Emphysema

Incidence in USA: 4.7 million.

Prevalence, incidence, and mortality increase with age.

Higher in males than females.

Higher in whites than nonwhites.

Intraop bronchospasm

N ₂ O expansion of bullae

Postop respiratory failure

Postop pulm infection

Worsening of baseline pulm function, caused by:

• Bronchospasm.

• Acute bronchitis or pneumonia.

• Pulm embolism.

Worsening of baseline cardiac function caused by right heart failure.

Most common comorbidities include ischemic heart disease, diabetes, skeletal muscle wasting, osteoporosis, and lung cancer.

Anatomic: Destruction of interalveolar septa and loss of pulm elastic recoil, leading to formation of bullae and development of irreversible expiratory airflow obstruction.

Remodeling of the small airway compartment and loss of elastic recoil result in progressive decline of FEV ₁ and lead to static and dynamic hyperinflation.

The “pink puffer” has dyspnea, hyperinflation, distant breath sounds, low diffusing capacity (decreasing D _L CO to <60% predicted).

The “blue bloater” has chronic bronchitis, leading to hypoxemia, polycythemia, and CO ₂ retention.

Hypoxia, hypercarbia, and cor pulmonale are late developments.

Mucociliary clearance is often worsened after inhalational anesthetics.

Diaphragmatic mechanics are impaired by anesthetics, sedatives, NMBs, interscalene blocks, and supine positioning.

According to the elastase-antielastase hypothesis, the lung is normally protected from injury to its elastic tissues by antielastases, including API, which is also called a ₁ -antitrypsin. According to this theory, emphysema may be acquired or genetic.

Acquired: Related to inhaled oxidants (cigarette smoke or other occupational exposures), which are believed to inactivate API, thus compromising lung matrix repair after injury.

Genetic: Absent or abnormal API, also known as a1-antitrypsin deficiency, which accounts for a small fraction of cases.