A. Introduction. Dyspnea is defined as a subjective experience of breathing discomfort. Because dyspnea can only be perceived by the patient’s experience, adequate assessment by the clinician relies on the patient’s self-report. Acute dyspnea—breathing discomfort occurring within hours to days—is a common cause of emergency department visits and hospital admissions and may be a sign of cardiorespiratory decompensation among hospitalized patients.
B. Causes of Acute Dyspnea. Dyspnea is the cardinal symptom in a variety of disorders, many of which can be immediately life-threatening (Table 14.1).
Table 14.1 Common Causes of Acute Dyspnea
Myocardial ischemia or infarction
Upper airway obstruction
Acute respiratory distress syndrome
i. Pneumothorax is a sudden event caused by accumulation of air in the pleural space. It is often accompanied by very acute dyspnea and pleuritic chest pain. The diagnosis should be considered carefully in patients with significant bullous lung disease or recent chest wall trauma, patients presenting with pain or hypoxemia after forceful coughing, and those on a mechanical ventilator.
ii. Pulmonary embolism is a difficult clinical diagnosis because of the poor sensitivity and specificity of the history and physical examination. Consider the diagnosis early because specialized testing is required (see Chapter 23).
iii. Airflow limitation should be suspected in patients with known obstructive lung disease, such as chronic obstructive pulmonary disease (COPD) or asthma (see Chapter 19). Airflow limitation leads to hyperinflation and air trapping in the lungs. Increased activation of pulmonary stretch receptors is perceived as dyspnea. Wheezing is the hallmark physical finding of airflow limitation.
iv. Aspiration should be suspected in patients with swallowing dysfunction, alcohol abuse, seizure disorder, or diminished level of consciousness for any reason. Always ask family members or nurses about witnessed aspiration. Remember, aspiration events are often not witnessed.
v. Pneumonia. Patients will usually have other symptoms of infection, including fever or hypothermia, rigors, or a productive cough. A localized infiltrate on the chest radiograph is diagnostic (see Chapter 21).
vi. Upper airway obstruction. Acute onset of inspiratory stridor with a report of dyspnea should prompt consideration of this diagnosis. Consider foreign body and/or upper airway edema as contributory causes.
vii. Acute respiratory distress syndrome (ARDS). ARDS is associated with bilateral infiltrates on the chest radiograph caused by noncardiogenic pulmonary edema. It commonly occurs in patients with sepsis, trauma, massive blood transfusion, or pancreatitis (see Chapter 25).
i. Myocardial ischemia or infarction (see Chapter 11). Dyspnea may occur in the absence of chest pain and may represent angina, also known as an “anginal equivalent.”
ii. Heart failure (see Chapter 12). In hospitalized patients with heart failure, acute dyspnea is often precipitated by fluid administration or myocardial ischemia leading to cardiogenic pulmonary edema. A significant elevation in brain natriuretic peptide (BNP), which is primarily released by atrial myocytes, may occur and suggests increased atrial wall stretch and a cardiogenic cause of dyspnea.
iii. Arrhythmias. Patients may have a history of palpitations. Specific etiologies cannot be reliably diagnosed on physical examination; a 12-lead electrocardiogram (EKG) or a rhythm strip is required (see Chapters 7 and 8).
iv. Cardiac tamponade is rare but should always be considered in patients with breast and lung cancer, renal failure, recent myocardial infarction, or blunt trauma to the chest.
i. Sepsis. Tachypnea and acute respiratory alkalosis may be the earliest findings in sepsis.
ii. Metabolic acidosis (see Chapter 42). Dyspnea is common because patients hyperventilate to compensate for their acidosis. Respiration with large tidal volumes, known as Kussmaul breathing, is a common breathing pattern associated with metabolic acidosis.
d. Hematologic. Acute anemia (from hemorrhage or hemolysis) can cause acute dyspnea due to the decreased oxygen carrying capacity of blood. Anemia can easily be missed on history and physical examination (see Chapter 62).
e. Psychiatric. Anxiety can be a primary cause of acute dyspnea; however, a diagnosis of primary anxiety should be considered only after ruling out the conditions listed above.
C. Approach to the Patient. The key to evaluating a patient with acute dyspnea is to focus on recognizing the most life-threatening disorders.
a. Patient history. There are four key areas of inquiry:
i. What was the speed of onset of the dyspnea?
ii. Are there associated symptoms (e.g., chest pain, cough, chills)?
iii. What happened immediately before the onset of the dyspnea? What medications or fluids was the patient receiving?
iv. What are the patient’s other medical problems? If hospitalized, what was the admission diagnosis?
i. Vital signs. Significantly abnormal vital signs in an acutely dyspneic patient may signify impending respiratory failure. An oxygen saturation should be obtained.
Remember, a normal oxygen saturation does not exclude the possibility of a serious disorder! Oximetry drops when the PaO2 is significantly low.
ii. Chest. Pay particular attention to the symmetry of breath sounds and the presence of wheezing or rales. Look for tracheal deviation (away from a pneumothorax or large effusion, toward a collapsed lung). Look for use of accessory muscles or paradoxical breathing (abdomen retracts with inspiration), which signify increased work of breathing and pending respiratory failure.
iii. Heart. A complete examination should be performed, focusing on the findings of right-sided and left-sided heart failure. Also note the heart rate (too fast? too slow?).
iv. Extremities. Look for edema (unilateral versus bilateral) and cyanosis. Cool extremities may suggest poor perfusion and a cardiac etiology.
v. Mental status. Evaluating the patient’s mental status is crucial for two reasons:
1. A significantly depressed level of consciousness may necessitate intubation for airway protection.
2. The finding of altered mental status in the setting of a dyspnea suggests a significant homeostatic insult.
c. Diagnostic studies. Four studies should routinely be performed when the patient is acutely dyspneic.
i. 12-Lead EKG
ii. Chest radiograph
iv. Arterial blood gas analysis (may not be required in all dyspneic patients)
D. Treatment. Treatment should be aimed at the underlying cause. The following are a few general principles:
a. Supplemental oxygen. Hypoxemic patients with acute dyspnea should be given supplemental oxygen, with the goal of normalizing oxygen saturation (>90%) and partial pressure of oxygen (PaO2> 60 mm Hg). A history of COPD or carbon dioxide retention should not prevent oxygen therapy for hypoxemic patients; however, patients at risk for carbon dioxide retention should be monitored closely. A maximum of about 40% fraction of inspired oxygen (FiO2) can be reliably delivered by standard nasal cannula. Up to 50% FiO2 can be delivered by Venturi mask and between 80% and 90% FiO2 with a non-rebreather face mask.
b. Diuretics. Cardiogenic pulmonary edema should respond rapidly to diuretic therapy. Other processes associated with excess lung water (e.g., ARDS) may also improve with diuresis.
c. β-agonists. Regardless of the cause, wheezing may improve with nebulized β-agonist therapy. Albuterol can be given continuously if indicated but may cause tachycardia. Ipratropium (an anticholinergic agent) may be used in conjunction with albuterol for COPD but should not be given more frequently than every 4 hours.
d. Noninvasive Positive Pressure Ventilation (NPPV). COPD exacerbation and pulmonary edema may be treated with this modality to avoid complications associated with intubation or ventilation. This will give time for acute therapies such as steroids and β-agonists for COPD and diuretics for pulmonary edema to work. Ventilation is delivered through a face mask rather than through an endotracheal tube. NPPV is triggered by airflow and delivers a constant pressure throughout inspiration.
1. Patients with hypercapnic ventilatory failure [e.g., an acute exacerbation of COPD] and hypoxemic respiratory failure from cardiogenic pulmonary edema may respond well to this mode of ventilation.
2. NPPV may help delay or avoid endotracheal intubation.
1. The face fit and amount of airflow/pressure applied by the machine mask may be uncomfortable for the patient.
2. It is difficult to deliver high levels of oxygen.
3. NPPV is difficult to administer if a patient is unable to control secretions or is uncooperative.
iii. NPPV is not appropriate for patients who have altered consciousness and cannot protect their airway.
e. Heated high-flow nasal cannula. Patients with acute hypoxemic respiratory failure without hypercapnia may benefit from this modality. This has been shown most convincingly in patients with severe hypoxemia (PaO2:FiO2 ≤200).
f. Mechanical ventilation (see Chapter 26). The need for mechanical ventilation should be carefully assessed in patients with severe dyspnea. Indications for mechanical ventilation include:
i. Refractory hypoxemia (PaO2 <60 mm Hg despite maximal oxygen therapy).
ii. Hypercapnia (generally manifested by an increasing Paco2 despite therapy).
iii. Inability to protect the airway.
iv. Impending upper airway obstruction.
v. Excessive work of breathing (this may signify impending respiratory failure and may happen before abnormalities appear on the arterial blood gas).
Hypoxemic or hypercapnic respiratory failure may respond to NPPV in patients who are alert and able to tolerate the pressurized mask. Inability to protect the airway requires immediate endotracheal intubation. Impending upper airway obstruction should be approached cautiously, with immediate percutaneous tracheostomy available in case endotracheal intubation proves impossible.
Suggested Further Readings
Frat JP, Thille AW, Mercat A, et al. High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. N Engl J Med 2015;372:2185–96.Find this resource:
Lindenauer PK, Stefan MS, Shieh MS, Pekow PS, Rothberg MB, Hill NS. Outcomes associated with invasive and noninvasive ventilation among patients hospitalized with exacerbations of chronic obstructive pulmonary disease. JAMA Intern Med 2014;174:1982–93.Find this resource:
Mahler DA, Baird JC. Are you fluent in the language of dyspnea? Chest 2008;134:476–7.Find this resource:
Parshall MB, Schwartzstein RM, Adams L, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med 2012;185:435–52.Find this resource:
Puntillo K, Nelson JE, Weissman D, et al. Palliative care in the ICU: relief of pain, dyspnea, and thirst—a report from the IPAL-ICU Advisory Board. Intensive Care Med 2014;40:235–48.Find this resource: