Physiological effects of Oxygen

[AWDennis]

It's all about homeostasis....

Let's talk about o2 use in trauma patients.

We all know that everyone dies from shock, one way or another. Whether it be hypovolemic, cardiogenic.... whatever.

Anyways, o2 is essential in trauma patients.

O2 is what keeps our cells working in aerobic metabolism, without it our body starts to work in anaerobic and that pyruvic acid that was being used by aerobic metabolism isn't being used anymore and is converted to lactic acid. Lactic Acid build up causes metabolic acidosis. Metabolic acidosis is lethal.

O2 also keeps the postcapillary sphincters closed, but once o2 reaches low levels those sphincters relax. And in trauma patients in decompensated shock, all that built up lactic acid and rouleax and waste is released into the body, this is known commonly as capillary washout. Capillary washout is also lethal

Finally o2 in trauma patients is essential to administer, in a attempt to hyperoxygenate the little blood that is being delivered to the vital organs is loaded with o2.

The major killer of post-trauma patients these days is Renal Failure. We can keep them alive but they die days after from renal failure, why? Bacause of the metabolic acidosis caused by ... inadequate oxygenation and off-loading of co2.

It all boils down to homeostasis,
Metabolic Acidosis, Inadequate Perfusion and Renal failure = No homeostasis
No homeostasis = A place to park my bike if we bury you upside down, right under the surface.

 

[Veneficus]

Let's talk about o2 use in trauma patients.

We all know that everyone dies from shock, one way or another. Whether it be hypovolemic, cardiogenic.... whatever.

Anyways, o2 is essential in trauma patients.

O2 is what keeps our cells working in aerobic metabolism, without it our body starts to work in anaerobic and that pyruvic acid that was being used by aerobic metabolism isn't being used anymore and is converted to lactic acid. Lactic Acid build up causes metabolic acidosis. Metabolic acidosis is lethal.

O2 also keeps the postcapillary sphincters closed, but once o2 reaches low levels those sphincters relax. And in trauma patients in decompensated shock, all that built up lactic acid and rouleax and waste is released into the body, this is known commonly as capillary washout. Capillary washout is also lethal

Finally o2 in trauma patients is essential to administer, in a attempt to hyperoxygenate the little blood that is being delivered to the vital organs is loaded with o2.

The major killer of post-trauma patients these days is Renal Failure. We can keep them alive but they die days after from renal failure, why? Bacause of the metabolic acidosis caused by ... inadequate oxygenation and off-loading of co2.

It all boils down to homeostasis,
Metabolic Acidosis, Inadequate Perfusion and Renal failure = No homeostasis
No homeostasis = A place to park my bike if we bury you upside down, right under the surface.

That is rather over simplified.

What about the pathologic effect of reperfusion injury?

Oxygen free radical damage in the lungs, liver, eyes, and kidney?

Oxygen free radical damage to RBCs

Would seem sort of counter productive to destroy the very "cell" that you need to carry and offload oxygen.

Speaking of RBCs they function on anaerobic metabolism all the time?

What about free radical damage to vascular endothelium causing patholigc coagulation when glutothione is depleted?

There is much more to the physiology and pathophysiology of hyperoxygen concentrations than you give it credit for.

 

[systemet]

Anyways, o2 is essential in trauma patients.

It's unclear what you're trying to say here. Can you expand this statement?

Lactic Acid build up causes metabolic acidosis. Metabolic acidosis is lethal.

Metabolic acidosis can be lethal, if it is severe enough / lasts for long enough. There's a basal level of anaerobic metabolism occurring in the body at rest. This can be detected by measuring lactate in healthy volunteers. I help run a lab where we do this, and we typically see values around 2 mmol/L, with the odd person running up as high as 4 mmol/L, which I suspect is probably a limitation of the testing device, but may be normal variation.

You've identified that hypoxia results in anerobic metabolism, which can result in lactic acidosis, if the H+ production exceeds the capacity of the buffer systems and respiratory compensation. But have you considered what sort of hypoxia you're dealing with?

In the trauma patient you're primarily looking at elements of stagnant (i.e. no/low blood flow) and hypemic (decreased oxygen carrying capacity, i.e. anemia) hypoxia. Supplemental oxygen will likely not produce flow to areas that are not currently perfused, and may decrease it in some regions -- so it's not much use against stagnant hypoxia. On the same level, it's not going to reverse the patients anemia, so if the patient is well saturated, only a small increase in arterial oxygen content is going to occur. So it's not that useful against hypemic hypoxia either.

Provided we've ensured an open airway and adequate oxygenation (+/-suction +/- OPA +/- BIAD +/- ETI, +/- needle decompression +/- securing flail / open pneumo +/- artificial ventilation), supplemental oxygen isn't going to fix the major issues of (1) Inadequate tissue perfusion, (2) Inadequate oxygen carrying capacity.

O2 also keeps the postcapillary sphincters closed, but once o2 reaches low levels those sphincters relax. And in trauma patients in decompensated shock, all that built up lactic acid and rouleax and waste is released into the body, this is known commonly as capillary washout. Capillary washout is also lethal

Capillary washout may be lethal. You're talking about local hypoxia being harmful because at a low enough pO2, enough acidosis / CO2, K+, adenosine etc., you may have a restoration of local flow. But to treat this, we need high enough perfusion pressures to restore local flow, and enough oxygen carrying capacity that the oxygen delivery meets local metabolic needs.

The treatment here is to prevent further blood loss, and to restore volume and oxygen carrying capacity.

Finally o2 in trauma patients is essential to administer, in a attempt to hyperoxygenate the little blood that is being delivered to the vital organs is loaded with o2.

But have you looked at how small a difference in oxygen content occurs when you hyperoxygenate? It's hemoglobin that carries oxygen, not plasma.

See #68 here: http://www.emtlife.com/showthread.php?t=28700&page=7

The major killer of post-trauma patients these days is Renal Failure. We can keep them alive but they die days after from renal failure, why? Bacause of the metabolic acidosis caused by ... inadequate oxygenation and off-loading of co2.

But here inadequate oxygenation occurs for several reasons:

(1) Renal blood flow drops dramatically in shock states as a result of sympathetic activation (amongst other things).

(2) Once the body is no longer able to compensate for volume loss by vasoconstriction and increases in heart rate and cardiac contractility, MAP falls, and this further decreases renal perfusion pressure.

(3) The oxygen carrying capacity of the blood that does perfuse the kidneys is markedly reduced due to loss of hematocrit.

The kidneys are particularly sensitive to this because of countercurrent perfusion, and the relative hypoxia of some regions under resting conditions. This problem is going to be addressed by surgical correction of the underlying injury, restoration of volume, and restoration of oxygen-carrying capacity.

Could hyperoxygenation improve this process? Maybe. But it could also create further injury and compound the existing problem. This isn't clear yet.

 

[AirMed44]

JP, I think you were misunderstanding the original point...

What I am arguing against is LOCAL vasoconstriction of the coronary vasculature. I'm not even arguing that net vasoconstriction will help the pathophysiology. That would be silly, as it would contradict my own initiative to give oxygen (active hyperemia would be more potent without O2).

What I am trying to say is that O2 causing vasoconstriction problems in the coronary vasculature is not a valid concern to me when I measure it against the possible benefits of raising global O2 Sats...

Sent from my DROID2 using Tapatalk

I presented on how we are killing people with high flow oxygen at the Critical Care Transport Medicine conference last year. It's not a theory, but a fact. The whole idea of giving high flow oxygen originated in a paper in 1900. By 1904 it was being questioned and by the 50's there was already research showing it was harmful in patient's with normal oxygen levels. The problem isn't when we give oxygen to people who are hypoxic. That is a definite must. It's when we are slapping non-rebreathers on chest pain patients who have normal oxygen levels.

McNulty, et al. study was the most graphic explanation for me. His group took patients to the cath lab and injected dye to look at their coronary vasculature. Once that was completed, they placed the patients on non-rebreather mask and shot dye again. It showed a 30% increase in coronary vasoconstriction and a 40% decrease in coronary blood flow. The study shows the pictures and it is unbelievable.

The way I look at it is if they don't need it, I am not going to give it to them. Dan Davis, MD (chairman of the ROC committee) once stated that if you were to try to run oxygen through the FDA now, it would have no chance of making it as an acceptable drug. I don't give epi if a patient doesn't need it (yeah, I know opening a whole other can of worms), I won't do oxygen that way either.

Just my two cents!