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Neural Mechanisms of Cardiac Pain
Author Biography
Introduction
Anterolateral System
Somatic vs. Visceral Nociceptive Processing
Angina Pectoris
Sympathetic Sensory Innervation
Referred Pain
Vagal Sensory Innervation
Other Ascending Pathways
Central Sensitization
Thalamus and Cerebral Cortex
Neurophysiology of Angina Pectorsis
Nausea and Vomiting

Currently selected section: Dyspnea
Summary


Chapter 25:Neural Mechanisms of Cardiac Pain: Dyspnea
        

Dyspnea

Another common symptom associated with angina pectoris is dyspnea. In this text, Schwartzstein and Harver (Chapter 23: Clinical Research on Dyspnea) discuss multiple mechanisms by which cardiac ischemia can lead to dyspnea.

Dyspnea probably occurs as a result of a mismatch between the heart's demand for oxygen versus the delivery of oxygen. Inadequate blood flow to the heart leads to cardiac ischemia and angina pectoris. In addition, inadequate blood flow leads to an inadequate cardiac output with consequent reduced oxygen delivery to the tissues. As a result of inadequate emptying of the heart, left ventricular pressure increases.

This increased pressure "backs up" into the lungs, which causes increased fluid retention in the lungs and decreased lung compliance, which are detected by afferents in the lungs. Lowered PO2 causes ischemia to respiratory and other muscles.

Hypoxia and hypercarbia stimulate chemoreceptors which will attempt to increase breathing but may exacerbate the problem. Anxiety about the chest pain activates limbic areas that receive respiratory input. The individual attempts to breathe harder to deliver more oxygen to the blood, but this is ineffective due to the low cardiac output. As a result the person feels short of breath.

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