Monday, October 27, 2025

The carbon dioxde balance in the blood in relation to the availability of oxygen to the tissues

The carbon dioxde balance in the blood in relation to the availability of oxygen to the tissues. By Graeme Ward


Oxygen is transferred from the finest arteries, known as arterioles, to where it is needed by the body through the capillary network. Arterioles branch into tiny capillaries, which are the smallest blood vessels and the primary site for exchange between blood and tissues. The walls of capillaries are extremely thin, composed of a single layer of endothelial cells, allowing for efficient diffusion of gases, nutrients, and waste products. Oxygen diffuses from the blood in the capillaries, where it is present at a higher concentration, into the surrounding tissue cells, where it is at a lower concentration, driven by the concentration gradient. This process occurs directly across the capillary walls, facilitated by the high surface area and permeability of the capillary endothelium. Once oxygen is delivered to the cells, carbon dioxide, a waste product of metabolism, diffuses from the cells into the blood in the capillaries to be transported away. This exchange is a key function of systemic circulation, which carries oxygenated blood from the left ventricle through the aorta and systemic arteries to the capillary beds in the body's tissues.


The lymph does not carry oxygen between arterioles and tissues. The delivery of oxygen to tissues is primarily the function of the blood system, specifically the plasma within capillaries, which leaks into the interstitial spaces to supply oxygen and nutrients to cells. Lymph, which forms from this interstitial fluid, does not transport oxygen; instead, it collects excess fluid, proteins, cellular debris, and pathogens from the tissues. The lymphatic system's main roles are maintaining fluid balance, absorbing dietary fats, and supporting the immune system by transporting antigens and immune cells to lymph nodes.


The statement that the delivery of oxygen to tissues is primarily the function of the blood system, specifically the plasma within capillaries, is inaccurate. While the blood system is indeed responsible for oxygen delivery, the primary transport of oxygen occurs not in plasma but within red blood cells. Oxygen is mainly transported bound to haemoglobin, a protein found inside red blood cells, with approximately 98% of oxygen in the blood being carried this way, while only a small fraction is dissolved directly in plasma. Red blood cells, which contain haemoglobin, are essential for carrying oxygen from the lungs to the body's tissues. Once the blood reaches the systemic capillaries, oxygen diffuses from the plasma into the tissue cells, driven by a partial pressure gradient. The capillary walls, composed of a single layer of endothelial cells, facilitate this diffusion, allowing oxygen to move from the blood into the interstitial fluid and then into the cells. Therefore, although plasma plays a role in the final step of oxygen transfer at the capillary level, the primary function of oxygen delivery is carried out by red blood cells, not plasma.


Oxygen diffusion from plasma into tissue cells is driven by a partial pressure gradient, not by osmotic pressure. This movement occurs because oxygen moves from areas of higher partial pressure (in the blood) to areas of lower partial pressure (in the tissues), following the principle of diffusion. The partial pressure gradient is established by the difference in oxygen concentration between arterial blood and the metabolically active tissues, where oxygen is continuously consumed. Osmotic pressure, which is primarily generated by plasma proteins and influences the movement of water across capillary walls, does not play a direct role in oxygen transport. Instead, osmotic pressure governs fluid movement, particularly the reabsorption of water at the venous end of capillaries. Therefore, the diffusion of oxygen is independent of osmotic pressure and is solely governed by the partial pressure difference.


Is blood that is present in the capillaries all diffused into the interstitial fluid.

No, not all blood present in the capillaries is diffused into the interstitial fluid. While fluid and solutes such as oxygen, nutrients, and waste products exchange between the blood in capillaries and the interstitial fluid, the blood itself—specifically the formed elements like red and white blood cells and large plasma proteins—does not leave the capillaries in significant amounts. The movement of fluid into the interstitial space is driven by hydrostatic pressure at the arterial end of the capillary, where capillary hydrostatic pressure (CHP) exceeds blood colloidal osmotic pressure (BCOP), leading to filtration. However, this process is balanced by reabsorption at the venous end, where BCOP exceeds CHP, drawing fluid back into the capillaries. Despite this, approximately 24 liters of fluid are filtered daily from capillaries, but only about 20.4 liters are reabsorbed, leaving a surplus of about 3.6 liters that is collected by the lymphatic system as lymph. This indicates that while a significant amount of fluid moves into the interstitial space, the majority of the blood components remain within the vascular system, and the interstitial fluid is primarily derived from plasma, not whole blood.


Is the oxygen present in the extremities of the arterial capillaries and is not needed by the surrounding tissues transferred via the interstitial fluid to the venous capillaries 

Oxygen is not transferred from the arterial end of capillaries to the venous end via the interstitial fluid if it is not needed by the surrounding tissues. Instead, oxygen diffuses from the blood in the capillaries into the interstitial fluid at the arterial end due to a concentration gradient, where oxygen levels are higher in the blood than in the tissue cells. This oxygen then diffuses into the surrounding cells for metabolic use. The process is driven by diffusion, which moves solutes like oxygen from areas of high concentration (blood) to areas of low concentration (tissues). If oxygen is not required by the tissues, it will not be taken up, and the excess will remain in the blood as it travels toward the venous end. At the venous end, the blood pressure is lower, and osmotic pressure becomes dominant, leading to reabsorption of fluid and solutes, including any remaining oxygen, back into the capillaries. Therefore, oxygen that is not utilized by the tissues is not actively transferred through the interstitial fluid to the venous capillaries; rather, it stays in the bloodstream and is carried back to the heart and lungs for re-oxygenation.


Are the arterial and venous capillaries connected to allow oxygen not used by the surrounding tissues to be carried back to the heart and lungs for recirculation or is the excess oxygen reabsorbed from the surrounding interstitial fluid that it was transferred to from the arterial capillaries.

The arterial and venous capillaries are connected through a network of microcirculatory units, where blood flows from arterioles into capillaries and then into venules, ultimately returning to the heart and lungs for recirculation. Oxygen that is not used by surrounding tissues is not reabsorbed from the interstitial fluid; instead, the deoxygenated blood, which has lower oxygen levels due to tissue consumption, exits the capillaries and flows into venules. This venous blood, now rich in carbon dioxide and depleted of oxygen, is carried back to the heart and lungs via the systemic veins and pulmonary circuit. In the lungs, carbon dioxide is expelled and oxygen is reabsorbed into the blood through gas exchange in the pulmonary capillaries. The primary mechanism for substance exchange in capillaries involves diffusion, filtration, and osmosis, driven by partial pressure gradients and hydrostatic and osmotic pressures. The net movement of fluid and solutes is regulated such that oxygen and nutrients leave the capillaries at the arteriole end, while waste products and carbon dioxide enter the capillaries at the venule end, with the majority of fluid returning to the capillaries near the venule end due to oncotic pressure. Excess fluid that does not return to the capillaries is collected by the lymphatic system and eventually returned to the venous system. Therefore, the oxygen not used by tissues is not reabsorbed from the interstitial fluid but is carried back in the venous blood for reoxygenation in the lungs.


Oncotic pressure, also known as colloid osmotic pressure, is the pressure exerted by plasma proteins—primarily albumin—in the blood vessels that draws water into the bloodstream from the surrounding tissues. This force is crucial for maintaining fluid balance between the blood vessels and the interstitial space, counteracting the outward push of hydrostatic pressure that forces fluid out of capillaries. The presence of large, impermeable proteins like albumin in the plasma creates an osmotic gradient, attracting water molecules across the semipermeable capillary membrane to prevent excessive fluid leakage into tissues. Normal oncotic pressure ranges from 20 to 30 mmHg, and a significant decrease—often due to low albumin levels from malnutrition, liver disease, or kidney disorders—can lead to edema, the accumulation of fluid in tissues.


Is the haemoglobin that is depleted of oxygen returned from the arterial capillaries via the venous capillaries to be recirculated.

Yes, haemoglobin that has released its oxygen, known as deoxygenated haemoglobin or deoxyhaemoglobin, is returned from the tissues via the venous capillaries to be recirculated back to the lungs. This deoxygenated blood travels through the systemic veins and eventually reaches the right side of the heart, which pumps it to the lungs via the pulmonary arteries. In the pulmonary capillaries, the haemoglobin binds with oxygen again, becoming oxygenated once more, and the cycle repeats. This process ensures continuous oxygen delivery to tissues and removal of carbon dioxide.


Is the interstitial fluid that is referred to that the oxygen moves into from the capillaries prior to being absorbed by the surrounding tissues the same as lymph fluid and does it occupy the same interstitial space

The interstitial fluid that receives oxygen from the capillaries before it is absorbed by surrounding tissues is the same fluid that, when collected by lymphatic capillaries, becomes lymph. This fluid occupies the same interstitial space between cells and tissues. Interstitial fluid bathes the cells, delivering oxygen and nutrients from the blood capillaries and collecting waste products, including carbon dioxide, from the cells. As blood pressure causes fluid to leak from capillaries into the interstitial spaces, this fluid is referred to as interstitial fluid. Most of this fluid is reabsorbed directly into the blood capillaries, but the remaining portion—approximately 3 liters per day—enters the lymphatic system and is then called lymph. Therefore, lymph is essentially interstitial fluid that has entered the lymphatic vessels, and both fluids originate from the same source and occupy the same interstitial space.


Is all of the carbon dioxide produced by the tissues released to be taken back to the lungs or does a percentage remain in the tissues to help facilitate the absorption of oxygen as it becomes available.

All carbon dioxide produced by tissues is transported to the lungs for elimination; none remains in the tissues to facilitate oxygen absorption. Carbon dioxide is a metabolic byproduct generated primarily in the mitochondria during cellular respiration and diffuses out of cells into the extracellular fluid due to a concentration gradient, where its partial pressure is higher than in the blood. This carbon dioxide then enters the bloodstream and is transported to the lungs via three main mechanisms: dissolved in plasma (about 5–7%), bound to haemoglobin as carbaminohaemoglobin (about 10%), and converted into bicarbonate ions (about 70–85%). The bicarbonate form is the most significant, as it allows for efficient transport while minimizing changes in blood pH through buffering by haemoglobin.

The process is tightly coupled with oxygen transport through the Bohr and Haldane effects. The Bohr effect describes how increased carbon dioxide levels in tissues lower blood pH, promoting oxygen unloading from haemoglobin to tissues. Conversely, the Haldane effect explains that when oxygen binds to haemoglobin in the lungs, it reduces haemoglobin’s affinity for carbon dioxide, facilitating its release and transport out of the blood. This ensures that as oxygen is loaded in the lungs, carbon dioxide is efficiently unloaded and exhaled, maintaining a continuous cycle of gas exchange.

Therefore, carbon dioxide is not retained in tissues to aid oxygen absorption; instead, it is rapidly removed from tissues and transported to the lungs for exhalation. The entire process is designed to maintain acid-base balance and support efficient gas exchange, with no residual carbon dioxide left in tissues to serve as a facilitator for oxygen uptake.


The Bohr effect describes how increased carbon dioxide levels in tissues lower blood pH, promoting oxygen uptake  from haemoglobin in the blood. Does the presence of residual carbon dioxide in tissues assist with the efficient absorption of oxygen by the tissues


The Bohr effect describes how increased carbon dioxide levels in tissues lower blood pH, which reduces haemoglobin's affinity for oxygen, thereby promoting the release of oxygen from haemoglobin into the tissues, not its uptake. The presence of residual carbon dioxide in tissues does not assist with the efficient absorption of oxygen by the tissues; instead, it facilitates the unloading of oxygen from haemoglobin in the capillaries surrounding metabolically active tissues. This mechanism ensures that oxygen is delivered where it is most needed, particularly in areas with high metabolic activity such as exercising muscles. The process is driven by the formation of carbonic acid from carbon dioxide and water, catalyzed by carbonic anhydrase in red blood cells, leading to an increase in hydrogen ions and a decrease in pH, which stabilizes the deoxygenated T-state of haemoglobin and promotes oxygen release. Therefore, residual carbon dioxide aids in oxygen delivery to tissues, not in the absorption of oxygen by the tissues themselves.


Does the blood normally have a percentage of carbon dioxide which is not diffused into the lungs and is constantly recirculated in the blood stream

The blood normally contains a percentage of carbon dioxide that is not fully eliminated during each passage through the lungs and is constantly recirculated in the bloodstream. Less than 10 percent of the total quantity of carbon dioxide carried in the blood is eliminated during a single passage through the pulmonary capillaries, which is insufficient to remove all carbon dioxide due to the short transit time—typically less than a second—within the lungs. This incomplete elimination means that a significant portion of carbon dioxide remains in the blood and is continuously recirculated until it is eventually exhaled over multiple cycles. The partial pressure of carbon dioxide in the blood is maintained through a dynamic equilibrium, with carbon dioxide entering the blood in tissues due to its higher partial pressure there compared to the blood, and being transported primarily as bicarbonate ions (about 85–88%), with smaller amounts bound to haemoglobin as carbamate (about 5–10%) or dissolved in plasma (about 5%). This recirculation is essential for maintaining stable blood pH and ensuring continuous gas exchange, as the body relies on the bicarbonate buffer system to regulate acidity, with the kidneys compensating for long-term changes in carbon dioxide levels. 

Oxygen-haemoglobin Dissociation Curve



Does the presence of carbon dioxide in the blood in any way help with the absorption of oxygen by tissues

Yes, the presence of carbon dioxide in the blood helps facilitate the absorption of oxygen by tissues through the Bohr effect. When carbon dioxide levels increase in the blood, such as in metabolically active tissues, it leads to the formation of carbonic acid, which dissociates into bicarbonate and hydrogen ions, thereby lowering blood pH. This decrease in pH reduces haemoglobin's affinity for oxygen, causing the oxygen-haemoglobin dissociation curve to shift to the right. As a result, haemoglobin releases oxygen more readily to the tissues, enhancing oxygen delivery where it is needed most. This mechanism ensures that oxygen unloading is increased in areas with high metabolic activity, where carbon dioxide production is elevated.



When a person hyperventilates the level of circulating carbon dioxide is significantly reduced. Does this reduced level of carbon dioxide and the increase in blood pH reduce the available oxygen to the tissues due to the oxygen-haemoglobin dissociation curve shifting to the left

When a person hyperventilates, the rate and depth of breathing increase, leading to the excessive elimination of carbon dioxide (CO2) from the lungs. This results in a significant reduction in the partial pressure of arterial carbon dioxide (PaCO2), a condition known as hypocapnia. The decrease in CO2 levels shifts the bicarbonate/carbonic acid equilibrium in the blood to the left, reducing the concentration of hydrogen ions (H+) and causing an increase in blood pH, a condition termed respiratory alkalosis.

This rise in pH causes the oxygen-haemoglobin dissociation curve to shift to the left. A leftward shift indicates that haemoglobin has a higher affinity for oxygen, meaning it binds oxygen more tightly at the lungs but releases it less readily to the tissues. As a result, despite adequate oxygen saturation in the blood, the delivery of oxygen to peripheral tissues is impaired because oxygen is not easily unloaded from haemoglobin. This physiological effect can contribute to symptoms such as dizziness, tingling, and even fainting. Furthermore, the reduced availability of oxygen to tissues is exacerbated by other effects of hyperventilation, including cerebral vasoconstriction and decreased cerebral blood flow, which can further compromise tissue perfusion.


 

What was discovered by Konstantin Buteyko in patients who were hyperventilating

 What was discovered by Konstantin Buteyko in patients who were hyperventilating by Graeme Ward

Buteyko discovered that chronic hyperventilation in elderly patients, like in other patients,

leads to low blood carbon dioxide levels (CO2) This state of hypocapnia can cause blood

vessels and airways to constrict, compromise oxygen delivery to tissues, and trigger

various symptoms, including those associated with asthma and hypertension. His theory

suggests these mechanisms lead to a range of symptoms and conditions that can be

alleviated by breathing exercises designed to restore normal CO2 levels and promote

slower, shallower breathing.

Buteyko's discoveries regarding hyperventilation and elderly patients

Hypocapnia and its effects: Hyperventilation causes a drop in blood CO2 levels

(hypocapnia), which leads to the body triggering defensive mechanisms.

Physiological consequences: These mechanisms include the constriction of

blood vessels and airways, which can increase blood pressure and contribute to

asthma symptoms like broncho-constriction.

Oxygen delivery issues: Despite there being plenty of oxygen in the blood, the

constricted blood vessels reduce the amount of oxygen that can be delivered to the

body's tissues.

Symptom trigger: Buteyko theorized that this cycle is a root cause of many health

problems, including heart conditions, high blood pressure, and anxiety, which are

common in the elderly population.

Potential for treatment: Based on these discoveries, Buteyko developed a

breathing technique that uses exercises to encourage slower, more controlled

breathing and nasal breathing, aiming to increase blood CO2 levels and alleviate

symptoms.

Konstantin Buteyko discovered that elderly patients with hyperventilation, or chronic over-

breathing, often developed more severe health conditions as their breathing rate

increased. By observing patients in a hospital setting, he found that the sicker the patient,

the faster and deeper their breathing became, a pattern that intensified as their condition

worsened.

Buteyko's key insight was that this dysfunctional breathing was not merely a symptom of

illness, but a contributing factor to it. He hypothesized that chronic hyperventilation, a state

of breathing more air than metabolically needed, leads to a cascade of negative

physiological effects.

Physiological effects of chronic hyperventilation

• Reduced carbon dioxide (CO2) levels: Over-breathing causes the body to exhale

excessive amounts of CO2, leading to a decrease in its blood levels (hypocapnia).

• Bohr effect impairment: CO2 is crucial for releasing oxygen from hemoglobin into

the body's tissues. With less CO2 available, oxygen delivery to organs is

compromised, causing tissue hypoxia.

• Blood vessel and airway constriction: Low CO2 levels can cause the smooth

muscles in blood vessels and airways to constrict, leading to conditions like high

blood pressure and asthma.

• Increased acidity: Despite the initial rise in blood pH (alkalosis) from low CO2, the

lack of proper oxygenation can lead to a buildup of acids like lactic acid, causing

fatigue and muscle pain.

• Overstimulated nervous system: Hyperventilation can trigger the "fight or flight"

response, leading to increased anxiety and other mental health symptoms.

The Buteyko method in practice

Based on these discoveries, Buteyko developed his breathing technique to help retrain

patients' breathing patterns to be slower and shallower. The goal is to correct chronic

hyperventilation and increase the body's tolerance to CO2. Key components of the

Buteyko method include:

• Nasal breathing: Encourages breathing through the nose to filter, warm, and

humidify the air, as well as to produce beneficial nitric oxide.

• Reduced breathing exercises: Consciously decreasing breathing volume to

trigger a mild "air hunger," which helps normalize CO2 levels.

• Breath-holding exercises: Techniques like the "Control Pause" (the comfortable

breath-hold time after an exhale) are used to monitor progress in restoring proper

breathing.

By controlling their breathing, Buteyko found that patients were able to alleviate symptoms

of chronic hyperventilation and improve conditions exacerbated by it.

This method retrains people to breathe in accordance to medical norms which in a healthy

person is around 4-8 litres of air per minute ( or minute volume). But the average person

these days is estimated to breathe 3 times what is healthy, and this sets up a situation of

chronic undetected hyperventilation. For asthmatics the minute volume can even get up to

around 25 litres.

His method gently retrains the respiratory centre in the brain, to not be triggered to take a

big gulp of air as soon as it detects an uncomfortable accumulation of CO2 in the lungs.

The retraining needs to be carried out slowly and gently along with muscular relaxation as

otherwise it could even exacerbate the over breathing due to stress, especially so in the

case for survivors of near drowning or choking.

The foregoing, as noted above, pertains to any cohort, not only the elderly.

A side note regarding asthma. There is evidence that asthmatics, like a large proportion of

the population are chronically dehydrated. This can often be the primary cause of

hyperventilation as a result of the body trying to conserve moisture being lost through the

breath. This causes broncho-constriction in the lungs resulting in hyperventilation

exacerbating all that is considered previously.


I experienced an unexpected and unexplained physiological event.

 After the event I experienced in March 2025. I went researching in an effort to better understand what had happened to me and what was the physiology surrounding it.

I spoke to many about my experience and nothing was forthcoming to explain what I'd suffered until one dear lady by the name of Tahnia mentioned the name Konstantin Buteyko. What he had discovered was that there can be a carbon dioxide imbalance in the blood, not too much but too little.

After much discussion with Tahnia and much time researching I finally put pen to paper as it were and cobbled together two short essays. These I've published separately.

"What was discovered by Konstantin Buteyko in patients who were hyperventilating" 

and

"The carbon dioxde balance in the blood in relation to the availability of

oxygen to the tissues"

Earlier in 2025 I experienced one of those unexpected days.

Some days just take a turn of their own.

A week ago today the day began much the same as any other, nothing out of the ordinary. After mowing some  of the lawn and moving some landscaping rocks I felt it was time for a rest. 

After resting for a short time I began to realise that there was something out of balance. Heart rate was high, blood pressure was way too high, started to feel really hot and had pain along my arms. I thought I’d said my morning prayers for the last time. So an SOS call to the ambulance.  Prompt response and a paramedic that I had known for some time turned up, that was very reassuring. She quickly had the ECG connected and it looks like a heart related event going on. I began to feel worse than I’d ever felt and thought if this is dying, I don’t want anything to do with it. 

Well, an hour or so later I was in hospital and in the catheter lab having angiograms  looking for the offending blockage in the coronary arteries. Zilch, no blockages found. By this time I almost felt as I usually feel, very well! Next day an ultrasound and an MRI, nothing really conclusive except the usual things one would expect of an old man, nothing immediately life threatening. 

I was then let out of hospital with the advice, “just be wary of what is happening and stop before the same thing happens again’. In other words don’t over do it.

So here I am at home, taking it easy, not over doing it and now learning what the new norm is in my life.

I’m so thankful to get another reprieve in life, thanks to the emergency and trauma care and technology that is now available here in this country.

Two days prior to all this happening I’d updated my training in applying CPR, I  thought how ironic it was that here I was lying there with real live gel pads clinging to my chest just in case I suffered a cardiac arrest.