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cardiac arrhythmia and atrial fibrillation

Strictly speaking, atrial fibrillation is also a specific type of cardiac arrhythmia. Arrhythmias can be seen in almost everyone. Normally, the sinus node in the atrium provides the "electrical ignition", which is then conducted via the atrial conduction system via the frequency filter, the AV node, to the heart muscle cells. The sinus node can be described as the body's own pacemaker, which is subject to the vegetative influences of the sympathetic and parasympathetic nervous system. The sympathetic nervous system is the fight and flight nerve that accelerates the heart rate. The parasympathetic nervous system is the relaxation nerve that slows the heartbeat, for example when sleeping. This already shows how stress and excitement can affect our heartbeat. In principle, every heart muscle cell can also act as a conductor for excitation. This makes the heart less susceptible to blockages in the conduction system.


Sometimes young people are concerned about the "palpitations" they feel. These arrhythmias are usually harmless and can be triggered by stress, overtiredness or exhaustion of the autonomic nervous system. There are also rare dangerous arrhythmias in young people like WPW syndrome (Wolff-Parkinson-White syndrome), but that's rare. These are additional pathways between the ventricles and the atrium. This leads to a menacing circling electrical excitement.

A basic distinction must be made between arrhythmias that arise in the area of the atrium and those that originate in the ventricles. If the form of the cardiac excitation shown in the ECG looks like normal excitation, this is an arrhythmia from the auricle area, since these use the normal conduction system after passing through the AV node and are not distorted as a result. If the complexes appear wider, the arrhythmia is developing in the heart chamber because the excitation propagation takes other paths. As a result, the current travels longer and the heart action appears wider due to the time axis of the ECG. Individual failures from the ventricle (ventricular extrasystoles) are not dangerous. However, when they pile up like a machine gun salvo, the risk increases. It is of particular concern if these bursts increase in frequency, ie if the intervals between the extrasystoles become shorter, since this can lead to ventricular flutter and ventricular fibrillation, which ultimately leads to cardiac arrest. It is also of concern if the arrhythmias increase under stress, for example with a stress ECG. They are then usually not noticed by the person concerned. This can be due to coronary heart disease or dilated cardiomyopathy, in which the arrhythmias are triggered by overload or lack of oxygen.

Arrhythmias from the atrial area are generally less of a concern, since ventricular fibrillation does not occur even with atrial fibrillation. Atrial fibrillation occurs when high-frequency electrical impulses are generated in the atrial area, which are then transmitted to the ventricles. The sinus node normally responsible for generating the excitation is then no longer relevant. Fortunately, there is the AV node, which does not transmit the predetermined rate of atrial fibrillation (350-600 per second) one-to-one. It holds back most   atrial stimuli so that only an occasional impulse is transmitted to the ventricle. this leads to a completely irregular heart rate. The frequency can therefore vary between 40 and 120/min per drum beat. If we didn't have the AV node, the one-to-one conduction would quickly lead to cardiac arrest. Even with atrial fibrillation, the frequency is not always in the optimal range. Sometimes there is bradycardia (a rate that is too slow, below 50 per minute) and sometimes absolute thachyarrhythmia, with a rate that is too fast, up to 170 per minute. This is where medication is needed. In the case of the low frequency, only the implantation of a pacemaker is often possible.


Electrical cardioversion is often recommended for new-onset atrial fibrillation. A powerful electric shock is given through the heart under short-term anesthesia, which restores the old sinus rhythm. For me, the method is not particularly convincing, since the atrial fibrillation often recurs. That's not surprising either, because once the atrial fibrillation has made its way, it will do it again. Cardiac catheter ablation has also been used more frequently in recent years. Here, a catheter is used to try to find the point in the atrium that is decisive for triggering atrial fibrillation. Then this place is electrically sclerosed. Success stands and falls with the experience of the cardiologist. This procedure was also unsuccessful in many patients. While atrial fibrillation itself is not that dangerous, it does carry certain risks.Sinus rhythm also excites the atrial area. As a result, the atrium contracts and supports the flow of blood into the left ventricle. When atrial fibrillation occurs, cardiac output decreases by approximately 20%. This is not a problem in itself, unless it occurs in the case of significant cardiac insufficiency, such as dilated cardiomyopathy. The fall in blood pressure can then become a concern for the patient.


However, there is another more common problem. Because the atrium no longer contracts during atrial fibrillation, clots can form in the flaccid atrium because the blood no longer flows through the atrium normally, but squirms around in it. Therefore, anticoagulants such as Marcumar or the new NOACs should be taken for atrial fibrillation. This in turn increases the risk of bleeding and I am not a friend of the stubborn implementation of the guidelines. From my point of view, two circumstances speak against the prescription of anticoagulants. Firstly in case of anemia (low blood count). I immediately discontinued the anticoagulants prescribed by the hospital for a patient after bypass surgery because the patient only had a hemoglobin (red blood pigment) of 8 mg% (lower normal limit 13 mg%). A single complication, such as a bleeding stomach ulcer or an accident, would be immediately life-threatening. Second, I think exceptions should be made if the atrial fibrillation is intermittent. There are always patients who suffer paroxysms of atrial fibrillation. The flickering then stops by itself. Patients do not always notice the arrhythmias. This is of course dangerous if you are not taking a blood thinner when the arrhythmia occurs. But the new smartwatches, i.e. wristwatches with all sorts of functions, including an ECG, make it possible to detect atrial fibrillation. In 2019 I was called for the first time by a patient who had diagnosed his own atrial fibrillation in this way. I was still a bit skeptical. After looking at the EKG, I was able to confirm the arrhythmia. In the past, an event recorder was needed to detect this arrhythmia. The patients had to wear it like a long-term ECG and press a button when they felt something. Then the arrhythmia was recorded. At the largest medical fair, the "Medica", I asked about such an event recorder. The representative told me that all companies had stopped developing because smartwatches had replaced devices.Apple employed 1,500 people to develop it. No medical device manufacturer can afford that.


In my opinion, smartwatches make better therapy possible for patients with intermittent atrial fibrillation. I advise you to take the new anticoagulants (Noaks) while the atrial fibrillation occurs. The fact that the anticoagulant takes a few hours to take effect is not a problem. It was previously agreed among cardiologists that clot formation, if it occurs at all, takes at least three days. Then it does not depend on 2 to 3 hours until the onset of action.

Another way to prevent clot formation is to occlude the left atrial appendage. This is an area in the left atrium where clot formation is particularly prone. The left atrial appendage can be closed and sealed with a catheter. The blood clots are feared because they cause vascular occlusions. In principle, this can be in any organ. Very often they are directed to the head and lead to strokes.

A special form of atrial arrhythmia is atrial flutter. Here the frequencies are between 220 and 350 per minute. As a rule, the AV node also works well here and, for example, only allows every third impulse to pass into the ventricle. However, there is a risk that if the AV node fails, every beat will be conducted, which can lead to ventricular flutter and ventricular fibrillation with cardiac arrest.

It can also happen that the sinus node fails completely. Then the AV node is the lifeline again, which itself takes over the pacemaker function. However, it only sends out a heart rate of 40 per minute. The patients do not feel well, but they survive. Any cause of a slow heart rate will require the implantation of a pacemaker unless the slow rate is caused by medication such as beta blockers, which can be stopped.

There are entire books on the multitude of arrhythmias. I was able to describe the most important ones at this point. In general, some medications can be used to treat cardiac arrhythmias. I've never been a friend of that. Because first you should find out why the heart reacts with arrhythmias. It is therefore important to treat the heart holistically and not simply to carry out an ECG cosmetic procedure. The drugs against cardiac arrhythmia are either negatively inotropic (weaken the pumping capacity) or have serious side effects, eg on the cornea or thyroid gland.  A comprehensive examination of the heart is the basis for a holistic therapy of the same using allopathic and naturopathic medicines and cell-specific therapy.

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