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.
Related Topics
Privacy Policy, Terms and Conditions, DMCA Policy and Compliant
Copyright © 2018-2023 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.