Welcome to Thrombophysiology

A Novel Study and Theory of Venous Blood Clots

by Dr Bode

Life is a fire,

Full of hot wet desire.

We laugh and cry,

And love until we die,

When metabolism goes awry,

And the final flames expire.

 

Metabolism is the fire of life that uses oxygen to burn sugar and fat deep inside our cells. The fire produces power, which energizes the muscles of the body and the nerve cells in the brain.

Thrombophysiology is a novel study of the formation of venous blood clots due to a malfunction of metabolism that produces acidosis from metabolic acid. Moreover, blood clots have a life cycle during which they cause mysterious syndromes as they migrate through the heart before they stop inside the lungs.

Blood clots are good when they stop bleeding after bicycle accidents and cover up abrasions. They prevent infection, and facilitate healing. Clots protect us in the beginning, but later, as old clots break loose from sore veins, they migrate into the heart and they turn towards the dark side of an invisible line that separates good health from sickness and disease.

Clots inside the heart cause premature beats with palpitations and skipped heartbeats (pulsus interruptus). 

Moreover, liquid clot (detritus) that stops inside the lungs clogs up small alveoli, which interferes with respiration. Detritus in alveoli prevents the absorption of oxygen, which causes oxygen desaturation and panic attacks.

Finally, big fat purple killer clots cause unexpected death when they obstruct the pulmonary valve and cause sudden cardiac arrest.

This website outlines the life cycle of blood clots and explains idiopathic syndromes associated with deep vein thrombosis (DVT), venous thromboembolism (VTE), paradoxical embolism (PDE), and pulmonary embolism (PE). 

Outline of the Life Cycle of Venous Blood Clots

1. Deep Vein Thrombosis (DVT)
2. Venous Thromboembolism (VTE)
3. Paradoxical Embolism (PDE)
4. Pulmonary Embolism (PE)

First: acidosis leads to hemothrombosis and DVT formation.

The venous blood clot life cycle begins because a malfunction of metabolism produces metabolic acid that triggers the coagulation of warm blue venous blood into deep vein thrombosis (DVT).

When we fall against the ground with severe force, the ground tears blood vessels and interrupts the flow of pink blood full of oxygen to cells. Stagnant blood (hemostasis) causes a lack of oxygen inside cells, which causes them to burn sugar and fat without oxygen (anaerobically). This produces metabolic acid that mixes with venous blood, which is resin full of proteins, platelets, water, and red blood cells. Acid is a catalyst that transforms blood (resin) into sticky, liquid, purple epoxy gel called detritus (thrombosis). Detritus forms a matrix that hardens over time into a blood clot (thrombus).

Blood clots have variable shapes and sizes, with different compositions. A thrombus is a solid or semisolid blood clot, however, part of thrombosis is amorphous liquid clot called detritus.

Acidosis plus DVT causes sore red inflamed veins and swollen, warm, weak muscles.

Moreover, DVT is the source of other venous blood clots including VTE, PDE, and PE.

The origin of DVT can be determined by using the pulse oximeter that measures carboxyhemoglobin (carbon monoxide in hemoglobin) because carboxyhemoglobin increases in tissue with acidosis. Thus, elevated SpCO (saturation percent of carbon monoxide in blood) identifies tissue with acidosis that is the origin of DVT. In other word, carboxyhemoglobin is a circulating pH biomarker and the pulse oximeter identifies extremities with acidosis.

Second: venous clots from DVT migrate into the heart as venous thromboembolism (VTE).

DVT is the source of venous thromboembolism (VTE), which is the second venous blood clot.

VTE is a piece of DVT that breaks loose from a sore vein because muscular contractions squeeze it out of the vein like toothpaste out of a tube.

VTE migrates through venous channels as liquid detritus and/ or a solid or/ semisolid clot. VTE flows back into the heart, which then pumps the material into the lungs.

VTE is the source of the final two parts of the venous blood clot life cycle: paradoxical embolism (PDE) and pulmonary embolism (PE).

Third: a paradoxical embolism (PDE) is a venous thromboembolism (VTE) that passes through a congenital hole in the heart (patent foramen ovale, PFO)

PDE formation requires the presence of a DVT that produces a VTE. Next, VTE migrates into the right atrium of a heart that has a congenital hole between the right and left atria called a patent foramen ovale (PFO). These holes exist in a small percentage of people.

Finally, a cough or some other external force increases right atrial pressure, which pushes VTE material through the PFO out of the right atrium into the left atrium, where VTE becomes PDE.

PDE material inside the left atrium migrates into the left ventricle and aorta and travels into smaller arteries that provide pink oxygenated blood to organs. PDE material reduces or obstructs blood flow into organs of the body, which causes pain and dysfunction.

PDE into a coronary artery of the heart causes sudden angina and embolic heart attack (myocardial infarction). Liquid or soft PDE that moves into the brain causes dizzy spells with transient ischemic attacks (TIA). Large solid PDE that moves into the brain causes a stroke (cerebral vascular accident, CVA).

Most people do not suffer from PDE because they do not have a congenital hole in the heart. However, patients who live with a hole in the heart, suffer mysterious syndromes, such as atypical angina, dizzy spells, or blurred vision. PDE are associated with prolapsed mitral valve syndrome.

Theory of Thrombodextracardia: VTE in the heart valves cause premature beats

Solid VTE inside the heart valves (thrombodextracardia) interfere with blood flow through the tricuspid and pulmonary valves, stimulating premature atrial or ventricular contractions.

This new theory postulates that pulmonary valve VTE cause the heart to skip a beat (pulsus interruptus) and change the pulse oximeter pattern, which records the pulse generated by the contraction of the left ventricle and the contraction of the aorta.

Novel theory of the EKG:

The electrocardiogram (ECG, EKG) records the electricity from the heartbeat and the normal contraction of the heart generates three waves (electric potentials) that are the P wave, QRS wave, and T wave.

Orthodoxy teach that depolarization of heart muscle cells during the heartbeat generate the P and QRS waves. Moreover, repolarization of the ventricle cells generate the T wave of the EKG.

Bodensteiner Medical Research (BMR) postulates that blood flow generates the electricity of the EKG.

Thus contractions by the two atria generate blood flows that generate the P wave. Next, contractions by the two ventricles generate blood flows that generate the QRS wave. Finally, contraction by the two great arteries (aorta and pulmonary artery) generate blood flows that generate the T wave of the EKG.

Thrombodextracardia and theory of the sick sinus syndrome

VTE in the right heart valves cause the tachy-brady rhythm known as the sick sinus syndrome.

First, VTE in the tricuspid valve causes supraventricular tachycardia (SVT). Second, VTE in the pulmonary valve cause ventricular bigeminy with bradycardia, flip flop palpitations, and skipped heartbeats (pulsus interruptus).

The combined effects of tricuspid and pulmonary valve VTE cause the sick sinus syndrome.

Fourth: pulmonary embolism (PE) is the final part of the venous blood clot cycle

After VTE pass through the heart, they stop inside the pulmonary arteries or lung alveoli and become pulmonary emboli (PE).

Pulmonary artery effect: theory of gastro esophageal reflux disease (GERD)

When solid or/ semisolid clots accumulate inside the pulmonary artery at the junction of the esophagus, the beating heart generates repeating pulsating thrusts of VTE or/ PE against the flexible tender esophagus, which sits in front of the thoracic vertebrae behind the heart.

Pulsating clots in the pulmonary artery irritate and constrict the esophagus, which causes nausea, gagging, and difficulty swallowing. Moreover, they stimulate aerophagia and burping. Thus, VTE or/ PE irritation of the esophagus during sleep causes burping at night that leads to GERD.

PE effects on the lungs and alveoli

Solid VTE in the lungs temporarily prevent the flow of blood into a small segment of the lung. PE cause sharp pleuritic pain underneath the ribs. which subsides into a dull ache and interferes with deep breathing.

Liquid PE detritus congests alveoli causing wheezing, and prevents the absorption of oxygen during inspiration and the exhalation of warm moist vapor full of carbon dioxide.

Detritus liquid PE alters pulmonary function and causes several syndromes and symptoms.

Failure to absorb oxygen causes hypoxemia (decreased SpO2, saturation percent of oxygen in blood) measured by the pulse oximeter. Hypoxemia causes panic attacks with anxiety.

Failure to expel carbon dioxide (CO2) leads to hypercapnea (elevated CO2), which causes drowsiness and narcolepsy (CO2 narcosis).

Failure to expel moisture (H2O) leads to water retention causing bloating, swollen fingers, and cerebral edema causing headaches, irritability, and difficulty sleeping.  

Failure to expel heat (warm vapor) leads to hyperthermia, which causes hot flashes and sweating.

Website Summary:

this website presents numerous novel postulates about the pathophysiology of venous blood clots.

First, anaerobic metabolism generates metabolic acidosis that triggers venous blood clot formation with inflammation. Moreover, carboxyhemoglobin is a circulating pH biomarker.  The pulse oximeter measures SpCO (saturation percent of carbon monoxide in blood hemoglobin) and identifies tissue acidosis that is the source of DVT, VTE, PDE, and PE.

Next, thrombodextracardia (blood clots in the right heart) explains the impact of blood clots circulating through the heart valves and explains premature atrial and premature ventricular contractions, as well as the sick sinus syndrome. A novel interpretation of the EKG monitor identifies VTE passing through the tricuspid and pulmonary heart valves.

Third, the effects of liquid detritus PE in lung alveoli explain exercise induced asthma and hypoxic panic attacks. The pulse computerized pulse oximeter identifies oxygen desaturation events caused by detritus in the lungs.

Finally, blood clots in the heart and lung explain cerebral dysfunction including fainting, as well as anoxic grand mal seizures. BMR (Bodensteiner Medical Research) postulates that unconscious grand mal convulsions perform CPR (cardiopulmonary resuscitation).

Case reports illustrate examples of DVT, VTE, PDE, and PE. Moreover, EKG or pulse oximeter data support the novel postulates that explain the mysterious, paradoxical pathophysiology of venous blood clots.

Thrombophysiology is complicated and it will melt your brain if you think of everything. Please begin by looking at metabolism and then take a break. Later study circulation, blood flow, and the heart valves. Notice how clots change blood flow and pressures inside the atria or ventricles. Finally examine respiration.

Take time to understand how the pieces fit together and 'see' the Gestalt, which is the whole picture. Enjoy each new discovery and find joy in your journey to a deeper understanding of blood clots.

Not everyone can go to medical school, but most of us can learn that lactic acid is a mysterious aseptic virus that transforms slippery bloody resin into sticky purple blood clot epoxy.

Blood clots are good when they stop bleeding but they have a dark side when they interfere with circulation and cause skipped heartbeats. Moreover, sticky liquid blood clot glue in the lungs during exercise causes asthma and anxiety.

Thank you for your interest and best wishes for improved health as you study thrombosis. We hope that improved sleep will reduce venous metabolic acid that causes detritus that leads to central sleep apnea.

 

Venous Blood Clot Life Cycle Video

 

 

 DVT and Pulmonary Embolism

 

Blood clot formation, migration, and resolution:

Dr Rudolf Virchow, a German physician, discovered that blood clots in the lungs were the same as blood clots in the legs. He theorized that clots formed in the legs and that pieces of clot from the legs broke loose and migrated through the heart into the lungs. Virchow called migrating venous clots embolia.

Virchow noticed that stasis, trauma, and hypercoagulability led to the formation of venous clots.

Ventricular Bigeminy: Skipped Heartbeats: Thrombodextracardia pulsus interruptus

 

It is theorized that a short semisolid VTE shaped like a torpedo about the size of a small golf pencil enters the pulmonary valve of the right ventricle.

As the clot enters the pulmonary valve, it reduces blood flow out of the right ventricle, which causes a premature rise of pressure inside the ventricle. This pressure stimulates a protective premature right ventricular contraction (PVC) that originates in the RVOT (right ventricular outflow tract).

The premature contraction causes the pulmonary 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. Thr ruptured neck of the clot releases sticky liquid detritus and decompresses the clot. As the clot becomes smaller, blood flows resumes out of the right ventricle into the pulmonary artery.  This allows a normal sinus rhythm (NSR) cardiac contraction. However, the powerful strong heartbeat following PVC pumps extra blood with clot and detritus into the pulmonary artery and causes flip-flop sensations.

Next, the trailing part of the elongated golf pencil shaped clot enters and re-obstructs the valve, which causes a second PVC. The second PVC causes the pulmonary 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 gel as the clot sac decompresses, which reopens the valve. 

A second powerful normal sinus rhythm heartbeat ( NSR) pumps extra blood plus the empty clot sac with detritus into the pulmonary artery, which carries the material into the lungs. Inside the lung, the gel interferes with the absorption of oxygen, which causes a desaturation event that starts 20 to 30 seconds following bigeminy. Desaturation continues for about 40 to 60 seconds as powerful pulmonary enzymes in the alveoli dissolve the detritus, which restores alveolar function and reverses the desaturation.

During bigeminy, the heart flips and flops because the right ventricle enlarges during isovolumetric right heart contractions (PVC) when the clot obstructs the right ventricular out flow tract (RVOT). During PVC, the left ventricle partially decompresses by pumping out a small volume of blood and the heart "flips" to the left. Later during normal sinus rhythm (NSR), the heart flops back to the right after the clot ruptures and releases detritus, which restores blood flow out of the heart decompressing the right ventricle. Thus PCV / flip to left, NSR / flop back to right / PVC flip to left / NSR flop back to right.

 

.

Thrombo Associated Diseases:

• Cancer
  
• Carbon monoxide poisoning:
  
• Chronic Fatigue Syndrome:
  
• Congestive heart failure:
  
• Exercise-induced asthma:
  
• Fainting
  
• Gastro esophageal reflux disease (GERD)
• Infection:
  
• Injuries: foot, leg, knee, or hip injury
  
• Headache
  
• Insomnia:
  
• Macular degeneration:
  
• Malignant hyperthermia:
  
• Migraine visual
  
• Narcolepsy:
  
• Panic attacks
  
• Peripheral neuropathy:
  
• Pleurisy:
  
• Premenstrual syndrome: hot flashes, headache, mild fever, insomnia
  
• Pyriformis syndrome:
• Restless leg
  
• Seizures, anoxic grand mal
  
• Sick Sinus Syndrome
  
• Sleep apnea:
  
• Syncope:
  
• Tinnitus:
  

Thrombo Symptoms

• Anxiety, panic attacks
• Brain Fog
• Bradycardia
• Choking
• Coughing
• Confusion
• Depression
• Dizzy spells
• Dyspnea (shortness of breath)
• Exercise-induced asthma
• Fainting
• Fatigue
• Fear of sudden death
• Fever
  
• Fluttering fast weak jugular palpitations, pulsus reversus
• Flip-flop pounding slow strong palpitations, pulsus interruptus
  
• Gagging
• Headaches
• Hot flashes
• Insomnia
  
• Irritability
• Phlebitis
• Premature beats
• Light-headed sensations
• Muscular dystrophy (weakness)
  
• Nausea
• Night sweats
• Palpitations
• Panic Attacks
• Racing heartbeat
• Restless leg
• Seizures / grand mal unconscious convulsions
• Shortness of breath
  
• Skipped heartbeats, pulsus interruptus
  
• Sleep arousal, tachycardia
• Slow pulse
  
• Sneezing
• Sudden cardiac arrest syndromes
• Sore legs
• Tachycardia
• Vertigo

Thrombo Diagnosis

• 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, 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
• Echo cardiogram: 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 (ETCO2) decrease corresponds to oxygen desaturation events (SpO2)

Treatment / Prevention of Blood Clots

• Eight hours of rest / sleep every night (decreases metabolic acidosis)
• Avoid excess drug and alcohol use
• Maintain 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 during airplane trips
• Ultrasound: helps resolve inflammation and phlebitis
• Vibration exercise
  

Thrombo Future: cell phone pulse oximeter / EKG apps

• Thrombophysiology is a novel study and theory of venous blood clots
• Compartment syndrome causes muscle acidosis with hemothrombosis
• Carboxyhemoglobin locates acidosis caused by decreased venous blood flow
• SpCO is a circulating pH biomarker
• Muscle DVT cause inflammation with pain, swelling, and redness
  
• Cardiac VTE cause the sick sinus syndrome
• Liquid detritus PE causes asthma, panic, hypercapnea, and narcolepsy
• Novel ECG interpretation can diagnose blood clots in the heart valves
• VTE in the tricuspid valve cause PAC and pulsus reversus
• VTE in the pulmonary valve cause PVC and pulsus interruptus
• Cell phone apps can evaluate SpO2 (oxygen saturation) and EKG patterns
  
• ECG apps can emit warning signals during consecutive PVC with pulsus interruptus
• Pulse oximeter apps can detect desaturation events that lead to narcolepsy
• Cell phone apps can emit warning signals and improve safety
• Everyone becomes happier as brain fog fades away and safety improves
• Thank you for your curiosity about blood clots