How do you assess a patient with acute respiratory failure?

Pathobiology

Abnormal gas exchange is the physiologic hallmark of acute respiratory failure, which can be classified in several ways (Table 96-2). Although gas exchange can be abnormal for either oxygenation or CO2 removal, significant hypoxemia is nearly always present when patients with acute respiratory failure breathe ambient air. If CO2 is retained at a potentially life-threatening level under these conditions, it will be accompanied by significant hypoxemia (see later). Thelife-threatening aspect of the condition places the degree of abnormal gas exchange in a clinical context and calls for urgent treatment.

The diagnosis of acute respiratory failure requires a significant change in arterial blood gases or arterial oxygen saturation from baseline. Many patients with chronic respiratory problems can function with blood gas tensions that would be alarming in a physiologically normal individual. Over time, patients with so-called chronic respiratory failure or chronic respiratory insufficiency develop mechanisms to compensate for inadequate gas exchange. Conversely, this chronic condition makes patients vulnerable to respiratory insults that could be easily tolerated by a previously healthy individual.

In acute respiratory failure, the O2 content in the blood (available for tissue use) is reduced to a level at which the possibility of end-organ dysfunction, as a result of inadequate oxygen delivery, increases. The value of the partial pressure of O2 in the arterial blood (Pao2) that demarcates this vulnerable zone is often considered to be the point of the oxyhemoglobin dissociation relationship at which any further decrease in the Pao2 results in sharp decreases in the amount of hemoglobin saturated with O2 (Sao2) and in the arterial blood O2 content (Cao2). Thus, acute respiratory failure is often defined in practice as occurring when the Pao2 is less than about 55 to 60 mm Hg (Fig. 96-1). However, it is important to note that the oxyhemoglobin dissociation curve of whole blood, which is the partial pressure at which O2 is being unloaded to the tissues, is a critical determinant of how much O2 is available for the cells and their mitochondria at a given PaO2. Conditions such as fever or acidosis can shift the curve rightward. Other than under conditions of an extremely hypoxic environment (e.g., in utero or on the summit of Mt. Everest), however, the enhanced ability to unload O2 at the tissue level more than compensates for small decreases in the amount of O2 picked up in the lungs when the oxyhemoglobin dissociation curve is shifted rightward. With a leftward shift in the curve, O2 is bound more tightly to hemoglobin, so less O2 is available for tissue delivery.

Conclusion

Acute respiratory failure implies an inability to maintain adequate oxygenation for tissues or adequate removal of carbon dioxide from tissues. The differential diagnosis should be informed by the radiographic appearance of the chest radiograph and by the patient's history and physical examination. A specific diagnosis should be pursued, which frequently requires ancillary studies such as blood or sputum cultures, bedside spirometry, perfusion lung scan, or a CT angiogram using multidetector scanners. This allows the physician to initiate specific therapy for the underlying cause of acute respiratory failure. These patients often require supportive therapy.

Acute Hypoxic Respiratory Failure

Hypoxic respiratory failure is conventionally defined as an arterial oxygen tension (PaO2) of less than 60 mm Hg. Because this definition ignores the inspired fraction of oxygen (FiO2), some favor a PaO2/FiO2 ratio of less than 300. To account for the arterial CO2 tension (PaCO2), others favor an alveolar–arterial (A–a) O2 gradient greater than 250 mm Hg, using the equation

A–aO2gradient=PAO2 −PaO2 =(713×FiO2)−(PaO2+PaCO2/0.8)

where 713 is the barometric pressure (760) minus the water vapor pressure. A normal A–a O2 is less than 10 mm Hg, but this threshold value increases with age. The determination of PaO2 requires an invasive test, an arterial blood gas. Oxygenation can be continuously monitored noninvasively by pulse oximetry, which provides an estimate of arterial oxygen saturation (SaO2). In general, an SaO2 of 0.90 corresponds to a PaO2 of 60 mm Hg, but the relation depends on temperature, pH, PaCO2, and 2,3-diphosphoglycerate (2,3-DPG). Accuracy is adversely affected by low perfusion states, dark skin pigmentation, nail polish, dyshemoglobins (e.g., carboxyhemoglobin, methemoglobin), intravascular dyes, motion, and ambient light.

1 What is meant by acute respiratory failure (ARF)?

ARF occurs when the respiratory system is unable to either adequately absorb oxygen (i.e., hypoxemia) or excrete carbon dioxide (i.e., hypercarbia). Although both hypoxemia and hypercarbia can occur together, one process frequently predominates. ARF may occur suddenly or as a gradual process. It can occur in both healthy patients and those with chronic pulmonary disease.

2 How is ARF defined by arterial blood gas (ABG) analysis?

Although no rigid criteria apply for all patients, it is generally accepted that hypoxemic respiratory failure is present when the arterial PO2 is less than 50 mmHg when breathing room air. Hypercarbic ARF is present when PCO2 is greater than 50 mmHg and the arterial pH is acidotic (pH < 7.30). Hypercarbia in the presence of a normal or alkalotic arterial (pH ≥ 7.40) is a normal compensatory reaction and does not constitute ARF.

3 How can ventilation (i.e., carbon dioxide excretion) be assessed noninvasively?

There is no widely available noninvasive test that can accurately assess the adequacy of carbon dioxide excretion. Transcutaneous or end-tidal carbon dioxide analyzers are available, but their accuracy can be poor in certain circumstances. An abnormally low or high respiratory rate can suggest that hypercarbic respiratory failure is present, but a normal or high respiratory rate cannot exclude the diagnosis. ABG analysis remains the gold standard for the diagnosis of hypercarbic ARF.

Gattas D, Ayer R, Suntharalingam G, Chapman M: Carbon dioxide monitoring and evidence-based practice—now you see it, now you don't. Crit Care 8:219–221, 2004.

Soubani AO: Noninvasive monitoring of oxygen and carbon dioxide. Am J Emerg Med 19:141–146, 2001.

4 What are the physiologic mechanisms of hypoxemic ARF? Which are reversible with supplemental oxygen?

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Low mixed venous oxygen

Alveolar hypoventilation

Ventilation perfusion mismatch

Right-to-left shunt

Diffusion limitation

Low inspired oxygen fraction (e.g., high altitude)

Most of these physiologic mechanisms are reversible with supplemental oxygen, with the exception of shunt. Because shunting occurs when blood travels from the venous to systemic arterial circulation without passing through ventilated lung, changes in inspired oxygen concentration will not affect the shunted blood.

Greene KE, Peters JI: Pathophysiology of acute respiratory failure. Clin Chest Med 15:1–12, 1994.

Levy MM: Pathophysiology of oxygen delivery in respiratory failure. Chest 128(5 Suppl 2):547S–553S, 2005.

5 What physiologic processes can cause hypercapnic ARF?

Hypercapnia is the result of alveolar hypoventilation. Mechanisms responsible may be:

Central-decreased respiratory drive

Neuromuscular-decreased neural transmission or muscular translation of the drive signal

Abnormalities of the chest wall

Abnormalities of the lungs and airways

Greene KE, Peters JI: Pathophysiology of acute respiratory failure. Clin Chest Med 15:1–12, 1994.

6 Which disease processes are associated with each type of ARF? Which are reversible?

The differential diagnosis of hypoxemic ARF can be delineated based on whether there is concomitant hypercapnia and whether infiltrates are seen on the chest radiograph. If the patient is normocapnic and the chest x-ray result is normal (i.e., “clear”), pulmonary embolus, circulatory collapse, or right-to-left shunt is likely. If the chest radiograph displays diffuse infiltrates, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, or pulmonary fibrosis is possible. If focal infiltrates are present, the patient may have pneumonia, atelectasis, or pulmonary infarction. If the chest radiograph is clear in patients with hypercapnia, then status asthmaticus, chronic obstructive pulmonary disease (COPD), or alveolar hypoventilation resulting from drug overdose, neuromuscular weakness, paralysis, or sleep apnea syndrome is likely. If the chest radiograph shows diffuse infiltrates, end-stage pulmonary fibrosis or severe ARDS is possible, whereas if the findings are localized, the patient could have pneumonia with underlying COPD or respiratory depression resulting from drugs or oxygen therapy. In general, most of the previously mentioned disease processes are reversible. However, severe COPD, sleep apnea syndrome, diseases of the respiratory muscles, cervical fracture leading to paralysis, and kyphoscoliosis may lead to chronic carbon dioxide retention and chronic respiratory failure. In patients with these underlying disorders, ARF due to other etiologies may occur and should be investigated.

Bartter TC, Irwin RS: Respiratory failure. Part I: A physiologic approach to managing respiratory failure. In Irwin RS, Rippe JM (eds): Irwin & Rippe's Intensive Care Medicine, ed 5. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 485–488.

7 What empiric therapy should be used emergently in patients with hypoxemic ARF?

Raising the PO2 to greater than 50 mmHg is the first goal of therapy. If the patient is alert and cooperative, supplemental oxygen and close observation in the intensive care unit may be adequate. Pulse oximetry or repeat arterial blood gas analysis should be monitored frequently to assess the adequacy of therapy. If the patient is stuporous or comatose or has a decreased gag reflex, then control of the airway by endotracheal intubation is warranted. In the case of suspected opiate overdose (e.g., respiratory depression, pinpoint pupils, and coma), naloxone should be administered.

Bartter TC, Irwin RS: Respiratory failure. Part I: A physiologic approach to managing respiratory failure. In Irwin RS, Rippe JM (eds): Irwin & Rippe's Intensive Care Medicine, ed 5. Philadelphia, Lippincott Williams & Wilkins, 2003, pp 485–488.

8 What are the indications for endotracheal intubation?

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Cardiopulmonary resuscitation with the need for complete control of the airway

Airway protection from aspiration of gastric contents

Need for mechanical ventilation

Control of copious airway secretions

Complete upper airway obstruction

9 What are the indications for mechanical ventilation?

Mechanical ventilation is required whenever the patient is unable to maintain adequate alveolar oxygenation or ventilation. Even in the setting of a normal PO2 and PCO2, excessive work of breathing may eventually lead to respiratory muscle fatigue and failure, thus necessitating mechanical ventilation. The decision for intubation and mechanical ventilation should be based on the clinical appearance of the patient and blood gas analysis results. Mechanical ventilation can also be used to provide hyperventilation to patients with head trauma to reduce intracranial pressure for the first 24–48 hours. An alternative to endotracheal intubation in patients with sufficient mental status to protect their airways is noninvasive positive pressure ventilation.

Caples SM, Gay PC: Noninvasive positive pressure ventilation in the intensive care unit: A concise review. Crit Care Med 33:2651–2658, 2005.

Fan E, Needham DM, Stewart TE: Ventilatory management of acute lung injury and acute respiratory distress syndrome. JAMA 294:2889–2896, 2005.

10 What is positive end-expiratory pressure (PEEP)? When should it be used?

PEEP is a technique used to mechanically correct hypoxemia by increasing lung volume. PEEP increases the expiratory threshold pressure, which prevents the patient's airway pressure from falling below a preset level during the respiratory cycle. This increases the volume of gas in the patient's chest at end-expiration (i.e., functional residual capacity). The treatment would therefore be expected to be beneficial in patients with restrictive lung diseases such as ARDS because the hypoxemia in this disorder may be due to alveolar collapse, filling, or both.

11 What is the significance of the patient who is “fighting the ventilator”?

The sudden onset of agitation and distress in a patient who previously was tolerating mechanical ventilation is a medical emergency and may signify acute deterioration in the underlying disease, malfunction of the ventilator, obstruction of the airway or endotracheal tube, or inadequate sedation. The patient should be disconnected from the ventilator and manually ventilated. Vital signs should be obtained, the chest examined, the airway suctioned, and ABG analysis and chest x-ray performed. If no etiology is found after these measures are taken, the ventilator setup may be incorrect for the patient's needs. Changes in the ventilator settings are appropriate so as to more closely match the machine to the patient's requirements. Increased sedation should usually only be used if other measures have failed.

12 When can patients be weaned from mechanical ventilation?

Patients' health should be clinically improved with stabilization and correction of any underlying conditions that may interfere with weaning (e.g., electrolyte disturbances, fluid overload, severe anemia, or severe pain requiring analgesics or sedatives). Patients should be alert with stable vital signs and should have an intact gag reflex. Some physiologic guidelines that can be used include the following: PO2 > 60 mmHg with the FiO2 < 50% and PEEP = 0–5 cm H2O, respiratory rate < 20, vital capacity > 10–15 mL/kg, tidal volume > 5 mL/kg, minute ventilation (VE) < 10 L/min, and negative inspiratory force of > −25 cm H2O. No single physiologic variable can completely predict the success of a trial of ventilator liberation. Some clinicians advocate the use of frequent protocol-driven spontaneous breathing trials. A composite variable such as the rapid shallow breathing index (i.e., respiratory rate/tidal volume < 100–130 breaths/min/L) can be used to assess the adequacy of pulmonary function during these trials.

Ely EW, Meade MO, Haponik EF, et al: Mechanical ventilator weaning protocols driven by nonphysician health-care professionals: Evidence-based clinical practice guidelines. Chest 120(6 Suppl):454S–463S, 2001.

13 What are some postextubation complications?

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Hoarseness

Difficulty swallowing and risk of aspiration

Severe glottic edema leading to airway obstruction (may be treated with racemic epinephrine 0.5 mL/3 mL saline via nebulized aerosol)

Key Points: Acute Respiratory Failure

The mechanisms involved in acute hypercapnic respiratory failure include decreased central drive to breathe, weakness of respiratory muscles, abnormalities of the chest wall, and abnormalities of the lung and airways.

Mechanical ventilation needs to be initiated when the patient is too weak to breathe or the work of breathing is too excessive.

Hoarseness, difficulty swallowing, and glottic edema can occur after the endotracheal tube is removed.

Noninvasive Ventilation (seeChapter 136)

Although initial medical therapy is usually effective in mild COPD exacerbations, it is often not sufficient in severe exacerbations. In severe exacerbations, tachypnea, dyspnea, and CO2 retention may persist or worsen despite initial medical therapy. Until the mid- to late-1990s, patients in such a predicament would usually be intubated and mechanically ventilated. If they declined intubation, they were kept comfortable while medical therapy was continued, but they often died. Invasive mechanical ventilation was successful in the majority of cases, but hospital mortality rates were substantial, averaging 30% in several studies.138 Complications of invasive mechanical ventilation were common, including upper airway trauma, pneumothorax, and nosocomial infection, all contributing to patient mortality.139

In 1990, Brochard and coworkers140 demonstrated that the noninvasive delivery of pressurized air into the lungs via a face mask was effective in providing partial ventilatory assistance during COPD exacerbations. Shortly thereafter, Appendini and colleagues141 showed that noninvasive extrinsic PEEP (to counterbalance the effects of intrinsic PEEP) combined with pressure support reduced diaphragmatic work of breathing even more effectively in COPD patients than either CPAP or pressure support alone. In this way, NIV restores the balance between supply and demand for the work of breathing, thereby serving as a “crutch” during COPD exacerbations and halting the progression of respiratory muscle fatigue while medical therapies are given time to work.

Since Brochard’s study, multiple randomized controlled studies and meta-analyses have demonstrated the efficacy of NIV to treat exacerbations of COPD.139 When compared with standard oxygen and medical therapy alone, NIV for severe exacerbations of COPD more rapidly improves dyspnea, respiratory and heart rates, arterial Pco2, and encephalopathy scores.142–144 In addition, intubation and mortality rates drop precipitously (from roughly 75% and 30% in controls to 25% and 10%, respectively, in NIV-treated patients).142,143,145 NIV also lowers complication rates and hospital lengths of stay compared with controls.142–144 Such benefit has not been shown in milder exacerbations, when work of breathing is not substantially increased.146,147

Several meta-analyses148,149 have concluded that NIV is effective in avoiding intubation (relative risk 0.42 and absolute risk reduction 28%, respectively), reducing mortality (relative risk 0.41 and absolute risk reduction 10%, respectively), and shortening hospital length of stay (by approximately 4 days). A more recent study on a large cohort of more than 25,000 patients with COPD exacerbations requiring mechanical ventilation showed reduced mortality, length of stay, and cost with NIV compared to invasive ventilation.150 On the basis of this evidence, current guidelines,148–155 including the most recent European Respiratory Society/American Thoracic Society guidelines from 2017,156 have recommended that NIV be used in patients with a COPD exacerbation and acute or acute-on-chronic ventilatory failure (pH <7.35) and should be started early in the course of moderate to severe COPD exacerbations. The European Respiratory Society/American Thoracic Society guideline also recommends against NIV use in patients with mild exacerbations (with pH ≥7.35) because of the studies showing lack of efficacy in this setting.146,147

ACUTE RESPIRATORY FAILURE—TYPES 1 AND 2

Acute respiratory failure is defined as the inability of the respiratory system to meet the oxygenation, ventilation, or metabolic requirements of the patient.1 Although the main function of the lungs appears to be related to gas exchange (i.e., oxygenation and ventilation), it should be remembered that the lung is a metabolically active organ as well.1,2 Respiratory failure has been divided into two main types. Type 1 is hypoxemic respiratory failure, and type 2 is hypercapnic with or without hypoxemic respiratory failure.2 More simply stated, type 1 respiratory failure is oxygenation failure and type 2 is ventilatory failure. Operationally, type 1 respiratory failure is defined by a partial pressure of oxygen in arterial blood (Pao2) less than 60 mm Hg and type 2 respiratory failure is defined by a partial pressure of carbon dioxide in arterial blood (Paco2) of greater than 50 mm Hg (Box 38-1). The respiratory failure can be acute or chronic in nature, related to the onset and duration of the failure.2,3 Some patients may present with an acute deterioration or worsening of their chronic respiratory dysfunction.4 This is termed acute-on-chronic respiratory failure.

Acute respiratory failure is commonly encountered in the intensive care unit setting and may be the primary diagnosis necessitating the admission or a complication of the patient's medical condition(s) or their treatment. Remembering that the respiratory failure may be the result of a variety of causes and may not directly involve the lungs or the respiratory muscles is important.2 It has been said the body is like a chain composed of links that represent the brain, peripheral nervous system, upper airway, lower airway, respiratory muscles, cardiovascular system, and lungs (Fig. 38-1).2 Respiratory failure may result when any of the links become sufficiently dysfunctional or weak. Like a chain, the body is only as strong as its weakest link and respiratory failure may result when a component of the chain becomes sufficiently compromised. Common causes of hypoxemic and hypercapnic respiratory failure are listed in Box 38-2. This chapter reviews the basic mechanisms and clinical manifestations of types 1 and 2 respiratory failure and concludes with a more in-depth discussion of acute lung injury and ARDS, which are clinical disorders in the type 1 category.

RECOGNITION AND EARLY INTERVENTIONS

Acute respiratory failure is often preceded by a compensated state in which the patient, through increased effort, is able to maintain adequate gas exchange at the expense of increased work of breathing. Normal values of frequently determined respiratory parameters (Table 13-5) and clinical signs of respiratory failure are listed (Table 13-6). Tachypnea is often the first manifestation of respiratory distress in infants. Increased work of breathing is manifest by chest wall retractions and flaring of the alae nasi. Inspiratory stridor is a sign of obstruction in the upper airway, occurring anywhere from the supraglottic space to the lower trachea. Common causes of stridor in the pediatric population are laryngomalacia, laryngotracheobronchitis (croup), epiglottitis, aspiration of a foreign body, and congenital airway abnormalities, such as vocal cord cysts. Prolonged expiration with wheezing is a sign of lower airway obstruction, most likely at the bronchial or bronchiolar level. Viral bronchiolitis and asthma are two conditions commonly associated with lower airway obstruction. Expiratory grunting is another clinical sign of respiratory failure in infants and children; it is caused by premature epiglottic closure accompanying active chest wall contraction during early expiration. Infants grunt to increase airway pressure, thus trying to preserve or increase functional residual capacity. Cyanosis is a fairly late sign of respiratory failure. It should be noted that since the presence of cyanosis depends on the quantity of desaturated hemoglobin in blood, respiratory failure can exist in the presence of anemia without any sign of cyanosis. Therefore, arterial blood oxygen saturation or tension should be measured whenever a question of serious respiratory impairment exists, even in the absence of cyanosis. It should also be noted that the manifestations of respiratory failure are not always clinically evident and that some of the signs and symptoms discussed earlier, when present, may have a nonrespiratory etiology. For instance, tachypnea without respiratory distress commonly results from an attempt to compensate for metabolic acidosis (e.g., the patient with diabetic ketoacidosis). Thus, clinical assessment of arterial hypoxemia and hypercapnia is not always reliable. The clinician should therefore have a low threshold for measuring arterial blood gases or performing a pulse oximetry study.

The goals in the management of respiratory failure are to anticipate and recognize respiratory problems and to support those functions that are compromised or lost. Although measurement of arterial blood gases and pH is necessary for obtaining precise information about gas exchange in the lung, in an emergency situation, clinical judgment is paramount and the clinician must be able to assess the patient for respiratory compromise and initiate therapeutic measures appropriately. Table 13-7 outlines the American Heart Association's rapid cardiopulmonary assessment, which should be applied to any child with suspected respiratory or circulatory insufficiency. Restoration of airway patency and institution of ventilation are the first steps in resuscitation of the patient with suspected respiratory failure. Initially, the airway should be cleared of secretions or mechanical obstructions, such as foreign materials. A child who shows signs of adequate gas exchange should be allowed to maintain a neutral “sniffing” position. Hyperextension of the neck should be avoided because it may increase upper airway obstruction. Artificial airways may be useful in maintaining upper airway patency in the pediatric patient. An oropharyngeal airway is useful in an unconscious infant or child, but may stimulate retching and vomiting in the conscious child. Nasopharyngeal airways, available commercially in a variety of sizes, are better tolerated by a conscious patient. In the absence of a commercial nasopharyngeal airway, an appropriately sized endotracheal tube (ETT) may be used. A complication of small-diameter nasopharyngeal airways is that they may become obstructed by mucus, vomitus, or the soft tissue of the pharynx.

Once airway patency has been achieved, assisted ventilation may be necessary if adequate air entry and breath sounds are not observed. Assisted ventilation should not be delayed until placement of an ETT is accomplished, because the vast majority of infants and children with respiratory failure can be successfully ventilated and oxygenated with a bag-valve-mask (BVM) device, even in the setting of airway obstruction as a result of conditions such as epiglottitis. Assisted ventilation with a BVM device must be done with caution while chest and abdominal motion is observed carefully because excessive pressure may produce pneumothorax, pneumomediastinum, or gastric distention, with subsequent vomiting. Facemasks are available in a variety of sizes; a proper facemask should provide an airtight seal on the face, enveloping the nose and mouth, but avoiding depression of the eyes. Gastric distention, with a subsequent increase in respiratory embarrassment, can be minimized during assisted ventilation by application of gentle cricoid pressure by an assistant. During assisted BVM ventilation, monitoring of inflation pressure with a manometer is also important to reduce traumatic complications, such as pneumothorax.

A laryngeal mask airway (LMA) may be used when a facemask is difficult to fit or tracheal intubation is difficult. An LMA is made of a silicone rubber tube connected to a miniature mask with an inflatable cuff. The LMA is placed in the larynx and used to lift the epiglottis away, leaving the airway lumen open. Rescue ventilation can be provided to the child with the LMA in place, or the trachea can be intubated through the LMA using a stylet or bronchoscope.

The patient with suspected respiratory failure should be administered high levels of oxygen. Methods of oxygen administration and maximal achievable Fio2 are listed in Table 13-8. The use of a nasal cannula as an oxygen delivery device is unsuitable in emergency situations for children with suspected respiratory failure, because the inspired oxygen concentration cannot be controlled adequately. Many children do not tolerate oxygen facemasks, although some may accept soft pediatric masks. Many times, a child may tolerate a face shield better than a mask. Oxygen concentration up to 40% can be delivered with high flow through the shield. When BVM ventilation is performed in an emergency situation, 100% oxygen should be used to flow through the bag. In addition to oxygen administration, rapid assessment of both respiratory drive and the ability to maintain an open airway is necessary in the child with suspected respiratory failure. As mentioned earlier, if the child is hypoventilating, administering high concentrations of oxygen to correct hypoxemia will mask the development of hypercarbia if the practitioner does not correctly assess inadequate alveolar ventilation or measure arterial Pco2 concentrations.

Endotracheal intubation is indicated in the patient with ARF who has continued severe hypoxemia despite supplemental oxygen administration, who has worsening hypercapnia with acidosis, or who requires airway protection (Table 13-9). By linking the respiratory system directly to a ventilator, therapies such as the use of high oxygen concentrations, hyperventilation, and the delivery of positive end-expiratory pressure (PEEP) can be administered. The equipment required for ETT intubation includes an appropriately sized ETT (and one size larger and one size smaller), a stylet, a laryngoscope with an appropriately sized blade and a functioning light, a resuscitation bag and mask connected to a high-flow oxygen source, and suction. Optimally, the patient should be monitored by pulse oximetry and a cardiorespiratory monitor, and the appropriate staff and equipment should be available in case cardiopulmonary resuscitation is needed. ETT size can be estimated with the use of a Broselow tape or the following formula:

ETTsize(inmillimeters)=(16+ageinyears)/4

Generally, a newborn infant would require an ETT with an internal diameter of 3.0 to 3.5 mm, and a 1-year-old child would need a 4.0-mm ETT. Children younger than 8 years old should, under most circumstances, be intubated with an uncuffed ETT, because their narrow subglottic space usually forms a good seal around an appropriately sized ETT. For placement of the ETT, in the absence of possible traumatic spine injury, the child's head and neck should be placed in a “sniffing” position to allow better visualization of the glottis. Preoxygenation with 100% oxygen should be performed next. At this time, premedications, such as atropine, may be given, and a sedative/amnestic, such as a benzodiazepine, should be given. If desired, and when appropriate, a muscle relaxant, such as succinylcholine (depolarizing muscle relaxant) or pancuronium, vecuronium, or rocuronium (nondepolarizing muscle relaxants), should be administered. After administration of a muscle relaxant, it is necessary to provide complete support of the patient's ventilation by BVM with 100% oxygen. Gentle cricoid pressure should be maintained during this time to prevent gastric distention. After suctioning, the glottis should be visualized and the ETT passed through the vocal cords. Intubation attempts should be limited to 15 to 30 seconds, depending on the patient's level of oxygenation and hemodynamic condition. If unsuccessful, the patient should again be preoxygenated with BVM ventilation before another attempt is made. After successful placement of the ETT, its proper position in the trachea should be assessed by use of a colormetric filter (attached to the ETT at the time of intubation) that shows a change in color from purple to yellow, by listening for equal breath sounds, by obtaining a chest x-ray, or by direct bronchoscopic visualization, if available.

Principles of Management

The most common clinical presentation of all types of acute respiratory failure is acute hypoxia.79 Early identification and appropriate management are critical in limiting adverse outcomes. In the non-intubated patient, evaluation includes a physical examination, a review of recent events, an inspection of any supplemental oxygen equipment, arterial blood analysis, chest radiography, and an electrocardiogram (selectively). Following this, management should be as indicated by the likely diagnosis.

In the intubated patient, the evaluation is more complex. An algorithm for the approach to the hypoxic intubated patient is found in Fig. 39.3.80 In this scenario, hypoxia is defined as a 5% decrease in continuous pulse oximetry (SpO2) or a 10% decrease in mixed venous oximetry (SvO2). After identification of hypoxia, the supplemental oxygen should be enhanced. The patient should be disconnected from the mechanical ventilator and hand ventilated. If there is a cuff leak, the tube should be repaired or replaced. If there is difficulty bagging the patient, an attempt at passing a suction catheter should be made. Inability to do so confirms obstruction. If this cannot be reversed by altering the patient’s head position, checking the tube’s position, or deflating the cuff, the tube should be replaced. If there is no evidence of obstruction, despite bagging difficulty, a tension pneumothorax should be ruled out. Assuming that the patient is hand ventilated easily, the mechanical ventilator and its circuitry should be inspected to exclude a mechanical flaw. Additional workup at this time should include a physical examination, review of recent events, blood gas analysis, a portable anteroposterior chest radiograph, and an electrocardiogram. Further diagnostic studies should be guided by the findings in the algorithm of Fig. 39.3.

DEFINITIONS

ARF is defined by arterial blood gas analysis. In a patient without underlying lung disease, ARF is defined by a arterial oxygen tension (Pao2) of less than 50 mm Hg (breathing fraction of inspired oxygen [Fio2] 0.21 at sea level).2 In a patient with COPD, it is difficult to define ARF by arterial blood gas analysis without knowledge of baseline arterial blood gas levels. Clinical data, such as worsening of daily baseline symptoms, cough, tachypnea, and deterioration of mental status, also must be considered. A decrease in Pao2 from baseline and an increase in arterial carbon dioxide tension (Paco2) with acidemia is a common presentation of ARF in COPD.

Respiratory

Acute respiratory failure (ARF) was reported in a 38-year-old Japanese female with newly diagnosed DM. The patient developed ARF one day after administration of vildagliptin 100 mg daily. The patient was admitted in a comatose state after several hours of dyspnea and hyperpnea. The patient was diagnosed with acute kidney failure and diabetic ketoacidosis (DKA) and received insulin and intravenous saline. Non-segmental ground-glass opacities in the lower lobes of both lungs were seen on chest computed tomography (CT), which was initially treated with empiric antibiotic therapy and oxygen. Pulmonary problems resolved within weeks. The patient fully recovered after discontinuation of vildagliptin. Of note, due to the development of DKA and insulin-deficient hyperglycemia, the patient met the diagnostic criteria for acute-onset T1DM [12A].