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 develop fast fluttering pulses followed by slow strong palpitations and these patients suffer 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 share new insights about the heart rhythm; and explain how blood clots in the heart change its rhythm by interfering with blood flow through the heart valves. Moreover, venous thromboembolism (VTE) in the pulmonary artery irritates the esophagus, which causes nausea, burping and difficulty swallowing. Burping while sleeping causes gastroesophageal reflux disease (GERD).
In 2005 Dr Bode became sick following inguinal hernia surgery, and a CT x-ray scan revealed a blood clot inside the iliac vein beneath the surgical site. Someone recommended that he use a venous compression sleeve to squeeze his sore leg because compression helps resolve blood clots and prevent the formation of new ones.
When Dr Bode squeezed his sore leg, he developed palpitations that were powerful flip-flop sensations inside the chest and these were mixed with fluttering jugular pulsations in his neck. Dr Bode used his stethoscope and listened to soft systolic murmurs at the pulmonary valve. It was easy to hear murmurs as the compression device squeezed his sore leg and turning off the compression sleeve stopped the palpitations and murmurs. Thus, it was easy for Dr Bode to "see" that blood clots from his sore leg were migrating into the heart, where they caused palpitations and murmurs as they passed through the pulmonary heart valve and moved into the lungs.
Next, Dr Bode attached a pulse oximeter to his finger, which showed patterns of bradycardia during flip-flop palpitations and desaturation patterns followed the arrhythmias.
Dr Bode's wife, a worried nurse, took him to the recovery room where the electrocardiogram showed a pattern called ventricular bigeminy during bigeminy and flip-flop palpitations.
Dr Bode consulted medical colleagues, but no one could explain palpitations or skipped heartbeats called premature ventricular contractions (PVCs). The tachy-brady pattern called the sick sinus syndrome is a paradoxical mystery.
There are no accepted relationships between venous thromboembolism and palpitations, arrhthmias, and oxygen desaturation events.
Thrombophysiology by Dr Bode
Dr Rudolf Virchow in 1859 discovered during autopsy 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 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.
Venous hemostasis changes metabolism from aerobic into anaerobic metabolism, which generates metabolic acid. This was first discovered by Professor Louis Pasteur around 1857.
Dr Pasteur discovered that anaerobic germ metabolism of milk sugar produced sour milk with lactic. Pasteur noticed that lactic acid caused milk protein to coagulates into cheese. The compartment syndrome of the body produces anaerobic metabolism and lactic acid.
Metabolic acid in venous blood denatures blood proteins, which combine with red cells to form sticky purple gel. This soft gel called detritus matures over time into a blood clot called a thrombus, which adheres to the inner walls of veins inside muscles and causes phlebitis.
Blood clots have a life cycle that starts inside muscles as deep venous thromboses (DVT). Later, pieces of DVT clot break loose and migrate out of sore legs during walking or exercise. Migrating clots become venous thromboembolisms (VTE) and circulate into the heart. Next They move into the lungs and stop in the alveoli, where they are called pulmonary emboli (PE).
Venous blood clots cause pathology and change vital signs.
The Life Cycle of Blood Clots is full of arrhythmias and idiopathic syndromes
Heart VTE, thrombodextrocardia in the right atrium obstruct blood flow through the tricuspid heart, which causes tachycardia with fluttering jugular pulsations (pulsus reversus)
Thrombodextrocardia in the right ventricle obstruct blood flow through the pulmonary valve, which causes bradycardia, PVCs, skipped beats (pulsus interruptus), and flip-flop palpitations.
Thrombodextrocardia in the pulmonary artery irritate the esophagus, which causes nausea, and burping, and difficulty swallowing. Burping while sleeping causes GERD.
VTE moves into the lungs and stop in pulmonary alveoli, where clots are called pulmonary emboli (PE).Detritus causes asthma, night sweats, hot flashes, panic attacks, and narcolepsy.
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 and shape 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.
Because the clot is long, the trailing part of the clot re-obstructs the valve, which causes a second PVC. The second PVC causes the valve to grip the middle of the clot, which causes a second rotating isometric contraction which extends the rupture of the clot all the way to its tail, 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 and the heart skips every other pulse during bigeminy because of isometric non-perfusing PVCs when the clot obstructs the pulmonary valve.
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.
Next, detritus is released from the clot rupture and 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.
Pulmonary detritus following bigeminy causes a delayed (ten to twenty seconds) oxygen desaturation event. It also causes hypercapnea (elelvated carbon dioxide) and delayed hyperthermia (fever). Elevated carbon dioxide causes narcolepsy and hyperthermia stimulates vasodilatation with sweating (hot flash or night sweats).
During bigeminy, the right ventricle enlarges during its rotating isometric contraction and the left ventricle 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 allows normal sinus rhythm (NSR) to pump out the ruptured sac plus extra blood.
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 following PVC.
The pulse slows down as the heart skips every other pulse during bigeminy so that the pulse rate during thrombobradycardia is one half of the speed of normal sinus rhythm.
The Gestalt is the whole picture
It takes time to understand how associated events are connected, so focus on one thing and then another, and take time to gradually "see" the whole picture.
Observe how an elongated soft purple thrombus initially sticks its nose inside the pulmonary valve opening of the outflow tract of the right ventricle.
The clot causes PVC that is followed by a rotating isometric contraction of the right ventricle that ruptures the neck of the clot, which release detritus and deompresses the 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 re-obstructs the valve causing 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:
Dr. Einthoven discovered in 1903 that the heartbeat generates electricity.
Electrophysiologist explain that cardiac cell depolarization and repolarization events generate the electricity of the electrocardiogram (ECG). However, there seems to be a fundamental misunderstanding of the ECG.
Moreover, there is an alternative 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 fabricated several left ventriicle/aorta simulators to evaluate the possibility of generatimg EKG like signal 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 different cardiac contractions generate three distinct electrolyte motion potentials during the heartbeat that occur each second of time.
First, two atria contract together and create electrolyte motion P wave potentials.
Next, two ventricles contract together and create electrolyte motion QRS wave potentials.
Last, the aorta and pulmonary artery contract together and pump blood, which generates electrolyte motion T wave potentials.
Blood clots alter blood flow through the heart valves, which changes the electrolyte motion, which changes the ECG pattern.
Pathological Q waves are caused by the downward outward bulge of the apex of the ventricles at the start of systole, and electrolyte motion explains the Q wave of the QRS.
Thus, VTE in the pulmonary valve cause PVC and a long QT with a wide split T wave.
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.
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: 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?
Thrombodextrocardia 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 electorkinetic potentials of the ECG and the ECG can diagnose blood clots in the heart valves. VTE in the tricuspid valve causes PAC, SVT, atrial flutter, and paradoxical atrial fibrillation. VTE in the pulmonary valve causes PVC, bigeminy, and the long QT.
Thrombo Future: The importance of pulse oximeter / ECG discoveries:
First, the ECG can diagnose blood clots in the heart valves
Next, the pulse oximeter can diagnose skipped heartbeats