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Section 10. Pulmonary Disorders
Chapter 79. Respiratory Failure
Topic:    Respiratory Failure

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Respiratory Failure

Impairment of gas exchange between ambient air and circulating blood, occurring in intrapulmonary gas exchange or in the movement of gases in and out of the lungs.

Respiratory failure can be defined with numeric constants, such as a partial pressure of oxygen (Pao2) < 60 mm Hg (hypoxemia) or a partial pressure of carbon dioxide (Paco2) > 45 mm Hg (hypercapnia). However, many patients function quite well with hypoxemia and chronic hypercapnia. Therefore, understanding and treating the continuum of the causative disease and the limited reserves and endurance of a patient are usually more valuable than relying on specific laboratory test values.

Etiology and Pathophysiology

The respiratory system can fail to eliminate CO2 (ventilatory failure), to bring in O2 (hypoxemia), or to defend the lung against damage and disease. It is rare for only one aspect to fail.

Ventilatory failure: Normal changes of aging, including decreased elastic recoil of the lung, loss of some of the supporting structure around the airways, stiffening of the rib cage, and decreased muscle mass, can predispose the elderly to ventilatory failure.

Ventilatory failure is synonymous with an inappropriate elevation in Paco2; the absolute level is less important. For example, a patient with a previous Paco2 of 30 mm Hg because of compensation for metabolic acidosis may be in respiratory failure when the Paco2 rises to 39 mm Hg because of respiratory muscle fatigue.

The most common cause of ventilatory failure in the elderly is probably the increased work of breathing associated with chronic obstructive pulmonary disease (COPD). Recognizing impending ventilatory respiratory failure can be difficult in such patients. A history of labile bronchospasm or of gradual worsening of symptoms (suggesting that the patient's pulmonary reserve is depleted), inherent in COPD, puts these patients at high risk of respiratory failure.

Other common causes of ventilatory failure include decreased respiratory muscle strength and impairment of the central drive to breathe, which can be caused by drug toxicity. Increased CO2 production as a result of fever or agitation or changes in metabolism based on dietary intake can induce respiratory failure in a patient with concomitant respiratory disease and limited pulmonary reserve.

Hypoxemia: Hypoxemia (decreased oxygen content of the arterial blood) may lead to hypoxia (decreased oxygen at the tissue level). The predicted Po2 for age can be estimated by subtracting one third of the patient's age from 105. Forms of hypoxia include hypoxemic hypoxia (reduced arterial oxygen content), anemic hypoxia (low Hb, which reduces oxygen-carrying capacity), circulatory hypoxia (inadequate cardiac output, leading to inadequate oxygenation of the tissues), and cytotoxic hypoxia (interference with intracellular oxygen transport, which can be caused by a poison such as cyanide). The most common cause of hypoxemia is ventilation/perfusion (V(dot)/Q(dot)) mismatch. Other causes include a decrease in the inspired oxygen concentration (as occurs at high altitude) and hypoventilation.

A common cause of hypoxic respiratory failure is capillary leak pulmonary edema as a result of adult respiratory distress syndrome (ARDS). ARDS represents a common pathway of lung injury, the cause of which may include aspiration of gastric contents, sepsis, hypotension, shock, and inhalation of toxic gas. Pulmonary edema is caused by a leaking at the alveolar capillary interface so that high-protein fluid moves from the vascular space into the interstitium and alveoli. Unlike cardiac edema, the mechanism is not hydrostatic pressure. Rather, it is a diffuse inflammatory process, a potent cause of shunt and refractory hypoxemia. In addition, the lung becomes stiff, and lung compliance decreases.

Inadequate lung defense: In elderly patients, the defense functions of the airway are altered, so that pneumonia is more common and often more serious than in younger patients. Pneumonia can lead to ventilatory or hypoxemic respiratory failure.

Diagnosis

Ventilatory failure is confirmed by the inability to eliminate CO2, resulting in elevation of Paco2. A pulsus paradoxicus (a greater-than-normal decrease in systolic blood pressure with inspiration) suggests that the work of breathing is increased. Measurement of peak flow can be helpful in difficult cases and in patients who minimize their symptoms. The response of flow rate to bronchodilator therapy is very important: peak flow that remains < 70% of predicted after bronchodilator therapy indicates serious disease that necessitates inpatient care; a flow rate remaining < 50% of predicted indicates critical disease that requires observation in an intensive care unit.

Hypoxemic respiratory failure may be difficult to diagnose in the elderly. Heart rate during hypoxemia may not increase because of blunted autonomic drive. Cyanosis may occur late in patients with anemia (because at least 5 g of unsaturated Hb is needed), although cyanosis may occur early in patients with chronic lung disease and polycythemia.

Arterial blood gases can help determine the severity of the process but not the cause. Patients in acute distress should not have their supplemental oxygen removed to obtain a room air blood gas for a baseline Paco2 measurement or because of concern about possible CO2 retention. Pulse oximeters, although useful, may give inaccurate readings in patients with poor perfusion. Heavy smokers or patients exposed to exogenous carbon monoxide may register falsely elevated Pao2 levels.

Chest x-rays and ECGs can identify causes of dyspnea, such as flash pulmonary edema or an unsuspected pneumothorax. ARDS often manifests as tachypnea and diffuse whitening of the lungs (due to increased lung water). It usually begins diffusely, although areas with prior emphysematous change are sometimes spared.

When inadequate lung defenses produce respiratory failure, pneumonia is almost always present. It can usually be diagnosed on the basis of typical symptoms and laboratory findings.

Treatment

Ventilatory failure: The usual therapy is assisted ventilation; other therapy is directed at the underlying problem that increases the work of breathing.

A nasal bilevel continuous positive airway pressure (BiPAP) mask (in which gas flow is delivered at a higher pressure during inspiration than during expiration) allows noninvasive ventilation. This method can temporarily assume some of the work of breathing while treatment is directed at the underlying disease. BiPAP is difficult to maintain with a patient who is uncooperative or whose mental status is altered. The patient must be closely monitored for persistent elevation of Paco2 or failure to tolerate the mask or pressure. Some patients need assisted ventilation at night only. Temporary ventilation with heliox, a mixture of helium (80%) and oxygen (20%), may increase mid-vital capacity flow rates by as much as 50%, substantially reducing the work of breathing.

More severe respiratory failure may require acute intervention with airway adjuncts, such as bag-and-mask ventilation. Ventilation with a bag may be easier when dentures are left in place, allowing a tighter seal. However, mechanical ventilation is usually started as quickly as possible using intubation. Special care must be taken to avoid unnecessary neck extension and damage to the jaw and teeth during efforts to place an endotracheal tube.

Hypoxemia: The primary goal is to restore proper delivery of oxygen to the tissues. The lowest concentration of oxygen that prevents hypoxia should be used. Oxygen concentrations > 60% can cause alveolar injury within 48 to 72 hours (through the generation of free oxygen radicals) and within 12 hours at 100% inspired oxygen fraction (Fio2). A 100% Fio2 can produce absorptive atelectasis, which can be avoided by using <= 90% Fio2. Bronchociliary function is impaired at oxygen concentrations as low as 30%.

Treatment with oxygen may require the use of a high-flow device (eg, ventimask), which provides a blended oxygen concentration, or a low-flow device (eg, nasal cannula) set at a particular flow rate (L/minute). High-flow devices provide more consistently delivered Fio2, but low-flow devices may be more comfortable. A close-fitting mask equipped with a reservoir bag and nonrebreathing valves over exhalation ports in the mask body provide the highest Fio2 (about 90%) without requiring intubation. Nebulizer masks with 100% oxygen delivered through a nebulizer bottle with water can provide the same high Fio2 with humidity, which can increase patient comfort.

The specific therapy for ARDS depends on the underlying cause. In most cases, therapies are mainly supportive, maintaining oxygen delivery to the tissues until the inflammatory process resolves, the capillary leak is reversed, and the alveolar fluid is cleared. Corticosteroids are not useful in the treatment of acute ARDS.

Inadequate lung defense: Therapy is directed at the underlying disorder and any subsequent infection. Defense may be further impaired by the presence of an endotracheal tube, which bypasses a number of respiratory defenses and eliminates the possibility of glottic closure and the initiation of an effective cough.

Intubation

Intubation should be considered early in the course of a respiratory illness, because if delayed, it may need to be performed as an emergency procedure. Oral endotracheal tubes generally allow better suctioning and produce less resistance but may be occluded by a patient who is biting or may be moved by the patient's tongue, resulting in malposition or additional trauma to the trachea. In addition, endotracheal tubes are often more difficult to secure in edentulous patients.

Intubation of some patients, particularly those in marked distress, is often followed by hypotension. This complication may be due to the loss of sympathetic tone when the work of breathing is quickly reduced, to sedative use, to alkalosis due to overventilation, or to increased positive intrathoracic pressures leading to diminished venous return and lower cardiac output. Elderly patients who are hypovolemic as a result of an underlying disease are particularly at risk of hypotension and its sequelae.

The endotracheal tube reduces the normal protective mechanisms that defend the airway from aspiration and colonization with bacteria. About 20% of patients with endotracheal tubes aspirate; elderly patients aspirate at a rate that may be as high as 70%. Other complications of prolonged endotracheal intubation include pressure necrosis on the tracheal mucosa from overinflated cuffs or from movement of cuffs with movement of the tube. The cuff pressure should not exceed 25 mm Hg because blood flow to the mucosa is decreased and necrosis may occur. The "minimal leak" approach, in which the cuff is inflated until there is no leak and then very slowly deflated, usually maintains pressure within the safe limit, but direct measurement of pressures in the cuff provides greater assurance.

When prolonged intubation (> 2 weeks) is necessary, a tracheostomy should be considered. Many patients feel more comfortable with a tracheostomy.

Mechanical Ventilation

Initially, most patients are best treated by a mode of mechanical ventilation that completely assumes the work of breathing and minimizes the patient's efforts. Minimizing airway pressure and providing the most uniform ventilation possible is an important goal, especially when stiff lungs limit maximum volume.

Most ventilators are volume-cycled: they provide inspiratory flow until a set volume is delivered. The frequency of breaths and the inspiratory flow are also programmed, leaving the inspiratory/expiratory ratio and the pressure in the airways as the resulting dependent variables. A ventilator in control mode delivers its set volume at a specific frequency and will not respond to the patient's efforts to take more frequent breaths. In assist-control mode, the ventilator provides a preset number of breaths at a given volume per minute, but in between these breaths, the patient can trigger the ventilator by making an inspiratory effort; the ventilator then resets its clock to wait for the next appropriate interval until another breath is given. A ventilator in pressure-support mode provides specific airway pressure during inspiration only. Pressure may be set high to do most or all of the inspiratory work of breathing or low to provide partial support. Pressure-support mode may be helpful during weaning efforts and when patients need only a minimal level of support and have an adequate respiratory drive.

Ventilator settings: Tidal volumes between 5 and 8 mL/kg and respiratory rates around 20 breaths/minute are usually recommended. Positive end-expiratory pressure (PEEP) allows airway pressure during expiration to remain at a small positive value; PEEP recruits and stabilizes damaged alveoli (as in ARDS), brings them to larger volume, and helps prevent complete alveolar collapse. However, PEEP increases the risk of barotrauma, diminishes venous return, may increase intracranial pressure, and may increase fluid retention through changes in antidiuretic hormone and atrial natriuretic factor.

Pharmacotherapy: Many patients placed on mechanical ventilation require sedation to be comfortable. Opioids decrease breathlessness but may cause hypotension and ileus. Benzodiazepines are effective and are commonly used. Patients must always receive adequate sedation when receiving neuromuscular blockade, which may be needed when patients have difficulty matching their respiratory pattern to the ventilator. Neuromuscular blockade may reduce airway pressures and risk of barotrauma.

Nutrition: Adequate nutrition during assisted ventilation is very important. Elderly patients with nutritional problems may have less muscle mass, especially the fast twitch fibers that may be related to inspiratory work. Nutritional deficiency may worsen host defenses. However, because carbohydrates produce more CO2 per calorie than fat, feedings with large proportions of carbohydrates require greater ventilation.

Complications: Complications from mechanical ventilation are often abrupt and dramatic. Problems include inadvertent disconnection of the patient from the ventilator; barotrauma-related events, such as pneumothorax or pneumomediastinum; and ventilator malfunction. When adequate ventilation is in doubt, the patient should be removed from the ventilator and immediately supported with bag ventilation at 100% O2. If bag ventilation is not successful and the examination does not suggest a pneumothorax, a quick attempt at endotracheal tube suctioning can be made to determine whether a large mucous plug is the problem. Larger mucous plugs that cannot be removed effectively by positioning or unguided suctioning may require bronchoscopy.

Weaning: The underlying disease that caused the respiratory failure should be under control, hemodynamics should be stable, mental status and neurologic function should be good, secretions should be minimal, nutritional support should be adequate, and sedating drugs should be stopped.

Determinants of a patient's readiness to be weaned from a ventilator include a negative inspiratory pressure more negative than 120, tidal volumes > 5 to 10 mL, vital capacities twice the associated tidal volume, and minute volumes < 10 L/minute. The patient should also be on minimal PEEP (5 cm) and on <= 50% Fio2. However, about one third of patients who meet these criteria cannot be weaned successfully. A "rapid-shallow" breathing index (calculated by dividing the respiratory rate by the tidal volume in liters) < 105 may predict successful weaning.

The patient should be well rested and positioned for maximal chest bellows effectiveness (eg, sitting partially upright). Weaning techniques include spontaneous breathing through a T-piece, synchronized intermittent mandatory ventilation with reduced machine-assisted breaths, and pressure support. Spontaneous breathing while intubated can be permitted by providing continuous gas flow through large-bore tubing and attaching the tubing to the end of the patient's endotracheal tube (T-piece ventilation). When performed with a ventilator, this spontaneous breathing is called CPAP (continuous positive airway pressure). A patient breathing spontaneously when the ventilator is set not to deliver any additional pressure other than what the patient generates is on a CPAP of zero.

Patients who do not wean successfully may be considered for transfer to a long-term care facility that accepts ventilated patients.

End-of-Life Issues

Some patients choose not to spend their last days in the hospital and prefer to die at home or in a nursing home. Supportive care can be arranged in both settings. Hospice care is an option in either setting. Families and caregivers should be taught how to treat worsening distress and what to do when death comes.

When a patient has made a decision to have mechanical ventilation withdrawn, the physician should ensure the patient's comfort during this process. Comfort measures may include the use of drugs to relieve pain or dyspnea, even though such use may hasten death.

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