed to a cool environment for hours. In addition, the
peripheral vasodilatory effect associated with most types of anesthesia can aggravate heat loss and further decrease body temperature. Although hypothermia lowers total body oxy- gen consumption, severe depression may be fatal. Other complications of hypothermia include myocardial dysfunc- tion, cardiac dysrhythmia, coagulopathy, and acidosis. Shivering during recovery may increase oxygen consumption as much as fourfold. During rewarming, circulatory collapse can occur if adequate fluid replacement is not provided to offset increased vascular capacitance.