Type 1 Respiratory Failure: Hypoxemic

Hypoxemic respiratory failure is typically associated with parenchymal lung diseases that affect oxygen exchange at the alveolar level. It is defined as a PaO ₂ less than 50 mm Hg on room air. Five pathophysiologic mechanisms can explain hypoxemia—low oxygen admixture, ventilation/perfusion (V/Q) mismatch, shunting, diffusion impairment, and alveolar hypoventilation. Shunt physiology is unique because it is nonresponsive to supplemental oxygen. Pulmonary edema and ARDS are two examples of hypoxemic respiratory failure and are discussed later in this chapter.

Type 2 Respiratory Failure: Hypercarbic With or Without Hypoxemia

Hypercapnic respiratory failure is associated with ventilatory failure and inadequate carbon dioxide elimination. It occurs when the arterial partial pressure of carbon dioxide (PaCO ₂ ) increases above 50 mm Hg in patients without chronic CO ₂ retention and may be associated with hypoxemia. There are three main causes of ventilation failure: depression of the respiratory centers in the brainstem, mechanical dysfunction of the respiratory muscles and associated structural tissues (e.g., the chest wall and diaphragm), and respiratory muscle fatigue associated with increased work of breathing. Depressed respiratory drive from medication effects (e.g., narcotics, inhalation anesthetics) is a classic cause of hypercapnic respiratory failure in the perioperative period. COPD is the most common cause of type 2 respiratory failure. Rare neuromuscular diseases (i.e., amyotrophic lateral sclerosis, muscular dystrophy, and myasthenia gravis) may lead to chronic hypercapnic respiratory failure.

Postoperative Respiratory Failure

Postoperative respiratory failure may be defined as unplanned intubation and mechanical ventilation within 48 hours of surgery. It is a serious complication associated with an 18-fold increased risk of death. Postoperative respiratory failure may be either hypoxemic or hypercarbic depending on the underlying pathophysiology. Patients may also require intubation for impending respiratory failure before hypercarbia or hypoxemia develops. Risk factors for postoperative respiratory failure are either patient related or procedure or anesthesia related. Patient factors include American Society of Anesthesiologists score greater than 3, older age, ethanol use, tobacco use, COPD, insulin-dependent diabetes mellitus, heart failure, hypertension, cancer, liver dysfunction, cachexia and weight loss, and morbid obesity (body mass index >40). Surgical and anesthesia factors include emergency surgery, medium- to high-risk surgery, surgery for sepsis, surgical location (upper abdominal or thoracic surgery), and surgery lasting longer than 2 hours. General anesthesia may pose a higher risk of postoperative respiratory failure versus regional or neuroaxial anesthesia, although this remains controversial. Residual neuromuscular blockade is an important risk factor for immediate perioperative respiratory failure.

Respiratory Failure in Circulatory Shock

Circulatory shock–associated respiratory failure develops when an imbalance between respiratory muscle oxygen supply and demand occurs. Respiratory compensation for a metabolic acidosis requires an increased minute ventilation to decrease the PaCO ₂ . Increased work of breathing requires greater oxygen supply, which is compromised in shock. Respiratory muscles fatigue and fail when the oxygen supply is insufficient to maintain the higher respiratory workload.

Pulmonary Edema

Starling forces control the net flow of fluid across the alveolar membrane and are proportional to the permeability and surface area of the alveolar membrane, as well as the balance between hydrostatic and oncotic pressures of both the capillaries and alveoli. In a normal lung, the extravasation of fluid from the capillaries into the alveoli is matched by the lymphatic system’s ability to drain the lung water. Imbalances in the Starling forces cause pulmonary edema and occur primarily from a high hydrostatic pressure in cardiogenic pulmonary edema or increased alveolar capillary permeability in noncardiogenic pulmonary edema. Restoration of the normal ebb and flow of alveolar lung water is often rapid in cardiogenic pulmonary edema because the elevated hydrostatic forces are normalized with diuresis and a negative fluid balance. In contrast, the resolution of noncardiogenic pulmonary edema can be prolonged and requires the restoration of the integrity of the alveolar membrane. A patient with pulmonary edema typically presents with tachypnea, dyspnea, and hypoxemia.

Cardiogenic Pulmonary Edema

Cardiogenic pulmonary edema can present with slowly progressive dyspnea or an acute dyspnea referred to as flash pulmonary edema. Slowly progressive edema is caused by a decline in cardiac function and progressive accumulation of intravascular and extravascular fluid. Contributing factors include medication effects (noncompliance or inadequate dose), renal dysfunction, and respiratory infection. Flash pulmonary edema is caused by abrupt physiologic derangement such as a sudden increase in blood pressure, acute myocardial ischemia, acute myocarditis, acute valve dysfunction (e.g., mitral regurgitation), or arrhythmia. Elevated filling pressures in the left heart cause an increase in pulmonary venous pressures and increased hydrostatic pressure in the pulmonary capillary bed. These changes force a transudative edema fluid into the interstitium and the alveoli when the left atrial pressure increases above 18 mm Hg. Alveolar fluid impairs oxygen exchange and results in hypoxemia.

Evaluation of the patient with pulmonary edema should focus on the severity of the respiratory distress and required respiratory support then shift to an assessment of etiology. Chest radiography and 12-lead electrocardiography are cornerstones of management, and laboratory evaluation should include cardiac troponins, complete blood count (CBC), complete metabolic panel (CMP), and brain natriuretic peptide level. Transthoracic echocardiography may be considered for better definition of cardiac structure and function.

Urgent treatment of pulmonary edema focuses on correction of hypoxemia and stabilization of respiratory distress. Patients with mild to moderate dyspnea and hypoxemia can often be treated with supplemental oxygen via nasal cannula; however, more severe dyspnea may require noninvasive or invasive mechanical ventilation. Noninvasive ventilation (NIV) may lead to quicker resolution of respiratory symptoms and decreased need for intubation. After respiratory stabilization, diuresis and afterload reduction should be considered. Loop diuretics are the mainstay of therapy for volume overload. Hypoxemia and respiratory distress improve as pulmonary edema resolves with a negative fluid balance. Afterload reduction with vasodilators reduces cardiac workload and may hasten recovery. Inotropes and advanced mechanical heart failure therapies may also be considered in the appropriate clinical setting.

Noncardiogenic Pulmonary Edema

The most important cause of noncardiogenic pulmonary edema is acute respiratory distress syndrome (ARDS). Less common etiologies of noncardiogenic pulmonary edema include neurogenic, diffuse alveolar hemorrhage, medication induced (e.g., naloxone), and negative-pressure pulmonary edema. Initial treatment includes stabilization of the respiratory distress with oxygen therapy, NIV, or invasive mechanical ventilation. Loop diuretics are often used for a negative fluid balance depending on patient stability.

Negative-Pressure Pulmonary Edema

Negative-pressure pulmonary edema occurs when extreme negative intrathoracic pressure (deep breath) occurs against an obstructed airway. The obstruction can be caused by an obstructed endotracheal tube, laryngospasm, or an upper airway obstruction. The large negative inspiratory force against an obstructed airway creates a vacuum effect and draws fluid into the alveoli, resulting in pulmonary edema characterized by pink, frothy sputum. The presentation can be immediate or delayed. There is misconception that negative-pressure pulmonary edema is typically associated with individuals who are capable of generating significant negative intrathoracic force; however, many of the patients who develop this disorder have preexisting cardiac disease.

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome is a common cause of respiratory failure, affects approximately 200,000 people a year, and is associated with 15% of all ICU admissions. ARDS is characterized by diffuse alveolar damage leading to increased alveolar capillary permeability, resulting in pulmonary edema, hypoxemia, and respiratory distress. The most common causes are pneumonia (viral or bacterial), sepsis, trauma, gastric aspiration, transfusion related, medications, and pancreatitis. The diagnosis of ARDS requires hypoxemia, bilateral opacities on chest radiographs, and pulmonary edema associated with a clinical insult and not fully explainable by cardiac function. ARDS severity is measured by the degree of hypoxemia using PaO ₂ /F _I O ₂ (fraction of inspired oxygen) ratio of mild, 200 to 300; moderate, 100 to 200; and severe, less than 100, correlating with increasing mortality rate (26%–35%). The cause of death in ARDS is most often related to multisystem organ failure and bacterial sepsis.

Treatment of ARDS is supportive and requires treatment of the underlying condition (e.g., antibiotics and source control for sepsis). The mainstay of therapy for ARDS is lung-protective ventilation and conservative fluid management. Lung-protective ventilation consists of low tidal volume ventilation (6 mL/kg), maintaining plateau pressures less than 30 cm H ₂ O, and permissive hypercapnia to avoid ventilator-induced lung injury (volume trauma and barotrauma). Conservative fluid therapy in ARDS begins after circulatory shock has resolved (no longer requiring fluid boluses or vasopressors for 12 hours). The goal for conservative fluid therapy is a net negative fluid balance of 500 mL/day achieved through diuresis and has led to decreased ventilator-dependent days and ICU length of stay. Several adjuvant therapies may lead to an additional decrease in mortality rate from severe ARDS, including short-term paralysis with cisatracurium, prone positioning in the ICU, and extracorporeal membrane oxygenation. Consultation with critical care specialists is recommended.

Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease is a very common disorder and is projected to be the third leading cause of death by 2020. Smoking is the leading risk factor, and 70% of patients with COPD have a cardiovascular comorbidity. COPD causes a constant, low-grade inflammatory response that accelerates atherosclerosis and is associated with a two- to threefold increased risk of cardiovascular death. Not surprisingly, COPD is a major risk factor for postoperative complications, including pneumonia, respiratory failure, myocardial infarction, cardiac arrest, sepsis, reoperation, and kidney injury or failure.

Chronic obstructive pulmonary disease is characterized as chronic and progressive airflow limitations from damage to the lung parenchyma or inflammation of the airways. Symptoms include dyspnea, respiratory signs of distress (i.e., accessory muscle use), increased sputum production, and chronic cough. Exposure to tobacco smoke is nearly universal, although there are other risk factors such as environmental exposures and rare genetic defects (α ₁ -antitrypsin). Common physical examination findings include expiratory wheezing, increased expiratory time, diminished breath sounds, and a barrel chest. Diagnosis is confirmed with spirometry. COPD severity is important because it directly relates to increased risk of exacerbation. The Global Initiative for Chronic Obstructive Lung Disease has developed a simple disease severity scale based on forced expiratory volume in 1 second (FEV ₁ ) with the assumption that the patient has an FEV ₁ /FVC (forced vital capacity) ratio less than 0.7. An FEV ₁ less than 80% predicted value is mild, FEV ₁ of 50% to 79% is moderate, FEV ₁ of 30% to 49% is severe, and FEV ₁ less than 30% is very severe. Other risk factors for exacerbation include gastroesophageal reflux disease, asthma, heart failure, cancer, and respiratory infections.

It is important for the anesthesiologist to recognize the severity of COPD in patients presenting for surgery. Preoperative pulmonary function testing should be considered for those who are at risk for COPD or have an established diagnosis of COPD. A specific level of functional status and spirometric data points have not been established for COPD patients who require an operation. Consultation with a pulmonologist should be considered. Standard medical therapies for COPD include smoking cessation and inhalers for symptom alleviation. Bronchodilator therapy with a β ₂ -agonist (i.e., albuterol, salmeterol) and/or an antimuscarinic (i.e., tiotropium) are commonplace, as are inhaled corticosteroids. Oxygen therapy is added when patients develop resting hypoxemia, pulmonary hypertension, or heart failure. It is beneficial that these medications are continued in the perioperative period.

Exacerbations of COPD are characterized by worsening of symptoms ranging from increased wheezing to hypercarbic respiratory failure. Treatment includes respiratory support with oxygen, noninvasive or invasive mechanical ventilation, and medical management. Noninvasive mechanical ventilation is the mainstay of therapy in severe COPD exacerbations and has been shown to decrease mortality rates, the need for intubation, and hospital length of stay. In the perioperative period, the anesthesiologist should be cognizant of the relative contraindications to NIV such as diminished mental status, ability to protect the airway or aspiration risk, recent and severe facial surgery or trauma, hemodynamic instability, and upper gastrointestinal (GI) surgery. After NIV has been initiated, frequent patient assessment is required. NIV failure is defined as no improvement or worsening of the respiratory acidosis within 1 hour of initiation, and intubation should be considered. Declining mental status and increased work of breathing are additional signs of NIV failure, suggesting that intubation and mechanical ventilation may be needed. Pharmacotherapy for acute COPD exacerbations includes antibiotics for respiratory infection, inhaled β-agonists (e.g., albuterol), and anticholinergic agents (e.g., ipratropium). Systemic corticosteroids also are recommended.