1. 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

2. 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.

4. 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.

6. 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.

7. Approach to the Patient: Dyspnea

8. 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