In this article, we will uncover centuries-old mystery of development of cardiac fibrillation due to various causes, including structural heart changes. You will learn about unique abilities of heart’s "transitional" cells, which are part of "antacid barrier" and simultaneously function as an "electrical barrier," preventing reentry wave from penetrating into other generating nodes, thereby blocking the reentry trigger. You will understand that dementia is directly related to a lack of electrical energy in brain, which should be supplied by heart. We'll explain correct process of depolarizing repolarization in the myocardium, leading to the formation of T and U waves. You'll understand how reentry mechanism for extrasystole is triggered. You'll understand that there's no such thing as sick sinoatrial node syndrome, but rather "strong sinoatrial node impulse syndrome" and "weak sinoatrial node impulse syndrome." We are not oncologists, but at the end of the article we will write our opinion on the mechanism of cancer development, which does not contradict the opinions of many researchers, but rather complements theirs.

We began searching for mechanism for the development of atrial fibrillation in 2014, and in 2016, we published our initial results in Journal of Atrial Fibrillation under title "Antiarrhythmic Effect of Antioxidants in Patients with Atrial Fibrillation" [1]. Even then, we had already practically delineated the correct mechanism for development of paroxysmal tachycardia, atrial flutter, and atrial fibrillation associated with structural heart changes. This mechanism was subsequently expanded upon, and in 2026, we published it in the Journal of Clinical Cardiology Interventions under title "Importance of the “antacid barrier” in heart fibrillation mechanism" [2]. We believed this to be ideal mechanism for development of paroxysmal tachycardia, atrial flutter, and atrial fibrillation associated with structural heart changes. But after analyzing all information, we realized that we had indeed written ideal mechanism for development of these arrhythmias for all causes, including structural changes in heart. However, we had overlooked something, and new interesting facts about electrical activity of heart came to mind, which we must share with you. We already wrote in a previous article (link 2) about the existence of an "anti-acid barrier" in heart, which consists of a connective tissue insulating sheath and transitional cells. One of main functions of "anti-acid barrier" is to protect the cardiac conduction pathways, along with the sinoatrial (SA), atrioventricular (AV), and other ectopic nodes of generation located along them, from acid stress (Figure 1).

Briefly, we will describe these mechanisms:

• Damage to distal portion of "anti-acid barrier" leads to myocardial interstitial fluid, which contains excess Na+, K+, and H+ ions, leaking into distal ectopic nodes during acid stress. This hyperacidity irritates several ectopic nodes and predisposes heart to fibrillation, and reentry electrical impulse triggers arrhythmia.
• In some cases, damage to connective tissue insulating sheath of "anti-acid barrier" can be extensive and located in the proximal conduction pathways. In this case, acidity will penetrate one of proximal ectopic nodes, where reentry electrical impulse will travel, and most of the electrical impulse will be released into myocardium, bypassing underlying conduction pathways and Purkinje fibers. This process will generate a large macro reentry wave in the myocardium, which will re-enter generating node, resulting in cardiac flutter.
• Damage to "anti-acid barrier" in proximal conduction pathways may be less significant than in cardiac flutter; this could be cracks or pores in the connective tissue sheath. In this case, acidity will penetrate the same ectopic generating node as in cardiac flutter, but electrical impulse will follow its normal path to distal Purkinje fibers, and paroxysmal tachycardia will appear on ECG.

Spontaneous occurrence of atrial fibrillation due to ectopic contractions originating from the pulmonary veins [5]. We support Mr. Haissaguerre M.'s observation that bronchopulmonary diseases such as pneumonia, chronic obstructive bronchitis, pulmonary embolism, etc., lead to right heart overload and myocardial remodeling, which can damage the anti-acid barrier and lead to acidosis—a direct pathway to arrhythmias described here. Accordingly, similar overload in pulmonary artery, vena cava, or aorta can lead to myocardial overload, which will lead to damage to anti-acid barrier and the development of the paroxysmal arrhythmias described here [6].Cardiac surgery [7]. As with structural changes in heart, cardiac surgery in most cases damages anti-acid barrier. Damage can occur due to direct impact of surgical instruments; ischemia, inflammation, and acidosis accompany any surgery.

Familial cardiac fibrillation [8]. Many authors believe that there are genes directly responsible for the development of familial cardiac fibrillation. We hasten to disappoint you: familial cardiac fibrillation cannot occur due to defects in genes responsible for development of this arrhythmia – such genes do not exist! The development of the aforementioned paroxysmal arrhythmias may be linked solely to mutations in genes leading to myocardial acidosis. Although there is no direct link, it is associated with indirect mechanisms, such as renal acidosis, which maintains acid-base balance of the entire body. Mutations causing distal renal tubular acidosis (for example, in the ATP6V1B1 and ATP6V0A4 genes) can lead to systemic acidosis, which negatively impacts all organs, including myocardium.

Patent foramen ovale (PFO) [9]. A PFO itself does not usually cause fibrillation, but it can indirectly lead to myocardial acidosis, as low blood oxygen levels can lead to lactic acid accumulation. This occurs due to hypoxemia (low blood oxygen levels), which switches the body to a state of anaerobic glycolysis, causing cells to produce more lactate for energy, leading to lactic acid accumulation. The procedure for closure of a PFO (endovascular occlusion) can trigger cardiac fibrillation in the first months after the procedure, as a reaction to the implant or tissue irritation, although this risk decreases in the long term. At the same time, rapid mouth breathing can lead to respiratory alkalosis, which can lead to ventricular tachycardia.

Adipose tissue [10]. Adipose tissue leads to fatty degeneration of the myocardium. This process occurs due to the replacement of muscle cells by fat cells (adipocytes), which can be caused by circulatory disorders, hypoxia, and neuroendocrine disorders. Adipose tissue also produces biologically active substances (cytokines, adipokines), which can influence metabolism and the development of acidosis. Nervous system dysfunction. It is believed that an imbalance between the sympathetic and parasympathetic nervous systems can provoke or maintain arrhythmia. In particular, sympathetic innervation, through stress reactions and excessive stimulation, releases catecholamines (epinephrine, norepinephrine) [11]. Paroxysmal catecholaminergic polymorphic ventricular tachycardia is characterized by the abrupt onset and termination of episodes triggered by physical or emotional stress [12] – it is considered an inherited genetic heart disease. We believe that this is a similar familial cardiac arrhythmia associated with a gene mutation leading to myocardial acidosis. Moreover, the heart rate can reach very high values, sometimes >200-250 bpm, therefore, it is paroxysmal. At the same time, non-paroxysmal polymorphic ventricular tachycardia exists – this is a dangerous rhythm disorder characterized by frequent (>100-150 bpm) irregular ventricular contractions with a constantly changing shape of QRS complexes. Unlike paroxysmal polymorphic ventricular tachycardia, this form can develop gradually and last longer. Our opinion is that this type of arrhythmia, non-paroxysmal tachycardia, is directly related to myocardial alkalosis. Heavy alcohol consumption [13] causes acidosis and adverse histological, cellular, and structural changes in the myocardium, while long-term alcohol abuse leads to cardiomyopathy. Interestingly, alcohol consumption doubles the likelihood of an episode of atrial fibrillation within 4 hours of consumption [14]. The link between the development of acidosis and alcohol consumption is clear.

WPW and CLC syndromes do not directly cause myocardial acidosis or alkalosis. However, the addition of acidosis or alkalosis to these syndromes, when the reentry mechanism operates along an additional pathway, leads to a double load on the myocardium, which is severely stressful for the heart [15]. Accordingly, with the addition of acidosis to WPW and CLC syndromes, transitional cells are damaged, which often leads to the development of paroxysmal supraventricular tachycardia or atrial fibrillation

Broken heart syndrome, or Takotsubo cardiomyopathy. Scientists have used MRI brain scans to prove that emotional and physical stress is directly linked to broken heart syndrome. Excessive stress triggers the release of hormones that provoke metabolic acidosis and literally deafen the heart. Takotsubo cardiomyopathy manifests itself on the ECG with changes similar to myocardial infarction: ST segment elevation and T-wave inversion (especially in V2-V6), QT prolongation, but without signs of acute coronary artery ischemia on angiography, with transient (temporary) dysfunction of the left ventricular apex (resembling an "octopus trap," hence the name) [16]. We believe that Takotsubo syndrome is directly related to alkalosis! It's important to consider that these patients experience a prolonged QT interval, which is a direct sign of alkalosis. Respiratory alkalosis in severe cases can lead to respiratory failure or distress requiring mechanical ventilation, highlighting the close relationship between stress-induced heart failure and breathing, sometimes requiring respiratory support [17]. The patient presented to the clinic for an urgent evaluation after two days of chest pain that began after the death of her dog. Initially, she experienced hyperventilation and acute pain in her left chest, radiating to her left shoulder; She rated the pain as a 6 on a scale of 1 to 10. She took 2 aspirin, but it did not help. The next morning, the pain subsided slightly, but after physical activity, it intensified so much that she took 3 ibuprofen tablets and 1 clonazepam tablet, but this also did not help. Due to persistent chest pain, the patient consulted the clinic with a pain level of 8/10 and was hospitalized. Deep breathing, coughing, and sneezing while lying on her back, with her knees pulled to her chest, increased the pain. Her blood pressure was 90/60 mmHg; heart rate 78 beats per minute; respiratory rate (regular and shallow) 20-28 breaths per minute; oxygen saturation 95%. (Respiratory alkalosis caused by hyperventilation increases the affinity of hemoglobin for oxygen (shifting the oxygen dissociation curve to the left), which improves oxygen saturation in the lungs but hinders its release to the tissues. This is due to low carbon dioxide (pCO2) levels and an increase in blood pH, which shifts the equilibrium and makes hemoglobin more likely to "hold" oxygen.) Physical examination was unremarkable except for the expected single second heart sound, consistent with the absence of a functional pulmonary valve. Electrocardiogram (ECG) revealed sinus rhythm of 95 beats/min with right bundle branch block, prolongation of the QTc interval, and profound T-wave inversions in leads V2–V6, II, and aVL (Figure 2).

The patient's echocardiogram performed a year prior to this incident revealed normal function of the single ventricle, and the most recent cardiac ultrasound showed typical enlargement of the apex. Segmental akinesia developed in the midventricular or apical regions of the heart, with elevated brain natriuretic peptide levels 12–24 hours after the onset of akinesia, elevated troponin levels 24–48 hours after the onset of akinesia, and resolution of segmental akinesia within a few days [18]. Metabolic acidosis and alkalosis are disturbances of the acid-base balance of the blood, when the pH falls below 7.35 (acidosis, excess acid or base deficiency) or rises above 7.45 (alkalosis, excess alkali or acid deficiency) [19]. We believe Brugada syndrome is directly related to acute myocardial acidosis. The shortening of the QT interval, as observed by specialists, must be taken into account. Transient right bundle branch block with ST segment elevation in the right chest is similar to Prinzmetal's vasospastic angina without coronary artery disease. Acidosis can be so rapid that it can temporarily paralyze electrical conduction in the right bundle branch or in the myocardial muscle itself. Please note the following (figure 3) [20], here the connection between acidosis and Brugada syndrome is clearly visible, in addition, very powerful cardiac complexes indicate the strength of the electrical impulse.

The most recently identified genetically determined syndrome is Bundgaard syndrome, also known as familial ST segment depression syndrome (described in 2018). We believe that this syndrome may be directly related to chronic acidosis (if the QT interval is shortened) or alkalosis (if the QT interval is prolonged). Here are the ECG signs of myocardial alkalosis: they include ST segment depression and/or T wave inversion (especially in the right/mid-chest leads V1-4), and QT interval prolongation. Now, look at the ECG of a patient with Bundgaard syndrome; these changes are similar (Figure 4) [21]. As you can see, the only difference may be the notch on the ascending portion of the ST segment depression. We noticed the following changes on the ECG: the PQ interval is shortened, which means that CLC syndrome is present (the researchers did not pay attention to this). In this case, a reverse retrograde conduction of electrical excitation occurs (from the ventricles to the atria along the myocardium, the James bundle), that is, the negative notch is a repeated excitation of the atria (negative P wave).

We conclude this section here, but we would like to share a case report of diabetic ketoacidosis:

A 68-year-old woman was admitted to the hospital with constipation, epigastric pain, vomiting, occasional "coffee-ground" emesis, and melena. Chest pain, osmotic symptoms, and weight changes were absent. She had a history of peptic ulcer disease and was not taking any medications other than over-the-counter fish oil. She had no diabetes or cardiovascular risk factors. Her sister had type 1 diabetes. Physical examination revealed dehydration, moderate tachycardia, and melena on rectal examination. Blood tests, including hemoglobin, coagulation, renal function, and electrolytes, were normal. Glucose was 37 mmol/L, ketones 4.3 mmol/L, and moderate acidosis was observed. She was treated with intravenous fluids, intravenous insulin, proton pump inhibitors, and antiemetics. An electrocardiogram revealed profound T-wave inversion in the inferolateral leads. Cardiac enzyme tests were normal, a chest X-ray was also normal, and an echocardiogram revealed normal left ventricular function. The ECG changes resolved within 24 hours. The patient was diagnosed with diabetes mellitus with high glycated hemoglobin levels, negative diabetes autoantibodies, and elevated C-peptide levels and was prescribed subcutaneous insulin therapy and metformin. Esophagogastroduodenoscopy revealed mild gastritis. ECG changes in diabetic ketoacidosis typically indicate myocardial ischemia or electrolyte disturbances. The literature describes abnormal changes in the ECG in the absence of the above-mentioned causes in patients with diabetic ketoacidosis, which are called “pseudoinfarction” [22].

Repolarizing depolarization of the myocardium, the mysterious U wave and the power of electrical impulses of the heart

The second function of transition cells is unique! We talk about the reentry mechanism and don't consider why all the electrical excitation that reaches the myocardium doesn't reenter the conduction pathways and ectopic nodes, thereby causing the arrhythmias described above in all healthy people? What obstacle stands in the way of the reentry mechanism? Unfortunately, we live in clichés; if it's written this way, then the reentry mechanism unimpededly triggers arrhythmia. We'll disappoint you; nothing simply reenters the conduction pathways; an "electrical barrier" blocks the reentry of the repolarization wave (electrical wave) in a healthy heart. Did you think repolarization was something abstract? No, repolarization is a fading wave of depolarization, and it would seem that it could, having bounced off the epicardium, reenter the ectopic nodes and cause arrhythmia without hindrance, but this doesn't happen! So, there's an "electrical barrier," and it's formed by transition cells. Let's first explain the repolarization process, and then the "electrical barrier." We know that the ventricular myocardium doesn't communicate with the atrial myocardium. The initial electrical excitation of the ventricles begins from left to right, forming the Q wave. Then, the main electrical current reaches the apex, which is the R wave. Then, both ventricles are excited along the lateral sections, forming the S wave. Then, some "wise guy" jumped to the myocardial wall and confused everyone about the repolarization process! But it should have continued like this: after exciting the lateral sections of both ventricles, the electrical wave encounters dead ends (obstacles) and begins to slowly roll back from three sides toward the apex of the heart, merging and re-exciting it (forming the T wave or repeated R2). This excitation is not as strong and does not lead to full myocardial contraction (Figure 5).

We know nothing about the strength of the heart's electrical impulse in millivolts (mV); no one conducts such studies! Meanwhile, every electrician, and you yourself, understand that electrical voltage, especially in our homes, is very important! If the voltage in the house is too high (280-300 volts), some of our equipment may burn out, and if the voltage is too low (100-140 volts), equipment may not work (we think everyone has encountered this problem). What makes the heart's electrical impulses powerful is acidosis, which significantly increases the concentration of Na+ and K+ in the intercellular space of the generating nodes and the myocardium. With acidosis, blood pH decreases (<7.35), which increases the concentration of hydrogen cations H+, which leads to competition with ????+ and ????????+ for channels and transport systems. ????+ displaces ????+ from the cell and competes with ????????+ for ????????+/????+ exchange, leading to ????????+ overload of pacemaker cells and myocytes, which increases the risk of cardiac arrhythmias. Such excess amounts of Na+, K+, and H+ enhance the power of depolarization and accelerate myocardial conduction, thereby shortening the QT interval. Hydrogen (in the form of the proton H+) is involved in the operation of the sodium-potassium pump. Research in 2010 showed that the proton factor in the mechanism of protein conformational change, passing between aspartate and glutamate residues, and can even pass the protein through a channel, synchronously with ion transport [23]. Accordingly, with alkalosis, the amount of Na+, K+ and H+ decreases, which reduces the power of depolarization and repolarization, and the QT interval lengthens. The resulting powerful electrical impulse in the cardiac conduction pathways discharges other generating nodes, including the SA node. Only after reaching the myocardium does the electrical impulse dissipate and lose its power, and can then reenter the conduction pathways (reentry trigger wave), stimulating any generating node. Now imagine that the heart's electrical impulse is powerful. In this case, after repeated excitation of the apex of the heart (the T wave or R2), the excitation wave again excites the lateral portions of the ventricles, but with a weakened impulse. On the electrocardiogram, this is reflected by a descending T wave. Then, the electrical wave again encounters dead ends and begins to slowly roll back from both sides toward the apex of the heart, where minor excitation occurs, forming the U wave or R3 (Figure 6).

What's wrong with a more powerful electrical impulse from the heart? We must understand that everything should be normal, and a more powerful electrical impulse from the heart is not normal! At the same time, powerful electrical impulses from the heart to the brain are very good, because they replenish the brain's battery, and its computer works actively. Many researchers believe that they see nothing dangerous in registering a U wave, but we believe that this wave often accompanies Short QT Syndrome. Short QT Syndrome was first described as a new clinical entity by Gussak . in 2000. Previously, shortening of the QT interval was noted only in the context of electrolyte imbalance (hyperkalemia, hypercalcemia), hyperthermia, acidosis, and endocrine disorders [24]. We also believe that this syndrome is associated with acidosis. Please note Figure 5, ECG of a patient with Short QT Syndrome. High-amplitude symmetrical T waves in V2–V4. QT = 220 Ms. This ECG is described in an article in the journal "Cardiological Bulletin" [25], but there is no mention of the U wave, although it is clearly visible on the ECG (Figure 7). A more powerful electrical impulse conducts electricity more quickly through the myocardium; it is capable of breaking through the "electrical barrier" (also known as the "anti-acid barrier") and conducting a reentrant trigger wave to the generating nodes. Accordingly, powerful impulses lead to myocardial hypertrophy and damage the "anti-acid barrier." Patients with short QT syndrome often die from cardiac fibrillation. Many of you already understand that if a strong electrical signal shortens the QT interval and forms a U wave, this is associated with myocardial acidosis, while a weak electrical signal prolongs the QT interval, which is associated with alkalosis and slower myocardial impulse transmission. Thus, Long QT Syndrome is directly related to chronic myocardial alkalosis! Metabolic alkalosis prolongs the QT interval, increasing the risk of dangerous cardiac arrhythmias, such as torsades de pointes, often associated with concomitant electrolyte shifts, such as decreased ionized calcium levels and sometimes magnesium/potassium imbalances, which affect cardiac repolarization. [26,27]. Non-paroxysmal ventricular tachycardia, including the "pirouette" type, in its fading form can resemble cardiac fibrillation (this is described as an instant transition to ventricular fibrillation).

Figure 1: The figure shows an approximate model of the "anti-acid barrier", let's assume that this is the Bachmann pathway. 2-5. Connective tissue sheath. 4. Transitional cells. 1. Ectopic nodes (1 distal and 4 proximal), 3. Purkinje fibers.

Figure 2: A) The patient's electrocardiogram 2 months before the diagnosis of Takotsubo cardiomyopathy shows sinus rhythm with right axis deviation and right ventricular hypertrophy. B) The patient's electrocardiogram upon presentation with Takotsubo symptoms shows sinus rhythm with new T-wave inversions in leads V2–V6.

Figure 3: A) 12-lead ECG on admission of a patient with severe diabetic ketoacidosis, showing tall, elevated T waves due to hyperkalemia. Note the Brugada type I pattern. B) A repeat ECG 8 hours later, after significant improvement in acidosis, showing resolution of the Brugada type I pattern.

Figure 4: A typical ECG in Bundgaard syndrome: concave-ascending ST segment depression in leads I, II, aVL, aVF, V2-V6. A notch (red arrows) is visible in the ascending portion of the ST segment depression, most pronounced in leads V3-V5.

Figure 5: Ventricular myocardium. The cul-de-sac edges of the ventricles are marked.

Figure 6: Triple excitation of the apex of the heart (R, R2, R3).

Figure 7: ECG of a patient with short QT syndrome. High-amplitude symmetrical T waves in V2–V4. QT = 220 ms.

Figure 8: A 10-year-old boy's ECG, recorded on a bedside monitor during an attack of ventricular tachycardia rapidly transforming to ventricular fibrillation. Following a precordial beat, asystole, the junctional rhythm gives way to an accelerated atrial rhythm with first- and second-degree atrioventricular block.

Figure 9: transmembrane potential, pre-depolarization phase.

Figure 10: The Earth's atmosphere is similar to an "electric barrier".

Figure 11: Supraventricular extrasystoles with an indication of the source of their occurrence.

Figure 12: The arrow indicates the end of depolarizing repolarization and the beginning of true repolarization of the ventricular myocardium.

Table 1: Influence of the brain and shifts in acid-base balance leading to arrhythmias.

Table 2: Differential diagnosis of dilated and hypertrophic cardiomyopathy.

Clinical Case [28]: On November 8, 2011, an ambulance brought a 10-year-old boy to the intensive care unit of Tushino Children's City Hospital No. 7, bypassing the emergency room. He was diagnosed with "Convulsions. Post-clinical death status. Stage 1 mental retardation." His medical history revealed that in the morning, caregivers at the boarding school where he lived found him unconscious and unable to breathe on his own. The ambulance team, responding to the call, performed a series of resuscitative measures, including tracheal intubation, chest compressions, defibrillation, and peripheral venous catheterization. During transport, mechanical ventilation, fluid therapy, and diazepam sedation were administered. Upon admission to the hospital, the child was in extremely serious condition; he was unconscious. He was unresponsive to examination and did not open his eyes. He remained sluggish in response to pain and an endotracheal tube. The pupils are equal in size, narrow, photoreaction cannot be reliably determined. The skin is pale pink, clean. Mucous membranes are moist, pink. Turgor is sufficient. Temperature is 36.2 °C. There are no microcirculatory disorders. Spontaneous breathing is shallow, up to 10 per minute. Mechanical ventilation was performed with an AMBU bag. Capillary blood oxygenation according to pulse oximetry data is SpO2 94-96% with FiO2 21%. Heart sounds are muffled; rhythm is regular. HR 100 bpm. BP 110/68 mmHg. The abdomen is soft, not distended, painless. The liver is at the edge of the costal arch. The spleen is not palpable. Intestinal peristalsis is sharply weakened. There was no stool or urination on admission. Unfortunately, the electrocardiogram data on admission did not note the prolongation of the QT interval at that time (Figure 8). After QT prolongation was detected, lidocaine, magnesium sulfate, and ?-blockers were prescribed.

The authors of this clinical case report conclude: Long QT syndrome is a life-threatening condition requiring differentiated medical and interventional treatment. New genetic discoveries make therapy more specific and effective, offering many patients the chance to return to normal life with some restrictions regarding physical activity and the use of certain medications. Currently, beta-blockers are the treatment of choice, with all other medications being complementary. For drug-resistant cases of long QT syndrome, implantable cardioverter-defibrillator (ICD) and left-sided sympathectomy are used.

Our conclusion: the boy's problems arose due to alkalosis, which has accompanied him since birth and manifests as long QT syndrome. Consequently, mental retardation (mental retardation) is associated with weak electrical impulses from the heart, and the brain does not receive the necessary electrical energy for the body's development. Due to the increased alkalosis at that time, the brain found itself in a critical situation and survived by triggering non-paroxysmal ventricular tachycardia in search of electrical energy! Note what happened after the non-paroxysmal ventricular tachycardia was terminated: non-paroxysmal atrial rhythm with first- and second-degree atrioventricular block developed. This also means that the brain is attempting to extract the electrical energy it needs through an accelerated atrial rhythm and first- and second-degree atrioventricular block. With a 2nd-3rd degree AV block, the brain takes electricity from the ventricles through the AV node. We wrote about this in the article "The brain's battery dependence on the heart's electrical charge."

An example of acute alkalosis. A 55-year-old man dependent on a gastrojejunostomy tube presented to the emergency department with altered mental status. The patient had metabolic alkalosis, electrolyte disturbances, and a prolonged QT interval on an electrocardiogram. Examination and history revealed that chronic gastric acid backflow through a faulty gastrojejunostomy tube led to severe alkalosis. The patient recovered with supportive care, electrolyte replacement, and gastrojejunostomy tube replacement [29]. So, dear colleagues, we're misinterpreting sick sinus syndrome! With sick sinus syndrome, the electrical impulses are powerful, overcharging the brain's battery. The brain doesn't like this, so it slows the heart rate (bradycardia). If the heart doesn't respond, it shifts rhythms and searches for a weaker brain charge, that is, slower replacement rhythms. If this doesn't produce the desired effect, the brain induces varying degrees of sinoatrial block, as the brain's battery has overheated. Episodes of tachy-brady syndrome indicate intermittent hyperacidity—these are manifestations of the new "strong sinus impulse" syndrome! Accordingly, there is also "weak sinus impulse" syndrome, associated with sinoatrial tachycardia, ectopic no paroxysmal tachycardias, and atrioventricular block, and sick sinus syndrome should be forgotten! Now we will try to regulate cardiac arrhythmias (Table 1). Continuing with the topic of weak and strong electrical impulses, imagine this: you began to do less intense daily activities, and your muscles became flabby. What would this lead to? And what would happen to the heart if the electrical impulses were weak? The myocardium would decrease contractility and gradually become flabby, leading to a diagnosis of idiopathic dilated cardiomyopathy! If the electrical impulses are powerful during acidosis, then it's idiopathic hypertrophic cardiomyopathy! Or perhaps many dilated and hypertrophic cardiomyopathies aren't so idiopathic after all? The differences between the two conditions are presented in (Table 2). Patients with early-stage dilated cardiomyopathy likely require permanent ventricular pacemakers to correct contractility problems, with a controlled electrical signal.

Amiodarone is a unique antiarrhythmic drug; it reduces heart rate and prolongs the QT interval (reducing acidosis and decreasing electrical impulse strength). Consequently, amiodarone increases blood iodine levels, which stabilizes pH, leading to prolongation of the QT interval.

Amiodarone, which contains 39% iodine, is a benzofuran derivative with a molecular structure similar to the hormone thyroxine. Thyroxine (T4) and other thyroid hormones indirectly affect the acid-base balance (pH) and can contribute to the development of alkalosis. Each 200 mg tablet of amiodarone hydrochloride also contains 81.6 mg of potato starch. Studies have shown that feeding rats a boiled potato diet (raw or boiled potatoes contain approximately 15% starch) can lead to urinary alkalinization, an increase in urinary pH, and citrate excretion, suggesting that potatoes help neutralize acidity. This effect is associated with an increase in short-chain fatty acids. A three-week boiled potato diet, after feeding wheat, resulted in significant urinary alkalinization (pH shifted from 5.5 to 7.3), along with increased citrate and potassium excretion. Calcium and magnesium excretion in urine accounted for 17% and 62% of the daily absorbed minerals, respectively, in rats [32]. Thus, we can conclude that the QT interval has significant diagnostic value for both heart disease and nervous system disorders! We must understand that the connection between the nervous and cardiac electrical systems is obvious; science has wasted several centuries isolating these two systems! Mental retardation and senile dementia are not so much a neurological problem as a cardiac one. The heart supplies insufficient electricity to the brain, which prevents it from functioning properly. You're probably wondering how the heart's electrical impulses are connected to the brain's electrical system. To find out, you should read the article "Battery Dependence of the Brain on Electrical Charging of the Heart" in the International Journal of Cardiology and Cardiovascular Disorder [33]. In this article, we argue that our body cannot have two independent electrical systems: the nervous system and the cardiac system! The electrical system is unified; the heart is the sole generator of our body, and the brain merely accumulates the electricity it receives! Now we'll tell you how electrical impulses from the nerves enter the sinoatrial node and excite the heart—this is a section not included in that article.

Dual excitation of the sinoatrial node ensures proper functioning of the "potassium-sodium pump."

We often talk about the influence of the parasympathetic or sympathetic nervous system on heart function. But how do you imagine this happening if information in the nervous system is transmitted by electrical impulses? It turns out that we say one thing and mean another – isn't it the nervous electrical impulse that enters the heart?

We posed a question to artificial intelligence: Are electrical impulses from the nervous system conducted to the heart?

Answer: No, impulses from the central nervous system (brain) are not conducted to the heart. The heart has its own internal conduction system, consisting of the sinoatrial node and other structures, which generates and distributes electrical impulses that cause its contractions. However, the nervous system influences the heart by changing the heart rate: sympathetic nerves accelerate the heart rate, while parasympathetic nerves slow it down.

We emphasized the word "affects"—that's the discrepancy. Of course, "electrical impulses from the nervous system are conducted to the heart," and we'll explain how this happens! Since the advent of electrocardiography, many have assumed that electrical impulses must enter the heart. But these specialists were immediately brought down to earth, explaining that, like a supraventricular extrasystole, which interrupts and discharges the sinoatrial node, a nervous electrical impulse will also interrupt the sinoatrial node—and this is logical, but incorrect! The scientific community has long debated whether the sinoatrial node is stimulated by chemical or electrical stimulation. However, it is hypothetically believed that the sinoatrial node can generate electrical impulses through neurochemical influences. We are confident in the neuroelectrical theory! The point is that the electrical impulses in the cardiac conduction pathways are more powerful in millivolts, so they can interfere with each other, and after reaching the myocardium, they become less powerful, like a reentrant wave. The nervous system also has weak electrical impulses, and they enter the sinoatrial node. Note Figure 8: it shows phase 4 of diastole of the sinoatrial node pacemaker cell; nothing is happening there. Furthermore, the teachers explained to us that ion channels open, and large influxes of Na+ and K+ rush into the pacemaker cell. This raises two questions: what stimulus causes the pacemaker cell's ion channels to open, and how do the influxes of Na+ and K+ rush in if the pacemaker cell is completely relaxed in phase 4 and all channels have been opened? It's like a person who's overfed and relaxed; try to force anything else into them, but it won't work! So, for the pacemaker cell to admit Na+ and K+ currents, the first neuroelectrical impulse must pass through it, stimulating a mild excitation with spasm of the sinoatrial node and electrical activation of Na+ and K+ (the pre-depolarization phase). During this phase, the pacemaker cell contracts (empties), rapidly leaking cytoplasm and then begins to rapidly recover, drawing in electrified Na+ and K+ currents. This will be the second (main) excitation of the pacemaker cell (phase 0 of the action potential), but this time, it will be more powerful, generating an electrical impulse in the sinoatrial node. Thus, an additional "pre-depolarization" phase should appear in Figure 9. Once again (for better understanding), the first neuroelectric impulse should contract the sinoatrial node and pacemaker cells, electrify the flows of Na+ and K+, and the second, powerful electrical impulse is formed inside and it does not contract anything, it expands the membrane of the pacemaker cells with an electrical explosion and throws out discharged flows of Na+ and K+ into the intercellular space. P.S. to this section. Before writing this section, we long struggled with the question of what triggers the sinoatrial node to begin functioning at the beginning of the fourth week of embryonic life. Currently, it is believed that this occurs spontaneously. As soon as we wrote this section, everything fell into place! It turns out that at the end of the first week after conception, the embryonic membrane attaches to the uterus, and the woman's brain receives information that she is pregnant. If there are no genetic defects, then at this stage, the correct electrical impulses begin to flow to the uterus via the autonomic nervous system, similar to those sent to one's own heart (many pregnant women feel "uterine pulsation" and tell their doctor). At the beginning of the fourth week (the embryo measures 1.5 to 3 mm), when the tubular heart of the embryo is formed, it is the maternal electrical impulses that "ignite the electric fire in the embryonic heart"! Next, up until the 11th week of pregnancy, the mother will teach her unborn baby how the heart should function properly. Then, the fetal membrane will harden (become covered with connective tissue, which blocks electrical impulses from reaching the fetus) and become the placenta. By this stage, the fetus should have learned its "maternal lessons" and begun to control the heart using its nervous system. These two stages are very dangerous; if there are genetic defects in the mother or fetus, dangerous pauses in the tiny creature's heart can occur (80% of all miscarriages occur in the first trimester of pregnancy). Of course, not all miscarriages are due to this cause; quite a lot.

"Electric barrier" and the formation of a reentry trigger wave

In previous articles, we attributed the discovery of transitional cells to Purkinje cells, but this may not be the case. Researchers Martinez-Palomo, Alanis, and Benitez are cited in foreign sources; in 1970, they identified specialized "transitional cells" [34] that serve as a link between the Purkinje fibers and the working myocardium. The researchers believed that these transitional cells were important for the proper transmission of electrical signals from the Purkinje fibers to the rest of the heart muscle. Although very little is known about transitional cells, it has been hypothesized that these cells may be a potential source of arrhythmogenic activity [35,36]. We have already explained the first important function of the "anti-acid barrier"; we would only like to add that telocytes play an important role in repairing damage to transitional cells. Now it's time to tell you about the second important function of transitional cells: the creation of an "electrical barrier," protecting against the reentrant trigger wave. The "electrical barrier" is also formed by transitional cells. These cells regulate the acid-base balance of the cardiac conduction pathways and ectopic nodes. Consequently, a large number of electrolytes are located near and within them: sodium (Na+), potassium (K+), calcium (Ca2+), and hydrogen (H+) ions. Transitional cells are located in the atria and ventricles, between the Purkinje fibers and the myocardium. In addition, transitional cells surround all generating nodes, which provides double protection against acid stress [37]. When an electrical wave passes through the Purkinje fibers to the myocardium, transitional cells become electrified (accumulate static electricity) and form a protective "electrical barrier," similar to how the Earth's atmosphere protects us from the harmful effects of short-wave electromagnetic radiation from the Sun (Figure 10).

The "electrical barrier" prevents the myocardial excitation wave from rolling back into the conduction pathways and entering the generating nodes. This depolarization wave should fully excite and contract the myocardium, and when it and the "electrical barrier" weaken, the recoiling excitation wave returns to the conduction pathways but does not enter the generating nodes unless their "anti-acid barrier" has been damaged by "acid stress" or dysfunction of transition cells. We understand that the phenomenon of the "electrical barrier" in tissues is difficult to understand, but physics explains it as follows: When an electric wave collides with an electric barrier, it is reflected and transmitted. The fraction of the wave reflected and transmitted depends on the ratio of the wave energy to the barrier height. For classical waves, reflection is complete if the wave energy is less than the barrier energy. In quantum mechanics, a tunneling effect is possible, in which a wave partially passes through a barrier even if its energy is less than the barrier energy [38,39]. We've already explained how the U wave is formed. This would be impossible without the "electrical barrier." The myocardial depolarization wave would fade according to our classical understanding of repolarization processes. Now we'll explain how the reentry mechanism initiates the paroxysmal arrhythmias we've described, and this will be further evidence of the existence of the "electrical barrier." Have you ever wondered why all supraventricular extrasystoles are located in the same place as ventricular extrasystoles, behind the preceding cardiac complex—the T wave (Figure 11)? It's clear why a ventricular extrasystole is located behind the T wave; depolarizing repolarization has just occurred, and the reentry trigger could have triggered it. But the refractory period in the atria has long since ended. In theory, if a reentry trigger had occurred there, a supraventricular extrasystole in the form of a P wave should have been superimposed on the ventricular QRS complex or ST segment. But this doesn't happen; they all appear at roughly the same point (behind the T wave)! Let me remind you that the ventricular myocardium is separated from the atrial myocardium-that's a fact! Electrical impulses can only be conducted from the ventricles to the atria via accessory pathways (the muscle bundles of Kent and James), and only in CLC or WPW syndromes, and the vast majority of people do not have these syndromes! To understand this phenomenon, we'll return to the "electrical barrier." We've already written that in most people, "depolarizing repolarization" ends at the apex of the T wave, where the "electrical barrier" and rebound wave weaken (this is the descent from the apex of the T wave). Meanwhile, the remaining weak electricity returns retrogradely into the ventricular conduction pathways and through the AV node to the atria. Along the way, it can enter any generating node if their "anti-acid barrier" has been damaged by "acid stress" or dysfunction of the transition cells. Accordingly, the first to be retrogradely discharged by the weakened electrical impulse are the ventricles, and only there do early ventricular extrasystoles (R to T) occur (Figure 12). This retrograde movement of a weakened wave along the conduction pathways is only possible after the primary excitation of the ventricles and the onset of true repolarization. Thus, the nervous system scans the integrity of the conduction pathways, the generating nodes, and the "anti-acid barrier," after which all remaining electricity is transferred via the efferent nerve pathways to the brain.  

Proposed mechanism of carcinoma development

The topic of the power of the heart's electrical impulses and the development of acidosis may surprise you, but bioelectrical processes are very important. Let's think about it this way: the bloodstream's delivery of vital elements to organs and tissues is crucial, but no oncology researcher considers the neural electrical pumping function. If we stop the heart, the person will die—that's a fact! But death isn't due to a lack of electricity; the brain can function for several more hours on artificial circulation! Not only the heart performs a pumping function, but also muscles, all organs and tissues, including the cell itself—everything moves and pumps under the influence of electrical impulses, primarily nerves. Acidosis is characteristic of the tumor microenvironment. It doesn't necessarily cause the initial mutation, but it significantly promotes the survival, growth, invasion, and metastasis of cancer cells by causing genetic instability, altering cell behavior, promoting stem cell development, and helping tumors evade the immune response, essentially making "acidic cells" more like "cancerous cells." This acidic state, often a result of the rapid metabolism of cancer cells, creates a vicious cycle in which acidity promotes malignancy, and malignant cells thrive in it. Carcinomas affect the epithelial tissues lining the skin, mucous membranes, and internal organs, including the lungs, gastrointestinal tract (stomach, intestines), mammary glands, prostate, kidneys, and liver. They can develop in ducts, glands, and on the surface of organs. They are the most common type of cancer, characterized by uncontrolled cell growth and the ability to metastasize. Other types of cancer (for example, sarcomas, leukemia) develop from other types of tissue (connective, hematopoietic). We believe that initially, a long-term disruption of metabolic processes (acidosis) plays a significant role in the development of carcinoma. A second stage involves a local increase in the intensity of nerve electrical impulses, as evidenced by the following information.

A study by UK scientists, published in the journal Communications Biology, has shown that the electrical voltage of the cell membrane of malignant cells fluctuates periodically. Dr. Amanda Foust explains: We don't yet know why electrical voltage fluctuates in cancer cells. Professor Chris Bakal explains: This is the first time we've observed such rapid fluctuations in electrical activity in malignant cells. Professor Mustafa Jamgoz explains: Of all the cells in the body, the term "excitability" is typically applied to neurons in the brain and cardiac muscle cells. But our study has revealed the existence of a hidden signaling network among cancer cells, and this network may play a significant role in their behavior and interactions with each other. We already know that electrical activity facilitates the spread of cancer cells in the body—the leading cause of cancer-related deaths [40].

We believe that powerful electrical impulses promote metastasis, both acidosis and cancer. Cancer moves toward the efferent neurons that carry electricity from the brain, and they require a battery.

The third stage is the introduction of an anaerobic infection into acidotic cells, and the fourth stage is the transformation of the cell into a foreign cell to the human immune system. The foreign anaerobic cells then survive by spreading to other acidotic cells. One of the hallmarks of a malignant tumor is a change in the metabolic properties of cells [41]. The acidic environment of the tumor microenvironment plays a critical role in the development of cancer with a more aggressive phenotype, but the underlying mechanisms remain unclear [42]. For the first time, researchers from the Norwegian University of Science and Technology (NTNU) have demonstrated how cancer cells are reprogrammed to produce lactic acid and tolerate the acidic environment that exists around tumors. This discovery could open a completely new avenue for cancer treatment. The breakthrough is the culmination of more than 13 years of work. The study results were published in the journal of the Federation of American Societies for Experimental Biology (FASEB). The next step in this research could completely change the approach to cancer treatment [43]. Evaluating this information, we believe that the topic of the power of nerve electrical impulses (mV) and the development of acidosis, and perhaps alkalosis, will become no less relevant for neurologists and oncologists.

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