CHRONIC INTRINSIC PULMONARY DISORDERS
Chronic intrinsic pulmonary disorders are also often referred to as interstitial lung diseases. Regardless of etiology, the disease process is generally character-ized by an insidious onset, chronic inflammation of alveolar walls and perialveolar tissue, and progres-sive pulmonary fibrosis. The latter can eventually interfere with gas exchange and ventilatory func-tion. The inflammatory process may be primarily confined to the lungs or may be part of a generalized multiorgan process. Causes include hypersensitivity pneumonitis from occupational and environmentalpollutants, drug toxicity (bleomycin and nitrofu-rantoin), radiation pneumonitis, idiopathic pulmo-nary fibrosis, autoimmune diseases, and sarcoidosis. Chronic pulmonary aspiration, oxygen toxicity, and severe ARDS can also produce chronic fibrosis.
Patients typically present with dyspnea on exertion and sometimes a nonproductive cough. Symptoms of cor pulmonale are present only with advanced disease. Physical examination may reveal fine (dry) crackles over the lung bases, and, in late stages, evi-dence of right ventricular failure. The chest radio-graph progresses from a “ground-glass” appearance to prominent reticulonodular markings, and, finally, to a “honeycomb” appearance. Arterial blood gases usually show mild hypoxemia with normocarbia. PFTs are typical of a restrictive ventilatory defect (see above), and carbon monoxide diffusing capac-ity is reduced.
Treatment is directed at abating the disease process and preventing further exposure to the causative agent (if known). Glucocorticoid and immunosuppressive therapy may be used for idio-pathic pulmonary fibrosis, autoimmune disorders, and sarcoidosis. If the patient has chronic hypox-emia, oxygen therapy may be started to prevent, or attenuate, right ventricular failure.
Preoperative evaluation should focus on determin-ing the degree of pulmonary impairment as well as the underlying disease process. The latter is impor-tant in determining the potential involvement of other organs. A history of dyspnea on exertion (or at rest) should be evaluated further with PFTs and arte-rial blood gas analysis. A vital capacity of less than 15 mL/kg is indicative of severe dysfunction (nor-mal is >70 mL/kg). A chest radiograph is helpful in assessing disease severity.
The management of these patients is complicated by a predisposition to hypoxemia and the need to con-trol ventilation to ensure optimum gas exchange; anesthetic drug selection is generally not critical. The reduction in FRC (and oxygen stores) predis-poses these patients to rapid hypoxemia following induction of anesthesia. Because these patients may be more susceptible to oxygen-induced toxicity, particularly patients who have received bleomy-cin, the inspired fractional concentration of oxygen should be kept to the minimum concentration com-patible with acceptable oxygenation (Spo2 of >88% to 92%). High peak inspiratory pressures during mechanical ventilation increase the risk of pneumo-thorax and should prompt adjustment of the venti-latory parameters. In patients with severe restrictive disease, using an I:E ratio of 1:1 (or even an inverse ratio ventilation) and dividing the minute ventila-tion to a higher respiratory rate (10–15 breaths/ minute) may help to maximize the inspiratory time per tidal volume and minimize the peak and plateau ventilatory pressures.
Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.