Dyspnea a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioural responses

Mechanisms of Dyspnea respiratory sensations consequence of interactions between the efferent, or outgoing, motor output from the brain to the ventilatory muscles (feed-forward) and the afferent, or incoming, sensory input from receptors throughout the body (feedback) as well as the integrative processing of this information occurring in the brain given disease state may lead to dyspnea by one or more mechanisms, some may be operative under some circumstances Motor Efferents Disorders of the ventilatory pump are associated with increased work of breathing or a sense of an increased effort to breathe. When the muscles are weak or fatigued, greater effort is required, even though the mechanics of the system are normal. The increased neural output from the motor cortex is thought to be sensed due to a corollary discharge that is sent to the sensory cortex at the same time that signals are sent to the ventilatory muscles. Sensory Afferents Chemoreceptors in the carotid bodies and medulla are activated by hypoxemia, acute hypercapnia, and acidemia. Stimulation of these receptors, as well as others that lead to an increase in ventilation, produce a sensation of air hunger. Mechanoreceptors in the lungs, when stimulated by bronchospasm, lead to a sensation of chest tightness. J-receptors, sensitive to interstitial edema, and pulmonary vascular receptors, activated by acute changes in pulmonary artery pressure, appear to contribute to air hunger. Hyperinflation is associated with the sensation of an inability to get a deep breath or of an unsatisfying breath. It is not clear if this sensation arises from receptors in the lungs or chest wall, or if it is a variant of the sensation of air hunger. Metaboreceptors, located in skeletal muscle, are believed to be activated by changes in the local biochemical milieu of the tissue active during exercise and, when stimulated, contribute to the breathing discomfort.

Association of Qualitative Descriptors and Pathophysiologic Mechanisms of Shortness of Breath Pathophysiology Chest tightness or constriction Bronchoconstriction, interstitial edema (asthma, myocardial ischemia) Increased work or effort of breathing Airway obstruction, neuromuscular disease (COPD, moderate to severe asthma, myopathy, kyphoscoliosis) Air hunger, need to breathe, urge to breathe Increased drive to breathe (CHF, pulmonary embolism, moderate to severe airflow obstruction) Cannot get a deep breath, unsatisfying breath Hyperinflation (asthma, COPD) and restricted tidal volume (pulmonary fibrosis, chest wall restriction) Heavy breathing, rapid breathing, breathing more Deconditioning Quality of Sensation As with pain, dyspnea assessment begins with a determination of the quality of the discomfort (Table 33-1). Dyspnea questionnaires, or lists of phrases commonly used by patients, assist those who have difficulty describing their breathing sensations. Sensory Intensity A modified Borg scale or visual analogue scale can be utilized to measure dyspnea at rest, immediately following exercise, or on recall of a reproducible physical task, e.g., climbing the stairs at home. An alternative approach is to inquire about the activities a patient can do, i.e., to gain a sense of the patient's disability. The Baseline Dyspnea Index and the Chronic Respiratory Disease Questionnaire are commonly used tools for this purpose. Affective Dimension For a sensation to be reported as a symptom, it must be perceived as unpleasant and interpreted as abnormal. We are still in the early stages of learning the best ways to assess the affective dimension of dyspnea. Some therapies for dyspnea, such as pulmonary rehabilitation, may reduce breathing discomfort, in part, by altering this dimension.

Likely Mechanisms of Dyspnea in Selected Conditions Asthma Increased sense of effort Stimulation of irritant receptors in airways Neuromuscular disease COPD Hypoxia Hypercapnia Dynamic airway compression Mechanical ventilation Afferent mismatch Factors associated with the underlying condition Pulmonary embolism Stimulation of pressure receptors in pulmonary vasculature or right atrium (possible) Heart Disease In patients with cardiac disease, exertional dyspnea occurs most commonly as a consequence of an elevated pulmonary capillary pressure, which in turn may be due to left ventricular dysfunction, reduced left ventricular compliance, and mitral stenosis. The elevation of hydrostatic pressure in the pulmonary vascular bed tends to upset the Starling equilibrium with resulting transudation of liquid into the interstitial space, reducing the compliance of the lungs and stimulating J (juxtacapillary) receptors in the alveolar interstitial space. When it is prolonged, pulmonary venous hypertension results in thickening of the walls of small pulmonary vessels and an increase in perivascular cells and fibrous tissue, causing a further reduction in compliance. The competition for space among vessels, airways, and increased fluid within the interstitial space compromises the lumina of small airways, increasing the airways’ resistance. Diminution in compliance and an increase in the airways’ resistance increase the work of breathing. In advanced congestive heart failure, usually involving elevation of both pulmonary and systemic venous pressures, hydrothorax may develop, interfering further with pulmonary function and intensifying dyspnea. Orthopnea, i.e., dyspnea in the supine position, is the result of the alteration of gravitational forces when this position is assumed, which elevates pulmonary venous and capillary pressures. These, in turn, increase the pulmonary closing volume and reduce the vital capacity.

Approach to the Patient: Dyspnea

Patterns of Abnormality in Cardiopulmonary Exercise Testing Cardiovascular limitation Respiratory limitation Heart rate 85% of predicted maximum Low anaerobic threshold Reduced maximal oxygen consumption Drop in blood pressure with exercise Arrhythmias or ischemic changes on ECG Does not achieve maximal predicted ventilation Does not have significant desaturation Achieves or exceeds maximal predicted ventilation Significant desaturation (90%) Stable or increase dead space–to–tidal volume ratio Development or bronchospasm with falling FEV1 Does not achieve 85% of predicted maximal heart rate No ischemic ECG changes Distinguishing Cardiogenic from Noncardiogenic Pulmonary Edema The history is essential for assessing the likelihood of underlying cardiac disease as well as for identification of one of the conditions associated with noncardiogenic pulmonary edema. The physical examination in cardiogenic pulmonary edema is notable for evidence of increased intracardiac pressures (S3 gallop, elevated jugular venous pulse, peripheral edema), and rales and/or wheezes on auscultation of the chest. In contrast, the physical examination in noncardiogenic pulmonary edema is dominated by the findings of the precipitating condition; pulmonary findings may be relatively normal in the early stages. The chest radiograph in cardiogenic pulmonary edema typically shows an enlarged cardiac silhouette, vascular redistribution, interstitial thickening, and perihilar alveolar infiltrates; pleural effusions are common. In noncardiogenic pulmonary edema, heart size is normal, alveolar infiltrates are distributed more uniformly throughout the lungs, and pleural effusions are uncommon. Finally, the hypoxemia of cardiogenic pulmonary edema is due largely to ventilation-perfusion mismatch and responds to the administration of supplemental oxygen. In contrast, hypoxemia in noncardiogenic pulmonary edema is due primarily to intrapulmonary shunting and typically persists despite high concentrations of inhaled O2. DIFFERENTIATION BETWEEN CARDIAC AND PULMONARY DYSPNEA In most patients with dyspnea there is obvious clinical evidence of disease of the heart and/or lungs. Like patients with cardiac dyspnea, patients with chronic obstructive lung disease may also waken at night with dyspnea, but, as pointed out above, this is usually associated with sputum production; the dyspnea is relieved after these patients rid themselves of secretions. The difficulty in the distinction between cardiac and pulmonary dyspnea may be compounded by the coexistence of diseases involving both organ systems. In patients in whom the etiology of dyspnea is not clear, it is desirable to carry out pulmonary function testing, for these tests may be helpful in determining whether dyspnea is produced by heart disease, lung disease, abnormalities of the chest wall, or anxiety (Chap. 235). In addition to the usual means of assessing patients for heart disease, determination of the ejection fraction at rest and during exercise by echocardiography or radionuclide ventriculography is helpful in the differential diagnosis of dyspnea. The left ventricular ejection fraction is depressed in left ventricular failure, while the right ventricular ejection fraction may be low at rest or may decline during exercise in patients with severe lung disease. Both left and right ventricular ejection fractions are normal at rest and during exercise in dyspnea due to anxiety or malingering. Careful observation during the performance of an exercise treadmill test will often help in the identification of the patient who is malingering or whose dyspnea is secondary to anxiety. Under these circumstances, the patient usually complains of severe shortness of breath but appears to be breathing either effortlessly or totally irregularly. Cardiopulmonary testing, in which the patient’s maximal functional exercise capacity is assessed while measurements of the electrocardiogram, blood pressure, oxygen consumption, arterial saturation (oximetry), and ventilation are carried out, is useful in the differentiation between cardiac and pulmonary dyspnea