Do you ever lie awake at night and wonder what makes the healthy 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.
Sick patients with flu symptoms often develop mystereious fast fluttering jugular pulsations in the neck that are followed by slow strong flip-flop palpitations that are felt inside the chest. Heart doctors who specialize in arrhythmias call the tachy-brady pattern of the electrocardiogram (ECG) the "sick sinus syndrome".
Patients with the tachy-brady rhythm suffer brain fog, confusion, weakness, light-headed dizzy spells, and sometimes develop fainting spells and anoxic epileptic convulsions.
No one seems to understand what causes the heart to suddenly beat fast or slow; and not much really matters to us unless it changes our financial condition or romantic relationships. No one really cares too much about the "sick sinus syndrome" until he or she ends up in the ICU with a fast or 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 change the heart rhythm by interfering with blood flow through the heart valves. Vital sign evidence leads Bodensteiner Medical Research to postulate that venous thromboembolism causes the sick sinus syndrome.
In 2005 Dr Bode became sick with phlebitis in his leg following inguinal hernia surgery, and a CT x-ray scan revealed a blood clot inside the superficial iliac vein beneath the surgical site.
Someone recommended to Dr Bode that he use a venous compression sleeve to squeeze his sore leg because this improves venous blood flow back to the heart, which 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 listened to his heart with a stethoscope and heard soft systolic murmurs at the pulmonary valve during flip-flop palpitations.
It was easy for Dr Bode to imagine that leg compression squeezed blood clots out of his sore muscle into his heart, which caused flip-flop palpitations and pulmonary valve murmurs. Turning off the compression sleeve stopped the palpitations and murmurs.
Next, Dr Bode used his anesthesia monitoring skills and attached a pulse oximeter to his finger, and an electrocardiogram (ECG) to his chest. The ECG showed patterns called ventricular bigeminy as the heart slowed down during flip-flop palpitations; and oxygen desaturation events followed the bradycardia.
Dr Bode consulted medical colleagues for ideas about the tachy-brady rhythm called the sick sinus syndrome, but no one has any idea that blood clots cause palpitations called premature ventricular contractions (PVC). And no one seems to know that oxygen desaturation events are associated with arrhythmias.
This confusing sad situation stimulated basic science research using the computerized holter elelctrocardiogram and computerized pulse oximeter. Computer science unlocks the mysteries of the ideopathic tachy-brady rhythm called the sick sinus syndrome.
A large amout of ECG and pulse oximeter data was collected and presented to cardiologists, pulmonologists, anesthesiologists and scientists from UCSF, Stanford, UCLA, and Loma Linda Medical Schools.
A New Interpretation of the Electrocardiogram
The electrocardiogram (ECG) was discovered in 1903 by Dr Einthoven and it has three important waves, which are interpreted by cardiologists. They believe that "re-entry circuits" explain arrrhythmias, and electrophysiologists use minimally invasive "ablation" therapy to treat atrial fibrillation, flutter, and supraventricular tachycardia.
There seems to be a fundamental misunderstanding of the ECG (EKG). Abnormal electric waves of the heart, which are recorded as 're-entry' electric potentials during arrhythmias, move near the speed of light, which is 186,000 miles per second, which blurs the vital sign evidence.
The heartbeat takes place during one second of time, which equals one thousand milliseconds, and it is not possible for electrophysiologists to isolate and separate nerve action potential events from other simultaneous events. No one seems to appreciate that cardiac muscle contractions generate electric friction potentials as blood rubs against the walls of the atria, ventricles, and great arteries (aorta and pulmonary artery).
The electricity of the electrocardiogram seems to be generated by three separate cardiac contractions, namely, atrial, ventricular and arterial.
Two atrial contractions generate the P wave, two ventricular contractions generate the QRS wave, and two arterial contractions (aorta and pulmonary artery) generate the electric potential recorded as the T wave opf the ECG.
The premature waves of the ECG are confusing because electrophysiologists teach that cell depolarizations or repolarizations generate electric potentials, and no one knows much about streaming electric potentials generated by water flow.
It seems that contracting heart muscle rubs against blood, which generates friction electric potentials in the same way that fast flowing air in dark clouds full of water droplets generate electric potentials that become lightning.
Electric potentials from the heartbeat dissipate through the body and create electric wave potentials that are transmitted to the arms, legs and chest into ECG wires of the ECG machine which records the electic wave potentials as the electrocardiogram.
Cardiac wave electric potentials are the same as lightning electric potentials generated by swirling winds that rub against water droplets inside dark clouds in the sky. Air friction against water droplets generates electric potentials that discharge to the ground as lightning bolts.
Dr Bode recorded hundreds of normal and abnormal ECG rhythms on patients by using a holter monitor; and compared the ECG data to simultaneous pulse oximeter data, which measures the pulse rate, pulse rhythm, oxygen hemoglobin saturation, and carbon monoxide hemoglobin saturation.
Dr Bode studied patients at rest, during treadmill exercise, and during sequential venous leg compression, and videotaped many projects.
Leg compression of sore legs with blood clots caused repeating patterns of skipped heartbeats followed by oxygen desaturation events. Furthermore, sore extremities with DVT had elevated carbon monoxide hemoglobin (carboxyhemoglobin) saturation above 10%. There appears to be a direct connection between altered blood flow and altered ECG rhythm.
Leg compression of healthy patients caused no ECG changes, no desaturation events, and the carboxyhemoglobin levels of the extremities were 0 – 1%.
Compression of sore legs altered the ECG rhythm and oxygen saturation, however
There are no accepted relationships between blood clots, arrhythmias, or desaturations,
No one has any idea what causes the sick sinus syndrome,
No one can explain slow strong flip-flop palpitations,
No one can explain fast weak fluttering jugular palpitations,
No one has any idea why sore legs have elevated carboxyhemoglobin saturation,
No one knows that cardiac contractions / blood friction generate electric waves, and
No one can explain PVC, Q waves, or the long QT of the ECG.
Dr Bode designed a thrombo theory to explain how venous compression of sore legs induces palpitations with premature cardiac contractions that make up the tachy-brady rhythm of the sick sinus syndrome.
Thrombophysiology by Dr Bode
Dr Rudolf Virchow discovered around 1859 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 stasis led to the formation of clots; and hemostasis is the main basis that stimulates blood to coagulate into sticky purple gel called detritus that hardens over time into a blood clot called a thrombus.
But why does hemostasis leads to hemothrombosis (blood clots)? Hemostasis changes metabolism from aerobic into anaerobic metabolism, which generates metabolic lactic acid, which was discovered by Professor Louis Pasteur around 1857.
Dr Pasteur discovered that anaerobic germ metabolism of milk sugar produced sour milk. Lactic acid was discovered to denature milk protein which coagulates into cheese in sour milk. In a similar way, lactic acid in blood causes blood protein to coagulate into blood clots.
Lactic acid causes venous blood to transform into purple gel, composed of water, proteins, platelets, and red blood cells. This soft gel called detritus forms an outer membrane and becomes 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. These migrating clots become venous thromboembolisms (VTE) and circulate through the right heart valves. They move into the pulmonary artery, and stop in the lungs, where they become pulmonary embolisms (PE).
Venous blood clots cause pathology and change vital signs.
First, DVT weaken sore muscles, which become warm, swollen, and red with increased carboxyhemoglobin in the toes, which is a biomarker of venous vascular congestion and hemostasis.
Next, VTE inside the heart (thrombo dextrocardia) cause arrhythmias and palpitations. VTE at the tricuspid valve cause premature atrial contractions (PAC), with fluttering jugular palpitations called pulsus reversus; and VTE at the pulmonary valve cause premature ventricular contractions (PVC) with pulsus interruptus (skipped heartbeat) and flip-flop palpitations. Thrombo dextrocardia causes the tachy-brady rhythm of the sick sinus syndrome; and furthermore, consecutive skipped heartbeats cause fainting, anoxic convulsions, and sudden death syndromes.
Next, VTE circulate into the pulmonary artery and squeeze the esophagus. Pulsating clots cause nausea, burping, difficulty talking or swallowing; and burping while asleep causes gastro esophageal reflux (GERD).
Finally, VTE flow into the lungs and become pulmonary embolisms (PE). Detritus in alveoli causes exercise-induced asthma; and prevents the absorption of oxygen and the exhalation of warm moist vapor full of carbon dioxide. Pulmonary malfunction causes desaturation, hypercapnea, and hyperthermia, which may lead to panic attacks, narcolepsy, hot flash fevers, night sweats, and anaphylactic suffocation.
The Life Cycle of Blood Clots is full of arrhythmias and idiopathic syndromes
First, DVT (deep venous thrombosis) usually form inside muscles and cause inflammation. Muscles become sore, swollen, weak, warm, and red. Walking causes pieces of DVT to break loose and migrate into venous circulation, where they become venous thromboembolism (VTE).
VTE move into the right atrium of the heart, where they interfere with blood flow at the tricuspid heart valve, which causes premature atrial contraction (PAC), and the obstructed valve forces blood to regurgitate upwards into the jugular vein during fast atrial contractions called atrial flutter. This process is thrombodextracardia pulsus reversus, and the fast heart rate is thrombotachycardia.
Next, VTE move into the right ventricle and obstruct blood flow through the pulmonary valve, which causes a premature ventricular contraction (PVC). PVC delays ventricular blood flow out of the heart, which changes the QRS of the ECG. The heart skips a beat (pulse) and this process is called thrombodextracardia pulsus interruptus, and the slow heartbeat is thrombobradycardia.
VTE move into the pulmonary artery, and squeeze around the esophagus, which is located in front of the spine and behind the heart and pulmonary artery. Pulsating clots inside the pulmonary artery physically compress and irritate the esophagus, which causes nausea, burping, difficulty talking or swallowing. At night, burping while asleep causes gastro esophageal reflux (GERD).
Finally, VTE moves into pulmonary alveoli and becomes pulmonary embolism (PE). Detritus interferes with respiration and causes "circulatory" asthma. Furthermore, detritus and PE prevent the absorption of oxygen or the exhalation of warm moist vapor full of carbon dioxide, which causes oxygen desaturation, hypercapnea, and hyperthermia. These cause panic attacks, fever, narcolepsy, hot flashes, night sweats, and rare anaphylactic suffocation.
Clots cause bigeminy with pulse deficits, palpitations, and more
It is theorized that compression of sore legs pumps DVT that are the size and shape of a golf pencil into venous circulation. These soft clots look like small purple worms, which migrate into the heart where they alter blood flow at the pulmonary valve and cause an ECG pattern called bigeminy.
Cardiac physiology has multiple simultaneous covariant processes going on during one second of time during the heartbeat. Please take time to focus attention on one thing at a time, and become familiar. Later study the next item. Gradually, you will 'see' the whole picture, which is the Gestalt.
First, focus on blood flow and electric potentials, which make up the waves of the electrocardiogram (ECG).
Cardiac contractions / muscle / blood flow friction generates electic potentials that make up normal and abnormal waves of the electrocardiogram (ECG). Blood clots change blood flow at the heart valves, which stimulates premature heartbeats that are recorded by the ECG.
For example, VTE at the pulmonary valve reduce blood flow out of the right ventricle, which stimulates a premature ventricular contraction. The pulmonic valve closes down on the clot and the right ventricle develops a rotating isometric contraction that alters the normal QRS electric potentials of the heartbeat. The ECG pattern changes from a narrow wave called NSR (normal sinus rhythm) into a tall wide bifid QRS wave called PVC (premature ventricular contraction).
Second, focus on the pressure inside the right ventricle which triggers a cardiac reflex.
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 fatal distention of the ventricle, which causes fibrillation.
Next focus on the muscular contraction during 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 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.
Refocus on the clot. 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 heartbeat skips every other pulse during bigeminy because of isometric non-perfusing PVC as the clot obstructs the pulmonary valve.
Next focus on blood flow sounds of the heart during 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.
Next, focus on detritus, which is released from the clot rupture and migrates into the alveoli, where the detritus gums up the capillaries, 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 causes a delayed (ten to twenty seconds) oxygen desaturation event. It also causes hypercapnea (elelvated carbon dioxide) and hyperthermia (fever). Elevated carbon dioxide causes narcolepsy and hyperthermia stimulates vasodilatation and sweating (hot flash).
Finally think about sensations of palpitations. 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.
Next focus on the pulse rate. 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.
Patients press the button on the holter monitor during bigeminy and write down "flip-flop" palpitation on the record sheet because clots cause strong rotating isometric contractions that are followed by extra strong beats that are needed to expel clot, debris and extra blood out of the right ventricle.
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 "see" the whole picture.
Gradually, "see" 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 cause palpitations and change the ECG.
More about the electrocardiogram and electric potentials during the heartbeat
The heart is composed of two pumps intimately connected like Siamese twins.
Two pumps have six connected pumping parts,
These parts include two atria, two ventricles, and two great arteries,
Four one-way reciprocating valves connect six pumping parts.
Three connected pairs of pumps have sequential synchronized rhythmic contractions,
First: two atria contract together and fill up the ventricles,
Next: two ventricles contract together and fill up two great arteries, and
Last: two great arteries contract and pump blood away from the heart.
Dr. Einthoven discovered in 1903 that the heartbeat generates electricity. Electrophysiologists teach that the cumulative effects of millions of cardiac cell depolarization and repolarization events generate the electricity of the electrocardiogram (ECG), which has three spikes or electric potentials called the P, QRS, and T waves.
The heartbeat electrocardiogram (ECG) has three waves: P, QRS, and T.
However, electric action potentials move at the speed of light, which blurs the evidence.
There is an alternative way to explain the electric potentials of the ECG. Blood contains water and srrong cardiac muscle contractions rub against the blood, which generates friction electricity inside the heart just like swirling air against water droplets in dark storm clouds in the sky create friction electric potentials that discharge to the ground as bolts of lightning.
Dr McEdwards is a member of the Board of Directors of Bodensteiner Medical Research. He is a hydrogeologist who explained 'streaming electric potentials" that are generated by moving or flowing water in a river or water fall. Dr McEdwards believes that cardiac muscle contractions generate electric potentials inside the heart in the same way that air flow against water droplets in the clouds creates lightning.
Sequential contractions by different parts of the heart generate distinct electric potentials that dissipate and create electric waves of the electrocardiogram (ECG) during each heartbeat.
First, two atria contract together and create the P wave.
Next, two ventricles contract together and create the QRS wave.
Last, the aorta and pulmonary artery contract together and pump blood away from the heart, which creates the T wave.
Blood flow generates the electric waves of the ECG and blood clots alter the blood flow through the heart valves, which changes the ECG pattern. Blood flow 'controls' the heartbeat and the rhythm of the ECG.
The "heartbeat" starts with the SA node, AV node and conduction fibers; and this neuromediated pacemaker system initiates coordinated contractions of the atria, and facilitates simultaneous "reverse peristaltic" contractions of the ventricles, which are followed by normal peristaltic contractions of the aorta and pulmonary arteries.
The T wave of the ECG is created by contraction of the aorta and pulmonary artery!
The bottom (apex) of the ventricles contract at the start of systole, as the heart pumps blood "up" towards the aortic and pulmonary valves, and pathological Q waves are caused by the downward outward bulge of the apex of the ventricles at the start of systole. This is "takotsubo" of the broken heart syndrome.
Cardiac contractions / hemodynamic electric potentials explain ECG physiology, and
Depolarization and repolarization theories need revision.
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 lactic acid; and Dr Pasteur made this discovery when he studied germ metabolism of milk.
Why does cancer cause clots? Abnormal cancer cell metabolism produces lactic acid; and Dr Otto Warburg made this discovery when he studied cancer cell glucose metabolism.
Why do runners get clots? Anaerobic muscle metabolism produces lactic acid which causes blood clots; and Dr Otto Meyerhof made the discovery that anaerobic muscle metabolism produces lactic acid.
How does lactic acid activate the blood clotting mechanism? Acid denature protein in the blood, which becomes like velcro, which causes red blood cells to coagulate with platelets and form clots.
What makes blood clots migrate (embolize) into heart valves? Exercise or walking squeezes clots out of sore veins (DVT) into circulation that goes 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 does bloody debris (detritus) cause exercise-induced asthma? Detritus adds liquid glue into the lungs which causes temporary swelling and reduces air flow into tiny alveoli.
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 convulsion.
How do blood clots cause sudden thrombocardiac arrest? VTE obstruct the pulmonary valve, which stops cardiac output.
How does CPR reanimate someone with cardiac arrest without defibrillation? CPR expels clot out of the obstructed valve, which reopens blood flow into the brain and lungs, which reverses acidsosis and reanimates the person suffering a 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?
Thrombo dextrocardia 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 electric waves of the ECG. Blood clots alter blood flow, and altered blood flow causes PAC and PVC. The ECG can diagnose blood clots in the heart valves.
Blood flow / cardiac contractions generates the waves of the ECG.
Peristaltic contractions of the aorta and pulmonary artery create the T wave.
The downward outward bulging of the apex of the ventricles at the start of systole create Q waves.
Thrombo dextrocardia at the pulmonary valve causes the "long QT" syndrome.
Old depolarization and repolarization ECG theories need to be updated.
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.