Posted on - April 27, 2021
It becomes important to understand the Electrical stability of the heart and the mechanisms behind it especially for those with cardiovascular disease. The rapid eye movement during sleep and dreams have a greater role in increasing the blockage of blood flow to the heart muscles (Myocardial infarction) and sudden death in patients with cardiovascular disease. It affects the heart's major blood vessels leading to heart failure in patients who suffer from respiratory disorders. The breathing repeatedly stops and starts during sleep (central sleep apnea) which results in snoring in patients who have a sudden slowing of heart rate and malfunctioning of ion channels. Ischemic heart disease leads to death in infants, adolescents, and adults with a median age of 59 years. Sleep influences cardiac symmetric response through alteration inactivity of the Nervous system (Central and Peripheral both). The triggering of arrhythmias is not only a function of the central nervous system but can also be because of the information that is obtained by the nerves. The second most important thing is that the triggering of arrhythmias by the central nervous system depends on the inner mechanism which includes the direct effect of transformation carriers neurons (neurotransmitters) on the muscular tissues of the heart and its specialized conducting system and changes the muscles pumping in the heart (myocardial perfusion) due to the alteration in the diameter of muscles or enhances the clumping of platelet in the blood. The internal part of the brain which is called the posterior hypothalamus is an important point of centrally induced arrhythmias. The stimulation of this increases 10 times more the incidence of an inadequate heartbeat can be due to the symptoms of heart attack, by blockage of the coronary artery. These findings report that brain-related activities like intracranial hemorrhage (bleeding inside the skull) influence the cardiac repolarization abnormalities causing life-threatening arrhythmias.
The sympathetic nervous system is the main reason for life-threatening arrhythmias in both animals and humans. Due to the fusion of catecholamine (hormones made by adrenal glands) and stress the cardiac vulnerability increases. This enhancement of Sympathetic activity increases ventricular fibrillation by the continuous occurrence of arrhythmia. Enhanced sympathetic activity increases the vulnerability of the heart, the major effect is due to the impaired oxygen supply or demand due to cardiac metabolic activity and narrowing of coronary vessels ( coronary vasoconstriction).
The Vagus nerve activation is responsible for parasympathetic control of the heart and has both benefits and harmful effects on the heart rhythm. The former occurs from showing ventricular pacemaker (which functions as an activation for the heart when the SA node is unable to generate impulse) and after the completion of a cycle length activity, especially when the sympathetic tone is heightened, this provokes new arrhythmia. Vagal tone reduces the ischemia-induced susceptibility to ventricular fibrillation by threatening heart rhythm and decreasing the heart rate. If the decreasing effect is excessive the benefit of vagal activity can be ruined because of the development of low blood pressure and impaired coronary blood pressure.
Arrhythmias, Vagal tone, vagus nerve activation, ventricular fibrillation, perfusion, heart rhythm, coronary disease, neurotransmitters, Myocardial Infraction, cardiovascular disease, central nervous system References: Verrier, Richard L., James E. Muller, and J. Allan Hobson. "Sleep, dreams, and sudden death: the case for sleep as an autonomic stress test for the heart." Cardiovascular research 31.2 (1996): 181-211