Tintinalli's Emergency Medicine - Just the Facts, 3ed.


Joshua T. Hargraves



images Dyspnea is a subjective feeling of difficult, labored, or uncomfortable breathing. It is a complex sensation, without a defined neural pathway.

images Mechanical factors include a sense of skeletal muscle effort dependent on work of breathing and intraparen-chymal stretch receptors.

images Chemoreceptors in the central medulla and carotid body respond to changes in CO2 and O2, respectively. Receptors in the atria and pulmonary arteries contribute, but in a poorly defined manner.

images Central and peripheral receptors send afferent neurons to the central nervous system (CNS), where the information is integrated in a complex manner.


images Patients may present with complaints of shortness of breath, air hunger, or dyspnea on exertion.

images Signs include tachypnea, tachycardia, difficulty speaking, use of accessory respiratory muscles, and/or stridor.

images The complaint of dyspnea must be rapidly evaluated with immediate identification of abnormal vital signs and abnormalities in the primary survey (airway, breathing, and circulation). Airway obstruction, poor respiratory effort, and altered mental status mandate immediate intervention.


images A detailed history and physical examination will often lead to an accurate diagnosis of dyspnea.

images Pulse oximetry provides an immediate assessment of oxygenation, but has poor sensitivity.

images Arterial blood gas analysis (ABG) is invasive, but has improved sensitivity over pulse oximetry. ABG results must be interpreted with consideration of the patient’s work of breathing.

images Chest radiograph (CXR), electrocardiogram (EKG), peak expiratory flows, and hematocrit may prove helpful.

images Elevated D-dimer and B-natriuretic peptide (BNP) may lead to specific diagnoses.

images Other ancillary tests, not usually available in the ED, include spirometry, cardiac and exercise stress testing, echocardiography, ventilation-perfusion scans, and lung biopsies.

images Table 31-1 lists a focused differential diagnosis of dyspnea.

TABLE 31-1 Differential Diagnosis of Consequence: Dyspnea



images Immediate priorities include maintaining the airway and supporting respiratory function. Supplemental oxygen is given to anyone in respiratory distress. Patients with chronic obstructive pulmonary disease (COPD) may tolerate lower Pao2 levels and must be treated symptomatically.

images Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and biphasic positive airway pressure (BiPAP) ventilation may be initiated.

images Bag-valve-mask ventilation followed by endotracheal intubation with mechanical ventilation can be used for critically ill patients, and allows for long-term support.

images Definitive treatment depends on the etiology.

images All patients with an unclear cause of their dyspnea and hypoxia require admission to a monitored bed. Admission otherwise depends on the exact cause of dyspnea.



images Hypoxia, the inadequate delivery of oxygen to the tissues, is arbitrarily defined as a Pao2 <60 mm Hg. Hypoxia is caused by one of five mechanisms:

images Hypoventilation: Rising Paco2 displaces O2 from the alveoli, decreasing the diffusion gradient across the pulmonary membrane.

images Right-to-left shunt: Unoxygenated blood enters the systemic circulation; this occurs with congenital heart abnormalities or perfusion of unoxygenated lung segments.

images Ventilation-perfusion mismatch: From abnormalities of ventilation or perfusion.

images Diffusion impairment: Caused by abnormalities of the alveolar-blood barrier.

images Low inspired O2: Only a factor at high altitudes.


images Signs and symptoms are nonspecific, ranging from tachycardia and tachypnea to CNS manifestations such as lethargy, seizures, and coma.

images At a Pao2 <20 mm Hg, there is a paradoxical depression of the respiratory drive.

images Dyspnea does not always occur with hypoxia, and cyanosis is a poor indicator of oxygenation.


images Pulse oximetry is quick and frequently useful, but direct ABG analysis of arterial oxygen levels defines the diagnosis.

images Tests used to determine the cause of dyspnea are also useful to elucidate the cause of hypoxia.


images Support, identify, and aggressively treat hypoxia, and try to maintain a Pao2 >60 mm Hg. Lower Pao2 levels may be tolerated in COPD.

images All patients require hospitalization in a monitored bed, until the underlying process is stabilized and/or a definitive diagnosis made.

images Frequent ABGs may require an arterial line for patient comfort and reduction of complications of multiple arterial punctures.



images Hypercapnia, defined as a Paco2 >45 mm Hg, is caused by a decrease in minute ventilation. Minute ventilation is dependent on respiratory rate and tidal volume; changes in either may lead to hypoventilation and hypercapnia.

images Hypercapnia is almost never due to increased CO2 production.

images Alveolar ventilation per minute is calculated as [respiratory rate] × [tidal volume minus the dead space volume]. Alveolar minute ventilation is an accurate ventilatory measure, but its calculation is impractical in the ED.

images Minute ventilation is controlled via a neural chem-oreceptor in the medulla. Efferent outputs control the respiratory rate and tidal volume.


images Signs and symptoms of hypercapnia depend on Paco2’s absolute value and its rate of increase.

images Acute elevations of Paco2 cause an increase in intracra-nial pressure, leading to confusion, lethargy, seizures, and coma. Asterixis may be found on physical examination.

images Acute elevations in Paco2 >100 mm Hg may lead to cardiovascular collapse.

images In acute hypercapnia, for every 10-mm Hg increase in CO2, the pH will decrease 0.1 unit.

images In chronic hypercapnia, patients may tolerate high levels of CO2. For every 10-mm Hg increase in CO2, the [HCO3-] increases 0.35 mEq/L (see Chap. 6).


images The diagnosis is made by clinical suspicion and confirmed on ABG analysis. Pulse oximetry plays no role in the identification of hypercapnia. Table 31-2 lists a focused differential diagnosis of hypercapnia.

TABLE 31-2 Differential Diagnosis of Consequence: Hypercapnia



images Aggressively support, treat, and identify causes of hypercapnia.

images Early identification of the etiology may make treatment options easier. For example, a patient with respiratory depression, pinpoint pupils, and altered mental status may have a heroin overdose that will respond to naloxone, while a patient with amyotrophic lateral sclerosis may require early assisted ventilation.

images Oxygen should be given to every patient with respiratory distress and not withheld over concern for decreasing the respiratory drive. Hypoxia will kill a patient, while only extreme hypercapnia will do the same.

images BiPAP or CPAP may be used to increase tidal volume and thus increase minute ventilation. However, if there is profound hypoxia or inability to control the airway, endotracheal intubation and mechanical ventilation may be required.

images Disposition depends on the underlying cause and frequently requires admission to a monitored bed or intensive care setting.



images Cyanosis is a bluish color of the skin and mucous membranes resulting from an increased level of deoxyhemoglobin.

images The level of deoxyhemoglobin necessary for development of cyanosis is variable, but is in the range of 5 grams/mL.

images Lighting and temperature affect the ability to detect cyanosis.

images Other factors that affect the ability to identify cyanosis include skin thickness, pigmentation, and microcirculation.


images The presence of cyanosis usually indicates hypoxia, but this is not always the case.

images The tongue is very sensitive for identifying cyanosis. The earlobes, nail beds, and conjunctiva are less reliable.

images Cyanosis may be central or peripheral. Central cyanosis is usually the result of deoxyhemoglobin. Peripheral cyanosis is the result of poor peripheral circulation, leading to increased oxygen extraction by the peripheral tissues.


images The presence of cyanosis must be taken in the context of the clinical situation (see Table 31-3).

images ABG analysis will confirm the presence of hypoxia as a cause of cyanosis.

images Other useful tests include a hematocrit to detect anemia or polycythemia vera, a CXR, and an EKG.

images Pseudocyanosis should be considered in any asymptomatic patient, but it should be a diagnosis of exclusion. Pseudocyanosis is caused by abnormal skin pigmentation, giving the skin a bluish or silver hue. Causative agents include heavy metals (iron, gold, lead, and silver) and certain drugs (phenothiazines, minocycline, amiodarone, and chloroquine).

images Methemoglobinemia, carboxyhemoglobin, and other acquired hemoglobinopathies, although rare, must be considered in certain clinical situations. Methemoglobinemia will turn blood a chocolate brown that will not normalize to red upon exposure to air Carboxyhemoglobin will cause an atypical cherry-pink cyanosis. It is important to identify these acquired hemoglobinopathies because they can be quickly and easily treated.

TABLE 31-3 Differential Diagnosis of Consequence: Cyanosis



images Aggressive support, treatment, and identification of cyanosis are always indicated. Supplemental oxygen is an appropriate first-line treatment. If the patient is unresponsive to supplemental oxygen, poor perfusion, acquired hemoglobinopathies, or large right-to-left shunts may be present.

images Specific antidotes for acquired hemoglobinopathies include methylene blue (1–2 milligrams/kg IV) for methemoglobinemia, and supplemental oxygen (possibly including hyperbaric therapy) for carboxyhemoglobin poisoning.

images All patients with an unknown cause of cyanosis require admission until the condition is stabilized and/or definitively identified.



images Pleural effusions result from the collection of fluid between the visceral and parietal pleura.

images Effusions are categorized as exudates or transudates.

images Exudative effusions have increased protein content and typically result from increased fluid production due to inflammatory process or neoplasm.

images Transudative effusions are due to imbalance in hydrostatic pressure and have low protein content.


images Effusions may be clinically silent or may cause dyspnea as fluid accumulates.

images Physical findings include percussion dullness and decreased breath sounds.


images Approximately 150 to 200 mL of pleural fluid are required to identify an effusion on upright CXR (see Fig. 31-1).

images A listing of the differential diagnosis of pleural effusion is listed in Table 31-4.

images Significant pleural effusions will be large enough to produce a >10-mm strip on a lateral decubitus CXR, or on thoracic ultrasound.

images Diagnostic thoracentesis can be performed on patients without an obvious cause of effusion.

images An effusion is considered an exudate if it has one or more of the following criteria:

image Pleural fluid/serum protein ratio >0.5 and/or

image Pleural fluid/serum LDH ratio >0.6 and/or

image Pleural fluid LDH > two-thirds of the upper limit of serum LDH


FIG. 31-1. A. This is a supine radiograph showing a right-sided pleural effusion. The right lung field is hazy compared to the left, and a small layer of fluid is noted inferiorly. B. CT scan of the patient in (A). A moderate pleural effusion is noted in the right lung field, and a small effusion not seen in the left lung field of the plain film is noted on the CT scan.

TABLE 31-4 Differential Diagnosis of Consequence: pleural effusion



images A therapeutic thoracentesis with drainage of 1.0 to 1.5 L is indicated if a patient has dyspnea at rest.

images Drainage of larger volumes has been associated with reexpansion pulmonary edema and should be avoided.

images Treatment of effusions varies widely. Empyema requires a large-bore thoracostomy tube, while treatment of parapneumonic effusions is controversial.

For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 65, “Respiratory Distress,” by John Sarko and J. Stephan Stapczynski.