dyspnea, shortness of breath

Dyspnea (shortness of breath)

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Dyspnea (shortness of breath)


Dyspnea is the subjective experience of difficulty breathing and may be characterized by patients as tightness in the chest, shortness of breath, breathlessness, or a feeling of suffocation. Up to half of people at the end of life may experience severe dyspnea.

Tachypnea: A respiratory rate greater than normal. Normal rates range from 44 cycles/min in a newborn to 14 to 18 cycles/min in adults.

Hyperpnea: Greater than normal minute ventilation to meet metabolic requirements.

Hyperventilation: A minute ventilation (determined by respiratory rate and tidal volume) that exceeds metabolic demand. Arterial blood gases (ABG) characteristically show a normal partial pressure of oxygen (Po2) with an uncompensated respiratory alkalosis (low partial pressure of carbon dioxide [Pco2] and elevated pH).

Dyspnea on exertion: Dyspnea provoked by physical effort or exertion. It often is quantified in simple terms, such as the number of stairs or number of blocks a patient can manage before the onset of dyspnea.

Orthopnea: Dyspnea in a recumbent position. It usually is mea-sured in number of pillows the patient must use to lie in bed (e.g., two-pillow orthopnea).

Paroxysmal nocturnal dyspnea: Sudden onset of dyspnea occurring while reclining at night, usually related to the presence of congestive heart failure.

dyspnea, shortness of breath

Causes of dyspnea

Dyspnea is primarily of respiratory or cardiac origin, with almost 90% of all cases being due to asthma, heart failure, myocardial ischaemia, chronic obstructive pulmonary disease (COPD), pneum­onia, and psychogenic disorders. In the South African (SA) context, where there is a high burden of HIV infection, a broader differential needs to be incorporated that includes infectious diseases such as tuberculosis, Pneumocystis pneumonia, aspergillosis and acute infective exacerbations of bronchiectasis. Furthermore, due to the high prevalence of interpersonal violence in SA, a significant proportion of patients presenting to emergency centers have dyspnea related to trauma, with the cause dependent on the mechanism of injury and organ system involved.

Pathophysiology

The actual mechanisms responsible for dyspnea are unknown. Normal breathing is controlled both centrally by the respiratory control center in the medulla oblongata, as well as peripherally by chemoreceptors located near the carotid bodies, and mechanoreceptors in the diaphragm and skeletal muscles. Any imbalance between these sites is perceived as dyspnea. This imbalance generally results from ventilatory demand being greater than capacity.

The perception and sensation of dyspnea are believed to occur by one or more of the following mechanisms: increased work of breathing, such as the increased lung resistance or decreased compliance that occurs with asthma or chronic obstructive pulmonary disease (COPD), or increased respiratory drive, such as results from severe hypoxemia, acidosis, or centrally acting stimuli (toxins, central nervous system events). Pulmonary stretch receptors also are thought to play a role.

Dyspnea due to diseases of the respiratory system

Bronchial asthma

The cause is chronic inflammation of the airways leading to variable airway obstruction. The patients complain of frequent attacks of shortness of breath, often at night as well. Multiple allergies may be present. The precipitating factors can include respiratory irritation, allergen ex-posure, exercise, weather changes, and (respiratory tract) infections.

Auscultation reveals expiratory wheezes due to obstruction. Spirometry shows a decrease in both the forced expiratory volume at one second (FEV1) and the peak expiratory flow (PEF), both of which may be normal in the asymptomatic interval between episodes. The obstruction, and the symptoms, improve markedly after the inhalation of a bronchodilator drug (β2-agonist or anticholinergic drug). Episodes of acute dyspnea in a patient with asthma are called exacerbations. Tachypnea, wheezes, and a prolonged expiratory phase are typical clinical findings.

Chronic obstructive pulmonary disease (COPD)

Chronic bronchitis is present, according to the definition of the World Health Organization, when cough and discharge have been present for at least three months in at least two consecutive years. In COPD, chronic inflammation leads to destruction of lung parenchyma and thereby to over inflation of the lungs and a decline in elastic restorative forces. COPD is usually characterized by a fixed obstruction of the lower airways. The affected patients are usually over age 40, and nearly all are smokers or past smokers Pulmonary function tests and body plethysmography afford further diagnostic help.

The Tiffeneau index (FEV1/IVC, where IVC is the inspiratory vital capacity) is typically under 0.7, and the residual volume may be elevated as an expression of over inflation of the lungs. Abnormally low CO diffusion indicates emphysema. A plain chest x-ray reveals flattened diaphragm shadows and often rarefaction of the pulmonary vasculature. The occurrence of exacerbations that necessitate hospitalization is associated with a worse outcome. COPD shares risk factors with left heart failure and is often found together with it.

Pneumonia

Dyspnea is the main symptom of pneumonia primarily in patients over age 65 (ca. 80%). Pleuritic pain, fever, and cough are typical accompanying symptoms. Examination reveals tachypnea, inspiratory rales, and sometimes bronchial breathing. Laboratory testing (inflammatory parameters; hypoxemia in arterial blood gas analysis, in severe cases), chest x-ray, and in some cases chest CT are diagnostically helpful.

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The CRB-65 score is used to assess the severity of pneumonia. One point is awarded for each item present: C stands for confusion of new onset, R for respiratory rate ≥ 30/min, B for systolic blood pressure <90 mmHg, diastolic blood pressure ≤ 60 mmHg, and 65 for age ≥ 65). This score can serve as a guide to the need for hospitalization. Patients with a score of 0 can generally be treated outside the hospital; those with a score of 1 should be hospitalized if they have hypoxemia and comorbidities; and those with a score of 2 or more should always be admitted to the hospital.

Interstitial lung diseases

Patients report chronic shortness of breath and nonproductive cough, and they are often smokers. Examination reveals crackling ales at the bases, and sometimes also digital clubbing and hourglass nails.

Pulmonary function testing reveals low vital capacity (VC) and total lung capacity (TLC), a high normal Tiffeneau index, and reduced CO diffusion. The differential diagnosis of interstitial lung diseases is complex, and the prognosis and treatment differ from one type of interstitial lung disease to another. Consultation with a pneumonologist is advisable

Pulmonary embolism

The clinical picture of acute pulmonary embolism is often characterized by dyspnea of acute onset. Patients often report pleuritic pain and sometimes have hemoptysis. Examination reveals shallow breathing and tachycardia. There is often evidence of a deep venous thrombosis of the lower limb as the source of the pulmonary embolism

Dyspnea due to diseases of the cardiovascular system

Congestive heart failure

Along with dyspnea, there are other symptoms including fatigue, diminished exercise tolerance, and fluid retention. The common causes are advanced coronary heart disease, primary cardiomyopathy, hypertension, and valvular heart disease. There is an important clinical distinction between heart failure with reduced ejection fraction (HFrEF), in which the left ventricular ejection fraction (LVEF) is less than 40%, and the almost equally common heart failure with preserved ejection fraction (HFpEF), with elevated cardiac filling pressure. There is also a newly described entity called heart failure with mid-range ejection fraction (HFmrEF, in which signs of diastolic dysfunction are combined with an LVEF between 40% and 49%). In all types of congestive heart failure, the stroke volume and cardiac output are diminished.

Coronary heart disease

Dyspnea can also be a symptom of coronary stenosis, even if it is not a “classic” symptom. It can be present simultaneously with angina pectoris, or as the predominant or sole symptom of coronary heart disease, e.g., in a patient with diabetes mellitus.
Dyspnea more typically arises as part of the constellation of symptoms in an acute coronary syndrome or myocardial infarction, as well as in cardiogenic shock as a consequence of low cardiac output

Differential Diagnosis

Urgent and emergent conditions causing acute dyspnea include pneumonia, COPD, asthma, pneumothorax, pulmonary embolism, cardiac disease (eg, HF, acute myocardial infarction, valvular dysfunction, arrhythmia, intracardiac shunt), pleural effusion, diffuse alveolar hemorrhage, metabolic acidosis, cyanide toxicity, methemoglobinemia, and carbon monoxide poisoning. Chronic dyspnea may be caused by interstitial lung disease and pulmonary hypertension.

Treatment

The treatment of urgent or emergent causes of dyspnea should aim to relieve the underlying cause. Pending diagnosis, patients with hypoxemia should be immediately provided supplemental oxygen unless significant hypercapnia is present or strongly suspected pending arterial blood gas measurement. Dyspnea frequently occurs in patients nearing the end of life. Opioid therapy, anxiolytics, and corticosteroids can provide substantial relief independent of the severity of hypoxemia. However, inhaled opioids are not effective. Oxygen therapy is most beneficial to patients with significant hypoxemia (Pao2 less than 55 mm Hg).

In patients with severe COPD and hypoxemia, oxygen therapy improves mortality and exercise performance. Pulmonary rehabilitation programs are another therapeutic option for patients with moderate to severe COPD or interstitial pulmonary fibrosis. A small study showed that patients with pulmonary hypertension had less dyspnea and lower plasma norepinephrine and interleukin-6 (IL-6) with slow paced respiration therapy. Noninvasive ventilation may be considered for patients with dyspnea caused by an acute COPD exacerbation, but the efficacy of this treatment is still uncertain.

Other non-pharmacological approaches.

Patients with dyspnea often report that movement of cool air reduces breathlessness, and laboratory studies have shown that cold air directed on the face decreases dyspnea induced in healthy individuals. Increased respiratory muscle effort, associated with high ventilatory demand relative to respiratory muscle capacity, may contribute to dyspnea in many patients with chronic respiratory disease. By reducing the demand on the respiratory muscles, non­invasive ventilation might reduce dyspnea. However, few studies of non­invasive ventilation have used dyspnea as an endpoint.

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