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Neural Mechanisms of Cardiac Pain
Author Biography
Introduction
Anterolateral System
Somatic vs. Visceral Nociceptive Processing
Currently selected section: 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

Dyspnea
Summary

 

Chapter 25:Neural Mechanisms of Cardiac Pain: Angina Pectoris
        

Angina Pectoris

Angina pectoris refers to pain originating from the chest (Figure 3).

This pain was first recognized as a clinical identity by Heberden in 1772, who defined the "agchonč" (the Greek root means "a rope to hang") on the chest ("pectoris") as "a strangling sensation with a feeling of anxiety" (Heberden, 1772).

How does the sense of pain originate directly from the heart?

In normal hearts undergoing stress, such as occurs in exercise, lactate and other metabolic substances are usually produced, at increasing rates, before oxygen supply and demand become metabolically imbalanced. The cardiorespiratory threshold that ultimately limits the exercise is determined by the onset of unpleasant sensations such as fatigue, shortness of breath, muscle tension, and weakness induced by these metabolically active substances (Jones and Killian, 2000). Despite these unpleasant sensations, if the heart is normal we do not sense that pain is originating from the heart.

In contrast, a patient with advanced coronary artery disease who exercises may experience a crushing, constrictive, suffocating discomfort or pain. The pain usually occurs in the upper substernal area, sometimes radiating to adjacent areas (predominantly left side) such as the arms, neck, throat, and the lower jaw. The sense of pain can occur before the person feels fatigue or shortness of breath.


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