Do you ever lie awake at night and wonder what makes the heart flip and flop like a fish out of water? Suddenly the heart flutters like a humming bird and then slows down with powerful pounding palpitations that cause hot flashes or night sweats.
Patients with fast fluttering pulses followed by slow strong palpitations frequently develop mysterious brain fog, confusion, weakness, and light-headed dizzy spells.
No one can explain why the heart suddenly 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 he or she ends up in the ICU with a fast / slow heart rate following a long night of drinking and dancing coupled with lack of sleep.
The purpose of this website is to explain how blood clots migrate into the heart and interfere with blood flow through the valves. This changes the heart rhythm pattern. Moreover, venous thromboembolism (VTE) in the pulmonary artery squeeze the esophagus, which causes nausea, burping and difficulty swallowing. Burping while sleeping causes gastroesophageal reflux disease (GERD).
In 2005 Dr Bode became sick following right inguinal hernia surgery, and a CT x-ray scan revealed a blood clot inside the iliac vein beneath the surgical site. He took blood thinners and used a venous compression sleeve to squeeze his sore right leg because gentle compression eliminates blood clots and prevents the formation of new ones.
Compression of the leg caused palpitations, which were different. Some were slow powerful flip-flop sensations inside the chest while others were fast sensations in the upper part of the heart associated with fluttering jugular pulsations in his neck. The palpitations stimulated feelings of nausea with the desire to swallow followed by burping.
Dr Bode heard murmurs with his stethoscope during palpitations. Turning off the compression sleeve stopped palpitations and murmurs. It was easy for Dr Bode to "see" that leg compression squeezed blood clots into his heart, where they caused palpitations and murmurs at the heart valves. Moreover, clots went into the pulmonary artery where they pulsated against the esophagus, which stimulated nausea with burping.
Next, Dr Bode attached a pulse oximeter to his finger, which recorded tachycardia, bradycardia and desaturation events.
However, relationships between blood clots, palpitations, heart arrhythmias, or desaturation events have never been established.
The goal of this website is to explain thrombodextacardia (blood clots in the heart), which cause the tachy brady rhythm called the sick sinus syndrome. Moreover, it will explain how blood clots in the pulmonary artery press against the esophagus and cause nausea with burping. Burping while sleeping causes gastroesophageal reflux disease (GERD).
Furthermore, contracting heart valves break clots into pieces of bloody debris called detritus, which move into lung alveoli. Detritus in the alveoli interferes with breathing and causes desaturations, hot flash fevers, night sweats, panic attacks and more.
Thrombophysiology by Dr Bode
Dr Rudolf Virchow discovered during autopsy that blood clots in the lungs were the same as blood clots in the legs. He theorized correctly in 1859 that pieces of clot in the legs broke loose, and moved through venous circulation into the lungs. Virchow called this process embolia.
Virchow noticed that trauma, stasis, or hypercoagulation led to the formation of clots.
At the same time that Virchow studied venous hemostasis, another famous scientist named Louis Pasteur discovered that metabolism of milk sugar without oxygen produced lactic acid. Pasteur published his observations in 1857.
Anaerobic germ metabolism of milk sugar produced lactic acid which made the milk taste sour. Furthermore, Pasteur noticed that lactic acid caused milk protein to coagulate into cheese.
Injury, infection, cancer or pregnancy causes poor venous blood flow, and the area with slow venous blood flow is called a 'compartment syndrome'. The compartment sydrome decreases oxygen supplied to cells, which causes anaerobic cell metabolism and produces metabolic acid. Excess bloody acid denatures bloody proteins and causes denatured proteins to coagulate with red blood cells and platelets into blood clots. This happens in the same way that milk lactic acid denatures milk protein, which coagulate into cheese. Red cells combine with sticky denatured blood proteins and form an adhesive purple gel called detritus. The purple gel matures over time into a blood clot called a thrombus, which adheres to the inner walls of veins inside muscles and causes phlebitis.
The life cycle of blood clots begins with formation of detritus followed by thrombus that forms inside muscles, where clots are called deep venous thromboses (DVT). Later, pieces of DVT clot break loose and migrate out of sore legs during walking or exercise. Migrating clots are called venous thromboemboli (VTE) as they circulate into the heart. Finally, they move out of the heart into the lungs and stop in alveoli, where they are called pulmonary emboli (PE).
Venous blood clots cause pathology and change vital signs as they form, migrate, and dissolve.
The Life Cycle of Blood Clots is full of inflammation, arrhythmias and idiopathic syndromes
DVT (deep venous thrombosis) inflame sore, swollen, weak, warm, and red muscles.
VTE in the heart, thrombodextracardia obstruct the tricuspid heart, which causes tachycardia with fluttering jugular pulsations, pulsus reversus, et pulsus erraticus
VTE obstruct the pulmonary valve, which causes bradycardia, PVCs, skipped beats (pulsus interruptus), and flip-flop palpitations
VTE in the pulmonary artery irritate the esophagus, which causes nausea, burping, and difficulty swallowing. Burping while sleeping causes GERD.
PE stop in the pulmonary alveoli, where detritus causes asthma, night sweats, hot flashes, panic attacks, narcolepsy and idiopathic syndromes
Clots in the pulmonary valve cause bigeminy with pulse deficits, palpitations, and more
It is theorized that compression of sore legs pumps DVT called VTE that are the size of a golf pencil into venous circulation. These soft clots migrate into the heart where they alter blood flow at the pulmonary valve and cause an ECG pattern called bigeminy.
As the clot goes through the pulmonary valve, it reduces blood flow out of the right ventricle which causes a premature rise of pressure inside the ventricle, which triggers a premature contraction of the right ventricle, which prevents distention of the ventricle, which leads to fatal fibrillation.
The premature contraction causes the 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 sac sack that is held by the closed valve. The clot ruptures, which releases sticky detritus and decompresses the clot and reopens the pulmonary valve, which allows a normal sinus rhythm (NSR) heartbeat that pumps extra blood, clot sac, and detritus into the pulmonary artery.
The trailing part of the elongated clot re-obstructs the valve, which causes a second PVC. The second PVC causes the valve to grip the middle part of the clot, which causes a second rotating isometric contraction which extends the rupture of the clot all the way to its tail. This releases bloody glue, which decompresses the clot and reopens the valve. Another normal sinus rhythm heartbeat ( NSR) pumps blood plus the empty clot sac out of the valve into the pulmonary artery.
The ECG pattern is NSR / PVC / NSR / PVC / NSR as the heart skips every other pulse during bigeminy.
If you listen to the heart with a stethoscope during bigeminy, you can hear a soft variable grade I - II systolic murmur at the pulmonary valve as the clot passes through the valve.
Detritus that is released from the clot rupture migrates into the alveoli. Detritus gums up the capillaries of the alveoli, which temporarily prevents the absorption of oxygen during inspiration and stops the exhalation of warm moist vapor full of carbon dioxide during exhalation.
Detritus also causes hypercapnea (elelvated carbon dioxide) with narcolepsy, and hyperthermia (fever), which stimulates vasodilatation with sweating (hot flash / night sweats).
During bigeminy, the right ventricle enlarges during isometric contraction and the left ventricle partially decompresses by pumping out a small volume of blood. The heart "flips" to the left during PVC and flops back to the right after the clot ruptures. This is followed by normal sinus rhythm (NSR), which pumps out the ruptured sac plus extra blood and the heart flops back to the right.
The heart repeats its "flip-flop" process during the second PVC, which is followed by a second normal sinus contraction (NSR). Powerful pounding sensations occur because the ventricle pumps with more force to expel clot with debris plus extra blood during NSR that follows PVC.
The pulse slows down as the heart skips every other pulse during bigeminy. Thus the pulse rate becomes one half of the speed of normal sinus rhythm, which is recorded by the pulse oximeter.
The Gestalt is the whole picture
It takes time to understand the connections between associated events, so focus on one thing and then another, and take time to "see" the whole picture.
Observe how an elongated soft purple thrombus about the size and shape of a golf pencil initially sticks its nose inside the pulmonary valve opening of the outflow tract of the right ventricle.
The tip of the clot obstructs blood flow, which causes PVC that is followed by a rotating isometric contraction of the right ventricle that ruptures the neck of the clot, which releases detritus and deompresses the leading upper part of the clot sac.
A normal sinus contraction pumps the decompressed sac through the valve. Next, the remaining clot sac full of bloody glue enters the valve and re-obstructs opening, which causes a second PVC with another rotating isometric contract, which extends the rupture of the clot sac all the way to its tail, which releases more sticky purple detritus.
This is followed by a normal sinus rhythm contraction, which pumps the remaining clot sac into the lungs. The bloody glue gums up alveoli, which causes an oxygen desaturation event and stops the exhalation of warm moist vapor, which causes narcolepsy.
Thrombophysiology is complicated, so take time to "see" the Gestalt and find joy in your journey as you learn how blood clots in the pulmonary valve cause bigeminy, desaturation events, palpitaions, and narcolepsy with hot flashes.
A New Interpretation of the Electrocardiogram: blood flow generates electric potentials
Dr. Einthoven discovered in 1903 that the heartbeat generates electricity.
Electrophysiologists explain that cardiac cell depolarization and repolarization events generate the electric potentials of the electrocardiogram (ECG). However, there seems to be a fundamental misunderstanding of the ECG.
Moreover, research suggests another way to explain the electric potentials of the ECG.
In 1977, Eugene Findl and Robert Kurtz published research titled Electrokinetic Potentials in a LeftVentricle/Aorta Simulator. They constructed left ventricle/aorta simulators to evaluate the possibility of generatimg EKG like signals by electorkinetic 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."
Blood flow from cardiac contractions generates three separate and distinct electrolyte motion potentials during the heartbeat, and these potentials are the P, QRS, and T waves of the ECG.
First, two atria contract together and generate electrolyte motion P wave potentials.
Next, two ventricles contract together and generate electrolyte motion QRS wave potentials.
Last, the aorta and pulmonary artery contract together and pump blood, which generates electrolyte motion T wave potentials.
Using a new interpretation of the ECG, blood clots alter blood flow through the heart valves, which changes electrolyte motion, which alters ECG patterns.
Thus blood clots in the pulmonary valve cause premature contractions (PVCs) of the ventricle. PVC alters blood flow patterns and electric potentials. Blood clots cause a wide notched QRS as they pass through the pulmonary valve.
Movever, inferior MI (myocardial infarction) causes pathological downward outward bulging of the apex of the ventricles at the start of systole. The altered movement of electrolytes during the start of ventricular systole explains Q waves of the ECG.
Finally, VTE in the pulmonary valve cause the long QT.
Thrombo Theory Questions & Answers:
What makes the heart skip a beat? VTE at the pulmonary valve causes PVC with pulse deficits.
How does a blood clot (thrombus) cause the heart to skip a beat? It interferes with blood flow through the pulmonary valve, which triggers a protective contraction of the ventricle.
What causes blood to form clots? Abnormal metabolism produces acid, which denatures protein, which causes blood to coagulate.
Why does abnormal anaerobic (hypoxic) metabolism make lactic acid? Metabolism without oxygen produces metabolic acid.
Why does cancer cause clots? Dr Otto Warburg discovered that cancer cell glucose metabolism produced lactic acid, and the acid causes blood clots.
Why do runners get clots? Dr Otto Meyerhof discovered that anaerobic muscle metabolism produces lactic acid, which causes blood clots in runners with 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 clots.
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 the heart.
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 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 coughing, nausea, gagging and sneezing? VTE inside the pulmonary artery accumulate at the junction where the artery passes in front of the spine. The esophagus touches the back of the heart and pulsating VTE in the artery choke the esophagus causing difficulty swallowing or talking, coughing, gagging, nausea, and sneezing.
Do blood clots or detritus cause panic attacks or internal 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, which reverses acidosis and reanimates someone suffering from sudden thrombocardiac arrest.
Thrombo Associated Diseases:
Cancer → lactic acid → blood clots (Warburg effect)
Carbon monoxide poisoning: detritus causes night time hypoxemia → carboxyhemoglobinemia
Ultrasound: helps resolve inflammation and phlebitis
Vibration exercise oscillates bloody clots out of heart valves
What do doctors know about carboxyhemoglobin, or the long QT?
Thrombodextracardia is a new theory that explains how VTE interfere with blood flow at the triscupid and pulmonary valves, which causes the tachy-brady rhythm of the sick sinus syndrome.
Blood flow from cardiac contractions generates the electrokinetic potentials of the ECG, and blood clots alter blood flow. The ECG can diagnose blood clots in the heart valves. VTE in the tricuspid valve causes pulsus reversus, PAC, SVT, atrial flutter, and paradoxical atrial fibrillation; while VTE in the pulmonary valve causes PVC, pulsus interruptus, and the long QT.
Thrombo Future: The importance of pulse oximeter / ECG discoveries:
Thrombophysiology: hemostasis alters metabolism and produces acidosis