Do you ever feel dizzy as your heart suddenly flutters like a humming bird. Sometimes it slows down with powerful flip flop sensations. Patients with fast fluttering jugular sensations followed by slow strong flip flop palpitations frequently develop brain fog with sleepy fatigue called narcolepsy.
There is no simple explanation why the heart beats fast or slow; and not much really matters unless it changes our financial condition or romantic relationships. No one cares too much about the tachy-brady syndrome until they end up in the ICU with strange mysterious arrhythmias.
This website describes blood as resin and metabolic acid as a catalyst / hardener that transforms slippery resin full of red cells, platelets, proteins and salty water into sticky purple epoxy glue that becomes a blood clot.
Moreover, when pieces of clot break loose, they migrate into the heart, where they interfere with blood flow through the valves. BMR theorizes that blood clots in the heart cause the mysterious sick sinus syndrone.
Next, migrating clots called venous thromboembolism accumulate in the pulmonary artery next to the esophagus, where they squeeze and pulsate with the heartbeat against the esophagus. Clots next to the esophagus cause nausea, stimulate burping and cause trouble with swallowing. Burping from blood clots (thrombo-ructus) while sleeping causes gastroesophageal reflux disease (GERD).
In 2005 Dr Bode developed a sore restless leg following hernia surgery. A CT scan revealed a blood clot inside the vein beneath the surgical site, and he took blood thinners to dissolve the clot. Later, he used a compression sleeve to squeeze his sore leg because gentle compression eliminates blood clots and prevents the formation of new ones.
Leg compression stimulated palpitations, desaturations, and burping spells. In addition, Dr Bode heard soft musical systolic murmurs with his stethoscope as he felt flip-flop palpitations inside his chest. Turning off the leg squeezer stopped the palpitations and murmurs.Thus, it was easy to 'see' that leg compression squeezed tiny clots into his heart, where they caused murmurs and palpitations as they moved through the heart valves.
This website outlines the life cycle of blood clots and explains symptoms and diseases caused by venous thromboembolism (migrating clots) and pulmonary embolism (clots in the lungs).
Blood clot formation, migration, and resolution:
Dr Rudolf Virchow, a German physician, discovered that blood clots in the lungs were the same as blood clots in the legs. He theorized that clots formed in the legs and that pieces of clot from the legs broke looseand migrated through the heart into the lungs. Virchow called migrating venous clots embolia.
Virchow noticed that stasis, trauma, and hypercoagulability led to the formation of venous clots.
Life Cycle of Venous Blood Clots: DVT, VTE, PDE, PE
Blood is resin and metabolic acid is the hardener that transforms blood into sticky glue called detritus that becomes a solid or semisolid clot called thrombus or DVT (deep vein thrombosis).
Trauma, exercise, infection, cancer, or sitting for a long time causes the formation of metabolic acid, which is the hardener that activates blood coagulation and DVT formation.
Later, muscular contractions during walking or exercise break off pieces of blood clot DVT. Pieces of clot called VTE (venous thromboembolism) migrate into circulation and move into the heart, where they cause palpitations, arrhythmias, and skipped heartbeats with paradoxical ideopathic syndromes.
VTE inside the right atrium of the heart is a potential source of paradoxical embolism (PDE). These are clots that pass through a congenital hole inside the heart between the right and left atria. VTE that move from the right atrium into the left atrium become PDE. Paradoxical emoboli are a potential cause of TIA (transient ischemic attack), ischemic CVA (cerebral vascular accident), or embolic heart attacks, MI (mycardial infarct).
Most VTE migrate through the right heart (thrombodextracardia) and pass into the lungs where they stop in alveoli. Migrating clots that stop in the lungs are pulmonary emboli (PE).
Venous Blood Clot Cycle Summary:
1. DVT (deep venous thrombosis): cause sore, swollen, weak, warm, and red muscles, source of VTE
2. PDE (paradoxical emoblism), VTE that pass through PFO into left atriam, thrombolevocardia
3. VTE (venous thromboembolism) in the right heart, thrombodextracardia
VTE in the tricuspid valve causes tachycardia with fluttering jugular pulsations
VTE in the pulmonary valve causes bradycardia with flip-flop palpitations
VTE in the pulmonary artery causes thrombo ructus, which leads to GERD.
4. PE (pulmonary embolism): VTE in the lungs cause congestion, difficulty breathing, wheezing, stop oxygen absorption, and prevent exhalation of warm moist vapor full of carbon dioxide
An elongated tubular clot passing through the pulmonary valve causes skipped beats with flip-flop palpitations.
It is theorized that a semisolid VTE shaped like a torpedo about the size of a small golf pencil enters the pulmonary valve of the right ventricle.
First, as the clot enters the pulmonary valve, it reduces blood flow out of the right ventricle, which causes a premature rise of pressure inside the ventricle. This pressure stimulates a protective premature right ventricular contraction (PVC).
The premature contraction causes the pulmonary valve to close and grip the nose of the clot as the right ventricle develops an isometric rotating contraction that ruptures the neck of the clot sack. Thr ruptured neck of the clot releases sticky liquid detritus and decompresses the clot. As the clot becomes smaller, blood flows resumes out of the right ventricle into the pulmonary artery. This allows a normal sinus rhythm (NSR) cardiac contraction. However, the powerful strong heartbeat following PVC pumps extra blood with clot and detritus into the pulmonary artery and causes flip-flop sensations.
Next, the trailing part of the elongated golf pencil shaped clot enters and re-obstructs the valve, which causes a second PVC. The second PVC causes the pulmonary valve to grip the middle part of the clot, which causes another rotating isometric contraction which extends the rupture of the clot sack towards its tail. This releases more liquid detritus, which decompresses the clot sack and reopens the valve.
A second powerful normal sinus rhythm heartbeat ( NSR) pumps extra blood plus the empty clot sac with detritus glue into the pulmonary artery, which carries the material into the lungs.
The ECG pattern is NSR / PVC / NSR / PVC / NSR as the heart skips every other pulse during an ECG pattern called ventricular bigeminy. Moreover, the pulse oximeter records an oxygen desaturation event when detritus glue from the ruptured clot gums up the alveoli.
Desaturation starts approximately 20 to 30 seconds following bigeminy. Desaturation continues for about 40 to 60 seconds as powerful pulmonary enzymes in the alveoli dissolve the detritus, which restores capillary circulation and reverses the desaturation event.
During bigeminy, the heart flips and flops because the right ventricle enlarges during isovolumetric right heart contractions (PVC) when the clot obstructs the right ventricular out flow tract (RVOT). During PVC, the left ventricle partially decompresses by pumping out a small volume of blood and the heart "flips" to the left. Later during normal sinus rhythm (NSR), the heart flops back to the right after the clot ruptures and releases detritus, which restores blood flow out of the heart decompressing the right ventricle. Thus PCV / flip to left, NSR / flop back to right / PVC flip to left / NSR flop back to right.
In 1903 Dr. Einthoven discovered that the heartbeat generates electricity. However, there seems to be a fundamental misunderstanding of the electricity of the heartbeat.
In 1977, Eugene Findl and Robert Kurtz published Electrokinetic Potentials in a LeftVentricle/Aorta Simulator. They constructed left ventricle/aorta simulators to evaluate the possibility of generating EKG like signals by electrokinetic methodology.
According to Findl and Kurtz, "The simulators produced pulsed turbulent flows, simulating mammalian heart pumping conditions. EKG like signals were generated by the motion of the electrolyte through the simulators."
BMR theorizes that blood flow generates electricity, which explains the waves of the ECG.
Blood flow from cardiac contractions generates three sequential distinct potentials during the heartbeat. These potentials are the P, QRS, and T waves of the ECG.
First, two atria contract together and generate P wave potentials caused primarily by retrograde flow of blood from the right atrium into the jugular vein.
Next, two ventricles contract together and generate QRS wave potentials.
The Q of the QRS starts at the beginning of systole during isovolumetric bulging of the apex of the conjoint ventricles. The Q wave is followed by blood flow out of the ventricles into the aorta and the pulmonary artery, which generates the RS of the QRS.
Last, the aorta and pulmonary artery contract together and pump blood, which generates T wave potentials that are mainly caused by blood flow into the carotid arteries.
Thrombo Arrhythmias, PAC, PVC, Q waves and broken heart syndrome, long QT
Blood clots alter blood flow through the heart valves, which alters ECG patterns because blood flow generates the ECG waves.
Blood clots in the tricuspid valve cause premature atrial contractions, atrial flutter, or atrial fibrillation.
Moreover, blood clots in the pulmonary valve cause premature ventricular contractions.
PDE (paradoxical emoblism) into the RCA (right coronary artery) cause inferior MI (myocardial infarction) that weakens the apex of the conjoint ventricles. This causes a pathological downward outward bulging of the apex of the at the start of systole (takotsubo effect / broken heart syndrome), which causes the Q wave.
Finally, pulmonary valve VTE causes a long QT.
Thrombo Theory Questions & Answers:
What makes the heart skip a beat? Pulmonary valve VTE causes PVC's with pulse deficits.
How does a solid blood clot (thrombus) cause the heart to skip a beat? It interferes with blood flow through the pulmonary valve, which triggers a protective premature contraction of the ventricle.
What causes blood to form clots? Anaerobic metabolism produces acid, which causes blood to coagulate.
Does cancer cause clots? Dr Otto Warburg discovered that cancer cell glucose metabolism produces lactic acid, so BMR theorizes that cancer causes clots and detritus.
Do runners get clots and PVC's? Dr Otto Meyerhof discovered that anaerobic muscle metabolism produces lactic acid, so BMR theorizes that lactic acid from strenuous running causes blood clots, PVCs and palpitations.
How does lactic acid activate the blood clotting mechanism? Acid denatures blood proteins, which becomes like velcro. Sticky proteins coagulate with platelets and red cells to form bloody glue called detritus that hardens over time into semisolid or solid thrombus (healing clot).
What makes blood clots migrate (embolize) into heart valves? Exercise or walking breaks off pieces of DVT and squeezes them out of sore veins into circulation.
What happens to the heart rhythm as clots pass through different heart valves? VTE at the tricuspid valve causes tachcardia and VTE at the pulmonary valve cause bradycardia.
Do blood clots cause fluttering or flip flop palpitations? Yes.
Why do arrhythmias cause low blood pressure with lightheaded dizzy spells? VTE reduces the cardiac ejection fraction, which reduces blood pressure and causes lightheaded dizzy spells.
Does partly clotted blood called detritus interfere with breathing? Yes.
How do blood clots cause nausea, gagging or trouble swallowing? Yes, VTE inside the pulmonary artery accumulate at the junction where the artery passes in front of the spine. The esophagus is contiguous with the back of the heart and pulsating VTE in the artery choke the esophagus causing difficulty swallowing, nausea, burping, and gagging sensations.
Do blood clots or detritus cause panic attacks or suffocation? Yes.
Do blood clots cause pulseless fainting? Yes.
How do blood clots cause epileptic seizures? VTE at the pulmonary artery stops the flow of blood into the brain and lungs, which triggers an anoxic convulsions.
Do blood clots cause sudden thrombocardiac arrest? Yes, VTE obstruct the pulmonary valve, which stops cardiac output.
How does CPR reanimate someone with cardiac arrest without defibrillation? CPR expels clots out of the obstructed valve, which reopens blood flow into the brain and lungs. Restoring blood flow into the lungs reverses acidosis and reanimates someone suffering from thrombocardiac arrest.
Theory of Thrombo Associated Diseases:
Cancer → lactic acid → blood clots (Warburg effect)
Carbon monoxide poisoning: detritus causes night time hypoxemia → carboxyhemoglobinemia