Cardiac Pain

Cardiac Pain

Pain originating in the heart as the result of acute myocardial ischemia is assumed to be caused by oxygen deficiency and the accumulation of metabolites, which stimulate the sensory nerve endings in the myocardium. The afferent nerve fibers ascend to the central nervous system through the cardiac branches of the sympathetic trunk and enter the spinal cord through the posterior roots of the upper four thoracic nerves. The nature of the pain varies considerably, from a severe crushing pain to nothing more than a mild discomfort

 

The pain is not felt in the heart, but is referred to the skin areas supplied by the corresponding spinal nerves. The skin areas supplied by the upper four intercostal nerves and by the intercostobrachial nerve (T2) are therefore affected. The intercostobrachial nerve communicates with the medial cutaneous nerve of the arm and is distributed to skin on the medial side of the upper part of the arm. A certain amount of spread of nervous information must occur within the central nervous system, for the pain is sometimes felt in the neck and the jaw.

Myocardial infarction involving the inferior wall or diaphragmatic surface of the heart often gives rise to discomfort in the epigastrium. One must assume that the afferent pain fibers from the heart ascend in the sympathetic nerves and enter the spinal cord in the posterior roots of the seventh, eighth, and ninth thoracic spinal nerves and give rise to referred pain in the T7, T8, and T9 thoracic dermatomes in the epigastrium. Because the heart and the thoracic part of the esophagus probably have similar afferent pain pathways, it is not surprising that painful acute esophagitis can mimic the pain of myocardial infarction.

Action Potentials (AP) in Cardiac Muscle- What made cardiac AP longer

Action Potentials (AP) in Cardiac Muscle

The Cardiac Muscle action potential averages about 105 mv.

It rises from about -85 mv (between beats) to about +20 mv (during each beat).

After the initial spike, the membrane remains depolarized for about 0.2 second (plateau phase).

Plateau is followed by abrupt repolarization The presence of plateau in AP causes 15 times longer  ventricular contraction than in skeletal muscle
.

What made cardiac AP longer

Skeletal muscle AP is caused by sudden opening of fast Na channels (open for a few thousandths of a second).

In cardiac muscle AP is caused by opening of two types of channels:

(1) fast Na channels (same as those in skeletal muscle)

(2) slow Ca channels (also called Ca-Na channels).

Ca channels are slower to open, remain open for tenths of a second, Large numbers of Ca/Na flow inside causing plateau.

Ca entering during plateau activates contraction (in skeletal muscle activated by Ca from sarcoplasmic reticulum (SR)).

The second major difference between cardiac & skeletal muscle is the immediate decrease in “K” ions permeability after onset of AP.

“K” permeability decreases about fivefold (does not occur in skeletal muscle), preventing early return of the AP voltage.

When slow Ca-Na channels close (0.2 to 0.3 second) & Ca – Na ions influx ceases, membrane permeability of K ions increases rapidly.

This rapid loss of K immediately returns the membrane potential to its resting level (repolarization) & ending the AP.

The presence of plateau in AP causes 15 times longer  ventricular contraction than in skeletal muscle