Oxygen Pressure Field Theory I

Oxygen Pressure Field Theory.

Authored by:  Gary Grist,  BS, RN, CCP, LCP   

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I would like to begin a perfusion discussion of a subject about which most perfusionists know nothing.  Yet, in my opinion, it is vital to the basic understanding of perfusion science.  The subject is known as Oxygen Pressure Field Theory.

This idea has become almost a religion to me because it is so very important for the application of long-term perfusion support. This subject is new, exciting and controversial.  Oxygen Pressure Field Theory begins where the textbooks end.  The theory suggests how it is possible to maintain a normal blood gas and hemodynamcis and still have the patient go into multiple organ failure.  The theory suggests new ways to assess perfusion and new ways to adapt our intervention strategies. The down side is that the theory is complicated with many variables.

It does not easily fit into our known concept of perfusion science.  The theory suggests that transfer of gases at the capillary level is more complicated than the simple unloading of oxygen and pick-up of CO2.  Large areas of hypoxic and normoxic tissue can exist side by side in the same capillary tissue bed.  Intracellular pH can be radically different from blood pH, even to the point of causing tissue death.  Ironically, the theory suggests that the best measurement of tissue oxygenation does not  necessarily include the measurement of oxygen.

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“I will begin the discussion by posting my basic understanding of Oxygen Pressure Field Theory in a multipart series.  I do not know how many parts there will be.  Each part will describe a basic concept in Oxygen Pressure Field Theory.”

Gary Grist

The Krogh Cylinder

The Krogh cylinder is a basic concept of Oxygen Pressure Field Theory and was first described by August Krogh in 1919.  Dr. Krogh proposed the idea that the microcirculation functions as if each capillary is surrounded by a cylinder of tissue.  The capillary is responsible for perfusing the tissues in the cylinder, providing O2 and nutrients and removing CO2 and other waste products.  Of course, the Krogh cylinder does not exist as an anatomical structure.  The randomization of the capillary system results in the distribution of oxygen in the tissues surrounding each capillary in a special pattern called an oxygen pressure field from which the theory gets its name.

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The numbers used in describing the Krogh cylinder are examples only and do not necessarily represent the actual values found in a living organism.  Many things can affect the oxygen pressure field and some of those will be described in a later posting. Envision a structure shaped like a hollow cylinder with the center of the cylinder representing the capillary and the walls of the cylinder representing a sleeve of tissue surrounding the capillary.The capillary radius is 5 microns.  Therefor the X-section of the capillary is about 78 square microns (from the formula: area = “pi” x radius squared ).  The cylinder radius, which includes the capillary and tissue sleeve, is 10 microns.  Therefor,  the X-section of the entire Krogh cylinder is 314 square microns.  The ratio of the capillary X-section to the X-section of the entire cylinder is 1/4.

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In this example, the arterial blood enters the capillary with a pO2 of 80 mmHg.  The venous blood exits the capillary with a pO2 of 40 mmHg.  As the arterial blood enters the capillary the oxygen that it is carrying expands from the confinement of the capillary.  The oxygen passes through the capillary wall and fills the cylinder space that is 4 times larger than the capillary alone.

Because the O2 must fill this increased tissue volume the partial pressure of the O2 drops as it expands.  In this case the median tissue pO2 drops to about 20 mmHg.  Oxygen continues to expand into the greater tissue volume as the blood flows through the capillary until it is again confined when it exits the capillary and enters the venous system. Near the venous end of the capillary the pO2 is 40 mmHg resulting in a median tissue pO2 of only 10 mmHg. The difference between the capillary pO2 and the tissue pO2 is the capillary-to-tissue gradient.  This gradient causes oxygen to flow from the capillary and into the tissues.

The movement of O2 directly from the capillary and into the tissue follows “radial vectors”, so called because the O2 moves radially from the axis of the capillary lumen and into the tissues.  The gradient is largest near the arterial end of the capillary where the difference between the capillary pO2 (80mmHg) and the median tissue pO2 (20 mmHg) is 60 mmHg.  Near the venous end the gradient is only 30 mmHg (40 mmHg — 10 mmHg = 30 mmHg).  This means that oxygen will move into the arterial-end tissues faster and  in greater quantity than it will in the venous-end tissues where the gradient is half as much.

The net effect is an oxygen pressure field in the tissue sleeve that has a wide range of values.  Tissues at the arterial end and nearest the capillary will have pO2 values almost equal to the arterial pO2.  Tissues at the venous end and farthest away from the capillary will have values approaching zero.  In fact, the presence of an oxygen pressure field with it’s wide range of values is no theory.  Physiologists have measured tissue pO2 values in animals and adults with the results being very close to what Dr. Krogh predicted.

For example, resting skeletal muscle in humans and brain tissue in laboratory animals breathing room air have a median tissue pO2 of 20 mmHg.  This means that 50% of all the tissues in the capillary beds have pO2 values greater than 20 mmHg (with the highest value equaling the arterial pO2) and 50% have values of 20 mmHg or less.  The average value (as opposed to the median value) is about 55 mmHg because the upper 50% of cells have a wide range in cluding many high values while the low 50% of the cells never exceed 20 mmHg.

Also interesting is the fact that about 5% of all the cells in the capillary beds have no measureable pO2 (that is < 1mmHg).  Therefor, at any given time 5% of all the brain cells, 5% of all the muscle cells, 5% of all the other tissues are on the edge of anoxia.  A saving circumstance is the fact that mitrochonria can function at a pO2 concentration of 1 mmHg or less.  So as long as oxygen supply is steady to resting tissue even at low concentrations, the cells will survive even though they are hypoxic by most definitions and on the verge of anoxia. Of course, the Krogh cylinder is not a static model.

The tissue pO2 value is determined by several factors.  An increase in oxygen consumption decreases the tissue pO2.  A decreased tissue pO2 increases the capillary-to-tissue gradient thus magnifying the radial vectors and driving more O2 into the tissues.  The opposite occurs when oxygen consumption decreases.  Changes in the tissue volume of the cylinder surrounding the capillary also change the tissue pO2.  An increase in the tissue volume will decrease the tissue pO2 because the ratio between the capillary X-section and the cylinder X-section changes.

If the amount of tissue around  a capillary doubles the  median tissue pO2 is cut in half,  if all other variables remain unchanged.  Changes in the length of the capillary can also affect the tissue pO2 as can the intracapillary velocity. In summary, the Krogh cylinder predicts a  wide range of tissue pO2 values called an oxygen pressure field surrounding individual capillaries. This prediction has been substantiated by testing.  As the relationship between the capillary and its surrounding tissue changes the oxygen pressure field also changes.


I hope that by studying Oxygen Pressure Field Theory perfusionists can gain new insight and a fresh perspective on common perfusion problems.  For example, one of the biggest challenges facing the perfusionist (and the patient) is the use of deep hypothermia with circulatory arrest.  Most perfusionists cool their patients to a specified temperature (often 18C) to reduce the oxygen consumption to less than 10% of normal.  After what experience has shown to be an adequate time period (usually 20 minutes or longer), the pump is stopped, the patient drained of blood and the repair made by the surgeon.

However, there is a limit to how long this arrest period can last without damage. Generally, up to 45 minutes is usually safe.  Once 45 minutes is exceeded morbidity begins to increase so that at 90 minutes of arrest the morbidity reaches 90%.   The safe period of arrest might be increased utilizing the concepts taught by Oxygen Pressure Field Theory.  Two facts are known.  At 18C oxygen consumption is about 1/10th or less of normal.  At 18C oxygen is 4 times more soluble (0.12 cc/mmHg/kg of H2O) than at 37C (0.03 cc/mmHg/kg of H2O). Conceivably oxygen could be stored in the very tissues where it will be used (not just on the hemoglobin in the blood but in the Krogh cylinders themselves) during the arrest period.  This could be done by filling up the cylinders with oxygen during cooling so that all the tissues within the capillary bed are saturated with O2.

If the average tissue pO2 of a 3k baby at 18C is 150 mmHg and the O2 consumption is 0.6 cc/kg/minute, then the tissue O2 supply should last for approximately 30 minutes of arrest  [ ( 0.12 ccO2/ mmHg/kg  x 150 mmHg) / 0.6 ccO2/kg/minute =  30 minutes ] .  However, tripling the average tissue pO2 to 450 mmHg would greatly increase the oxygen supply and potentially increase the safe arrest period  [ (0.12 ccO2/mmHg/kg  x  450 mmHg )  / 0.6 ccO2/kg/minute =  90 minutes].  The average tissue pO2 can usually be estimated at 1.5 x the pvO2.

Therefore, the best parameter indicating when to arrest after 18C is reached  may be the estimated tissue pO2 based on a value of 1.5 x pvO2. As you can see, an understanding of Oxygen Pressure Field Theory can provide new insight into perfusion techniques.  As far as I know, no one has yet tested in a clinical study the idea of extending safe arrest periods as suggested above.  The reader is invited to do so, if interested.