Chapter 47 - Dyspnea

Question 1

Define dyspnea (American Thoracic Society).

Answer 1

“The American Thoracic Society defines dyspnea as a “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors and may induce secondary physiological and behavioral responses.”

Question 2

Dyspnea is a symptom but might also be considered a sign.

True or False?

Answer 2

False.
“Dyspnea, a symptom, can be perceived only by the person experiencing it and must be distinguished from the signs of increased work of breathing.”

Question 3

Summarize the mechanisms involved in dyspnea.

Answer 3

“Afferent information from the receptors throughout the respiratory system projects directly to the sensory cortex to contribute to primary qualitative sensory experiences and to provide feedback on the action of the ventilatory pump. Afferents also project to the areas of the brain responsible for control of ventilation. The motor cortex, responding to input from the control centers, sends neural messages to the ventilatory muscles and a corollary discharge to the sensory cortex (feed-forward with respect to the intructions sent to the muscles). If the feed-forward and feedback messages do not match, an error signal is generated and the intensity of dyspnea increases. An increasing body of data supports the contribution of affective inputs to the ultimate perception of unpleasant respiratory sensations.”

Question 4

What are the pathways that explain dyspnea due to increased motor efferent output? Why is it that this input might be increased?

Answer 4

“Disorders of the ventilatory pump - most commonly, increased airway resistance or stiffness (decreased compliance) of the respiratory system - are associated with increased work of breathing or the sense of an increased effot to breathe. When the muscles are weak or fatigued, greater effor is required, even though the mechanics of the system are normal. The increased neural output from the motor cortex is sensed via a corollary discharge, a neural signal that is sent to the sensory cortex at the same time that motor output is directed to the ventilatory muscles.”

Question 5

Name the condition that is typically associated with “air hunger”.

Answer 5

Congestive heart failure.

Question 6

Which receptors are associated with “air hunger” dyspnea?

Answer 6

Chemoreceptors and J-receptors (a type of mechanoreceptor).

Question 7

Describe the location and function of chemoreceptors.

Answer 7

“Chemoreceptors in the carotid bodies and medulla are activated by hypoxemia, acute hypercapnia, and acidemia. Stimulation of these receptors and of others that lead to an increase in ventilation produce a sensation of “air hunger.”

Question 8

Chest tightness or constriction, which might occur in asthma or congestive heart failure due to bronchoconstriction and interstitial edema, respectively, is correlated to mechanoreceptor activation stimulated to bronchospasm.
True or False?

Answer 8

True.

Question 9

What is the function of metaboreceptors?

Answer 9

“Metaboreceptors, which are 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 breathing discomfort.”

Question 10

Explain the pathophysiology of dyspnea due to efferent-reafferent mismatch.

Answer 10

“A discrepancy or mismatch between the feed-forward message to the ventilatory muscles and the feedback from receptors that monitor the response of the ventilatory pump increases the intensity of dyspnea. This mismatch is particularly important when there is a mechanical derrangement of the ventilatory pump, as in asthma or chronic obstructive pulmonary disease (COPD).”

Question 11

Acute anxiety in obstructive diseases might aggravete hyperinflation, which increases work and effort of breathing and thus increasing dyspnea.
True or False?

Answer 11

True.
“Acute anxiety or fear may [also] increase the severity of dyspnea either by altering the interpretation of sensory data or by leading to patterns of breathing that heighten physiologic abnormalities in the respiratory system.”

Question 12

Which types of dyspnea pattern are associated with pulmonary fibrosis?

Answer 12

“Air hunger” and “Inability to get a deep breath, unsatisfying breath”.

Question 13

Which mechanisms of dyspnea are shared between a cardiogenic versus a noncardiogenic pulmonary edema?

Answer 13

• Shared mechanisms: increased work of breathing and drive to breath; hypoxemia and stimulation of pulmonary receptors.
  (stimulation of vascular receptors only occur in cardiogenic pulmonary edema)

Question 14

Name the conditions associated with dyspnea due to stimulation of metaboreceptors.

Answer 14

• Anemia and deconditioning, exclusively.

- Cardiogenic Pulmonary Edema, along other mechanisms.

Question 15

Give examples of scoring scales for dyspnea.

Answer 15

• Modified Borg scale.
• Baseline Dyspnea Index
• Chronic Respiratory Disease Questionnarie.

Question 16

“Laboratory studies have demonstrated that air hunger evokes a stronger affective response than does increased effort or work of breathing. Some therapies for dyspnea, such as pulmonary rehabilitation, may reduce breathing discomfort, in part, by altering this dimension.
True or False?

Answer 16

True.

Question 17

What are the mechanisms for dyspnea in asthma and chronic obstructive lung disease (COPD)? Are there any different mecahsnisms responsible for dyspnea between these diseases?

Answer 17

“Asthma and COPD, the most common obstructive lung diseases, are characterized by expiratory airflow obstruction, which typically leads to dynamic hyperinflation of the lungs and chest wall. Patients with moderate to severe disease have both increased resistive and elastic loads (a term that relates to the stiffness of the system) on the ventilatory muscles and experience increased work of breathing. Patients with acute bronchoconstriction also report a sense of tightness, which can exist even when lung function is still within the normal range. These patients are commonly tachypneic; this condition leads to hyperinflation and reduced respiratory system compliance and also liits tidal volume. Both the chest tightness and the tachypnea are probably due to stimulation of pulmonary receptors. Both asthma and COPD may lead to hypoxemia and hypercapnia from ventilation-perfusion (V/Q) mismatch (and diffusion limitation during exercise with emphysema); hypoxemia is much more common than hypercapnia as a consequence of the different ways in which oxygen and carbon dioxide bind to hemoglobin.”

Question 18

Diastolic dysfunction, characterized by a very stiff left ventricle, may lead to severe dspnea with relatively mild degrees of physical activity, particularly if it is associated with mitral regurgitation.
True or False?

Answer 18

True.

Question 19

Describe the pathophysiology and response to oxygen in diseases of the pulmonary vasculature.

Answer 19

“Pulmonary thrombombolic disease and primary diseases of the pulmonary circulation (primary pulmonary hypertension, pulmonary vasculitis) cause dyspnea via increased pulmonary-artery pressure and stimulation of pulmonary receptors. Hyperventilation is common, and hypoxemia may be present. However, in most cases, use of supplemental oxygen has only a minimal impact on the severity of dyspnea and hyperventilation.”

Question 20

Regarding the diseases of the pericardium, which mechanisms might explain dyspnea?

Answer 20

“Constrictive pericarditis and cardiac tamponade are both associated with increased intracardiac and pulmonary vascular pressures, which are the likely cause of dyspnea in these conditions. To the extent that cardiac output is limited (at rest or with exercise) metaboreceptors may be stimulated if cardiac output is compromised to the degree that lactic acidosis develops; chemoreceptors will also be activated.”

Question 21

Explain the mechanisms that might explain dyspnea in obese patients.

Answer 21

“The breathlessness associated with obesity is probably due to multiple mechanisms, including high cardiac output and impaired ventilatory pump function (decreased compliance of the chest wall).”

Question 22

Make the correlation of the following symptoms with the differential diagnosis that should be considered: (i) orthopnea; (ii) nocturnal dyspnea; (iii) acute, intermitent episodes of dyspnea; (iv) chronic dyspnea.

Answer 22

(i) congestive heart failure (CHF), mechanical impairment of the diaphragm associated with obesity, or asthma triggered by esophageal reflux;
(ii) CHF or asthma;
(iii) myocardial ischemia, bronchospasm, or pulmonary embolism;
(iv) chronic obstructive disease, interstitial lung disease and chronic thromboembolic disease.

Question 23

Name two conditions associated with platypnea.

Answer 23

Hepatopulmonary syndrome and left atrial myxoma.

Question 24

What would you look for in physical examination in a patient with increased work of breathing? What do these findings mean physiopathologically?

Answer 24

“Evidence of increased work of breathing (supraclavicular retractions; use of accesory muscles of ventilation; and the tripod position, characterized by sitting with the hands braced on the knees) is indicative of increased airway resistance or stiffness of the lungs and the chest wall.”

Question 25

Paradoxical movement of the abdomen: inward motion during expiration is a sign of diaphragmatic weakness, and rounding of the abdomen during inspiration is suggestive of pulmonary edema.
True or False?

Answer 25

False.

Inspiration and exhalation, respectively.

Question 26

Summarize the different findings in chest imaging that might indicate an etiology for dyspnea.

Answer 26

“The lung volumes should be assessed: hyperinflation indicated obstructive lung disease, whereas low lung volumes suggest interstitial edema or fibrosis, diaphragmatic dysfunction, or impaired chest wall motion. The pulmonary parenchyma should be examined for evidence of interstitial disease and emphysema. Prominent pulmonary vasculature in the upper zones indicates pulmonary venous hypertension, while enlarged central pulmonary arteries suggest pulmonary arterial hypertension. An enlarged cardiac silhouette suggests dilated cardiomyopathy or valvular disease. Bilateral pleural effusions are typical of CHF and some forms of collagen-vascular disease. Unilateral effusions raise the specter of carcinoma and pulmonary embolism but may also occur in heart failure.”

Question 27

How many patients tested formally for reactive airway and asthma diagnosis do not actually meet asthma criteria?

Answer 27

Up to one-third.

Question 28

While investigating a patient with severe dyspnea, why is it that brain natriuretic peptide levels might be very limited as a differential diagnosis?

Answer 28

“Measurement of brain natriuretic peptide levels in serum is increasingly used to assess for CHF in patients presenting with acute dyspnea but may be elevated in the presence of right ventricular strain as well.”

Question 29

How does one distinguish between a cardiovascular from a respiratory system cause of dyspnea?

Answer 29

“If, at peak exercise, the patient achieves predicted maximal ventilatio, demonstrates an increase in dead space or hypoxemia, or develops bronchospasm, the respiratory system is probably the cause of the problem. Alternatively, if the heart rate is >85% of the predicted maximum if the anaerobic threshold occur early, if the blood pressure becomes excessively high or decreases during exercise, if the O2 pulse (O2 consumption/heart rate, an indicator of stroke volume) falls, or if there are ischemic changes on the elctrocardiogram, an abnormality of the cardiovascular system is likely the explanation for the breathing discomfort.”

Question 30

Summarize the general treatment for dyspnea.

Answer 30

“The first goal is to correc the underlying problem responsible for the symptom. If this is not possible, an effort is made to lessen the intensity of the symptom and its effect on the patient’s quality of life. Supplemental O2 should be administered if the resting O2 saturation is less or equal to 89% or if the patient’s saturation drops to these levels with activity. For patients with COPD, pulmonary rehabilitation programs have demonstrated positive effects on dyspnea, exercise capacity and rates of hospitalization. Studies of anxiolytics and antidepressants have not documented consistent benefit. Experimental interventions - e.g., cold air on the face, chest wall vibration, and inhaled furosemide - aimed at modulating the afferent information from receptors throughout the respiratory system are being studied. Morphine has been shown to reduce dyspnea out of proportion to the change in ventilation in laboratory models.”

Question 31

While hypoalbuminemia favors movement of fluid into the tissue for any given hydrostatic pressure in the capillary, it is usually not sufficient by itself to cause interstitial edema.”
True or False?

Answer 31

True.

Question 32

State the findings that you would expect to find in either physical examination and radiographic testing in a patient with cardiogenic pulmonary edema.

Answer 32

“Early signs of pulmonary edema include exertional dyspnea and orthopnea. Chest radiographs show peribronchial thickening, prominent vascular markings in the upper lung zones, and Kerley B lines. As the pulmonar edema worsens, alveoli fill with fluid; the chest radiograph shows patchy alveolar filling, typically in a perihilar distribution, which then progresses to diffuse alveolar infiltrates. Increasing airway edema is associated with rhonchi and wheezes.”

Question 33

What is the pathophysiology of noncardiogenic pulmonary edema?

Answer 33

“In noncardiogenic pulmonary edema, lung water increases due to damage of the pulmonary capillary lining with consequent leakage of proteins and other macromolecules into the tissue; fluid follows the protein as oncotic forces are shifted from the vessel to the surrounding lung tissue. This process is associated with dysfcuntion of the surfactant lining the alveoli, increased surface forces, and a propensity for the alveoli to collapse at low lung volumes. Physiologically, noncardiogenic pulmonary edema is characterized by intrapulmonary shunt with hypoxemia and decreased pulmonary compliance leading to lower functional residual capacity.”

Question 34

What are the pathological characteristics of noncardiogenic pulmonary edema?

Answer 34

Hyaline membranes and inflammation that could lead to fibrosis.

Question 35

Characterize the physical and imagiological findings in noncardiogenic pulmonary edema.

Answer 35

“Clinically, the picture ranges from mild dyspnea to respiratory failure. Auscultation of the lungs may be relatively normal despite chest radiographs that show diffuse alveolar infiltrates. CT scans demonstrate that the distribution of alveolar edema is more heterogeneous than was once thought.”

Question 36

Categorize the causes of noncardiogenic pulmonary edema.

Answer 36

• Direct injuries, such as aspiration and blunt chest trauma;
• Indirect injury, which is the consequence of mediators that reach the lung via the bloodstream;
• Conditions that may result from acute changes in pulmonary pressures, such as neurogenic and high-altitude pulmonary edema or sudden swings of pleural pressure as well as transient damage to the pulmonary capillaries, such as in reexpansion pulmonary edema.

Question 37

Name all the causes of noncardiogenic pulmonary edema by categories.

Answer 37

• Direct injury to lung: chest trauma, pulmonary contusion; aspiration; smoke inhalation; pneumonia; oxygen toxicity; pulmonary embolism, reperfusion;
• Hematogenous injury to lung: sepsis; pancreatitis; nonthoracic trauma; leukoagglutination reactions; multiple transfusions; intravenous drug use (e.g.: heroin); cardiopulmonary bypass;
• Possible lung injury plus elevated hydrostatic pressures: high-altitude pulmonary edema; neurogenic pulmonary edema and reexpansion pulmonary edema.

Question 38

Summarize how to distinguish cardiogenic from noncardiogenic pulmonary edema.

Answer 38

“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 pulmonar edema tipically shows an enlarged cardiac sillhouette, vascular redistribution, interstitial thieckening, 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 pulmonar edema is due largely to V/Q to 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 despide high concentrations of inhaled oxygen.”