Sometimes you just know…
It was gonna be a long pump run, huge patient, and the CT surgeon is a slow AND meticulous surgeon, an artist of self imposed preciseness that pre-emptively puts down 4.5 LPM as the standard for every bypass run. No rhyme or reason- his perfect universe ran at 4.5 liters per minute- come hell or high water- that’s going to be the ship you are sailing.
You look at huge muscular thighs that always tell you when you will be pushing your oxygenator to the limit, invariably the T-Rex thigh guys always come with incipient baggage- the heparin resistant kind. That’s not to suggest that all T-Rex thighs imply an AT3 deficiency- but this week it seemed like a Walmart sale on Heparin.
Todays run was going to be a PacMan game– where the bad guys are munching up O2 like popcorn, and thermoregulation is your only defense to stay ahead of that curve- The Oxyhemoglobin Dissociation Curve.
So in a nutshell- we have a big patient- roughly 2.6 BSA- very muscular- and under 60. That translates into a a review of your oxygenator’s capabilities, size and O2 transfer rate. The one variable not on the table? Speed in this case was non-negotiable. This was going to be a 3 hour pump run- assuming no mitigating or unexpected issues emerge during the on-bypass phase of the operation.
The physiology of the Oxyhemoglobin Dissociation Curve as it impacts CPB is a board question that comes to the fore pretty much on all written exams we take on our way to becoming certified. And certainly as we forge ahead and actually put all those patients on bypass- we rarely have to actually challenge ourselves when it comes to issues of potential hypo-perfusion. Our oxygenators are too good at this point- thoroughly vetted, so we rely on an empiric belief- that they will sustain almost any patient.
And that predisposed confidence has become pretty mainstream- when in the past it was a question you asked every day. “Can I adequately meet the perfusion demands for this patient?” – That uncertainty Is no longer even a baseline concern.
So our comfort zone has expanded. We increasingly rule out the potential for malfunction or under-performance- and so for now- addressing the the obvious process of dealing with a potentially overwhelmed oxygenator is a clinical inclination that hovers less prominently, yet lingers as something that in my opinion should probably be in the forefront of your game plan before engaging bypass and a reasonable review during morning coffee.
Typically I like to listen to music as I write about our lives’ in the operating room and the challenges we encounter.
This particular environment has no music- because the operations are bland, unimaginative, and basically meat and potato’s. The outcomes are always good- so no issue there. At least the outcomes are good.
Getting Back to the Clinical Presentation and Discussion
Although I realized that there might be an O2 transfer issue as we rewarmed, I was actually surprised at how significantly this patient was challenging the Oxy- as well as the fact that increasing Q wasn’t having any sort of impact in terms of improving O2 % or PaO2s based on our CDI.
I tried the usual, opened a shunt to hyper-oxygenate the venous reservoir- which hurt more than helped in all reality. The Pts’ Hgb was 12.0 mmHg so I diluted with an additional 750 ml of crystalloid which brought PO2’s from the low 200’s to roughly 280 torr. At this point however- we hadn’t started rewarming from 34 C. It was obvious there would be an O2 debt issue for when we did go into full rewarm mode. Cerebral saturations basically mirrored what I was doing- so there was an established baseline of reliability
At the command to rewarm, I bumped the heater cooler to 37 C- and maintained Q- the XC was still to come off, and 3 proximals left on the menu. That basically represented at least 45 minutes after the XC was off- and it was still not off.
This is when knowing your environment and the tendencies of your surgeon come into play.
At 35 C, and rewarming- I was already in the 200 range for PO2’s and watched them drop to about 176.
It was obvious to me that even at 100% FiO2 and despite increasing my LPM sweep- I was getting dangerously close to an unacceptable position in terms of failure to oxygenate. I obviously considered the possibility of adding a parallel Oxygenator to the circuit- but felt that would have been too aggressive and destabilizing at that particular moment.
I communicated that to the MDA and expressed my strategy to cool down to 34 C and wait until we finished the last proximal anastomosis- and go go into full rewarm once that partial XC came off. I factored in the speed of the surgeon.
I maintained PO2’s in the 170’s, as we rewarmed- and rewarmed quickly.
As soon as Anesthesia started ventilating- PO2’s bumped up to the 350-500 range.
We came off bypass – and no clinical issues. 37 C.
The point to be made here?
Most bypass runs are academic. That is not to diminish the risk or dedication to the task- but its a basic reality- assuming competence of all involved in the process.
Outliers such as the one described? That is when you define yourself- and sometimes its the angry process of having to get the experience- as scary as it may be- to believe in yourself enough to make the right decisions.
The more significant aspect of what we do? Our decisions to act are not really the question: Our decisions to evaluate and choose how and what we communicate is ultimately what saves lives.
How we process what we see in front of us- THAT is what truly makes the difference.
I have a lot of cases under my belt- but my firm belief has always been: “You are only as good as your last case”. It doesn’t matter what your resume’ says.
In this case? Experience payed off- Communication and a solid rationale are manifestly incumbent because they are the ingredients that although risky to rely on- the final equation amounts to having the finite courage to live and go forward with making THAT decision.
What factors affect hemoglobin’s oxygen affinity?
The oxyhemoglobin dissociation curve describes the relationship between arterial oxygen tension (partial pressure of oxygen in the arteries, PaO2) and the amount of oxygen bound to hemoglobin—the hemoglobin saturation. As arterial oxygen tension increases, the amount of oxygen loaded onto hemoglobin increases curvilinearly, creating a sigmoid- shaped graph—the result of enhanced oxygen-binding after the initial binding of oxygen occurs.
Figure 1. The oxyhemoglobin dissociation curve describes the relationship between arterial oxygen tension (e.g., partial pressure of oxygen in the arteries, PaO2) and the amount of oxygen bound to hemoglobin (e.g., hemoglobin saturation). The flat portion (A) shows that increases in PaO2 at higher concentrations does not result in significant increases in hemoglobin saturation. The steep portions (B) shows that at lower concentrations, small changes in PaO2 has greater effects on oxyhemoglobin concentrations.
The upper portion of the curve (PaO2 > 60 mmHg) is flat (A), indicating that further increases in arterial oxygen tension do not result in significant increases in hemoglobin saturation. The lower and middle portions of the curve are steep (B), indicating major changes in oxyhemoglobin concentration with small changes in arterial oxygen tension.
P50 of hemoglobin
A useful parameter to describe the overall positioning of the curve is the P50—the arterial oxygen tension at which hemoglobin is 50% saturated. Normal P50, measured at 37°C and an arterial pH of 7.40, is 26.6 mmHg.
Figure 2. Overall positioning of the oxyhemoglobin dissociation curve can be determined from the P50, which is the arterial oxygen tension at which hemoglobin is 50% saturated.
As hemoglobin’s affinity for oxygen decreases, oxygen is more readily unloaded at the tissue level. This is reflected in a rightward shift of the curve and a higher P50. A decrease in P50 indicates greater hemoglobin avidity for oxygen and decreased oxygen release.
Figure 3. Shifts in hemoglobin’s oxygen affinity are associated with shifts in the oxyhemoglobin dissociation curve’s P50. Decreases in hemoglobin affinity for oxygen is associated with a higher P50, while increases in hemoglobin affinity are associated with decreased P50.
Physiological factors that can shift the oxyhemoglobin
Changes in pH and the Bohr effect
Changes in the position of the curve with changes in red blood cell (RBC) intracellular hydrogen ion concentration constitute the Bohr effect. Decreases in pH shift the curve to the right, while increases shift the curve to the left.
Figure 4. Changes in pH are associated with changes in hemoglobin’s oxygen affinity. Decreases in pH shift the curve to the right, while increases shift the curve to the left.
Carbon dioxide increases hydrogen ion concentration and lowers tissue pH. As a consequence, hemoglobin’s affinity for oxygen decreases and oxygen release to tissues is facilitated. Opposite changes occur in the lung.
Figure 5. Changes in carbon dioxide (CO2) are associated with shifts in hemoglobin’s oxygen affinity. Increases in CO2 decrease hemoglobin saturation, while decreases in CO2 increase hemoglobin saturation.
During glycolysis, red blood cells generate organophosphates, particularly 2,3-diphosphoglycerate (2,3-DPG). In red cells, due to the absence of mitochondria, 2,3-diphosphoglycerate is used for energy generation. In the setting of diminished oxygen availability (e.g., anemia, blood loss, chronic lung disease, high altitude, or right-to-left shunts), organophosphate production in red cells is increased, shifting the oxyhemoglobin curve to the right, thereby facilitating unloading of oxygen in peripheral tissues.
Figure 6. Increased organophosphates shift the oxyhemoglobin curve to the right, which facilitates oxygen unloading into peripheral tissues.
Changes in temperature
Hyperthermia shifts the curve to the right. Opposite changes occur with hypothermia.
Figure 7. Changes in temperature are associated with changes in hemoglobin’s oxygen affinity. Hyperthermia shifts the curve to the right, while hypothermia shifts the curve to the left.
Carbon monoxide levels
Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left, impeding oxygen unloading in peripheral tissues. This effect is in addition to the effect of carbon monoxide in binding to hemoglobin and preventing oxygen loading in the lungs.
Figure 8. Carbon monoxide shifts the oxyhemoglobin dissociation curve to the left, preventing oxygen unloading in peripheral tissues.
Methemoglobin is the result of oxidation of the iron moiety of hemoglobin from the ferrous to the ferric state. Intracellular enzymatic reductive pathways normally maintain methemoglobin levels of less than three percent.
Figure 9. Oxidation of the iron moiety of hemoglobin from the ferrous to ferric state results in methemoglobin.
In the presence of congenital deficiencies of reductive enzymes, or in the presence of oxidant drugs (e.g., antimalarials, dapsone, local anesthetics), methemoglobinemia may develop.
Methemoglobin shifts the oxyhemoglobin curve to the left, impairing oxygen release in peripheral tissues.
Figure 10. Methemoglobinemia shifts the oxyhemoglobin curve to the left, impairing oxygen release in peripheral tissues.
Presence of abnormal hemoglobins
Finally, the presence of abnormal hemoglobins—such as fetal hemoglobin in an adult—can have an effect on the oxygen-hemoglobin binding curve. Fetal hemoglobin, hemoglobin F, consists of two gamma chains replacing the normal two beta chains.
The oxyhemoglobin curve is shifted to the left in the presence of hemoglobin F, enhancing hemoglobin’s affinity for oxygen, an advantage during fetal life when arterial oxygen tension is low.
Figure 11. Abnormal hemoglobin shifts the oxyhemoglobin curve to the left, enhancing hemoglobin’s affinity for oxygen.
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