Which nerve is responsible for the sensation of pain in a myocardial infarction (heart attack)?

Sympathetic Nerves Are Responsible for Pain Sensation in Myocardial Infarction

The sympathetic nerves (option D) are responsible for the sensation of pain in a myocardial infarction. The cardiac sympathetic afferent fibers serve as the essential pathway for transmitting cardiac pain signals during ischemic events 1.

Neuroanatomical Basis of Cardiac Pain

Cardiac pain during myocardial infarction is transmitted through the following pathway:

• Primary pathway: Cardiac sympathetic afferent fibers that run through sympathetic nerves 2, 1
• Sensory innervation: Both atria and ventricles are abundantly supplied with sympathetic sensory innervation 1
• Signal transmission: Pain signals travel via sympathetic afferents to the spinal cord, where they converge with somatic inputs from thoracic structures onto ascending spinothalamic neurons 1

Mechanisms of Pain Generation During MI

Cardiac sympathetic afferents are activated during myocardial ischemia through several mechanisms:

1. Chemical activation: During ischemia and reperfusion, multiple chemical mediators stimulate sympathetic nerve endings:

   • Reactive oxygen species, particularly hydroxyl radicals 2
   • Serotonin released from activated platelets 2
   • Bradykinin, prostaglandins, adenosine, histamine, and potassium 1
   • Changes in local pH from lactic acid accumulation 2

2. Mechanical activation: Abnormal wall motion (bulging) of the ischemic left ventricle stimulates mechanical receptors through passive stretching 1

3. Combined mechanism: Algogenic chemicals sensitize mechanical receptors, lowering their threshold for nociception 1

Clinical Manifestations of Sympathetic Activation

The activation of cardiac sympathetic afferents during MI results in:

1. Pain characteristics:

   • Diffuse pain over the anterior chest wall rather than localized 3
   • Radiation to left/right arm, neck, and back 3
   • Described as "tearing, intolerable, terrifying" 3

2. Autonomic responses:

   • Sympathetic activation causing vasoconstriction 3
   • Increased workload on the heart 3
   • Manifestations include pallor, sweating, and cool skin 3

3. Referred pain phenomenon:

   • Pain is often referred to the neck, lower jaw, or left arm 3
   • This occurs due to convergence of cardiac and somatic inputs on the same spinothalamic neurons 1

Why Other Nerves Are Not Primary Pain Pathways in MI

• Phrenic nerve (A): Primarily a motor nerve to the diaphragm with some sensory function, but not the primary pathway for cardiac pain
• Vagus nerve (B): While it contains afferent fibers from the heart, vagal afferents primarily mediate depressor reflexes and may modulate pain threshold rather than transmitting the pain sensation itself 2, 1
• Intercostal nerves (C): These nerves supply the chest wall but not the heart directly

Clinical Implications

Understanding that sympathetic nerves mediate cardiac pain has important therapeutic implications:

• Pain management: Opioids are effective for MI pain because they counteract the sympathetic activation 3
• Autonomic effects: Relief of pain is crucial not only for comfort but also because pain-related sympathetic activation increases cardiac workload 3
• Diagnostic value: The pattern of pain radiation follows sympathetic pathways and helps distinguish cardiac from non-cardiac chest pain 3

The sympathetic nervous system not only transmits the pain of MI but also undergoes remodeling after infarction, with nerve sprouting and sympathetic hyperinnervation that can contribute to arrhythmogenesis and sudden death 4.