Anesthesia and pulmonary diseases

1. Anesthesia and pulmonary diseases Dr abdollahi

2. Thoracic and upper abdominal operations are a particular risk for patients with chronic pulmonary disease.

3. Obstructive airway diseases • Asthma and chronic obstructive pulmonarydisease (COPD), the two major categories of obstructive airway disease, affect millions of Americans and cause significant morbidity and mortality worldwide.

4. Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction, airway inflammation, and bronchial hyperresponsiveness.

5. In contrast, the airflow obstruction in COPD is defined as progressive and not fully reversible. The chronic inflammation of the airways and lung parenchyma in COPD is most often secondary to cigarette smoke exposure.

6. Together, asthma and COPD constitute a major public health concern, and a basic understanding of these diseases is important when caring for patients who receive anesthesia.

7. ASTHMA • Asthma is a disease that is defined by the presence of: • (1) Chronic inflammatory changes in the submucosa of the airways • (2) Airway hyperresponsiveness • (3) Reversible expiratory airflow obstruction.

8. Airway hyperresponsiveness characterizes this disease, even in asymptomatic patients, and is demonstrated by the development of bronchoconstriction in response to stimuli (allergens, exercise, mechanical airway stimulation) that have little or no effect on normal airways. Airway hyper responsiveness elicited during methacholine bronchoprovocation and airway bronchodilation in response to inhaled albuterol help diagnose asthma.

9. Clinical Symptoms • The classic symptoms associated with asthma are cough, shortness of breath, and wheezing. However, symptoms of asthma may vary and range from cough with or without sputum production to chest pain or tightness. Chronic, • nonproductive cough may be the sole initial complaint.

10. Some asthmatics also experience symptoms exclusively • with exertion ("exercise-induced asthma"), and this diagnosis • is a consideration in the pediatric and young adult population.

11. The presence or absence of wheezing on physical examination is a poor predictor of the severity of airflow obstruction. Thus, the presence of wheezing suggests airway narrowing, which should be confirmed and quantified by spirometry.

12. Degrees of obstraction are defined according to the FEV1 % predicted . • Reversibility of obstruction after the administration of a • bronchodilator suggests a diagnosis of asthma.

13. An increase in FEV1 % predicted of more than 12% and an increase in FEVl of greater than 0.2 L suggest acute bronchodilator responsiveness and variability in airflow obstruction. • In contrast, the airways of patients with COPD do not demonstrate reversibility of airflow obstruction to the same degree as do those with asthma, a characteristic that can help distinguish these two causes of airflow obstraction.

16. During severe asthma exacerbations, intravenous therapy • with glucocorticoids is the mainstay of therapy. In rare • circumstances, when life-threatening status asthmaticus • persists despite aggressive pharmacologic therapy, it may • be necessary to consider general anesthesia (isoflurane or • sevoflurane) in an attempt to produce bronchodilation.

17. Management of Anesthesia • Pulmonary function studies (especially FEV1) obtained • before and after bronchodilator therapy may be indicated • in a patient with asthma who is scheduled for a thoracic • or abdominal operation. Measurement of arterial blood • gases before proceeding with elective surgery is a consideration • if there are questions about the adequacy of ventilation or arterial oxygenation.

18. All asthmatics who have persistent symptoms should be treated with either inhaled or systemic corticosteroids (depending on the severity of their airflow obstruction), in addition to scheduled dose of inhaled beta agonists. Therapy should be continued throughout the perioperative period. Supplementation with cortisol may be indicated before major surgery for corticosteroid-dependent asthmatics because of suppression of the hypothalamic-pituitary-adrenal axis.

19. REGIONAL ANESTHESIA • Regional anesthesia may be preferred when the surgery is • superficial or involves the extremities. Notably, however, • bronchospasm has been reported in asthmatics who have received spinal anesthesia, although it is generally accepted that regional anesthesia is associated with lower complication rates related to bronchospasm in the asthmatic population.

20. GENERAL ANESTHESIA • The goal during induction and maintenance of general anesthesia in patients with asthma is to depress airway reflexes in order to avoid bronchoconstriction in response to mechanical stimulation of the airway. Before tracheal intubation, a sufficient depth of anesthesia should be • established to minimize bronchoconstriction with subsequent • stimulation of the airway. Rapid intravenous induction of anesthesia is most often accomplished with the administration of propofol or thiopental. Propofol • may blunt tracheal intubation-induced bronchospasm in • patients with asthma.

21. ketamine (1 to 2 mg/kg IV) is an alternative selection for rapid induction of anesthesia because its sympathomimetic effects on bronchial smooth muscle may decrease airway resistance. The increased secretions associated with the administration of ketamine, however, may limit the use of this drug in patients with asthma. • Sevoflurane and isoflurane are potent volatile anesthetics that depress airway reflexes and do not sensitize the heart to the cardiac effects of the sympathetic nervous system stimulation produced by beta-agonists and aminophylline.

22. Bronchodilation with sevoflurane and isoflurane depends on the ability of the normal airway epithelium to produce nitric oxide and prostanoids. Halothane is also an effective bronchodilator but may be associated with cardiac dysrhythmias in the presence of sympathetic nervous system stimulation. • Desflurane may be accompanied by increased secretions, • coughing, laryngospasm, and bronchospasm as a result of • in vivo airway irritation.

23. Although case reports suggest that bronchodilation follows the intravenous administration of lidocaine, the clinical significance of this response is unclear and the data are equivocal.

24. In asthmatic patients undergoing tracheal intubation, premedication with inhaled albuterol should be the first choice of therapy to prevent intubation-induced bronchoconstriction. • Neuromuscular blocking drugs that are not associated with endogenous histamine release may also be used in patients with asthma .

25. Although histamine release has been attributed to succinylcholine,there is no evidence that this drug is associated with increased airway resistance in patients with asthma.

26. Intraoperatively, Pao2 and Paco2 can be maintained at • normal levels by mechanical ventilation of the lungs at • a slow breathing rate (6 to 10 breaths/min) to allow • adequate time for exhalation, an important maneuver • in patients with increased airway resistance. This slow • breathing rate can usually be facilitated by the use of a • high inspiratory flow rate to allow the longest possible • time for exhalation. Positive end-expiratory pressure • (PEEP) should be used cautiously because of the inherent, • impaired exhalation in the presence of narrowed airways.

27. At the conclusion of elective surgery, the trachea may be extubated while the depth of anesthesia is still sufficient to suppress airway reflexes. After the administration of anticholinesterase drugs to reverse the effects of nondepolarizing neuromuscular blocking drugs, bronchospasm may occur but is not usual, which may reflect the protective effects (decreased airway resistance) of simultaneously administered anticholinergics. When extubation is delayed for reasons of safety until the patient is awake (possible presence of gastric contents), intravenous administration of lidocaine may decrease the likelihood of airway stimulation as a result of the endotracheal tube in an awake patient.

28. IntraoperativeBronchospasm • Airway instmmentation can cause severe reflex bronchoconstriction and bronchospasm, especially in asthmatic patients with hyperactive airways. The bronchospasm that occurs intraoperatively is usually due to factors other than acute exacerbation of asthma. The frequency of perioperative bronchospasm in patients with asthma is low, especially if their asthma is asymptomatic at the time of surgery.

29. It is important to first consider mechanical causes of obstruction and inadequate levels of anesthesia before initiating treatment of intraoperative bronchospasm. • Fiberoptic bronchoscopy may be useful to rule out mechanical obstraction in the tracheal tube. Asthma related • bronchospasm may respond to deepening of anesthesia with a volatile anesthetic.

30. If the bronchospasm is due to asthma and persists despite an increase in the concentration of delivered anesthetic drug, albuterol should be administered by attaching a metered-dose inhaler to the anesthetic delivery system. When bronchospasm persists despite B2- agonist therapy, it may be necessary to add intravenous corticosteroids.

31. CHRONIC OBSTRUCTIVE PULMONARY DISEASE: EMPHYSEMA AND CHRONIC BRONCHITIS • COPD consists of two entities, emphysema and chronic • bronchitis. The Global Initiative for Chronic Obstructive • Lung Disease (GOLD) guidelines provide criteria • for diagnosis and classification of severity in patients with • symptoms of chronic cough, sputum production, or exposure • to cigarette smoke .

33. Emphysema is characterized by loss of elastic recoil of the lungs, which results in collapse of the airways during exhalation and increased airway resistance.

34. Chronic bronchitis is defined by the presence of cough and sputum production for 3 months in each of 2 successive years in a patient with risk factors, most commonly cigarette smoking. It has been estimated that 25% of surgical patients smoke and a further 25% are ex-smokers, thus making COPD an important diagnosis to consider in any patient undergoing anesthesia.

35. Prediction of Postoperative Outcome • The need for preoperative pulmonary function studies • in patients with COPD is controversial because of the • questionable correlation of these tests with postoperative • outcome. Although the FEV! % predicted has been used • to grade the severity of airflow obstraction, data have • shown that using a multidimensional grading system to • assess the respiratory and systemic extent of COPD is a • better predictor of mortality than using FEV, % alone.

36. BODE index. • This grading system is based on four variables- • 1=Body mass index (B) • 2=Severity of airflow obstraction (0) • 3=Functional dyspnea (D) • 4=Exercise capacity as assessed by the 6-minute walk test (E)

38. Patients with higher BODE scores were at higher risk for death. Hypercapnia and hypoxemia, as detected by arterial blood gas analysis, may also characterize patients with moderate to severe airflow obstmction. Chronic hypoxemia may lead to • pulmonary hypertension and cor pulmonale. Preoperative • detection plus treatment of hypoxemia-induced cor • pulmonale with supplemental oxygen is an important • part of preoperative management.

39. Management of Anesthesia • The presence of COPD does not dictate the use of specific • management of anesthesia. If general anesthesia is selected, a volatile anesthetic with humidified inhaled gases and mechanical ventilation of the lungs is useful. drugs or techniques (regional or general) for the management of anesthesia.

40. Nitrous oxide may be used, but potential disadvantages include • limitation of the inhaled concentrations of oxygen and passage of nitrous oxide into emphysematous bullae. • Nitrous oxide could lead to enlargement and rupture of these bullae and result in the development of tension pneumothorax.

41. Opioids are acceptable but are less ideal for maintenance of anesthesia because of the frequent need for high inhaled concentrations of nitrous oxide to ensure amnesia and associated decreases in inhaled concentrations of oxygen. To avoid this problem, administration of a volatile anesthetic at a low concentration may be substituted for nitrous oxide. Postoperative depression of ventilation may also reflect the residual effects of opioids administered intraoperatively.

42. MANAGEMENTOF VENTILATION • Patients with COPD are ventilated in a manner similar to • those with asthma. Small tidal volumes may be delivered • to decrease the likelihood of gas trapping and barotrauma. • Slow breathing rates are used to permit maximal time for • exhalation. Continued tracheal intubation and mechanical • ventilation of the lungs in the postoperative period are • often necessary after major surgery in patients with severe • emphysema. Postoperative depression of ventilation may • also reflect the residual effects of opioids administered.

43. Hypercapnia secondary to chronic hypoventilation should not be corrected intraoperatively because it may then be difficult to wean the patient from mechanical ventilation as a result of the decreased respiratory drive in patients who chronically hypoventilate.

44. Pulmonary HYPERTENSION • Pulmonary hypertension is defined as an elevation in • mean pulmonary artery pressure to levels higher than • 25 mm Hg at rest or higher than 30 mm Hg with exercise. • Most cases of pulmonary hypertension are secondary to • cardiac or pulmonary disease; in a minority of cases, the • etiology is unknown and the pulmonary hypertension is • considered primary.

45. Classification • The World Health Organization has proposed a classification • of pulmonary hypertension that includes pulmonary • hypertension secondary to left heart disease, pulmonary • disease, vascular disease, and primary pulmonary hypertension. • Indicators of disease severity include dyspnea at rest, hypoxemia, syncope, metabolic acidosis indicating • low cardiac output, and signs of right heart failure on • physical examination (elevated jugular venous pressure, • hepatomegaly, and peripheral edema).

46. Diagnostic Evaluation • Diagnostic evaluation for pulmonary hypertension includes • the electrocardiogram; echocardiogram; chest roentgenogram; • assessment for secondary causes such as pulmonary • embolism (computed tomographic angiography or • ventilation/perfusion scanning), underlying pulmonary • disease (pulmonary function testing), collagen vascular • disease, or liver failure; and right heart catheterization.

47. Right heart catheterization is the gold standard for diagnosis • because it provides data on the severity of pulmonary • artery hypertension, as well as pulmonary venous pressure • and cardiac output, which have prognostic significance. • In addition, right heart catheterization is a necessary part • of testing for vasodilator response, the first step in the • algorithm to determine appropriate therapy for pulmonary • artery hypertension.

48. Pathophysiology • Chronic elevation of pulmonary artery pressure leads to • elevated right ventricular systolic pressure, hypertrophy • and dilatation of the right ventricle, and resultant right • ventricular failure. Right ventricular preload and pulmonary • blood flow are dependent on venous return in this setting.

49. Management of Anesthesia • Intraoperative considerations for a patient with severe pulmonary hypertension include maintaining adequate preload, minimizing tachycardia and cardiac dysrhythmias that may decrease cardiac output, and avoiding arterial hypoxemia and hypercapnia, which can increase pulmonary vascular resistance (PVR). Cardiac output from a failing right ventricle is critically dependent on filling pressure from venous return and pulmonary pressure.

50. Options for treatment of pulmonary hypertension during surgery include inhaled nitric oxide (10 ppm), inhaled prostacyclin (either intermittent or continuous), and phosphodiesterase inhibitors such as milrinone. Pulmonary artery catheters have been used for intraoperative monitoring.