Skip to Content
Interactive Textbook on Clinical Symptom Research Logo


Home Button

 

Clinical Research on Dyspnea
Author Bios
What is Dyspnea?
What Provokes Dyspnea?
The Nature of Dyspnea
Language of Dyspnea
Clinical Application
Research Application
Variability in Sensations
Challenges in Study
Mechanical Loads and Sense of Effort
Chemoreceptors
Mechanoreceptors
Neuro-Mechanical Dissociation
Phase of Respiration and Dyspnea
Physiology of Dyspnea
Respiratory System
Currently selected section: Cardiovascular System
Measuring Dyspnea
Scaling Issues
Qualitative Aspects
Reliability and Validity Overview
Reliability and Validity
Sensitivity and Specificity
Scales
Sensation vs. Perception vs. Symptom
Treating Dyspnea
Why Measure?
Cluster Analysis
Statistical vs. Clinical Significance
Standard Error of Measurement
Measuring Fatigue
Measuring Depression
Measuring Anxiety and Hyperventilation
Measuring Quality of Life
Conclusion

 

Chapter 23: Dyspnea: Clinical Physiology of Dyspnea: Cardiovascular System
        

The role of the cardiovascular system, taken in its broadest sense, is to deliver oxygenated blood to the tissue where the oxygen is utilized to support aerobic metabolism, and return the blood with byproducts of metabolism to the liver and lungs. This process can be analyzed in terms of oxygen content, cardiac function (the pump), and oxygen use (conditioning).

Oxygen delivery to the tissues is compromised when systolic cardiac function is diminished, when anemia is present thereby reducing oxygen content of the blood, or when there are focal obstructions in the peripheral vasculature. The mechanism by which reduced oxygen delivery is perceived and processed to produce breathing discomfort remains unclear since there is no apparent apparatus within the body that monitors oxygen content (as opposed to partial pressure of oxygen) of the blood or delivery of oxygen to the tissue.

To the extent that insufficient oxygen delivery to metabolically active tissue may result in local anaerobic metabolism and production of lactic acid, there may be stimulation of "metaboreceptors" in the tissue that send signals to the brain that are perceived as dyspnea.

Altered cardiac function, whether systolic or diastolic, is typically associated with elevated pulmonary capillary wedge pressure. This may lead to stimulation of pulmonary vascular receptors and, to the extent that fluid passes into the pulmonary interstitium, C-fibers may also be stimulated. Furthermore, the production of interstitial fluid reduces pulmonary compliance and may increase airway resistance, thereby imposing an increased load on the ventilatory muscles and the ventilatory pump. Hypoxia and hypercapnia may follow in severe cases. Cardiac valvular disease clearly can contribute to these physiological derangements.

 

Page 25 of 47
      Previous Section