Welcome to Thrombo.Info
by Dr Bode
The Happy Heart
The happy heart beats like a clock.
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.
Doctors observe patients with fast fluttering pulses followed by slow strong palpitations and call this condition the "sick sinus syndrome". These patients suffer brain fog, confusion, palpitations, weakness, and light-headed dizzy spells.
Dr Bode used sequential venous compression sleeves to squeeze sore legs of patients with phlebitis and deep venous thrombosis (DVT); and discovered that leg compression changed the ECG rhythm; and he noticed oxygen desaturation events and abnormal high levels of carbon monoxide in sore extremities.
The relationship of VTE to arrhythmias, desaturation, and carboxyhemoglobin was unknown in 2005, and so Dr Bode studied sick and healthy patients.
The Trillium holter recorded the ECG rhythm, the Wristox pulse oximeter recorded the pulse and oxygen saturation, and the Masimo pulse oximeter measured the carboxyhemoglobin levels in the fingers and toes.
BMR theorizes that compression of sore muscles with DVT squeezes DVT (clots) into venous circulation. DVT become venous thromboembolism (VTE) as it goes into the heart; and it appears that VTE alters blood flow and changes the heart rhythm when it passes through the heart valves.
Thrombodextracardia describes VTE (clot) passing through the tricuspid and pulmonary valves.
First, VTE causes fast atrial contractions as it goes into the right ventricle through the tricuspid valve. Next, VTE causes slow skipped heartbeats called "premature ventricular contractions" (PVC) as it pass through the pulmonary valve and moves into the pulmonary artery.
Thrombodextracardia explains the sick sinus syndrome. Fast fluttering premature atrial beats plus slow PVC's equals the idiopathic "tachy-brady" rhythm of the sick sinus syndrome.
Discovery: Oxygen Desaturation Events during bigeminy and elevated carboxyhemoglobin levels lead to the VTE theory of PVC
Is there a relationship between VTE, PVC, and carboxyhemoglobin? VTE causes cardiac PVC and pulmonary desaturation events; and carboxyhemoglobin is a biomarker that locates the origin of VTE!
In 2005, BMR discovered that venous thromboembolism (VTE) changed the heart rhythm and theorized that VTE specifically interferes with blood flow through the pulmonary valve, which causes a flip-flop non-perfusing premature contraction of the heart!
This personal discovery led to research studies on sick and healthy patients. Leg compression of non-smoking healthy patients does not change the ECG rhythm or the oxygen saturation; and carboxyhemoglobin levels range between 0 - 1% in the fingers and toes.
Venous compression of patients with sore legs with DVT changed the heart rhythm. Patients complained about flip-flop palpitations when the ECG recorded ventricular bigeminy with pulse deficits that were followed by an oxygen desaturation event. The toes of sore legs with DVT had carboxyhemoglobin levels between 12 - 22%, while the fingers of the same patients recorded levels between 1 - 5%.
Compression-induced bradycardia with flip-flop palpitations and pulse deficits and delayed desaturations was a paradoxical mystery; and elevated carboxyhemoglobin levels were ideopathic.
How could blood clots (VTE) change the rhythm of the ECG with slow alternating skipped heartbeats and flip-flop palpitations plus cause a delayed desaturation event on the pulse oximeter? And what metabolic condition altered the extremities of sore legs, which increased the carboxyhemoglobin (SpCO) level?
VTE appeared to cause slow alternating premature ventricular contractions (PVC) called bigeminy; and the QRS of the ECG was wide and long with a notch in the middle. The QRS was followed by a bizarre looking T wave. The changes in the ECG during PVC forced the author to research the theory of electric potentials that make up the electric waves of the ECG.
And the abnormal cardio-pulmonary events forced the author to research the life cycle of blood clots.
First, the Blood Clot Life Cycle
Clots are made out of blood, which contains water, red blood cells, and sticky proteins. Many factors are associated with blood clot formation including strenuous exercise, trauma, poor circulation, travel, pregnancy, diabetes, germ infection, drug abuse, cancer, alcohol, dehydration, and other factors. Each factor causes metabolic changes, which produce acidotic toxins that start the blood clotting cycle.
Blood clots have a life cycle that includes their formation into deep venous thrombosis (DVT) followed by migration called venous thromboembolism (VTE) followed by pulmonary embolism (PE).
Pathological events during the life cycle of Venous Blood Clots
- First, venous blood clot begin its life cycle as deep venous thrombosis (DVT), and usually cause sore, swollen, weak, warm, and red muscles.
- Next, exercise or walking squeezes clot into venous circulation and it become venous thromboembolism (VTE). VTE move into the tricuspid heart valve where it causes fast fluttering jugular palpitations, paradoxical atrial arrhythmias (flutter / fibrillation), and thrombotachycardia.
- Next, VTE move into the pulmonary valve and causes premature ventricular contraction (PVC), slow flip-flop palpitations, skipped heartbeats, pulse deficits, fainting spells, anoxic grand mal seizures, and rare sudden unexpected death syndromes.
- Next, VTE move into the pulmonary artery, and squeezes the esophagus next to the spine. Pulsating clot causes nausea, burping, difficulty swallowing, and gastro esophageal reflux (GERD).
- Finally, VTE become pulmonary embolism (PE) and finishes its life cycle, when it stops in lung alveoli, where PE causes panic attacks, exercise-induced asthma, hyperthermia, narcolepsy, hot flashes, night sweats, and rare anaphylactic suffocation.
Ventricular Bigeminy, Thrombobradycardia, Desaturation, and elevated carboxyhemoglobin
Elongated clots are surrounded by thin flexible membranes that contains sticky glue called detritus. Clots change the heart rhythm and cause flip-flop sensations as they go through the pulmonary valve. Isometric heart contractions rupture clots, which releases detritus that causes a delayed desaturation event. Flip-flop sensations during bigeminy develop when clot obstructs the pulmonary valve, which causes the right ventricle to enlarge while the left ventricle decompresses. This creates a "flip" senstion. After the clot ruptues and passes through the valve, the ventricle rotates to the right, which causes a "flop" sensation.
Why does the heart develop premature contractions? When the nose of the clot enters the pulmonary valve, it narrows the aperture. Decreasing the aperture by 20% reduces flow by 50%, which triggers a protective premature ventricular contraction (PVC). Premature beats prevent fatal dilation and stretching of the ventricle, which leads to sudden unexpected fatal fibrillation.
As the valve closes down on the clot, blood flow stops and the right ventricle develops an isometric rotating contraction. The ventricle squeeezes while the valve grips the nose of the elongated clot. The torque from the isometric heart contraction tears open the clot's membrane, which releases sticky purple detritus. As the clot decompresses, the valve opens up. Next, an extra strong normal sinus contraction pumps blood and detritus out of the heart.
Next, the trailing part of the elongated clot moves into the valve, which obstructs blood flow causing a second PVC. This causes another isometric rotating contraction that squeezes more detritus out of the remaining clot. After the clot decompresses, the distended right ventricle pumps the rest of the clot out of the valve into the pulmonary artery. The ECG records normal sinus rhythm and the pulse oximeter records an extra strong heartbeat.
Ten to twenty seconds after the ECG records bigeminy, detritus from the ruptured clot enters the pulmonary alveoli. Bloody glue clogs up alveoli, which stops the absorption of oxygen and causes an oxygen desaturation events that is recorded by the pulse oximeter.
Pulmonary enzymes quickly digest detritus, which restores oxygenation and the desaturation event stops. There is a concurrent decrease in exhaled carbon dioxide during the oxygen desaturation event because detritus prevents the exhalation of warm moist vapor full of carbon dioxide.
It takes time to understand these events so take your time and focus on one thing at a time. Later, you will understand how soft sticky detritus interferes with pulmonary alveolar function, which prevents the absorption of oxygen and the exhalation of warm moist vapor full of carbon dioxid. Thrombus causes bigeminy and detritus causes oxygen desaturation.
Discovery: Carboxyhemoglobin Pulse Oximetry Data leads to theory of venous stasis / acidosis
New pulse oximeters measure the carboxyhemoglobin level. Venous acidosis caused by abnormal hypoxic metabolism changes the carboxyhemoglobin level, and there seems to be quantitative and qualitative relationships between SpCO levels (carboxyhemoglobin) and phlebitis in patients who suffer DVT's with sore weak warm red swollen muscles. Carboxyhemoglobin appears to be a circulating biomarker that evaluates slow venous blood flow, which causes hypoxic venous acidosis. Venous acidosis leads to blood clots, phlebitis, and peripheral neuropathy. Carboxyhemoglobin locates venous vascular stasis with hypoxic acidosis that seems to be the main basis of hemothrombosis. Carboxyhemoglobin (SpCO) is a biomarker of peripheral neuropathy and locates the origin of clots.
Hemodynamic Electrocardiac Theory: A New Interpretation of the Electrocardiogram
- The heart is composed of two pumps intimately connected like Siamese twins.
- The two pumps have six connected pumping parts.
- These parts include two atria, two ventricles, and two great arteries.
- Four one-way reciprocating valves connect the six pumping parts.
Focus on the ventricles, heart valves, and blood flow as the heartbeats each second of time.
- 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.
- 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.
- Action potential depolarization / repolarization explain ECG physiology.
- However, electric action potentials move at the speed of light, which blurs the evidence.
Electric events during the heartbeat move near the speed of light; and there is an alternative way to explain the different electric potentials of the ECG. Blood contains water and fast flowing blood generates friction electricity inside the heart just like swirling water droplets in dark storm clouds create electric charges, which discharge as lightning.. BMR concludes that swirling blood flow patterns generates electricity in the same way that swirling water droplets create lightning electricity in the sky.
Different contractions of different parts of the heart generate distinct electric charges that dissipate and create three different electric waves of the electrocardiogram (ECG) during the 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.
- Depolarization occurs first, cardiac contractions second, and blood flow electricity third.
- Blood flow causes electrical potentials that explain ECG waves and "reentry" circuits.
- Atrial contractions generate blood flow
- Blood flow friction from atrial contractions creates the P wave.
- Ventricular contractions generate blood flow.
- Blood flow friction from ventricular contractions generates the QRS wave.
- Aortic and pulmonary artery contractions generate blood flow
- Blood flow friction from arterial contractions creates the T wave.
- Hemodynamic friction electric potentials explain ECG physiology.
- Depolarization and repolarization theories need revision.
Thrombo Questions & Answers:
- What makes the heart skip a beat? VTE at the pulmonary valve.
- How does a blood clot (thrombus) cause the heart to skip a beat?
- What causes blood to form clots? Metabolic acid.
- Why does abnormal anaerobic (hypoxic) metabolism make lactic acid?
- How does lactic acid activate the blood clotting mechanism?
- What makes blood clots migrate (embolize) into heart valves?
- What happens to the heart rhythm as clots pass through different heart valves?
- Do blood clots cause fluttering or flip flop palpitations? Yes.
- Why do arrhythmias cause low blood pressure with lightheaded dizzy spells?
- Does partly clotted blood called detritus interfere with breathing? Yes.
- How does bloody debris (detritus) cause exercise-induced asthma?
- How do blood clots cause coughing, nausea, gagging and sneezing?
- Why do blood clots accumulate in the pulmonary artery next to the esophagus?
- 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?
- How do blood clots cause sudden thrombocardiac arrest? Obstruct pulmonary valve.
- How does CPR reanimate someone with cardiac arrest without defibrillation? Expels the clot out of the obstructed valve.
Thrombo Associated Diseases:
- Cancer → lactic acid → blood clots (Warburg effect)
- Carbon monoxide poisoning: night time hypoxemia → carboxyhemoglobinemia
- Chronic Fatigue Syndrome
- Congestive heart failure: right heart failure, valve malfunction, low ejection fraction
- Exercise-induced asthma: pulmonary embolism (PE) of detritus
- Infection: anaerobic germ metabolism muscle: glucose → lactic acid → blood clots
- Injuries: foot, leg, knee, or hip injury → blood clots
- Gastro esophageal reflux disease (GERD): emboli in pulmonary artery compress the esophagus between heart and vertebra, stimulates burping during sleep → GERD
- Headaches: pulmonary detritus ↓ water exhalation → brain edema, headache
- Insomnia: PE at tricuspid valve → thrombotachycardia → sleep arrousal
- Macular degeneration: micro emboli
- Malignant hyperthermia: PE → atelectasis, fever, VTE arrhythmias
- Migraine headaches
- Narcolepsy: PE detritus → ↓ exhalation of CO2 → hypercapnea → CO2 narcosis
- Panic attacks: PE of detritus, desaturation, dyspnea
- Peripheral neuropathy: venous vascular acidosis → neuropathy, restless leg
- Pleurisy: PE into alveoli causes sharp ischemic pain
- Pre-menstrual syndrome: PE of detritus, hot flashes, headache (edema), mild fever
- Seizures: VTE at pulmonary valve, sudden hypoxia, convulsions perform CPR
- Sick Sinus Syndrome: VTE at tricuspid and pulmonary valves
- Sleep apnea: PE detritus → internal hypercapnea with central CNS depression
- Syncope: short runs of continuous skipped beats, VTE at pulmonary valve
- Tinnitus: emboli of detritus into sensitive area of inner ear
- Anxiety, panic attacks
- Brain Fog
- Dizzy spells
- Dyspnea (short of breath)
- Exercise-induced asthma
- Fear of sudden death
- Fever (fever seizures, night sweats, hot flashes)
- Fluttering fast palpitations
- Flip-flop pounding strong palpitations
- Hot flashes
- Insomnia with fast racing heartbeats
- Irregular pulse
- Premature beats
- Light-headed sensations
- Muscular dystrophy
- Night sweats
- Panic Attacks
- Racing heartbeat
- Restless leg
- Seizures / grand mal unconscious convulsions
- Shortness of breath (dyspnea)
- Skipped heartbeats
- Sleep arousal
- Slow pulse / flip-flop palpitations / skipped heartbeats
- Sudden cardiac arrest syndromes
- Sore legs
- History: fluttering / flip-flop palpitations, night sweats with racing heartbeats, insomnia, panic attacks with choking, coughing, sneezing with shortness of breath, chronic fatigue, chronic bronchitis, ‘flu’ syndrome, fast weak irregular heartbeat / slow strong 'pounding' heartbeats, peripheral neuropathy
- Physical Examination: slow strong ventricular heartbeats mixed with fast weak atrial heartbeats, soft musical grade I – II systolic murmur, mild fever
- Pulse Oximetry: oxygen desaturation events, elevated peripheral carboxyhemoglobin in sore extremities with phlebitis & peripheral neuropathy
- Electrocardiogram: premature atrial beats, atrial flutter / fibrillation, premature ventricular beats, tachy-brady / brady-tachy / sick sinus syndrome
- Echocardiogram: pulmonary valve insufficiency / tricuspid valve regurgitation
- Arterial Blood Gas (ABG): elevated carbon dioxide saturation (hypercapnea), low oxygen saturation, elevated carboxyhemoglobin
- Capnography: end tidal expired carbon dioxide decrease corresponds to oxygen desaturation events
Treatment / Prevention of Bloody Clots
- Eight hours of rest / sleep every night (decreases metabolic acidosis)
- Avoid excess drug and alcohol use
- Adequate water intake, avoid exercise-induced dehydration
- Diet & Nutrition: control how much and what you eat
- Moderate aerobic exercise: golf, sex, bowling, gardening, walking, yoga, tai chi
- Sequential venous compression treats & prevents blood clots
- Ultrasound: helps resolve inflammation and phlebitis
- Vibration exercise oscillates bloody clots out of heart valves
What do doctors know about thrombodextracardia, carboxyhemoglobin, or the T wave of ECG?
Thrombodextracardia is a new blood clot theory: VTE causes the sick sinus syndrome!
Blood flow generates the electric waves of the ECG, and the pulse oximeter evaluates decreased venous blood flow, which leads to venous acidosis, which causes venous blood clots.
- Cardiac muscle contractions cause blood flow.
- Moving blood generates hemodynamic electric charges that become 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 creates Q waves.
- Thrombodextracardia at the pulmonary valve causes the "long QT" syndrome.
- Old depolarization and repolarization ECG theories need to be updated.
The importance of pulse oximetry discoveries & a new interpretation of the ECG:
- First, the ECG or pulse ox can diagnose blood clots at the tricuspid or pulmonary valves.
- Second, the pulse ox can evaluate peripheral carboxyhemoglobin.
- Carboxyhemoglobin locates venous acidosis and evaluates neuropathy.
- Carboxyhemoglobin locates the origin of blood clots.
- Blood clots at the pulmonary valve cause skipped heartbeats.
- Skipped heartbeats lead to fainting, anoxic seizures, and sudden cardiac arrest.
- Cell phones can diagnose skipped heartbeats and predict grand mal seizures!
- PE of detritus causes exercise-induced asthma and narcolepsy.
- Cell phone monitors can predict fainting spells and emit warning signals!
- Airline pilots, truck drivers, and train engineers can avoid accidents caused by mysterious narcolepsy or fainting spells.
- We can all improve our life style and become happier as brain fog fades away.
- Thank you for being curious.