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Anesthesia for the patient with respiratory compromise (Proceedings)
Because the airway extends from the oral or nasal cavity to the alveoli, respiratory compromise has numerous manifestations. Complications can be encountered in both the upper and lower airways.
Because the airway extends from the oral or nasal cavity to the alveoli, respiratory compromise has numerous manifestations. Complications can be encountered in both the upper and lower airways. Anesthesia can cause further complications since anesthetic drugs and equipment can exacerbate or even cause airway difficulties. Patients with compromised airways may present for surgery of the respiratory system or may present for surgery of other organ systems with airway compromise as a complication. Regardless of the reason for presentation, the patient should be critically evaluated before induction to anesthesia. The location, extent, and severity of the problem should be carefully assessed and the degree of respiratory dysfunction should be determined. During the evaluation, the patient should be handled quietly and carefully to avoid stress or fear-induced tachypnea with subsequent increased work of breathing and possible further respiratory dysfunction. Tranquilization is often necessary to keep the patient calm and analgesia is required for any painful patients. Oxygen should be administered to all patients during handling. For induction to and maintenance of anesthesia, the choice of anesthetic drugs is not necessarily dictated by the presence of respiratory compromise, but rather by the overall health of the patient. The choice of anesthetic technique (eg, method of induction, method of intubation, use of positive pressure ventilation, etc.), on the other hand, is often critical. For all patients, anesthesia should be thought of as 4 distinct and equally important phases (preanesthesia, induction, maintenance and recovery) and a plan should be developed for each phase.
Anesthesia for Patients with Upper Airway Dysfunction or Disease
Preanesthesia: Patients presenting for surgery of the upper airway are often at risk for airway obstruction. Stress, pain or fear-induced tachypnea, with subsequent increased work of breathing, will cause a tremendous increase in negative pressure in the airway and this negative pressure can cause or exacerbate airway collapse or obstruction. Acid-base derangements and hypoxia will occur due to ineffective ventilation through the narrowed airway and negative-pressure pulmonary edema can occur. Thus, the patient should be adequately sedated prior to examination or handling. Acceptable sedatives include the opioids, acepromazine and benzodiazepines. Alpha-2 agonists may be appropriate in some patients. Low dosages should be used in order to avoid excessive respiratory depression and the patient should not be left unobserved after sedation. Analgesia should also be provided and the opioids are generally the most logical choice.
Administration of oxygen via face mask or nasal cannula is recommended, and sometimes critical. Delivery of 100% oxygen for 2-5 minutes ('preoxygenation') allows the functional residual capacity (or 'reservoir' of air in the lungs) to fill with oxygen. With this technique, the patient can be apneic for 3-4 minutes without becoming hypoxemic. Patients that are not preoxygenated will become hypoxemic following approximately 90 seconds of apnea.
The use of anticholinergics in the preoperative period is controversial. Laryngeal manipulation can cause a profound vagally-mediated bradycardia, thus, anticholinergics are often used in brachycephalic breeds and other patients in whom intubation might be difficult. The use of anticholinergics as antisialagogues and to decrease respiratory tract secretions is generally not recommended, although exceptions exist. Anticholinergics change secretory composition from a watery fluid to a thick mucous. This mucous may not be adequately cleared by the mucociliary system and may remain in the respiratory tree. A major drawback to the use of anticholinergics is the subsequent tachycardia which increases cardiac work and cardiac oxygen demand. Cardiac oxygen demand may not be met by oxygen supply (creating an oxygen debt) if ventilation is impaired in any manner, including airway obstruction (ie, upper airway disease) and/or decreased diffusion of oxygen across alveolar walls (ie, lower airway disease).
Following adequate sedation, the patient should be rapidly induced to anesthesia and immediately intubated. Propofol or ketamine/diazepam will achieve the goal of rapid induction and both are acceptable in patients with airway compromise. Induction with inhalant anesthetic agents is too slow to ensure expedient control of the airway without undue stress and is not acceptable in patients with airway compromise.
In all patients, the larynx should be visualized at intubation and the endotracheal tube should be observed passing between the arytenoids. Esophageal intubation is a common complication and will further delay delivery of oxygen and anesthetic gases to the patient. If laryngospasms occur, a few drops of lidocaine should be placed on the arytenoids and the patient placed back on oxygen for 1-2 minutes before again attempting to intubate. Small boluses of propofol (1-2 mg/kg) have been used to improve laryngeal relaxation in human beings. However, propofol is a potent respiratory depressant and this technique should be used cautiously. If orotracheal intubation is not possible within a prudent time frame or if an orotracheal tube would interfere with the surgical approach, an endotracheal tube should be placed through a tracheotomy or pharyngotomy. Once intubated, the endotracheal tube cuff should be carefully inflated only to the point where leaks are prevented at 15-20cm H20 positive pressure. To prevent cuff damage to the trachea, patients should be disconnected from the machine if they are moved or repositioned.
Either sevoflurane or isoflurane are appropriate for maintenance. Although propofol infusions are sometimes used for upper airway surgery in patients that cannot be intubated, long-term maintenance with injectable anesthesia is not recommended since recovery from anesthesia, with subsequent respiratory depression, could be prolonged. Analgesia should be readdressed in the maintenance period. Appropriate analgesic techniques include the bolus or infusion administration of opioids or other analgesic drugs. Local blockade can be used in some surgeries. The provision of analgesia allows a decrease in the dose of inhalant anesthettic drugs. Diligent monitoring and patient support during the anesthetic period are imperative and these topics are addressed in the last section of the notes.
A stress-free recovery is absolutely essential in patients with upper airway dysfunction. Excitement and pain, with subsequent increased ventilation and increased peak inspiratory pressure, can severely constrict the patient's airway. Thus, patients should be adequately sedated (eg, acepromazine) and analgesed (eg, opioids). Opioids should be a part of the protocol since they provide pain relief and decrease the incidence of coughing, which could be detrimental to the surgical repair. The patient should remain intubated for as long as it will tolerate the endotracheal tube (if orotracheally intubated) or as long as the upper airway might reobstruct (if intubated through a tracheostomy site). In all instances, reobstruction should be anticipated and the anesthesiologist should be prepared to reanesthetize and reintubate the patient. The administration of a single dose of short-acting corticosteroids is often recommended to alleviate or attenuate obstruction of the airway from postoperative swelling. If upper airway edema is present, a diuretic (eg, 1 mg/kg furosemide) should be administered in addition to the corticosteroids.
Anesthesia for Patients with Lower Airway Dysfunction and/or Intrathoracic Surgery
Preanesthesia:Patients with lower airway dysfunction may present with metabolic derangements including acid-base imbalance and hypoxemia. Preoperative tranquilization to prevent stress is recommended and preoperative oxygen administration to prevent oxygen debt is virtually essential. Acepromazine, opioids & benzodiazepines are generally good choices for sedation. Alpha-2 agonists may be appropriate in some patients.
The use of anticholinergics is, again, controversial, although these drugs do have a bronchodilating effect. Bronchodilation occurs due to antagonism of acetylcholine effects on airway smooth muscle and the effects are most prominent in large and medium-sized airways. This effect leads to lowered airway resistance, but also to increased dead space, particularly in patients with bronchial asthma or chronic bronchitis. The possible beneficial effects of bronchodilation should be weighed against the detrimental effects of tachycardia and inspissation of secretions.
Any of the rapidly acting injectable anesthetic agents are acceptable choices for induction of anesthesia. Ketamine and propofol both have mild bronchodilating effects and this may reduce bronchospasm in asthmatic patients. Although propofol produces apnea similar to that produced by barbiturates, the effects of propofol are quickly dissipated, allowing ventilation to rapidly return to normal. Propofol can easily be titrated 'to effect'.
Inhalant anesthesia with controlled ventilation is generally the safest method for anesthetic maintenance of patients with lower airway disease. Inhalant anesthetic agents (eg, sevoflurane & isoflurane) are good choices for several reasons. First, these drugs have a nonspecific bronchodilating effect. This is especially beneficial in patients who have reactive and /or constricted airways (e.g., cats with asthma) and in those who may have their airways directly manipulated during surgery. Second, these drugs are rapidly eliminated (especially sevoflurane), thereby allowing the patient to recover and resume normal ventilation. However, inhalant anesthetic agents are not benign and will cause a dose-dependent decrease in alveolar ventilation. Thus, excessive anesthetic depth must be avoided. Appropriate analgesia will allow a decrease in inhalant gas requirements. Supplemental doses of opioids, constant rate infusions & local anesthetic blocks should all be considered during maintenance. Analgesia is described in detail in the recovery section below.
Intermittent positive pressure ventilation (IPPV) is generally recommended in patients with lower airway disease in order to maximize alveolar function. IPPV is imperative in patients with an open thorax. IPPV should be instituted at 10-15 breaths per minute, a tidal volume of 10 ml/kg and a peak inspiratory pressure of 10-20cmH20. Positive end expiratory pressure (PEEP) is occasionally necessary to maintain adequate gas exchange, especially in patients with an open thorax. In general, the application of IPPV and PEEP will improve arterial oxygen concentration in small animal patients. However, inappropriate use of IPPV and PEEP may cause collapse of the vena cavae with a subsequent decrease in preload. This in turn will lead to decreased cardiac output. It is important to support both ventilation and perfusion in order to obtain an optimal degree of tissue oxygenation. If a positive-pressure ventilator is not available, a staff member should be dedicated to maintaining ventilation in the patient by manual intermittent squeezing of the breathing circuit reservoir bag.
Thoracic surgical patients are at high risk for development of postoperative pulmonary complications, including atelectasis and/or pneumonia. There are three major causes of thoracic surgery induced postoperative pulmonary complications. First, the incidence of postoperative respiratory complications after any surgery is positively correlated with the degree of preoperative respiratory dysfunction. In patients with chronic lung disease, compared with normal healthy patients, there is a 20-fold increase in the incidence of postoperative pulmonary complications. Second, anesthesia / surgery can impair lung function in any patient. The dependent lung is especially vulnerable to the development of atelectasis and edema. Atelectasis provides the ventilatory and mucociliary stasis conditions necessary for the development and growth of pathologic organisms and can lead to pneumonia. Third, thoracotomy and upper abdominal incisions are very painful and cause patients to resist deep breathing and coughing in the postoperative period, leading to retained secretions, atelectasis and pneumonia. Postoperative pulmonary complications should be anticipated and attenuated by 1) appropriate preoperative therapy designed to decrease respiratory dysfunction (eg, antibiotic therapy of respiratory tract infection), 2) appropriate intraoperative support of respiratory function (eg, use of intermittent positive pressure ventilation) and 3) adequate postoperative pain control.
Monitoring and support of both respiratory and cardiovascular function should continue well into the recovery period. Support should include administration of oxygen, maintenance of circulating fluid volume through the administration of intravenous fluids and normalization of electrolyte and acid-base status. Following thoracotomy, a chest drain should be maintained until negative pressure can be consistently achieved with minimal to no aspiration of air, blood or fluid.
Provision of adequate post operative analgesia is absolutely imperative for return of normal ventilatory function. Pain causes "splinting" or tensing of the abdomen, active exhalation, and failure to cough. These actions intensify respiratory dysfunction by promoting retention of secretions, airway closure and atelectasis. Following thoracotomy, intraoperative blockade of the intercostal muscles with local anesthetic agents may provide analgesia for 60-360 (depending on the local anesthetic drug used) minutes postoperatively. In human beings, long-term pain relief is achieved by cryoablation of the intercostal nerves but this is not a technique currently used in veterinary medicine. Infusion of local anesthetics directly into the chest will also provide some degree of analgesia and this technique should be a part of a multimodal analgesic protocol. However, this technique may not be effective if used alone because fluid and blood in the chest will dilute the agents and decrease their efficacy, the patient may need to lie with the surgery site dependent (this may be uncomfortable for the patient) so that the local anesthetic actually comes in contact with the incision and large volumes of anesthetic agent may be necessary in order to cover adequate surface area. Large volumes of anesthetic agent may be toxic, especially in cats. Constant IV infusions of opioids, ketamine and/or lidocaine are easy to use and will also provide effective analgesia The administration of opioids through epidural catheters that are advanced into the thoracic region, a pain relief technique commonly used in human beings, is also an effective way to provide thoracic analgesia to veterinary patients. NSAIDs should be used in all patients that don't have NSAID contraindications since inflammatory pain will be a major part of the overall pain syndrome following any type of surgery.
Monitoring and Support for Patients with Respiratory Disease
Attentive monitoring throughout the anesthetic episode is absolutely crucial. A blood pressure monitor, ECG, pulse oximeter and end-tidal (ET)CO2 monitor should be utilized. Arterial blood gas (pH, PaO2, PaCO2) monitoring is ideal but not always practical. Hemoglobin saturation should be maintained at >90% (PaO2 at > 60mmHg on room air and >200 mm Hg on 100% O2). This recommendation is based on the shape of the oxygen-hemoglobin saturation curve, from which we determine that PaO2 values < 60mmHg lead to rapid desaturation and hypoxemia. PaO2 can be improved by: increasing the inspired concentration of O2 (FIO2); assisting or controlling ventilation; increasing cardiac output to improve perfusion of the lungs; and changing the patient's position (if possible) as dorsal recumbency generally causes greater respiratory impairment than lateral recumbency. End-tidal CO2 (and PaCO2) should be maintained between 35-55 mmHg. Ventilate for the patient if CO2 increases.
Preanesthesia: Opioid other sedative; Preoxygenate
Induction: Use rapidly acting injectable like propofol or diazepam/ketamine
Intubate rapidly (but carefully)
Maintenance: Sevoflurane or isoflurane
Readdress analgesia with boluses of opioids, local blockade or constant rate infusions
Use positive-pressure ventilation in patients with lower airway disease
Monitor and support the respiratory and cardiovascular systems
Recovery: MUST BE QUIET AND SMOOTH, especially for patients with upper airway dysfunction
Readdress analgesia, sedate if necessary; Monitor and support until full