The notion that blood pressure is the “driving force” of blood flow is all wrong. Blood flow is regulated by a capillary gate mechanism that determines microvascular flow resistance.

Carbon dioxide is the primary regulator of the capillary gate. For example, exercising muscle produces carbon dioxide, and rising levels of CO2 directly release nitric oxide (NO) from the vascular endothelium in the muscle tissues, which opens the capillary gate, lowers flow resistance, and increases perfusion and oxygen delivery to the exercising muscle. This explains why breathing air supplemented with carbon dioxide dramatically increases venous return to the heart as well as cardiac output and cardiac efficiency.

Autonomic balance is the secondary regulator of the capillary gate. Sympathetic nervous activity releases von Willebrand Factor (VWF) from the vascular endothelium, which generates insoluble fibrin that increases microvascular flow resistance. Parasympathetic nervous activity releases NO from the vascular endothelium, which disintegrates insoluble fibrin and reduces microvascular flow resistance. This explains how autonomic balance governs organ function.

Blood pressure, as measured by conventional instruments, is the lateral force generated by the traveling turbulent pulse waves that propagate throughout the arterial tree in the aftermath of each cardiac contraction. The lateral force of the turbulent pulse wave gradually increases as arterial diameter decreases toward the periphery, so that blood pressure measures higher in the fingers than in the aorta. The pulse wave is also altered by arterial bifurcations and curvatures as it travels, which explains why blood pressure measurement is never the same in separate locations.

Closing the capillary gate increases microvascular flow resistance, which exaggerates the lateral forces generated by the turbulent pulse wave and exaggerates conventional blood pressure measurement. Opening the capillary gate reduces microvascular flow resistance, which mitigates the lateral forces generated by the turbulent pulse wave, and decreases conventional blood pressure.

The concept of “vasopressors” and “vasodilators” is all wrong. Mammalian blood is a “non-Newtonian” fluid that exhibits decreasing flow resistance when it is accelerated by cardiac contraction. This enables the mammalian heart to expel its contents with little effort within a tenth of a second. The muscular arterial tree functions as a “secondary heart” that expands to accommodate the blood expelled by the heart during systole, and then slowly contracts to restore its resting diameter during diastole. This gently propels blood toward capillary beds. Thus, the tiny pressure that propels blood cannot be measured by conventional instruments. “Vasopressors" harmfully close the capillary gate, reduce cardiac output and tissue perfusion, and elevate measured blood pressure and pulse rate. This explains why tachycardia and hypertension go hand in hand. “Vasodilators” beneficially open the capillary gate, increase cardiac output and tissue perfusion, and lower blood pressure.

You can obtain a more complete explanation of hemodynamic physiology in my book called “50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism” that is available via Amazon.com.

Dear Lewis S Coleman!

I have read your answer.

First of all, I would like to say that the body is much smarter than all of us doctors in the world put together. You describe everything at the molecular level in such a way as if we ourselves created these compensatory mechanisms in order to normalize various deviations from the norm. You write that there are situations when the pressure in the fingers is higher than in the aorta, with which I do not agree - then there would be a reverse flow of blood - this is not reasonable. Unlike people, the organism (nature) never does unreasonable things. Even if an atomic bomb is blown up on the street, blood (water, oil, gas, and so on) will flow along the pressure gradient, these are the laws of physics and they do not depend on etiology, sex, weight, age.

I insist, for example, that in refractory, vasopressor-resistant shock, hypotension is a compensatory mechanism to decrease the increased blood flow to the heart due to hypervolemia (protects the heart from overload, measure the volume of circulating blood in this shock and you will see that there is hypervolemia). Therefore, with vasodilator (warm) shock, it is necessary to fight not with hypotension, but with hypervolemia, and this normalizes blood pressure without vasopressors.

We have not learned how to manage hemodynamics, but we are boldly discussing what pathological changes occur during shocks at the molecular level, which I consider unreasonable at this stage in the development of medicine. They came up with complex invasive methods of hemodynamic monitoring, which give conflicting results and which we are starting to abandon.

I sent you my work, it concerns monitoring of hemodynamics and is based on a retrospective analysis of the case histories of 229 sick children with severe polytrauma. Since the physical laws of hemodynamics do not depend on the etiology of the disease, gender, age, etc., the work is also suitable for the diagnosis and treatment of other critically ill patients. The work allows, on the basis of simple indicators of hemodynamics - arterial and central venous pressure, the "white spot" symptom and their changes in dynamics against the background of infusion therapy, to establish the type of hemodynamic disorder, to diagnose the body's volemic status.

The work also allows you to find out if the patient has hypovolemia or hypervolemia, is there bleeding, has it stopped or not?, the approximate intensity of bleeding (in case of injury), whether infusion therapy, vasoactive and / or cardiac drugs are indicated.

If you have questions, objections or wishes, write, I will answer your questions.

I sent my work to many eminent hemodynamic researchers around the world, but they either do not read, or read and do not answer - they do not know how to object to me?, so they avoid discussing with me or do not want to admit it were they wrong? Usually they don't answer.

Sorry, I don't know English, but I know Georgian, Russian and Google translator

I will be glad if you answer.

Thank you for your attention

Best regards, Jumberi Kiladze

Dear Dr. Kiladze,

How do you explain the fact that blood pressure measures higher in the fingers than in the aorta? How do you explain why blood pressure varies between any two points in the circulatory system?? How do you explain the observation that atherosclerosis begins on the outer curvatures and bifurcations of the large proximal arteries and almost never occurs in the fingers??? How do you explain the palpable pulse?? How do you explain the superior exercise tolerance of mammals compared to reptiles, lizards, and amphibians???

Dear Lewis S Coleman!

Thanks for answering

You ask me how I will explain that the pressure in the fingers is higher than in the aorta; on the contrary, I can ask: how do you prove that the pressure in the fingers is higher than in the aorta?

Physical laws are the same, as I wrote to you before, regardless of etiology, gender, age, and so on, so I can’t believe that the pressure in the vessels of the finger is greater than in the aorta. I will not answer the rest of the questions - I am not an expert in this area.

I came across a medical history - in a patient before discharge after stopping intra-abdominal bleeding in a completely normal condition, the resuscitator found that the central venous pressure was very low, when measuring the volume of circulating blood, it turned out to be 180% of the norm. having stopped infusion therapy against the background of polyuria, the CVP returned to normal and the patient was safely discharged home. I was able to explain this "paradox". In practice, I was convinced many times that I was right. I am now 73 years old, I have worked as an emergency surgeon all my life and my conclusions have never let me down. I did this job 40 years ago. For objective reasons, I was unable to complete the work. After retiring and studying how things are in the issue of monitoring hemodynamics and the questions to which I received answers 40 years ago, they still cannot be answered until now. There is no way to bring my work to the medical community and it would be a pity if all this is lost.

I don't know what else to write about. If you read the work and you have questions, I will answer.

Yours respectfully Jumbury