Acute Respiratory Failure


Respiratory failure occurs when the lungs fail to oxygenate the arterial blood adequately and/or fail to prevent carbon dioxide retention. Although the definition does not contain any absolute values, an arterial O 2 of less than 60 mmHg and an arterial CO 2 of more than 50 mmHg are often regarded as of consequence. However, values should be considered in the context of an individual patient.

Hypoxemic Respiratory Failure

There are four main causes of hypoxemic respiratory failure:

  • 1.


  • 2.

    Diffusion impairment

  • 3.


  • 4.

    Ventilation-perfusion (V/Q) mismatch

Of these, V/Q mismatch is the most frequently encountered. Most of these abnormalities improve with supplemental oxygenation, except for a shunt. A “true shunt” develops when portions of the lung are perfused in total absence of ventilation. The most frequent causes of a shunt in the postoperative patient are consolidated pneumonia, lobar atelectasis, and the later phases of the acute respiratory distress syndrome (ARDS). Other causes of hypoxemic respiratory failure in the postoperative population include pulmonary edema, chronic obstructive pulmonary disease (COPD), pneumothorax, pulmonary embolism, and pulmonary hypertension.

Hypercapnic Respiratory Failure

The four basic mechanisms underlying hypercapnic respiratory failure are:

  • 1.

    Inability to sense increasing arterial CO 2 (hypoventilation)

  • 2.

    Increased CO 2 production

  • 3.

    Increased dead space

  • 4.

    Decreased tidal volume

The common causes of each in the postoperative patient are listed in Box 39.1 .

Box 39.1

Common causes of type II respiratory failure in postoperative patients.

Inability to Sense an Increasing PaCO 2

  • Anesthetic agents

  • Benzodiazepines

  • Narcotics

Increased CO 2 Production

  • Hypermetabolic states

    • Fever

    • Sepsis

    • Multiple organ failure

    • Burns

    • Trauma

  • Excessive carbohydrate intake

  • Hyperthyroidism

Decreased Tidal Ventilation (V T )

  • Post-traumatic flail chest

Increased Dead Space Ventilation (V D )

  • Adult respiratory distress syndrome (ARDS)

Acute Respiratory Failure in the Perioperative Patient

Identification of risk factors for postoperative acute respiratory failure is helpful in that it identifies those patients who may benefit from preoperative optimization and increased postoperative vigilance. Many studies have been undertaken to identify predictors of postoperative acute respiratory failure and other pulmonary complications. Nijbroek et al. reviewed 21 different studies attempting to derive predictive scores and concluded that only the ARISCAT score was adequately externally validated.

The Assess Respiratory Risk in Surgical Patients in Catalonia (ARISCAT) investigators conducted a prospective multicenter observational random-sample cohort study of 2464 patients undergoing non-obstetric procedures under general, neuroaxial or regional anesthesia in southern Spain. The overall incidence of postoperative pulmonary complications (PPCs) was 5% and 30-day mortality was increased in those who developed PPCs compared with those who did not (19.5 versus 0.5%). Seven factors were found to be independently predictive of the development of PPCs: low preoperative arterial oxygen saturations when breathing room air and lying supine, acute respiratory infection associated with a fever and the need for antibiotic therapy during the preceding month, age, preoperative anemia, upper abdominal or intrathoracic surgery, a surgical duration longer than two hours, and emergency surgery. The derived ARISCAT score was able to classify patients as low (score < 26), intermediate (score 2–44) or high (score > 45) risk for PPCs. Although obesity and asthma did not emerge as independent predictors, other studies have shown that preexisting comorbidities are important contributors. However, their importance may be lessened by preoperative optimization.

Subsequent investigators have validated the ARISCAT score for predicting the risk of developing PPCs, including a recent study of 1170 patients undergoing noncardiac surgery, which showed that patients with intermediate and high risk based on ARISCAT were found to have increased risk of PPCs.

Some factors can be optimized prior to undertaking elective surgical procedures. Warner and coworkers documented that smoking cessation 8 weeks prior to elective surgery led to a decreased incidence of postoperative acute respiratory failure. Systematic review of the impact of preoperative smoking interventions by the Cochrane collaboration found that there was heterogeneity between intensive and brief behavioral interventions, with significant impact of intensive intervention on PPCs and wound complications.

There are also data suggesting that the manner in which both emergency and elective surgical patients are mechanically ventilated during surgery can be associated with the development of PPCs. Several studies have shown that for patients receiving tidal volumes less than 8 mL/kg IBW (ideal body weight), increased driving pressure or peak inspiratory pressure are associated with increased development of PPCs. These findings have also been reproduced in an individual patient meta-analysis of data from 2250 patients from 17 clinical trials.

The association between intraoperative tidal volume and PPCs is less straightforward, but a meta-analysis of 2127 patients from 15 studies suggested that low tidal volume ventilation is associated with a decreased incidence of PPCs, but has no impact on mortality of length of hospital stay. However, this finding was not reproduced in more recent clinical studies.

Postoperative Factors

After surgery, all patients are at risk of acute respiratory failure. Some of the more common etiologies are atelectasis, bronchospasm, pulmonary aspiration, anesthetic effects, pulmonary edema, pulmonary embolism, and ARDS.


The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as alveolar collapse with reduced intrapulmonary air. It is the most common PPC, with radiographic evidence in up to 70% of patients undergoing a thoracotomy or a celiotomy. If left untreated, it can result in pulmonary gas exchange alterations leading to severe hypoxemia and acute respiratory failure. The mechanisms leading to atelectasis are multifactorial and include alterations in ventilatory mechanics, changes in the mechanical properties of the thoracic wall, stagnation of bronchial secretions, and airway obstruction.

The alterations in ventilatory mechanics seen postoperatively include diminished vital capacity (VC), diminished V T , increased respiratory rate, and diminished functional residual capacity (FRC), resulting in atelectasis. The primary cause of these alterations is postoperative diaphragmatic dysfunction. Stagnation of bronchial secretions is also a mechanism leading to atelectasis. This problem is normally prevented by mucociliary clearance and coughing. When these functions are inhibited, stagnation of bronchial secretions occurs, and atelectasis can develop.

Mucociliary clearance is significantly diminished during mechanical ventilation. Coughing may be suppressed secondary to mechanical ventilation, opioids, diaphragmatic dysfunction, pain, altered mental status, and airway obstruction. A final mechanism of atelectasis is airway obstruction. In this case, atelectasis is either passive or absorptive. Passive atelectasis is secondary to external or internal compression of a lung segment (e.g., pneumothorax, hemothorax, abdominal distention). Absorptive atelectasis occurs when the inhaled gas is rich in oxygen and poor in nitrogen. In this instance, oxygen diffuses rapidly into venous blood, leading to alveolar collapse.

Risk factors for atelectasis are shown in Box 39.2 . The type of surgical procedure performed has tremendous influence on the occurrence of postoperative atelectasis. Thoracic and upper abdominal surgeries pose a greater risk for atelectasis than do other procedures. Several studies have documented progressive deterioration of pulmonary gas exchange during the course of thoracic and abdominal surgeries. Likewise, cardiopulmonary bypass surgery increases the risk of atelectasis more than other surgeries (including noncardiac thoracic surgeries). In addition, midline celiotomies have an increased risk of atelectasis relative to transverse or subcostal abdominal incisions.

Box 39.2

Risk factors for atelectasis.

  • Very young age (infants and young children)

  • Obesity

  • Smoking

  • Preexisting pulmonary disease

  • Dehydration

  • Anesthetic agents

  • Mechanical ventilation

  • Types of surgery

    • Cardiopulmonary bypass surgery

    • Thoracic surgery

    • Upper abdominal surgery

    • Midline incisions

    • Prolonged anesthesia

Clinical Manifestations

Clinically, atelectasis ranges from asymptomatic to severe hypoxemia and acute respiratory failure. The variability in presentation depends on the rapidity of onset, the degree of lung involvement, and the presence of an underlying pulmonary infection. In the worst-case scenario with rapid onset, major airway collapse, and underlying infection, atelectasis presents with sudden dyspnea, chest pain, cyanosis, tachycardia, and an elevated temperature. On physical examination, the patient often exhibits diminished chest wall excursion, dullness to percussion, and diminished or absent breath sounds. In the less severe presentations, elevated temperature on the first postoperative day may be the only manifestation of atelectasis.


The diagnosis of atelectasis is generally made from radiographic findings of diminished lung volumes in the presence of the aforementioned clinical manifestations. On chest radiographs, findings indicative of atelectasis relate to volume loss and include displacement of the lobar fissure, retracted ribs, an elevated hemidiaphragm, mediastinal or tracheal deviation to the affected side, and over-inflation of the unaffected lung. The exact radiographic findings depend on which portion of the lung is involved and to what degree, in addition to how the surrounding structures compensate for the volume loss. On arterial blood gas (ABG) analysis, significant atelectasis results in hypoxemia. Atelectasis also may be identified by means of chest computed tomography (CT) or lung ultrasound.


For postoperative atelectasis, prevention is the key. Because tobacco use and underlying pulmonary disease processes are predictors of postoperative atelectasis, preoperative optimization is essential. Both smoking cessation and improved bronchial toilet preoperatively should be encouraged. During anesthesia induction, the use of positive end-expiratory pressure (PEEP) has been shown to be beneficial. Rusca and coworkers documented significantly decreased atelectasis and improved oxygenation by applying 6 cm H 2 O of positive end expiratory pressure (PEEP) on induction. In addition to this, long-acting anesthetics and those with significant post-anesthesia narcosis should be limited.

During the postoperative period, a number of measures can be taken to prevent atelectasis ( Fig. 39.1 ). Control of postoperative pain is critical. Insufficient analgesia results in pleural and parietal pain, causing inadequate coughing and expectoration. However, because narcotics depress the cough reflex, excessive doses should be avoided. The traditional intermittent dosing of narcotics at 3- to 4-hour intervals is insufficient. The patient cycles from overdosing after administration (over-sedation with resultant poor coughing and expectoration) to pain and anxiety before receiving the next dose. This cyclical pattern may be avoided by using patient-controlled analgesia (PCA). Another alternative is neuroaxial or regional analgesia, which is very effective. A meta-analysis supports the view that postoperative atelectasis is decreased when patients receive epidural opioids instead of systemic opioids.

Fig. 39.1

Prevention and treatment algorithm for postoperative atelectasis. CPAP , Continuous positive airway pressure; FFB , flexible fiberoptic bronchoscopy; IPPB , intermittent positive-pressure breathing; IS , incentive spirometry; PEEP , positive end-expiratory pressure.

Just as pain control is critical, so is meticulous nursing care. In non-intubated patients, several steps should be taken to prevent atelectasis. Early ambulation and techniques that encourage deep breathing are important.

Incentive spirometry (IS) is the most widely used postoperative pulmonary therapy. Its purpose is to imitate the natural sighing or yawning that healthy individuals perform regularly. The simplicity of IS and its lack of required personnel account for its popularity. A meta-analysis suggests that IS, intermittent positive-pressure breathing (IPPB), and chest physiotherapy are all equally efficacious in decreasing PPCs after upper abdominal surgery. Chest physiotherapy encompasses deep breathing and coughing, postural drainage, and chest percussion.

Continuous positive airway pressure (CPAP) can be used as a last means in attempting to prevent intubation. In a randomized controlled trial, Squadrone and colleagues documented that CPAP decreases the incidence of PPCs (including endotracheal intubation) in patients who develop hypoxia after major elective abdominal surgery. If these maneuvers are unsuccessful and the patient continues to progress to acute respiratory failure, the patient should be intubated and consideration given to whether a flexible fiberoptic bronchoscopy may be of benefit.


Pulmonary aspiration of gastric contents is generally preventable with meticulous anesthesia technique and critical care. Despite this, the incidence varies from 1 in every 3900 elective surgical cases to 1 in every 895 emergent surgical cases. The number increases dramatically to 8% to 19% during emergent intubations without anesthesia.

Aspiration of gastric contents results in chemical pneumonitis, which develops in four stages. Initially, the aspirate causes mechanical obstruction of the airways, with distal collapse. Obstruction alters ventilatory mechanics, leading to increased shunt, loss of FRC, and increased work of breathing. In the second stage, chemical injury occurs in response to the acidity of the aspirate. The pattern of injury includes mucosal edema, bronchorrhea, and bronchoconstriction, all resulting in an increased risk of bacterial infection. The third stage in the pathophysiology of aspiration is the inflammatory response. The release of tumor necrosis factor, interleukin 1, leukotrienes, and thromboxane A 2 contribute to mucosal edema and bronchoconstriction resulting in lung inflammation. The final phase is progression to infection if appropriate interventions are not performed. Risk factors for pulmonary aspiration are shown in Table 39.1 .

Table 39.1

Risk factors for pulmonary aspiration.

Modified from Metheny NA. Risk factors for aspiration. JPEN J Parenter Enteral Nutr 2002;26(Suppl 6):S26-S31.

Risk factor Clarification / Examples
Endotracheal intubation The cuff does not prevent aspiration.
Decreased level of consciousness GCS < 9, alcohol or drug overdose/withdrawal, excessive analgesics or sedatives, chemical paralysis
Neuromuscular disease and structural abnormalities of the aerodigestive tract Diabetic gastroparesis, Parkinson’s disease, scleroderma, gastroesophageal reflux disease, esophageal cancer
Recent cerebrovascular accident Within 4–6 weeks
Major intra-abdominal surgery Less than 5 days postoperatively
Persistently high gastric residual volume (GRV) GRV > 500 mL
Prolonger supine positioning Spinal fractures
Persistent hyperglycemia Blood glucose > 140 mg/dL

Clinical Manifestations

Hypoxemia is the most consistent finding in aspiration. In addition, patients present with increased temperature, tachypnea, tachycardia or bradycardia, cyanosis, and altered mental status. On physical examination, the pulmonary findings include crackles, rales, and decreased breath sounds. The extent of these manifestations depends on the degree of aspiration.

The outcome varies widely from asymptomatic to rapid death. Fortunately, many patients improve rapidly within several days without further treatment. A second subset of patients improves initially and then deteriorates over the following 2 to 5 days. These patients develop increased temperature, productive cough, and hypoxemia and progress from aspiration pneumonitis to aspiration pneumonia. The remaining patients do not improve from their initial pneumonitis and progress to diffuse pulmonary infiltrates, refractory hypoxemia, and ARDS.


After a witnessed pulmonary aspiration, the diagnosis is clear. However, in other situations, the diagnosis of aspiration is based on the clinical symptoms and a high index of suspicion. On laboratory evaluation, significant aspiration results in hypoxemia and leukocytosis. Aspiration may also be identified by means of chest radiography. There are no pathognomonic radiologic features; however, infiltrates in gravity-dependent lung regions are the most consistent finding. The most common sites of infiltration are the superior segment of the right lower lobe and the right middle lobe. However, depending on the aspirate volume and the patient’s position during aspiration, left and bi-lobar aspiration is possible. Flexible fiberoptic bronchoscopy may also be used for diagnosing aspiration.


As in atelectasis, prevention is the key. During the preoperative assessment by the anesthesiologist, patients at risk of aspiration need to be identified ( Fig. 39.2 ). These include patients requiring emergency procedures, patients with diabetes mellitus, and pregnant patients. In these instances, an experienced anesthesiologist is required. If feasible, regional anesthesia should be entertained. The American Society of Anesthesiology have produced guidelines on the duration of preoperative fasting required under various circumstances ( Table 39.2 ).

Jun 9, 2021 | Posted by in ANESTHESIA | Comments Off on Acute Respiratory Failure
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