bloodgases

  1. 0
    I am a medsurg nurse moving to ICCU, I have never been good at understanding blood gases. Anyone have any tricks to help me to understand them better?
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  4. 0
    at a very basic level:

    First, look at the pH value: if < 7.4 it's an acidosis

    next, check the pCO2 and the HCO3 for the cause of the acidosis: if pCO2 is > 45, it's respiratory; if HCO3 is < 22, it's metabolic
    and, if both conditions exist, it's a mixed acidosis

    and vice versa for an alkalosis.

    This is very simplistic and there are many, many "acute on chronic" situations that are more complicated. Hope this helps.
  5. 0
    Oops. Addendum to the prior post. ABG's are also used to assess oxygenation. I'll let someone else talk about that.
  6. 1
    i think the last couple posts are really useful.

    also you want to see the o2sat and the pao2. the sat on the abg and the spo2 on the monitor will be pretty close. you want the sat>90%.
    sat is the % of hgb saturated with 02. Cardiac output, arterial sat and hgb/hct are three important factors affecting o2 delivery. on the other end of it you can look at lactic acid or svo2 to see if the supply is meeting demand. if someone has a high lactate (metabolic acidosis) or low svo2 they need more o2 delivery.

    pao2 is the partial pressure of 02 is arterial blood (oxygen that's not bound to hemoglobin).
    pao2 on room air in a normal person is around 90. so if someone is on o2 and their pao2 is low you know they aren't oxygenating well. also if you see a pao2 of 300 you'll know you need to turn down the fio2.
    but for me the sat is the important part of the equation if you have an unstable patient.
    JulieL likes this.
  7. 0
    Thanks all of that really helps!
  8. 0
    pH determines whether the patient has an acidemia or alkalemia.
    CO2 determines the respiratory component, HCO3 determines the metabolic component, being an acidosis or alkalosis.
    You can have a normal pH with a concurrent acidosis or alkalosis. Stated differently, acidemia or alkalemia do not need to be present to have an acidosis or alkalosis.
    With normal lungs, your PaO2 should be 5x your FiO2 (P:F ratio of 400-500 is normal). You can also do things like the A-a gradient, which give you additional information.
    There is a great podcast on iTunes. Search "ICU Rounds". Lots of great info there.
  9. 0
    Something I learned as a student that helped me was the acronym ROME.

    Respiratory Opposite, Metabolic Equal

    Like PetERNurse said, pCO2 is related to respiratory and HCO3 is related to metabolic. So, a basic way to look at a blood gas is, if the pH is down and the pCO2 is up it's respiratory acidosis. Or, the other way around, if pH is up and pCO2 is down then respiratory alkalosis. pH and pCO2 are opposite - Respiratory Opposite.

    When pCO2 is WNL and HCO3 is off: pH down and HCO3 down then it's metabolic acidosis. pH up and HCO3 up = metabolic alkalosis. Metabolic Equal.

    You can later delve into more than that but ROME helped me as a foundation for looking at ABGs.
  10. 0
    some good answers.

    but it aint if it is less than 7.4 as that is out of context. If all values are within 'normal limits', we dont ask that question--that question is used primarily to determine patial/complete compensation issues.

    'normal' values (it is relative, as this may not be normal for a given disease process, in which case Hx is needed for proper context):

    ph: 7.35 -7.45 (some books use 7.37)
    pco2 35-45
    hco3 22-26
    p02 80-100 (not 60)
    sa02 95-100 (not 90%, not 92%. something physiological/environmental is in place if it is less than 95)
    Base excess (BE) -2 to 2
    anion gap, without potassium, 12-16 (unlike the poster, acidosis does not have to be lactate, so we use this gap to look for poisoning, ie ethylene glycol, etc, and then check direct osmolality, should be less than 295-300mOsm)

    first first: if all values are wnl, dont procede with the analysis below

    first:
    ph less than 7.35 = acidosis
    ph more than 7.45 = alkalosis

    write answer down on paper

    second:
    pco2 less than 35 = alkalosis
    pco2 greater than 45 = acidosis
    explanation: co2 in the blood forms with hco3 to form h2co3, or carbonic acid. If we can increase the respiratory rate or volume (alveolar minute ventilation--said this for a reason, not just minute ventilation as it does not compensate for dead space), we can remove this co2 so it does not form carbonic acid and thus increase acidosis. this system kicks in within minutes-hours (carbonic system and protein system actually in seconds)

    write answer down on paper, labeled respiratory ______, as i just explained it is tied to the resp. system

    third:
    hc03 less than 22, acidosis
    hc03 greater than 26, alkalosis

    explanation: kidneys can excrete Hydrogen (thus it can not form with co2) and retain K or Na accordingly. Therefore this is 'metabolic' control, kicks in within several hours to few days

    label it, metabolic ________

    note: you may have a mixed metabolic and respiratory component if they are in the both direction, ie both acidotic or both alkalotic

    This next step is where we use 7.4 as the ABSOLUTE value. 7.4 is used to determine partial compensation or complete compensation

    If there is an acidosis or alkalosis, and the ph is exactly 7.4, we have complete compensation. Rare.

    If it is respiratory acidosis, but the hco3 is above 26, we have partial compensation (the metabolic system is trying to make the blood alkalotic to make the ph 'normal', ie 7.35 to 7.39)

    if it is respiratory alkalosis, but the hco3 is below 22, we have partial compensation (the metabolic system is trying to make the blook more acidotic to make the ph 'normal')

    if it is metabolic acidosis, but the pco2 is below 35, we have partial compensation (the respiratory system is hyperventilating trying to blow off co2 so it can not form carbonic acid, thus resp. alkalosis)

    if it is metabolic alkalosis, but the pc02 is above 45, we have partial compensation (lower rate or volume of breathing, trying to retain co2 to make more acid to make more normal ph). metabolic alkalosis is almost always BAD NEWS--be forewarned and on guard.


    It gets more complicated than this, but i dont want to type more and cause more confusion


    I believe my answer is the best thus far.

    I could be wrong.



    it should get u 95% accuracy.

    if the sa02 as measured via abgs is below 90, as far as the texts are concerned, we have hypoxia, as is the case with p02 60 or below, we correlates with the beforementioned on the oxyhemoglobin dissassociation curve. but it is more than this. use the other poster's formula with the fio2 multiply-er to determine what the true po2 should be.

    personally, i feel u should be wary if it is below 95% and 80mmhg on the po2 assuming room air.

    to determine the underlaying cause of the hypoxia, consider ketones, lactate, anion gap to assist in determining said underlaying cause, in addition to ventilation/perfusion mismatch or shunt and poisonings (carbon monoxide, cyanide, drug od like tricyclics, ethanols/ethylenes, etc)

    furthermore, as the other poster stated, we need to determine:
    adequate heart rate (HR)
    adequate cardiac output
    adequate hemoglobin (not hematocrit) (ie 12-18, but rarely transfuse until below 8mg/dl)
    adequate 2,3 diphosphoglycerate (banked blood is depleted, thus massive transfusions with be deficit and the blood will not want to release the oxygen off the hgb, a shift in the oxy-hgb curve, increasing affinity of hgb and o2)

    all the beforementioned is best evaluated as the poster said, not via oxygen delivery:
    cardiac output X HGB X 1.34 (or 1.37 depending on book)

    but by oxygen consumption

    this is because THIS patient may NEED more oxygen.

    the delivery equation assumes normalcy. would you want a 'normal' oxygen delivery if you were on a treadmill running as fast as you could for 1 hour?

    No. you would need a much HIGHER delivery, and thus the correct measure is the extraction ratio, usually quickly calculated by considering the abg sao2 and the svo2 subtraction

    However, the equation estimation is thus, based on FICK:

    (cardiac output X sao2) - (cardiac output X mixed venous blood o2 (obtained via pulminary capillary wedge port, wedged)

    as u can see, that roughly correlated with the beforementioned sa02 - sv02



    that is all i can think of at the moment during my work break.

    be well
  11. 0
    part 2, in brief:

    let's assume we want to improve the oxygen consumption ratio, we do this by addressing oxygen delivery, and thus the original equation i posted

    1. we can increase the heart rate, to a point, as
    CO = HR X stroke volume

    2. we can increase the 'contractility' of the heart, thus improving ejection fraction. for some, that is digoxin

    3. we can increase preload, the volume returning to the heart, thus a crystalloid (pref. isotonic), colloid (hespan, hetastarch, albumin 5/25%) or prbc's. more volume, more stretch, starlings law (but this may cause a reflex bradycardia via baroreceptors in the aortic arch etc thus may need to address this). blood has the advantage of increasing hgb, oxygen carrying capacity

    4. we can reduce afterload, the pressure the heart has to push against (aorta in case of left ventricle), think lowering blood pressure etc. this is the SVR, or systemic vascular resistance. One option may be dobutamine, which slightly increases HR, slightly reduces afterload (svr, bp). In the case of a chronic CHF patient he may have experienced 'dowregulation' (unfortunately, beta receptor sites on cells can 'uncouple'/disassociate and even be reabsorbed--in which case steroids may be in order to get mRNA involved to make new receptor sites). In the meantime, we use phosphodiesterase inhibitors (amrinone, milrinone, etc) and go thru the back door, increasing cAMP within the cardiac cell itself.

    5. we can reduce the pressure the right heart has to push against thru the pulmonary vasculature (PVR) via monitoring pulmonary congestion, etc--dont let the cvp get too high, assuming competent valves and normal compliance

    6. dont let the pcwp get too high or low, which reflects the pressure of the left ventricle at end diastole, assuming competent valves and normal compliance. if the pressure is too low, think starling law. if the pressure is too high, the increasing pressure in the venticle will back up to the right side, right heart very weak, and also the ventricular wall pressures may cause subendocardial ischemia and further dysfunction

    keep in mind that we have to balance these inotropes, chronotropes, vasodilators etc with myocardial oxygen consumption--if we have coronary artery occlusions increasing these values too much, even within 'normal limits', will increase myocardial oxygen consumption, reducing glycogen stores within the heart, increasing ischemia/cellular acidosis, further contributing to reduced ejection fractions, reduced cardiac output, cardiogenic shock etc

    we can recruit more alveoli via peep--watch for overcomliance of lungs, which may compress heart, reducing cardiac output--consider increasing preload to ability to counteract

    we can increase the tidal volume, keeping plateau pressure below 30-35, depending on the client

    we can increase the ventilator rate, to a point, but volume first, usually

    we can reduce oxygen consumption of client by maintaining normothermia, at times mild hypothermia, in case of head injury, etc. possibly barbituate coma, sedation, etc

    we can paralyze/sedate and consider reverse IE ratio

    we can consider high frequency oscillatory ventilation


    it is a science that must be balanced
    Last edit by zcoq72mehs on Nov 27, '11 : Reason: forget primary resp
  12. 1
    Just need to clear a few things up..

    first:
    ph less than 7.35 = acidosis
    ph more than 7.45 = alkalosis
    pH does not determine whether the patient has an acidosis or alkalosis (sorry pet peeve of mine). pH determines whether the patient has an acidemia (increased H+ concentration) or alkalemia (decreased H+ concentration).

    explanation: co2 in the blood forms with hco3 to form h2co3, or carbonic acid. If we can increase the respiratory rate or volume (alveolar minute ventilation--said this for a reason, not just minute ventilation as it does not compensate for dead space), we can remove this co2 so it does not form carbonic acid and thus increase acidosis. this system kicks in within minutes-hours (carbonic system and protein system actually in seconds)
    CO2 combines with H2O (not bicarb) to form carbonic acid, which then dissociates into bicarb and a hydorgen ion. This is mediated by carbonic anhydrase (yes the reaction takes seconds, rather slow for a chemical reaction), which under normality maintains homeostasis.

    explanation: kidneys can excrete Hydrogen (thus it can not form with co2) and retain K or Na accordingly. Therefore this is 'metabolic' control, kicks in within several hours to few days
    The kidneys excrete fixed acids, not hydrogen ions (technically). If there is an increase in H+ ions, there is a decrease in bicarb due to buffering of the H+ ions, forming carbonic acid. The carbonic acid then dissociates into H2O and CO2 in the lungs, which is then exhaled. Again this homeostasis, and is all mediated by carbonic anhyrdase.

    If it is respiratory acidosis, but the hco3 is above 26, we have partial compensation (the metabolic system is trying to make the blood alkalotic to make the ph 'normal', ie 7.35 to 7.39)
    Actually the metabolic system isn't "trying to make the blood alkalotic" (you mean alkalemic), it is simply decreasing the buffer (bicarb) excretion, and increasing fixed acid secretion (mostly NH4+). This decreases urine pH, and increases blood pH. There will never be an overcompensation causing the blood to be alkalemic.

    f it is respiratory alkalosis, but the hco3 is below 22, we have partial compensation (the metabolic system is trying to make the blook more acidotic to make the ph 'normal')
    Again, the body isn't trying to make the blood acidemic, the body is increasing renal excretion of the buffer (bicarb) and decreasing excretion of acids (NH4+).

    I believe my answer is the best thus far.
    Not bad...

    to determine the underlaying cause of the hypoxia, consider ketones, lactate, anion gap to assist in determining said underlaying cause, in addition to ventilation/perfusion mismatch or shunt and poisonings (carbon monoxide, cyanide, drug od like tricyclics, ethanols/ethylenes, etc)
    There are 5 causes of hypoxemia:
    1: hypoventilation
    2: V/Q mismatch (shunt)
    3: V/Q mismatch (dead space)
    4: Low FiO2
    5: Diffusion impairment
    Usually not that hard to narrow down, but obviously requires diagnostic imaging to dx.

    adequate 2,3 diphosphoglycerate (banked blood is depleted, thus massive transfusions with be deficit and the blood will not want to release the oxygen off the hgb, a shift in the oxy-hgb curve, increasing affinity of hgb and o2)
    Keep in mind your pH also shifts the curve. Acidemia = decreased affinity, alkalemia = increased affinity.
    Banked blood also has decreased NO2, which mediates capillary vasomotor tone. In hypoxia, RBCs release NO2, which dilates the capillaries to increase DO2. Banked blood doesn't do this, which decreases DO2 to these tissues. Banked RBCs are also rigid and act like sludge in the narrow capillaries, further decreasing DO2.

    5. we can reduce the pressure the right heart has to push against thru the pulmonary vasculature (PVR) via monitoring pulmonary congestion, etc--dont let the cvp get too high, assuming competent valves and normal compliance
    CVP doesn't affect RV afterload, but PAP does.
    we can recruit more alveoli via peep--watch for overcomliance of lungs, which may compress heart, reducing cardiac output--consider increasing preload to ability to counteract
    Inspiratory maneuvers recruit FRC, expiratory maneuvers maintain FRC. PEEP is an expiratory maneuver, and therefore doesn't recruit alveoli, but maintains FRC. PEEP will cause decreased myocardial compliance, and you may need to increase your CVP in order to maintain appropriate RV filling.

    we can increase the tidal volume, keeping plateau pressure below 30-35, depending on the client

    we can increase the ventilator rate, to a point, but volume first, usually
    This depends on the underlying pathophysiology. I WOULD NOT increase Vt or PIP in a patient with increased pulmonary compliance, as this will cause volutrauma.

    we can paralyze/sedate and consider reverse IE ratio
    THIS is an inspiratory maneuver, and recruits FRC/alveoli.

    it is a science that must be balanced and understood.
    Too many people driving vents are treating the ABG and vent, instead of treating the patient. Have to base tx changes on physiology not numbers.
    Last edit by PetERNurse on Nov 27, '11 : Reason: typo
    highlandlass1592 likes this.


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