How does anesthesia affect the respiratory function of animals?
In a normal state of consciousness, the total airway resistance of the nasal cavity, pharynx and larynx to breathing accounts for more than 50%. During general anesthesia, the muscles of the nose and pharynx relax.
Anesthesia may cause upper airway obstruction
In a normal state of consciousness, the total airway resistance of the nasal cavity, pharynx and larynx to breathing accounts for more than 50%. During general anesthesia, the muscles of the nose and pharynx relax. With the deepening of the anesthesia plateau, the cough reflex disappears. This eventually results in upper airway obstruction in animals, especially those with brachycephalic breed syndrome. In these animals, unless endotracheal intubation is performed, severe and potentially fatal upper airway obstruction can occur under general anesthesia. Experience has shown that endotracheal intubation is the better option for all anaesthetized dogs, in addition to preventing upper airway obstruction, as well as preventing aspiration of esophageal and gastric secretions or contents into the lungs. The premise is that no airway damage is caused during endotracheal intubation.
If there is significant upper airway obstruction in anesthetized animals, and the anesthesia is not too deep, the animal will usually exhibit abdominal labored breathing; if the degree of upper airway obstruction is moderate or severe, the chest wall may even be inhaling (paradoxically). Inward movement during respiration) and is also observed under very deep anesthesia, usually before the drive to breathe has completely ceased (apnea).
Cats are more likely than other species to keep their airways open unless drugs that increase secretions and/or laryngospasm are used (ether, etc.), and intubation requires a deeper platform of anesthesia than some minor surgical or diagnostic procedures , and after anesthesia, when the larynx is injured during intubation, or when the tracheal intubation used by the animal has been cleaned with detergents or disinfectants, but not sufficiently rinsed, the irritation is more prone to laryngospasm. This laryngospasm occurs. Injury to the body and trachea may result in anesthetized death of animals during early recovery. Therefore, whether to intubate cats under short-term anesthesia has been controversial. However, it is undeniable that, like other species, cats will have good benefits after tracheal intubation, such as mechanical ventilation, reduced risk of aspiration, and easier removal of exhaust gas with inhalation anesthesia. In cats, laryngeal desensitization with lidocaine may help reduce spasticity and injuries associated with placement of endotracheal tubes. Placement of the endotracheal tube should be based on an assessment of the risk of airway damage to the individual animal prior to anesthesia and the potential benefit of airway patency. If the animal is not intubated, the anesthesiologist should ensure that an emergency airway and oxygen are readily available and continuously monitor airway patency.
Anesthesia changes ventilation control
Awake animals can achieve the regulation of respiratory drive, respiratory rate, VT and VA through complex neuromodulation mechanisms. In awake animals, VEmin and VAmin are primarily determined by the response of central chemoreceptors to PaCO2 levels, which are located on the ventral surface of the cerebrospinal fluid and are very sensitive to changes in PaCO2 levels (CO2 readily diffuses into the cerebrospinal fluid and central chemical sensor cells). Changes in PaCO2 were ultimately detected as changes in pH within the chemoreceptor cells. Decreased pH in arterial blood also stimulates respiration through central and peripheral chemoreceptors. Peripheral chemoreceptors are located in the carotid artery and aortic body, and usually only play an important role in respiratory drive when PaO2 levels are below 60 mmhg.
In anesthetized animals, reduced resting lung volume and functional residual capacity, reduced lung compliance, and significantly increased respiratory system resistance will affect the animal's ventilation level; if oxygen-enriched gas is not given (inspired oxygen 30-40%) is prone to hypoxia; prolonged atelectasis during general anesthesia can also lead to anesthetic hypoxemia; and the ratio of dead space to tidal volume (VD/VT) will also increase during anesthesia (approximately 50% or more), hypoxemia due to respiratory perfusion mismatch is also very common. In addition, some drugs can also affect minute ventilation, which we describe in detail later.
Apnea threshold is the PaCO2 level at which ventilation becomes zero (no spontaneous breathing) (due to loss of respiratory center drive, such as low PCO2 or high pH in the spinal respiration center). Apnea can occur in hyperventilated awake animals or in anesthetized and sedated animals (artificial positive pressure ventilation) when the PaCO2 level is 5-9 mmHg lower than normal. Regardless of the depth of anesthesia, the difference between the resting PaCO2 level and the apnea threshold is relatively stable (i.e. 4-6 mmHg), and the anesthesiologist uses the apnea threshold to control breathing (i.e. cancel spontaneous breathing) when administering the ventilator to the animal ).
In fact, any depth of anesthesia can cause apnea when PaCO2 levels are significantly reduced. This means that "ventilatory control" may be required once hypercapnia has been corrected. That is, when EtCO2 is too high, the anesthesiologist will attempt to lower the EtCO2 level with intermittent manual positive pressure ventilation, but only temporary improvement can be achieved, and once the apnea threshold is reached (eg, from 50 mmHg to 40 mmHg), the animal will Apnea occurs. Spontaneous breathing does not resume until the respiratory threshold is crossed again, at which point the animal typically exhibits hyperventilation. Therefore, ventilatory control is an effective strategy in the event of apnea during prolonged anesthesia or the use of respiratory depressant drugs.
Another clinical feature associated with apnea threshold is when animals resume spontaneous breathing after mechanical ventilation. Before spontaneous breathing can resume, CO2 accumulation in the body must gradually build up to bring PaCO2 levels back to the asphyxia threshold level. Therefore, an apnea time proportional to the depth of anesthesia and the degree of hypocapnia produced during IPPV will be required before the animal begins to breathe spontaneously. Recognizing this fact, most anesthesiologists will reduce inhalation anesthesia concentration and respiratory rate before attempting to switch animals from IPPV to spontaneous breathing.
The effect of drugs on ventilation
Anesthetics and some pre-anaesthetics alter the ventilation of anesthetized animals by altering central and peripheral chemoreceptor responses to CO2 and O2 in a dose-dependent manner. Fortunately, hypoxia caused by anesthesia-related inhibition of peripheral chemoreceptors is less pronounced in dogs and cats than in humans.
All currently used general anesthesia drugs show a dose-dependent decrease in CO2 response. For common inhalants, the CO2 response is nearly flat at a minimum alveolar concentration of 2.0. When animals breathe spontaneously, PaCO2 levels also increase with increasing doses of anesthesia. Under mild anesthesia (eg, minimum alveolar concentration of 1.2), PaCO2 generally remains moderately elevated but stable for several hours after anesthesia. With the different types and degrees of surgical stimulation, the degree of hypercapnia under an equal dose of inhaled (or intravenous) anesthetics will vary.
When injectable anesthetics are used before inhalation anesthesia, the respiratory depressive effects of the two drugs may be superimposed. General anaesthetics (at least inhalation anaesthetics) also significantly reduced hypoxia-driven sensitivity in a dose-related manner. Therefore, in most inhalation anesthesia protocols, the high oxygen levels used may inhibit ventilation to some extent, but ensure that the oxygenation level is appropriate.
Many full μ receptor agonists suppress minute ventilation, suppress respiratory rate or tidal volume, or both, by affecting mechanical effects in and near the brainstem. Clinically, opioids, when administered in large doses as part of a balanced anesthesia regimen, depress the respiratory center and superimpose with the respiratory depression of general anesthetics, potentially leading to hypercapnia and even apnea.
In addition, dogs are prone to rapid and shallow breathing (especially before a plateau in surgical anesthesia) when using full μ-agonists, which may interfere with subsequent inhaled anesthetic uptake. Using an epidural route of administration helps ensure minimal postoperative respiratory depression in high-risk patients. Mixed antagonist-agonist opioids do not have significant respiratory depression. In fact, mixed antagonist-agonists (eg, butorphanol) can partially reverse the respiratory depression of full mu agonists and retain some analgesia.
Phenothiazine and benzodiazepine sedatives generally reduce respiratory rate, especially when animals are somewhat excited prior to use, but do not produce significant changes in arterial oxygen content. However, these mild respiratory depression effects may be amplified when used in combination with other anesthetic/analgesic drugs or in animals with respiratory disease.
Alpha-2 receptor agonists have a relatively large effect on respiration in ruminants, but have little effect on dogs and cats. The respiration rate may decrease, and the PaCO2 level may increase slightly, but the PaO2 level remains well. Peripheral cyanosis has been reported in up to one-third of dogs sedated with medetomidine and is thought to result from decreased peripheral capillary and venous blood flow rather than decreased arterial saturation. It is also important to note that when the agonist is used with other sedatives or anesthetics, the degree of respiratory depression of the alpha-2 agonist will increase (usually substantially), usually the decrease in PaO2 levels is associated with hypoventilation and V// This correlates with an increase in Q dispersion and, therefore, when alpha-2 agonists are used in combination with other sedatives or injectable anesthetics, the use of a mask or endotracheal tube for oxygen delivery is recommended, especially when dealing with elderly or sick animals.
Other effects on the lungs
General anesthetics, especially inhalation anesthetics, interfere with airway ciliary activity and mucus clearance during and after anesthesia. However, it is not entirely clear how much of this effect is due to the anesthetic drug itself, or changes in airway humidity, or the effect of concomitant oxygenation, and changes in tidal volume due to mechanical ventilation may also be a factor. In addition, under anesthesia, the respiratory system is also less resistant to infection, which may be the result of immunocompromised animals or an underlying clinical or subclinical pulmonary infection.