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.
This website presents a new theory that venous blood clots migrate into the heart and interfere with blood flow through the valves. Clots in the valves change 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 leg because gentle compression eliminates blood clots and prevents the formation of new ones.
Compression of his leg stimulated palpitations, arrhythmias, desaturations, and burping spells. Dr Bode heard heart murmurs with his stethoscope during palpitations. Turning off the compression device stopped the palpitations.Thus, it was easy to conclude that leg compression squeezed tiny mobile clots into the heart, where they caused murmurs at the heart valves. Moreover, clots in the pulmonary artery thumped against the esophagus during the heartbeat, which stimulated nausea and burping.
This website outlines the life cycle of venous blood clots and explains how clots cause problems during their formation, migration, and resolution.
Thrombophysiology: the study of blood clots
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, or pregnancy decreases venous blood flow, which decreases tissue oxygen. This lack of oxygen forces cells to develop anaerobic metabolism, which produces metabolic acid. Moreover, cancer cell metabolism is abnormal and produces metabolic acid.
Metabolic acid causes blood proteins to coagulate with red blood cells and platelets to form blood clots. Blood acid burns the lining of veins which become sticky, which causes blood clots to adhere to the inside walls of veins. Blood clots cause phlebitis.
Life Cycle of Venous Blood Clots
The life cycle of blood clots begins with hemostasis, altered metabolism, and the formation of detritus (liquid bloody glue) 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), which move into the heart. Sometimes, VTE pass through a congenital hole in the heart and become paradoxical embolim (PDE) inside the left atrium. PDE cause pain and infarction (tissue death). PDE in coronary arteries cause angina and heart attacks (MI), while cerebral (brain) PDE cause TIAs (transient ischemic attacks) and CVAs (cerebral vascular accidents).
Next, it is theorized that VTE in the heart cause the sick sinus syndrome and GERD.
Finally, VTE move 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.
1. DVT (deep venous thrombosis): cause sore, swollen, weak, warm, and red muscles.
2. PDE (paradoxical emoblism) = VTE migrate through PFO into the left atrium and cause ischemia / infarction
3. VTE in the 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: VTE congests lungs, stops oxygen absorption, prevents CO2 exhalation, causes asthma, panic, and narcolepsy.
The heart skips a beat: pulsus interruptus
It is theorized that a semisolid VTE shaped like a torpedo and about the size of a small golf pencil enters the pulmonary valve of the right ventricle. This decreases blood flow out of the right ventricle at the and causes an ECG pattern called bigeminy.
First, 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 systolic murmur at the pulmonary valve as the clot passes through the valve.
Detritus (liquid clot) that is released from the semisolid clot migrates into pulmonary alveoli. PE congests the capillaries of the alveoli, which causes wheezing and difficulty breathing.. Moreover, detritus in the alveoli temporarily stops the absorption of oxygen during inspiration and prevents 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), which explains the sweating from hot flashes during PMS (premenstrual syndrome) or night sweats in patients with lymphoma.
During bigeminy, the heart flips and flops because the right ventricle enlarges during isometric contractions as 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, which restores blood flow out of the heart. 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, debris, and extra blood during NSR that follows PVC.
The pulse slows down as the heart skips every other pulse during bigeminy because the heart contracts isometrically without pumping blood during pulsus interruptus.Thus the pulse rate becomes half of the speed of the ECG rhythm The pulse oximeter records a pulse deficit as the ECG records a non-perfusing PVC.
A Novel ECG Interpretation: blood flow generates electricity
In 1903 Dr. Einthoven discovered that the heartbeat generates electricity.
Cardiac electrophysiologists explain that cardiac muscle cell depolarization and repolarization events generate the electric potentials of the electrocardiogram (ECG). However, there seems to be a fundamental misunderstanding of the ECG.
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 generatimg 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."
It makes more sense to explain the T wave of the ECG in terms of blood flow generated by the contractions of the aorta and pulmonary artery. In addition, the Q wave can be explained as the downward outward bulging of the conjoint ventricles at the start of systole. Finally, ectopic pacemaker "re-entry" circuits observed inside the left atrium during supraventricular tachycardia (SVT) or atrial fibrillation make more sense if retrograde blood flow into pulmonary veins generates "re-entry" circuits.
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 P wave potentials caused by retrograde flow of blood from the right atrium into the jugular vein.
Next, two ventricles contract together and generate QRS wave potentials caused by blood flow from the left ventricle into the aorta plus blood flow from the right ventricle into the pulmonary artery.
Last, the aorta and pulmonary artery contract together and pump blood, which generates T wave potentials that are mainly caused by blood flow upwards towards the carotid arteries.
Blood clots alter blood flow through the heart valves, which alters ECG patterns because blood flow generates the ECG waves, and altering blood flow will change the wave patterns.
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 (PVCs). Blood clots cause a wide notched QRS as they pass through the pulmonary valve.
Movever, 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 of the 'broken heart syndrome). The downward movement of blood during the start of ventricular systole explains the Q waves of the QRS of the ECG caused by embolic myocardial infarction.
Finally, pulmonary valve VTE cause the long QT because blood flow out of the pulmonary artery is delayed, which delays and lengthens the T wave of the ECG.
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 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 metabolic acid causes blood clots.
Why do runners get clots and PVC's? Dr Otto Meyerhof discovered that anaerobic muscle metabolism produces lactic acid, which causes blood clots, PVCs and palpitations in runners.
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. Early CPR prevents ventricular muscle dilation, which requires powerrful defibrillation to reverse.
Theory of 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, the sick sinus syndrome 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.
Novel ECG Interpretation: Findl and Kurtz
Blood flow from cardiac contractions generates the electrokinetic potentials of the ECG. Because blood clots alter blood flow, which alters the ECG pattern, 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.
Novel circulating pH Biomarker:
SpCO (carboxyhemoglobin) identifies extremities with acidosis, which causes DVT formation and peripheral neuropathy with restless leg syndrome.
Thrombo Future: The importance of pulse oximeter / ECG discoveries:
Thrombophysiology: hemostasis alters metabolism and produces hemoacidosis