The problem with that statement is that the 100% is only measured on the hemoglobin itself. The rest of the blood is not measured, and if there are free radicals, which is oxygen molecules that are not attached to any blood cell, then you create ozone, which is toxic in the blood. And there is more than 100% in that instance.
In the case of a left shift, you can have a higher than correct value on your pulse oximeter.
Right.....Sp02/Sao2 are measures only of the percentage of bound hemoglobin, not dissolved oxygen. My point was that since dissolved oxygen makes up only about 1% of the total arterial oxygen content, you can increase oxygen delivery very little by continuing to add supplemental oxygen when Sp02 is already adequate.
This is true regardless of whether a right or left shift is present. A left shift represents a greater affinity of hgb for oxygen, but this is not changed by increases or decreases in Pao2 or Sa02.
A left shift will not affect your pulse oximetry readings. It simply describes how readily oxygen leaves the hemoglobin to diffuse into the tissues.
What we really need to think about when considering supplemental oxygen is oxygen delivery:
Oxygen delivery (D02) is Cardiac output (CO) x Arterial oxygen content (Ca02):
- Ca02 is the oxygen carried on hemoglobin + the oxygen dissolved in plasma, or [1.39 x Hb x SaO2 + (0.003 x PaO2)]
- CO, of course, is HR x SV, and SV is affected by preload, contractility, and afterload.
- The complete oxygen delivery equation looks like this: DO2 = Ca02 [1.39 x Hb x SaO2 + (0.003 x PaO2)] x CO [HRxSV]
Being that there are only 2 parts to the equation, there are only 2 things that can be manipulated to improve oxygen delivery: cardiac output and oxygen content.
The primary ways to improve oxygen content are increasing hgb levels (giving PRBC's), and increasing oxygen saturation. If you calculate the equation out using different values, you'll see that increasing Pa02 has a very negligible effect on oxygen delivery, and increasing Sp02 has a small effect as long as it is already above ~95%. Increasing hemoglobin generally has a large effect, however.
The basic first step is to always maximize the Ca02 side of the equation first, which simply means ensuring an adequate hemoglobin level and Sp02.
But, what about the tissue perfusion? In the ICUs we are able to see the SaO2, PaO2, ScvO2 or SvO2. We adjust fluids and pressors according with the O2 in place until we know we can improve delivery.
When you manipulate fluids and pressors in the ICU, you are simply manipulating the other side (the CO side) of the equation. Scv02/Svo2, CVP, SVR, SVV, lactate, etc are simply clues to help you decide whether CO needs to be manipulated, and if so, which component of CO (HR, SV, preload, or SVR) will have the biggest impact.
Changes in Pa02 have very little impact on total oxygen delivery. Assuming, of course, that abnormal forms of hemoglobin or other blood toxicities (methemoglobin or cyanide toxicity) are not present. Also, pulmonary problems that can make it difficult to properly oxygenate the blood (ARDS), or deleterious effects of certain therapies (increased Mv02 or renal or splanchnic hypoperfusion due to vasopressor therapy, etc.) obviously need to be assessed and managed.
It also does not take into account the effects of a serious right or left shift, but that is a problem separate from blood oxygenation. Shifts are avoided primarily by maintaining normal C02 and pH level, not by manipulating Fi02.