Myocardial Oxygen Balance

Myocardial Oxygen Balance

Maintaining the blood’s oxygen carrying capacity to vital organ structures and peripheral vascular beds is the primary consideration for cardiovascular perfusion.

Oxygen content is defined as the number of cc’s contained in 100 cc of whole blood.  This value is derived from a combination of physical and physiological parameters that can be expressed by the equation:
CaO2 = (Hb x 1.34) x (SaO2) + (PaO2 x 0.003)

Where:
Hb    = gm of hemoglobin per dl (1/3 of hematocrit).
1.34    = number of cc of O2 bound to 1 gm of saturated hemoglobin.
SaO2    =% oxyhemoglobin to total hemoglobin, fractional saturation.
0.003    = oxygen solubility in plasma.

If the hemoglobin is 100% saturated the oxygen content of blood with 15 gm/dl of hemoglobin is 20 cc/dl,  then the O2 content can be quickly approximated as being slightly less than half (45%) of the hematocrit; assuming the hemoglobin is fully saturated.

For oxygen to be utilized in the tissue it must be circulated.  The rate of overall circulation (cardiac output) averages 5 liters/minute (70 cc/kg) for an adult at rest.  The cardiac output is determined as the product of heart rate and stroke volume .

The rate of oxygen transport to the body (oxygen delivery) is the product of cardiac output and oxygen content, (1,000 cc/minute).

The tissue extraction rate is 5 cc of oxygen per 100 cc of blood flow (25%) and result in a mixed venous oxygen saturation of 75% (15 cc of oxygen per 100 cc of blood).

As the hematocrit decreases the tissues may either extract more oxygen if blood flow remains constant, increase blood flow if the volume of oxygen to be extracted is to remain constant, or decrease oxygen consumption.  The primary components of cardiac output are preload, afterload, contractility, compliance, and heart rate.

Blood flow may increase through acceleration of heart rate or through an increase of stroke volume.  Since blood viscosity decreases with hematocrit and decreases with increasing flow rate (blood is a non-newtonian fluid), normovolemic anemia decreases cardiac afterload thus facilitating increasing cardiac output.

This assumes intravascular volume is maintained and there is an ample cardiac reserve.  Afterload is defined and can be related to systemic arterial pressure as being a determinant of the tension that cardiac fibers must develop before they can shorten.

References

Mohrman DE, Heller LJ. Cardiovascular Physiology. 3rd ed. New York, NY.     McGraw Hill; 1991:175-188.