Chapter 29. Respiratory Distress

Causes of respiratory distress are multifactorial and include the findings of dyspnea, hypoxia, hypercapnia, and cyanosis. Despite the increasing reliance on ancillary studies and technology, the evaluation of respiratory distress depends on a careful history and physical examination.

Dyspnea is the subjective feeling of difficult, labored, or uncomfortable breathing. There is no single pathophysiologic mechanism that causes dyspnea. However, most patients with dyspnea have a cardiac or a pulmonary cause.

Clinical Features

The initial assessment of any patient with dyspnea should be directed toward identifying respiratory failure. Dyspnea is a subjective complaint difficult to quantify. Vital signs (including pulse oximetry) and general impression will identify those in significant distress. Tachycardia, tachypnea, stridor, and the use of accessory respiratory muscles point to significant respiratory distress. Other significant signs include lethargy, agitation, altered mental status, and inability to speak due to breathlessness. In patients with any of these signs or symptoms, oxygen should be administered immediately. When there is no improvement, the need for aggressive airway management and mechanical ventilation should be anticipated. Lack of these significant signs and symptoms indicates a lesser degree of distress, thereby allowing for a detailed history and physical examination that often may help identify the etiology of dyspnea.

Diagnosis and Differential

The history and physical examination should be the primary aids in identifying the etiology of dyspnea. However, ancillary testing may aid in determining the severity and specific cause (Table 29-1). Overall clinical gestalt is important, as are specific findings of an S3 gallop and jugular venous distention. Pulse oximetry is a rapid but insensitive screen for disorders of gas exchange. Arterial blood gas (ABG) analysis has improved sensitivity but does not take into account work of breathing. ABG analysis may also demonstrate a metabolic acidosis, which can be a common cause of hyperpnea. A chest radiograph may identify pulmonary and cardiac causes of dyspnea. In addition, an abnormal electrocardiogram or elevated cardiac enzymes may point toward a cardiac cause of dyspnea. A peak expiratory flow rate may indicate reactive airway disease. Additional laboratory tests that may prove helpful include a complete blood count, B-type natriuretic peptide, and D-dimer assay. Uncommonly, the cause of dyspnea may not be identified. Specialized testing that may be indicated include computed tomography of the chest, echocardiography, pulmonary function testing, cardiac stress testing, nuclear medicine scans, or combined cardiopulmonary exercise testing.

Emergency Department Care and Disposition

Just as there is no single cause of dyspnea, there is no single treatment. The following are general treatment guidelines for dyspnea.

1. Patients identified as having impending respiratory failure will need aggressive airway management and mechanical ventilation. Noninvasive ventilation techniques, such as continuous positive airway pressure and biphasic positive airway pressure, should be considered.

2. The goal of therapy is to maintain the Pao2 above 60 mm Hg or the oxygen saturation above 90%. Lower goals are appropriate in those with long-standing lung disease such as chronic obstructive pulmonary disease (COPD).

3. After oxygenation has been insured, disorder-specific treatment and evaluation can be pursued.

4. The disposition of patients with dyspnea depends on its etiology. Any patient with hypoxia and an unclear cause of dyspnea requires hospital admission.

Hypoxia is the inadequate delivery of oxygen to the tissues. Oxygen delivery is a function of cardiac output, hemoglobin concentration, and oxygen saturation. Hypoxemia is arbitrarily defined as a Pao2 below 60 mm Hg, where oxygen saturation and blood oxygen content drop quickly. Hypoxemia results from a combination of five distinct mechanisms: (a) hypoventilation hypoxia in which lack of ventilation increases Paco2, thereby displacing oxygen from the alveolus and lowering the amount delivered to the alveolar capillaries; (b) right-to-left shunt in which blood bypasses the lungs, thereby increasing the amount of unoxygenated blood entering the systemic circulation; (c) ventilation/perfusion mismatch in which areas of the lung are perfused but not ventilated; (d) diffusion impairment in which alveolar-blood barrier abnormality causes impairment of oxygenation; and (e) low inspired oxygen, such as occurs at high altitude.

Clinical Features

Signs and symptoms of hypoxemia are nonspecific. Acute physiologic responses to hypoxemia include pulmonary arterial vasoconstriction and increases in minute ventilation and sympathetic tone manifesting as tachypnea, tachycardia, and an initial hyperdynamic cardiac state. The predominant features can be neurologic, and may include headache, somnolence, lethargy, anxiety, agitation, coma, or seizures. Chronic hypoxemia may result in polycythemia, digital clubbing, cor pulmonale, and changes in body habitus (eg, the “pink puffer” or “blue bloater” presentations of COPD). Cyanosis may be present but is not a sensitive or specific indicator of hypoxemia.

Diagnosis and Differential

The diagnosis of hypoxemia requires clinical suspicion and objective measurement. Formal diagnosis requires ABG analysis, but pulse oximetry may be useful for gross abnormalities or trends. As is the case with dyspnea, the etiology of hypoxemia can be multifactorial. Determination of the exact cause is facilitated by thorough, careful history and physical examination. Hypoxemia may be quantified, and clues to its etiology may be obtained, by calculation of the Alveolar-arterial oxygen gradient (“A-a gradient,” where the capital “A” represents alveolar oxygen tension and “a” indicates arterial oxygen level). The formula for calculating A-a gradient while breathing room air at sea level is:

The A-a gradient is increased in cases of right-to-left shunts, ventilation-perfusion mismatch, and diffusion impairment. The normal value for a 20 year old nonsmoker is 5 to 10; the upper limit of normal increases by 1 for each decade of life.

Emergency Department Care and Disposition

Regardless of the specific cause of hypoxemia, the initial approach remains the same. The following are general treatment guidelines for hypoxia:

1. Supplemental oxygen is administered to achieve an O2 saturation greater than 90%.

2. The airway is managed aggressively as needed (see Chapter 1).

3. Cause-specific treatment and evaluation should be pursued.

4. All patients with new hypoxemia should be admitted and monitored until their condition is stabilized.

Hypercapnia is arbitrarily defined as a Paco2 above 45 mm Hg and is exclusively due to alveolar hypoventilation. Factors that affect alveolar ventilation include respiratory rate, tidal volume, and dead space volume. Alveolar ventilation is tightly controlled by the body to maintain Paco2 in a narrow range. Hypercapnia is almost never caused by increased co2 production.

Clinical Features

The signs and symptoms of hypercapnia depend on Paco2's absolute value and rate of change. Acute elevations result in increased intracranial pressure, prompting patient complaints of headache, confusion, and lethargy. Coma, encephalopathy, and seizures may be present in cases in which the Paco2 acutely rises above 80 mm Hg; similar Paco2 levels may be well tolerated if elevations are chronic.

Diagnosis and Differential

The diagnosis requires clinical suspicion and ABG analysis, pulse oximetry may be completely normal. In acute cases, the ABG will demonstrate an elevation in Paco2 with a respiratory acidosis and minimal metabolic compensation. Common causes of hypercapnia include COPD, respiratory center depression from drugs (eg, opiates, sedatives, anesthetics), neuromuscular impairment from disease (Guillain-Barré syndrome) or toxin (botulism), and finally thoracic cage disorders (morbid obesity, kyphoscoliosis).

Emergency Department Care and Disposition

Treatment of acute hypercapnia requires aggressive measures to increase minute ventilation. The following are general treatment guidelines for hypercapnia:

1. Airway maintenance is crucial and mechanical ventilation may be indicated (see Chapter 1).

2. A trial of biphasic positive airway pressure or continuous positive airway pressure may prove helpful and improve minute ventilation. In some cases treatment should include condition-specific therapies such as bronchodialators for COPD, or reversal agents for opiate overdose.

3. Disposition depends on etiology, but many patients with hypercapnia require hospital admission and monitoring.

Cyanosis is a bluish color of the skin or mucous membranes, resulting from an increased amount of deoxyhemoglobin. The detection of cyanosis is highly subjective and not a sensitive indicator of arterial oxygenation. Traditional teaching purports that cyanosis develops when the deoxyhemoglobin level exceeds 5 milligrams/dL, but this is greatly variable.

Clinical Features

The presence of cyanosis suggests tissue hypoxia. The presence of cyanosis with a normal Pao2 suggests an abnormal hemoglobin such as methemoglobin. Cyanosis is divided into central and peripheral. Central cyanosis, which is most reliably observed under the tongue or on the buccal mucosa, is due to inadequate pulmonary oxygenation or abnormal hemoglobins. Peripheral cyanosis is cyanosis of the distal extremities due to diminished peripheral blood flow.

Diagnosis and Differential

The causes of cyanosis may be multifactorial (Table 29-2). In some cases, diagnosis is confounded by coexistence of central and peripheral cyanosis. Pulse oximetry is easily available for continuous monitoring, but it may overestimate oxygen saturation when there is dyshemoglobinemia. ABG analysis with cooximetry is the gold standard for diagnosis of cyanosis, since ABG alone may be misleading in the presence of abnormal hemoglobin. Methemoglobinemia and carboxyhemoglobinemia may cause cyanosis with a normal Pao2. Methemoglobinemia is associated with blood that has been described as chocolate brown, and which does not change color with exposure to room air. Classically, carboxyhemoglobin produces a cherry-red mucous membrane discoloration. A hematocrit may demonstrate polycythemia vera or severe anemia, both of which may contribute to cyanosis.

Emergency Department Care and Disposition

Patients with cyanosis require aggressive treatment and rapid identification of the underlying etiology. The following are general treatment guidelines for cyanosis:

1. Patients should be started on supplemental oxygen to achieve an oxygen saturation greater than 90%. Those with central cyanosis should improve rapidly. If there is no improvement, suspect impaired cardiac circulation, abnormal hemoglobin or pseudocyanosis.

2. Peripheral cyanosis should respond to therapy directed at the specific condition causing the cyanosis.