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.
There is no simple explanation 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 they end 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 present a new theory that venous blood clots migrate into the heart and interfere with blood flow through the valves. This changes the heart rhythm pattern and causes palpitations. Moreover, venous thromboembolism (VTE) in the pulmonary artery squeeze the esophagus, which causes nausea, burping and difficulty swallowing. Burping (thrombo-ructus) while sleeping causes gastroesophageal reflux disease (GERD).
In 2005 Dr Bode became sick with 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 restless leg because gentle compression eliminates blood clots and prevents the formation of new ones.
Compression of his leg immediately caused palpitations and burping spells. Dr Bode heard heart murmurs with his stethoscope during palpitations and noticed abnormal changes on a portable electorcardiogram (ECG). Turning off the compression sleeve stopped palpitations and arrhythmias. Thus, it was easy to conclude that leg compression squeezed blood clots into the heart, where they caused murmurs at the heart valves. Moreover, clots moved into the pulmonary artery and thumped against the esophagus during the heartbeat, which stimulated burping with nausea.
The goal of this website is to outline the life cycle of venous blood clots and explain how clots cause a large number of problems during their formation, migration, and resolution.
Thrombophysiology by Dr Bode
Dr Rudolf Virchow was a German physician who discovered that blood clots in the lungs were the same as blood clots in the legs. He theorized that pieces of clot in the legs broke looseand migrated through the heart into the lungs and called migrating venous blood clots embolia.
Virchow noticed that trauma, stasis, or hypercoagulation led to the formation of venous clots.
Injury, infection, cancer or pregnancy decreases venous blood flow, which causes hemostasis. This decrease oxygen used during cell metabolism, and lack of oxygen forces cells to change into anaerobic metabolism, which produces metabolic acid.
Metabolic acid changes blood proteins, which coagulate with red blood cells and platelets to form blood clots. Moreover, acid in the blood injures the lining of veins which become sticky and blood clots adhere to veins, which causes phlebitis.
Thus, the life cycle of blood clots begins with hemostasis, altered metabolism, the formation of detritus (loose bloody debris) followed by thrombus formation called deep venous thromboses (DVT).
Later, pieces of DVT clot break loose and migrate out of sore legs during walking or exercise. Migrating clots become known as venous thromboemboli (VTE) and they move into the heart. Sometimes, VTE pass through a congenital hole in the heart and move into the left atrium. VTE inside the left atrium become PDE (paradoxical embolism). PDE embolize and cause pain from decreased perfusion (ischemia) and infarction, tissue death. PDE into the heart cause angina and heart attacks (MI), while PDE into the brain cause TIAs (transient ischemic attacks) and CVAs (cerebral vascular accidents).
It is theorized that VTE in the heart cause the sick sinus syndrome and GERD.
Finally, VTE move out of the heart into the lungs where they stop in alveoli and are called pulmonary emboli (PE).
Venous blood clots (DVT, PDE, VTE, and PE) cause pathology and change vital signs as they form in muscles, migrate through the heart, and dissolve inside the lung.
The life cyle of venous blood clots has inflammation, arrhythmias and syndromes
DVT (deep venous thrombosis): sore, swollen, weak, warm, and red muscles.
PDE / VTE migrates through PFO into the left atrium and cause ischemia / infarction
VTE at 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 causes GERD.
PE: VTE congests lungs, stops oxygen absorption and CO2 exhalation, causes asthma, panic, and narcolepsy.
Pulmonary valve VTE cause bigeminy, pulse deficits, palpitations, and desaturations
It is theorized that cardiac VTE shaped like a torpedo and about the size of a small golf pencil decrease blood flow out of the right ventricle 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 stimulates a protective premature right ventricular contraction (PVC).
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 clot sack. This ruptures the neck of the clot, which releases sticky liquid detritus and decompresses the clot, which reopens blood flow through the pulmonary valve, which allows a normal sinus rhythm (NSR). The heartbeat following PVC pumps extra blood with clot sack and detritus into the pulmonary artery.
Next, the trailing part of the elongated golf pencil shaped 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 another rotating isometric contraction which extends the rupture of the clot sack towards its tail. This releases more liquid detritus, which decompresses the clot and reopens the valve.
A second strong normal sinus rhythm heartbeat ( NSR) pumps extra blood plus the empty clot sac and detritus into the pulmonary artery, which carries the material into the pulmonary artery and lungs.
The ECG pattern is NSR / PVC / NSR / PVC / NSR as the heart skips every other pulse during an ECG pattern called ventricular 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 pulmonary embolism (PE) congests the capillaries of the alveoli. This causes wheezing and difficulty breathing.. Moreover, detritus in the alveoli temporarily prevents the absorption of oxygen during inspiration and stops the exhalation of warm moist vapor full of carbon dioxide during exhalation.
Detritus PE causes desaturation, hypercapnea (elevated carbon dioxide) with narcolepsy, and hyperthermia (fever) 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.
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