Trouble with understanding pH-related death

  1. I'm having trouble understanding what effects acidemia and alkalemia have on the body that LEADS TO death.

    I have scoured the internet to no avail. I was told by my preceptor that both acidemia and alkalemia affects the conduction of the electrical stimulation of the body and they can impact the cellular extraction of oxygen off heme molecules.

    Is this true?

    So is it that the worse the pH gets one way or the other than the pt is more prone to arrhythmias and hypoxia?

    Is there a difference in effects leading to death from alkalemia versus acidemia, or are the effects the same that cause death of these things?

    Thanks sooooo much for all your help fellow nurses, as I am confused:
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    Joined: Sep '09; Posts: 23


  3. by   Esme12
    The body is a delicate balance systems extremes can cause death. The extremes cause system failure. Acidosis is more quickly fatal that alkalosis. Both will cause electrical failure of the cardiac system and respiratory failure as well as cell death at the molecular level.

    I am not sure what you are looking for about the difference in effects leading to death. What are you looking for?
    Last edit by Esme12 on Sep 9, '12
  4. by   Susie2310
    I think that a medical or nursing reference book that explains basic blood gas abnormalities along with medical conditions that can cause these abnormalities would be helpful. For example, metabolic acidosis, which according to my reference is a pH less than 7.35, with CO2 34-45 (normal), bicarbonate less than 22, base less than minus 2, can be caused by shock, sepsis, renal failure, diarrhea, DKA, and shortage of oxygen. Symptoms can be hyperkalemia, confusion, lethargy and coma. Studying the pathophysiology of medical conditions such as shock, sepsis, renal failure and DKA should clarify at a cellular level how metabolic acidosis can lead to death; it is a multistage process. Then you can study metabolic alkalosis, respiratory acidosis, and respiratory alkalosis in the same way.

    I hope this answers your question.
  5. by   mlbdestined
    thank you both for the responses. It helped. I guess I need to focus on the MODS picture that I'm guessing acidemia/alkalemia causes. I just was confused b/c the specific things I was told was that acidemia causes the heme molecules to give up O2 more readily to tissues, causing a drop in PaO2, but at the same time, not necessarily causing tissue hypoxia (which is what it would look like when just looking at an ABGs PaO2).

    So I was confused when my preceptor said "Acidosis doesn't cause hypoxia, which is what it looks like," and then later the shift said " the tissue hypoxia that extremes in pH can cause leads to cell death (which also goes along with the abnormalities of electrical conduction)". SO if I knew which one she meant I could say that MODS can lead to death r/t acidemia/alkalemia.

    So can any of you help me sort this out or confirm that acidosis does or does not cause tissue hypoxia?

    Thanks again all!
  6. by   Susie2310
    If we are speaking about hypovolemic shock for example, being the cause of metabolic acidosis, my understanding is that the tissue hypoxia causes the acidosis.
  7. by   Caffeinated RN
    Well, one easy way to think of it is to remember that the proteins in your blood require a certain pH. Messing up that pH can alter the shape of proteins, rendering them less effective or simply non-functional.
  8. by   BelgianRN
    I think your preceptor was indicating the oxygen hemoglobin dissociation curve. It's true that acidosis causes the curve to shift to the right thereby decreassing the "bond" between oxygen and the heme group in hemoglobin. In the lungs this isn't a real issue because you have ample time to saturate your hemoglobin fully in general terms. But on the tissue level this causes oxygen to come loose from the heme group much easier then in normo-pH states.

    The rational behind this is that acidosis caused by tissue hypoxia is a condition quickly leading to death so the body "designed" a mechanism to counter this. This wouldn't cause much of a change in paO2/saO2 due to the fact that in the arterial blood you are on the flat part of the curve. But in the tissues where the oxygen is used up you'll have noticably higher values for pO2 for a certain saturation level due to being on the steep part of the curve. And dissolved oxygen (pO2) is available for diffusion into the tissues/cells, where "bound" hemoglobin is not.
    There are certain other situations that cause right shift of this curve. And I love Wikipedia(R) for their "CADET, face right" indicating that increased CO2, Acidosis, 2,3-DPG, Exercise and increased Temperature cause right shift of the curve.

    I agree with with NBB2013 that failure of your proteins (read everything functional in your body) is a much more likely cause of death. Everything just stops functioning properly the more your pH deviates from 7,40 (wether it is up or down). Think about things like DIC, membrane destabilization, failure of your immune system that can be caused by pH abnormalities and you have your causes of death.

    And OP I like to stress the benefit of central venous/mixed venous blood gasses as well. An ABG shows you how well the lungs are capable of taking up oxygen and getting it into the arterial system. PaO2/SaO2 is basically what you are getting into the body, where I like to keep in mind that your hemoglobin carries your oxygen so saturation is much more indicative of the amount of oxygen available than paO2 is.
    For tissue hypoxia to be causing a drop in paO2/saO2 it would require such an depletion of oxygen in your tissues that your lungs don't have the diffusion capacity anymore to fill up nearly all your hemoglobin molecules with oxygen. Knowing that our body has about a 3 - 4 fold reserve capacity for diffusion capacity (in healthy lungs) you are looking at a (nearly) dead patient before you will see tissue hypoxia causing a normal paO2/SaO2 to drop.

    Central venous blood gasses or mixed venous blood gasses give you much more information. The blood collecting in your superior vena cava/right atrium is coming from the body (for the most part) if you determine the ScvO2 on that blood you can see exactly what's left over in terms of oxygen after it has been used by the body as a whole. Normally about 25% of our oxygen gets depleted so normal values are around 75%ish.
    Either it comes back as too high then there is decreased uptake due to decreased metabolism (usually not a problem), increased supply (hyperdynamic states) or due to a failure of oxygen to get into the tissues (problem, you will see other signs of tissue hypoxia like increased lactate levels).
    Or it comes back as way too low (much more common) which means the tissues take up more oxygen then usual. Increased metabolism (can be a problem especially when there isn't a lot of oxygen to begin with like ARDS patients breathing on their own), decreased supply (hydodynamic or hypovolemic or hypoxemic).
    Mixed venous gives you about the same information but in the mixed venous blood from the pulmonary artery there is also a big factor of venous blood coming from the heart itself.
    Keep in mind that venous blood is a pooling from all the tissues and it is entirely possible to miss signs of localized tissue hypoxia if your other tissues are receiving enough oxygen.
  9. by   mlbdestined
    Wow Belgian thanks! That really helps my understanding of the whole picture. I haven't seen these scvo2 catheters yet. Are they like continuous co measuring devices in that they give you a constant update on the scvo2 via a monitor?
  10. by   Esme12
    Belgian beat me to the punch!! Well said!!!!
  11. by   Esme12
    Quote from mlbdestined
    Wow Belgian thanks! That really helps my understanding of the whole picture. I haven't seen these scvo2 catheters yet. Are they like continuous co measuring devices in that they give you a constant update on the scvo2 via a monitor?
    Yes there are SVO2 Swan Ganzs and CCO (continous cardiac output) as well
  12. by   BelgianRN
    You have caths measuring it but if I don't have them in my patient I'll just draw blood from a central line or Swan Ganz and determine the SO2 myself via our blood gas analyzer.
  13. by   haji
    I think you would need to know a lot about physiology to understand why a low pH kills patients. I don't understand it really, but from what I've read at some point your body cannot carry out the cellular functions necessary to sustain life once your pH gets to low. Supposedly acidosis depresses cardiac function as well. Also you will hear that pressors don't work once the pH gets really low.

    I think it makes lots of sense to think about scvo2 when you have a sick patient (and how to increase it). The rivers trial showed a lot of benefit with this approach in septic patients. look up "early goal directed therapy" and "rivers"

    also it will help if you understand how to interpret abg's.
  14. by   rkealy
    Quote from haji
    Also you will hear that pressors don't work once the pH gets really low.

    That is true. Thats why after complete fluid resucitation fails, and levophed begin to become ineffective switch to Vasopressin ASAP. Vasopressin is a hormone that works much differently. Ideally you would begin CRRT Immediatly when noticing metabolic acidosis in septic shock