Dyspnea: General Considerations

DefinitionTop

Dyspnea is a subjective sensation of breathlessness or difficulty breathing. Dyspnea can be characterized by its acuity and association with exertion and positioning as:

1) Acute, intermittent or paroxysmal, and chronic dyspnea.

2) Dyspnea at rest and exertional dyspnea.

3) Orthopnea, which refers to dyspnea occurring in the recumbent position and improving when sitting or standing.

4) Platypnea, which refers to dyspnea increasing in the sitting or standing position.

Dyspnea severity scales help quantify breathlessness or disability associated with breathlessness. Examples:

1) Modified Medical Research Council (mMRC) dyspnea scale (available at mdcalc.com): A 4-point scale for evaluating activities that generate dyspnea as ranging from strenuous exercise (0 points) through walking up a slight hill (1 point), walking slower than peers (2 points), running out of breath after a few minutes’ walk on level ground (3 points), to getting dyspneic when dressing (4 points).

2) Borg scale (0, no dyspnea; 5, severe dyspnea; 10, maximal dyspnea).

3) Disease-specific scales: The New York Heart Association (NYHA) scale used to evaluate dyspnea in heart failure (see Table: New York Heart Association (NYHA) classification of heart failure), ranging from dyspnea with strenuous exertion (stage 1) through dyspnea with ordinary physical activity (stage 2) to dyspnea with less than ordinary activity (stage 3) and dyspnea at rest (stage 4).

Causes and PathogenesisTop

1. Causes of dyspnea according to the underlying pathophysiology: The pathophysiology of dyspnea is complex and often involves interaction between pulmonary and extrapulmonary (cardiovascular, neuromuscular, and oxygen delivery) systems. Underlying mechanisms can be broadly categorized as impaired gas exchange (both at the level of the lungs and tissue) or impaired ventilatory drive, in either case leading to perception of breathlessness.

1) Pulmonary: Abnormal gas exchange may arise from dysfunction at the level of the alveoli, bronchi, lung parenchyma, pleura, or pulmonary vasculature. Alveolar disease processes may include infection, inflammation, and alveolar fluid (eg, in congestive heart failure). Bronchial disease processes include inflammatory conditions such as chronic obstructive pulmonary disease (COPD) and asthma. Examples of parenchymal disease include infection, inflammatory or collagen vascular diseases, malignancy, and interstitial lung disease. Pleural disease includes pleural effusions and malignancy, while pulmonary arterial diseases include pulmonary hypertension and pulmonary embolism.

2) Extrapulmonary:

a) Cardiovascular: Dyspnea in cardiovascular disease is often driven by decreased cardiac output (shock or heart failure). Further categorization of specific causes includes cardiac ischemia, cardiac arrhythmia, valvular disease, and myopericardial disease.

b) Neuromuscular: This predominantly affects ventilatory drive and effort in the absence of gas exchange abnormalities. Neuromuscular causes of hypoventilation can arise at the level of the muscle (myopathy or respiratory muscle/diaphragmatic weakness), neuromuscular junction (neuromuscular conduction abnormalities such as myasthenic crisis), or nerve conduction abnormalities (Guillain-Barré syndrome). Other etiologies of hypoventilation and hypercarbia include mechanical causes such as chest wall deformities, obesity hypoventilation syndrome (OHS), and metabolic causes outlined below.

c) Metabolic: This includes sensation of breathlessness caused by nonrespiratory acidosis (eg, lactic acidosis, diabetic ketoacidosis, renal tubular acidosis), thyrotoxicosis, stimulation of the respiratory center by endogenous toxins (toxins originating in the liver, uremic toxins) and exogenous toxins (salicylates).

d) Other: Abnormal tissue gas exchange can result from impaired oxygen binding by hemoglobin (eg, carbon monoxide poisoning and methemoglobinemia) or decreased cellular oxygen utilization (eg, with cyanide poisoning). Anxiety and strenuous exercise in healthy individuals are more benign considerations.

2. Causes of specific presentations of dyspnea:

1) Acute dyspnea (and differential diagnosis): Table 1.

2) Chronic dyspnea (initially exertional, subsequently also at rest): COPD, bronchiectasis, chronic heart failure, interstitial lung disease, posttuberculous lesions in the lungs, primary and secondary lung tumors, anemia, neuromuscular disorders.

3) Paroxysmal nocturnal dyspnea and orthopnea: Left ventricular failure; chronic pulmonary diseases causing impaired sputum evacuation during sleep (COPD, bronchiectasis), ventilation abnormalities increasing in the recumbent position (interstitial lung disease) or increase in airway resistance during sleep (obstructive sleep apnea, in some cases asthma or COPD).

4) Platypnea: Dyspnea in the upright position that is relieved in the recumbent position. This is usually related to intracardiac or intrapulmonary (eg, hepatopulmonary syndrome) shunting (see Cirrhosis).

Also see Dyspnea in Palliative and End-of-Life Care.

DiagnosisTop

Assess the vital signs (temperature, respiratory rate, oxygen saturation, heart rate, blood pressure) and take a history. Perform physical examination (differential diagnosis based on the time of onset of dyspnea and accompanying symptoms: Table 1), complete blood count, chest radiography, and, as needed, blood gas analysis. Depending on the suspected cause, perform further cardiovascular (electrocardiography [ECG], echocardiography, venous ultrasonography, chest computed tomography [CT] angiography) or respiratory (pulmonary function tests, chest CT) investigations. Additionally, measure serum levels of electrolytes, glucose, ketones, and lactate, and perform renal function tests (especially in patients with acidosis), liver function tests, tests for hemoglobinopathy, and neurologic examination when appropriate.

TreatmentTop

Treatment of dyspnea depends on the underlying etiology. For most causes, there are disease-specific treatments that are discussed in relevant chapters.

In patients with acute hypoxemia, starting oxygen therapy is warranted, even before establishing the cause. If patients are not hypoxic there may be no role for supplemental oxygenation. We recommend avoiding oxygen supplementation achieving saturation >94% to 96%.Evidence 1Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness. Chu DK, Kim LH, Young PJ, et al. Mortality and morbidity in acutely ill adults treated with liberal versus conservative oxygen therapy (IOTA): a systematic review and meta-analysis. Lancet. 2018 Apr 28;391(10131):1693-1705. doi: 10.1016/S0140-6736(18)30479-3. Epub 2018 Apr 26. Review. PMID: 29726345. Caution is warranted when administering oxygen to patients with chronic carbon dioxide retention; in such situations the goal of supplemental oxygen should be to achieve an oxygen saturation level between 88% and 92%. Patients with hypoxia, hypoventilation, or hypercarbia may require noninvasive positive-pressure ventilation (high-flow nasal oxygen, continuous positive airway pressure [CPAP], or bilevel positive airway pressure [BiPAP]). In patients in whom noninvasive ventilation has failed or those who are unable to maintain their airway, endotracheal intubation and mechanical ventilation may be warranted.

TablesTop