COPD and Anesthesia
Management of anesthesia for COPD patient
Studies in patients with COPD suggest that there is a higher incidence of postoperative respiratory failure in patients who have general anesthesia, but whether this reflects the nature or complexity of the surgery and/or the operative site or the selection of anesthetic drugs or technique is unclear.
The management principles for patients with reactive airways are enumerated in Table 2.19.
Table 2.19: The key management principles for anesthesia for patients with reactive airway disease
-
Preoperative optimization of bronchodilation.
-
Minimal (or no) instrumentation of the airways.
-
Instrument the airways when necessary only after appropriate depth of anesthesia with a bronchodilating anesthetic (propofol, ketamine, sevoflurane).
-
Maintenance of anesthesia with a bronchodilating anesthetic.
-
Appropriate warming and humidification of inspired gases. An endotracheal tube bypasses nearly the entire natural airway humidification system. So humidification of inspired gases and use of low gas flows will be needed to keep airway secretions moist.
-
Regional anesthesia is suitable for operations that do not invade the peritoneum and for surgical procedures performed on the extremities. Lower intraabdominal surgery can also be performed using a regional technique. General anesthesia is the usual choice for upper abdominal and intrathoracic surgery.
Premedication
It must be appreciated that COPD patients can be extremely sensitive to the ventilatory depressant effects of sedative
drugs like opioids and benzodiazepines. Elderly patients may be especially susceptible to this depression of ventilation.
The most important aspect of preoperative medication is to avoid inadvertent withdrawal of those drugs that are taken for concurrent medical conditions.
Ensure that a perioperative program of intensive chest physiotherapy is initiated preoperatively.
Regional anesthesia
Regional anesthesia via peripheral nerve block such as an axillary block carries a lower risk of pulmonary complications than either spinal or general anesthesia. Regional anesthesia is a useful choice in patients with COPD only if large doses of sedative and anxiolytic drugs will not be needed. Often small doses of a benzodiazepine, such as midazolam, in increments of 1 to 2 mg IV, can be administered cautiously without producing undesirable degrees of ventilatory depression. Regional anesthetic techniques that produce sensory anesthesia above T6 are not recommended because such high blocks can impair the ventilatory functions requiring active exhalation such as expiratory reserve volume, peak expiratory flow, and maximum minute ventilation. Clinically, this is manifested as a cough that is inadequate to clear airway secretions.
The key advantage of regional anesthesia for COPD patients are enumerated in Table 2.20.
Table 2.20: Advantages of regional anesthesia in COPD patients
-
Avoids airway manipulation, which may cause bronchospasm
-
Reduces the requirement of sedatives/opioids with ventilatory depressant effects
-
Excellent analgesia
-
Increase in functional residual capacity (FRC); normalization of FRC and closing capacity (CC) ratio
-
Preservation of phrenic nerve activity (Inhibition of phrenic nerve function via spinal reflex arcs appears to be responsible for the diaphragmatic muscle dysfunction seen after upper abdominal and thoracic surgery)
-
Reduced incidence of deep vein thrombosis
-
Reduces postoperative pulmonary complications
-
Avoiding positive pressure ventilation is advantageous in patients with “bullae”
-
When combined with general anesthesia, significant reduction in postoperative intubation time (i.e. early extubation) and requirement for mechanical ventilation after major abdominal and thoracic surgery.
General anesthesia
-
Volatile anesthetics
-
Can obtund airway reflexes.
-
Rapidly eliminated through the lungs—Residual ventilatory depression during the early postoperative period is thereby minimized.
-
Can produce bronchodilation.
-
Allows delivery of a high FiO2 (Fraction of inspired oxygen) without lightening the plane of anesthesia 3⁄4 Reasonable degree of cardiovascular stability (upto 1 MAC—Minimum Alveolar Concentration)
-
Inhibition of hypoxic pulmonary vasoconstriction is more or less comparable to intravenous anesthetics (during one-lung ventilation)
-
-
Nitrous oxide
-
Potential for passage of this gas into pulmonary bullae, leading to enlargement or even rupture of the bullae resulting in development of a tension pneumothorax.
-
Another potential feature of nitrous oxide is the limitation on the inspired oxygen concentration that it imposes.
-
Nitrous oxide/oxygen (N2O/O2) mixtures are more prone to cause atelectasis in poorly ventilated lung regions than oxygen by itself.
-
-
Opioids
-
Can be associated with prolonged ventilatory depression
-
Even the duration of ventilatory depression produced by drugs such as thiopental and midazolam may be prolonged in patients with COPD compared to normal individuals.
-
Diminish the amount of volatile anesthetics to achieve surgical level of anesthesia.
-
No significant adverse hemodynamic effects.
-
Short-acting agents may be used for a smooth transition from surgery to postoperative period.
-
Permit optimal oxygenation during one-lung ventilation.
-
-
Ketamine
-
Sympathomimetic properties – inhibition of reuptake of noradrenaline at sympathetic nerve endings; may contribute to the reduction and inhibition of the vagal reflex pathway at high doses
-
Reduce bronchospasm in asthmatic patients
-
No significant effect on hypoxic pulmonary vasoconstriction.
-
Anesthesiologists must be very aware of the possibility of dynamic hyperinflation whenever general anesthesia is induced in a patient with emphysema.
-
The primary methods to avoid hemodynamic instability in these patients are ventilatory management:
-
Thorough preoxygenation prior to induction,
-
The use of small tidal volumes, slow respiratory rates and long expiratory times, and
-
Tolerance of hypercarbia until the patient recovers from the vasodepressant effects of induction drugs.
Also important for these patients are: Large-bore intravenous access, vasopressors and inotropes immediately available and intravenous preloading with colloids or crystalloids.
Many patients with moderate or severe COPD develop cystic air spaces in the lung parenchyma known as bullae. These bullae will often be asymptomatic unless they occupy more than 50% of the hemithorax, in which case the patient will present with findings of restrictive respiratory disease in addition to their obstructive disease. Previously, it was thought that bullae represented positive pressure areas within the lung which compressed surrounding lung tissue. It is now appreciated that a bulla is actually a localized area of loss of structural support tissue in the lung with elastic recoil of surrounding parenchyma. The pressure in a bulla is actually the mean pressure in the surrounding alveoli averaged over the respiratory cycle. This means that during normal spontaneous ventilation the intra-bulla pressure is actually slightly negative in comparison to the surrounding parenchyma.6 However, whenever positive- pressure ventilation is used the pressure in a bulla will become positive in relation to the adjacent lung tissue and the bulla will expand with the attendant risk of rupture, tension pneumothorax and bronchopleural fistula. Positive- pressure ventilation can be used safely in patients with bullae provided the airway pressures are kept low and there is adequate expertise and equipment immediately available to insert a chest drain and obtain lung isolation if necessary.
Many COPD patients have an elevated PaCO2 at rest. Among moderate and severe COPD patients it is not possible to predict from history or physical examination which patients are ‘‘CO -retainers’’. Perioperative arterial blood gas analysis is required to set goals for intra- and postoperative ventilation. This CO -retention seems to be primarily related to an inability to maintain the increased work of respiration and not due to an alteration of respiratory control mechanisms.
The PaCO rises in these patients when supplemental oxygen is administered not due to a decrease of minute ventilation, but because a high FiO2 causes a relative increase in alveolar dead space by the redistribution of lung perfusion and also due to the Haldane effect. However, supplemental oxygen must be administered to these patients postoperatively to prevent hypoxemia. The attendant rise in PaCO2 should be anticipated and monitored. Hypercarbia is usually well- tolerated in the absence of intracranial pathology and if the vasodepressant effects of acidosis can be managed.10 In addition to arterial blood gas monitoring, the best monitor of dangerous hypercarbia is the patient’s level of consciousness. At levels >80–100 mm Hg PaCO2 carbon dioxide begins to have a sedative and anesthetic effect. If spontaneous breathing is permitted during anesthesia in patients with COPD, it should be appreciated that the ventilatory depression produced by volatile anesthetics may be greater in these patients than in normal individuals.
Postoperative management
COPD patients are susceptible to development of acute respiratory failure during the postoperative period. Continued tracheal intubation and mechanical ventilation may be necessary, particularly after upper abdominal or intrathoracic surgery. Alternatively, postoperative analgesia with neuraxial opioids that permits pain-free breathing may permit earlier tracheal extubation.
Prophylaxis against the development of postoperative pulmonary complications is based on maintaining adequate lung volumes especially FRC and facilitating an effective cough. Identification of the FRC as the most important lung volume during the postoperative period provides a specific goal for therapy.
Postoperative neuraxial analgesia with opioids may permit early tracheal extubation. The sympathetic blockade, muscle weakness, and loss of proprioception that are produced by local anesthetics are not produced by neuraxial opioids. Therefore, early ambulation is possible. Ambulation serves to increase FRC and improve oxygenation, presumably by improving ventilation-to- perfusion matching. Neuraxial opioids may be especially useful after intrathoracic and upper abdominal surgery. Breakthrough pain may require treatment with systemic opioids administered by bolus or via patient-controlled analgesia. Sedation may accompany neuraxial opioid administration and delayed respiratory depression can be seen, especially when poorly lipid-soluble opioids such as morphine have been used.
The quality of neuraxial analgesia (epidural or spinal) may be superior to that provided by parenteral administration of opioids, but it has not been possible to document that neuraxial analgesia decreases the incidence of clinically significant postoperative pulmonary complications or is superior to parenteral opioids in this regard. Postoperative neuraxial analgesia is recommended after high-risk thoracic, abdominal, and major vascular surgery. Intermittent or continuous intercostal nerve blocks may be an alternative if neuraxial analgesia is ineffective or technically difficult.
Chest physiotherapy
The actual removal of secretions may be accomplished by a combination of postural drainage (several different positions may be required), coughing, and chest percussion and vibration (common methods include tapping with cupped hands and the use of electric vibrators) for 15 to 20 minutes several times a day.
Chest physiotherapy moves peripheral bronchial secretions to more central airways for expectoration by coughing. The reason that coughing alone cannot clear peripheral airways is that an effective cough must attain a high enough airflow rate so that it shears secretions away from the airway wall. In patients with chronic lung disease, flow rates are low (especially peripherally), and shearing of secretions by cough may well be limited to the trachea and perhaps just the first two airway generations. Obviously, with either chest physiotherapy or cough it will be much easier to expel the secretions if the airways have already been dilated and the secretions loosened.
Chest physiotherapy is relatively contraindicated in patients with lung abscesses, metastases to the ribs, a history of significant hemoptysis, and an inability to tolerate the postural drainage positions.
The forced expiration technique (FET) is increasingly being regarded as more effective in removing secretions than a cough is. FET consists of a forced expiration starting from midlung volume (50% of inspiratory reserve lung volume) to a low lung volume, usually residual volume, followed by a period of relaxation and diaphragmatic breathing. This forceful expiration maneuver differs from a cough in that it is performed without closure of the glottis and without the accompanying compressive phase that characterizes a cough. Because transpulmonary pressure is less during FET than during a cough, airway compression is less and proximal and distal clearance of bronchial secretions is better than with a conventional cough. FET is now commonly used as an alternative to cough during chest physiotherapy.
Lung expansion maneuvers (deep breathing exercises, incentive spirometry, chest physiotherapy, positive- pressure breathing techniques) are of proven benefit for preventing postoperative pulmonary complications in high-risk patients. These techniques decrease the risk of atelectasis by increasing lung volumes. Preoperative education in lung expansion maneuvers decreases the incidence of pulmonary complications to a greater degree than if education begins after surgery, but there is no evidence that instituting lung expansion maneuvers preoperatively is of value.
Incentive spirometry (or sustained maximum inspiration) is simple and inexpensive and provides objective goals for and monitoring of patient performance. It is simply a visual and/or audiofeedback device that encourages slow, deep inspiration. Patients are given a particular inspired volume as a goal to achieve and hold. This provides sustained lung inflation, which is important for reexpanding collapsed alveoli. Generally incentive spirometry is performed frequently, up to every hour and its purpose is to treat and prevent atelectasis, especially in postoperative thoracic and abdominal patients. The major disadvantage of incentive spirometry is the need for patient cooperation to accomplish the treatment.
Intermittent positive-pressure breathing can decrease the incidence of postoperative pulmonary complications, but its cost and complexity have resulted in a decline in its use. Continuous positive airway pressure is reserved for the prevention of postoperative pulmonary complications in patients who are not able to perform deep-breathing exercises or incentive spirometry. Nasal positive airway pressure can minimize the expected decrease in lung volumes after surgery but less costly lung expansion maneuvers are available.
Postoperative Pulmonary Complications (PPCs)
A major PPC will be defined as a postoperative pneumonia, respiratory failure or inability to extubate within 48 hours of surgery, or the need for reintubation after extubation at the end of an anesthetic, either within the operating room, recovery room, or intensive care unit (ICU). Minor pulmonary complications include but are not limited to atelectasis, bronchospasm, laryngospasm, and the unanticipated need for supplemental oxygen therapy beyond the initial postoperative period.
PPCs are significant source of morbidity and mortality. Postoperative changes include diaphragmatic dysfunction, V/Q mismatch, and reductions in functional residual capacity (FRC), which, while measurable, have an unclear relation to morbidity and mortality. The etiology of PPCs is complex and poorly understood.
The risk factors for PPCs are given in the following Table 2.21.
Table 2.21: Risk factors for PPCs
Patient-related factors
-
Age > 60 years
-
ASA class > 2
-
Goldman class 2-4
-
COPD
-
Cigarette use < 8weeks before surgery
-
Dependent functional status
-
Albumin < 3 gm/dl
-
Blood urea nitrogen > 30 mg/dl
-
Abnormal chest radiograph
Surgery-related factors
-
Surgical site:
– Thoracic surgery
– Abdominal aortic aneurysm surgery
– Upper abdominal surgery
– Neurosurgery
– Peripheral vascular surgery
-
General anesthesia
-
Emergency surgery
-
Duration of surgery >3 hours
Many of the risk factors for PPC are nonmodifiable. So emphasis is on generic risk reduction strategies and postoperative surveillance. When possible, clinicians should also implement interventions that are specific to the particular risk factor. Pre- and postoperative pulmonary rehabilitation has been shown to decrease PPC in moderate to high-risk patients undergoing upper abdominal surgeries. Lung expansion maneuvers including cough, deep breathing, incentive spirometry, positive end-expiratory pressure (PEEP), and CPAP (continuous positive airway pressure) reduce PPC rates.
Patients with COPD may have chronically fatigued respiratory muscles. Impaired nutrition, electrolyte, and endocrine disorders contribute to respiratory muscle weakness and should be corrected before surgery. Patients with COPD should be examined for unrecognized cor pulmonale; if present, it should be treated before surgery. One modality of potential value in patients with COPD is respiratory muscle training. Patients that demonstrate increased respiratory muscle strength after respiratory muscle training have fewer PPCs than those who do not increase their respiratory muscle strength. Determination of exercise capacity may also be of benefit in identifying patients at risk for PPCs.
Patients with chronic hypoxemia benefit from short- term oxygen administration, which usually results in lessening of pulmonary hypertension, reduction in signs and symptoms of heart failure, and improvement of mentation. A preoperative finding of hypoxemia should prompt further investigation. Even if hypoxemia is chronic, but the patient is not receiving oxygen at home, continuous oxygen administration should be started and elective surgery deferred to allow improvement in pulmonary hypertension and heart function.
The risk reduction strategies according to PPC risk is given in the following Table 2.22.
