metabolic acidosis and tachypnea

  1. 0
    A patient was found down after an unknown, but believed prolonged over 3-6 hrs, unconscious. EMSd to hospital, intubated. Severe metabolic acidosis, with initial pH of 7.1, CO2 70s, pO2 60s on 100% FiO2. Obvious aspiration pneumonia. Sedated with propofol, PRVC rate of 24. Despite adequate comfort sedation, patient respirations averaging 30-45 BPM. Low dose bicarb gtt in use.
    It was suggested to increase patient sedation to the point of overcoming respiratory drive. Just wondering if this is common practice. I thought allowing the patient to remain tachypnic would reduce CO2. Also thinking that oxygenation would not be responsive to reduced resp rate as the patient was not 'bucking' or fighting the ventilator breaths.
    Do you generally allow the patient to breath instinctively, or block spontaneous respirations in initial recovery?
    I am new in dealing with Med ICU patients and would appreciate any education and insight!
  2. 12 Comments so far...

  3. 1
    I'm not sure how to answer the question about how commonplace it is to sedate someone to the point of overcoming the respiratory drive and controlling ventilatory effort after that, but I would love to take this time as a learning opportunity, if I may.

    The ABG you described doesn't sound like metabolic acidosis to me. I am probably wrong, and if I am I hope that someone corrects me and explains everything to me. In metabolic conditions, as I understand it, the bicarbonate is primarily affected (elevated or decreased, with a normal carbon dioxide level, unless the patient has started to compensate), while, in respiratory conditions, the carbon dioxide is primarily affected (elevated or decreased, with a normal bicarbonate level, unless the patient has started to compensate). This patient's pH was low, making it acidosis, but the high carbon dioxide makes me think respiratory acidosis. In metabolic acidosis, as I understand it, you would expect to see a low pH and a low bicarbonate with normal carbon dioxide levels. In respiratory acidosis, as I understand it, you would expect to see a low pH and a high carbon dioxide level with normal bicarbonate levels. If I am wrong about this, someone please explain to me so that I can gain a better understanding.

    I don't want to seem rude, or come off as though I am telling you that metabolic acidosis isn't the correct diagnosis for this patient, because that is not how I feel at all. I am just slightly confused, and would love to use this situation as a learning opportunity.
    Last edit by NCRNMDM on Jan 5, '12
    fiveofpeep likes this.
  4. 1
    It sunds like respiratory acidosis to me too due to the carbon dioxide level. However, the bicarbonate level wasn't mentioned so we really don't have a complete picture.
    Biffbradford likes this.
  5. 1
    OP, do you have an HCO3 or serum CO2 level for us? I'm guessing the HCO3/serum CO2 was low because they started the pt on a NaHco3 gtt? Pt. elderly? COPDer?
    fiveofpeep likes this.
  6. 10
    Quote from vic_rn
    a patient was found down after an unknown, but believed prolonged over 3-6 hrs, unconscious. emsd to hospital, intubated. severe metabolic acidosis, with initial ph of 7.1, co2 70s, po2 60s on 100% fio2. obvious aspiration pneumonia. sedated with propofol, prvc rate of 24. despite adequate comfort sedation, patient respirations averaging 30-45 bpm. low dose bicarb gtt in use.
    it was suggested to increase patient sedation to the point of overcoming respiratory drive. just wondering if this is common practice. i thought allowing the patient to remain tachypneic would reduce co2. also thinking that oxygenation would not be responsive to reduced resp rate as the patient was not 'bucking' or fighting the ventilator breaths.
    do you generally allow the patient to breath instinctively, or block spontaneous respirations in initial recovery?
    i am new in dealing with med icu patients and would appreciate any education and insight!
    respiratory acidosis is caused by any condition which increases the pco2 (hypercapnia).2 while increased production of co2 (hyperthermia, cardiopulmonary arrest) is a possible cause of hypercapnia, the vast majority of cases are due to impaired removal of co2 through the lungs. hypoventilation, ventilation-perfusion mismatch and impaired alveolar gas exchange can all lead to hypercapnia. therefore, the broad categories of disease which can lead to respiratory acidosis include: respiratory center depression, neuromuscular disease, restrictive extrapulmonary disease, intrinsic pulmonary and small airway disease, large airway obstruction, and increased co2 production with impaired alveolar ventilation.

    causes of metabolic alkalosis include loss of acidic chloride-rich fluids from the body and chronic administration of alkali. in small animal practice, most cases of metabolic alkalosis are caused by vomiting of stomach contents. abomasal reflux of hydrochloric acid (hcl) into the rumen will cause metabolic alkalosis in ruminants.
    there are two types of metabolic acidosis. both are characterized by a decrease in the[hco3] but they differ in how that decrease occurs. secretional metabolic acidosis is caused by a direct loss of bicarbonate-rich fluid such as diarrhea or saliva. titrational metabolic acidosis is caused by the presence of non-co2 acids that titrate bicarbonate causing a decreased [hco3].
    http://www.vet.uga.edu/vpp/clerk/morse/index.php

    you have a few things occurring here. this very sick patient has both metabolic and respiratory acidosis as well as remaining hypoxic. the rest of the vent settings are just as important as to whether sedating the patient's inate respiratory drive is prudent. what is the tidal volume, is there pressure support and peep? what is the patients bicarb and ion gap....what is the base excess.

    it's obvious that the patient is trying to assist the metabolic acidosis and blow off co2 by increasing the respiratory rate. if however the patient continues to work so hard to breathe there will be a further build up of lactic acid. this patient needs moderately aggressive resuscitation with bicarb as well as ventilation to decrease the co2 thereby increasing the ph and correcting (hopefully) the hypoxia which further contributes to the acidosis.

    what is the patients lactic acid? how long after intubation were these gasses? the supression of the respiratpry drive, because it's assisting with acid base correction, needs to be done cautiously but if the patient's increase drive it contributing to the build up of lactic acid then the ventilation needs to be meticuously controlled with the patient's drive shut down to allow the interventions have their theraputic effect.

    abg tic tac toe part 1.doc‎ (52.5 kb, 4412 views)
    abg tic tac toe part 2.doc‎ (94.0 kb, 2476 views)
    http://allnurses.com/nursing-student...gy-387179.html

    this patient needs to be adequately ventilated first, to drop the pco2 level and increase the po2 and by correcting these at the same time correcting the metabolic acidosis with bicarb

    being new to critical care you may find this helpful........http://www.ccmtutorials.com/index.htm

    the bird's eye-view, two components:

    • respiratory: when breathing is inadequate carbon dioxide (respiratory acid) accumulates. the extra co2 molecules combine with water to form carbonic acid which contributes to an acid ph. the treatment, if all else fails, is to lower the pco2 by breathing for the patient using a ventilator.

      metabolic when normal metabolism is impaired - acid forms, e.g., poor blood supply stops oxidative metabolism and lactic acid forms. this acid is not respiratory so, by definition, it is "metabolic acid." if severe, the patient may be in shock and require treatment, possibly by neutralizing this excess acid with bicarbonate, possibly by allowing time for excretion/metabolism.

      that's it! the whole of acid-base balance in six sentences. as you explore this site, keep this bird's eye-view in mind. we will also have to deal with low levels of metabolic and respiratory acid (alkalosis) - but this initial overview helps to keep the subject in focus.
      http://www.acid-base.com/

      http://www.vectors.cx/med/apps/abg.cgi


      i am sure this made it clear as mud.....i hope it helped some.
  7. 0
    The patient had a definite respiratory acidosis, but without more information it's difficult to say if a given strategy makes sense or not.
  8. 3
    As said before the ABG's are incomplete to make a definitive statement. Furthermore the ventilatory settings are incomplete as well. For this patient I would factor in following settings/measurements as well: PEEP, tidal volume setting, peak pressures, I:E ratio and if the patient manages to exhale completely before the inhalation starts. All these would balance in with my decision to sedate the patient more or allow his ventilatory drive to keep kicking in.

    With a pH of 7.1 and a paCO2 of 70 mmHg (assuming his baseline is normal or only slightly elevated) its obvious his current settings are not clearing enough CO2. You somehow need to increase his ventilation. One way of doing this is fully sedating the patient and up the pressures on the vent and change other settings to less agreeable conditions for the patients (e.g. increasing inspiratory time/decreasing expiratory time - providing he still has time to exhale, increasing PEEP all in an effort to recruit parts of the lung) but these setting tend to cause dissynchrony between vent and patient and result in a combative patient if not sedated enough.

    Even with permissive hypercapnia you can't manage this patient at this pH level. His pH needs to come up one way or another or he will get overwhelmed with infection in a few days to name one of the complications of prolonged acidosis.

    I know the trend in ARDS is allowing patients to have their own respiratory efforts as well. But we all have seen the patients that everytime they breath in between the vent breaths their respiratory mechanics just come crashing down and you spend about an hour getting them back up. Only to see them do it again.
  9. 3
    Addendum: In a spontaneously breathing patient you would accept tachypnea as it is the compensatory mechanism for metabolic acidosis. You accept this as long as the patient isn't getting exhausted and he effectively compensates for his acidosis. There comes the breaking point however where his respiratory efforts will become less effective and paCO2 levels start to rise (then you get a combined respiratory and metabolic acidosis). A patient generally needs to be intubated at that point (or pref before getting to that point) to prevent a catastrophy.
    esie, MomRN0913, and fiveofpeep like this.
  10. 1
    "I don't want to seem rude, or come off as though I am telling you that metabolic acidosis isn't the correct diagnosis for this patient, because that is not how I feel at all. I am just slightly confused, and would love to use this situation as a learning opportunity. "

    Not at all, this is exactly what I'm here for. I appreciate all the answers and it has given me a lot to think about.

    Thank you, too, for the links.

    I am glad to receive so much input. I am learning a lot and hope to one day be the person who is able to help educate others!
    fiveofpeep likes this.
  11. 1
    It's not as simple as saying the pH is X and the PCO2 is Y, therefore the disorder is N. It's not like a hemoglobin, where if it is low the disorder is anemia. You need a complete ABG to evaluate acid-base (pH, PCO2, HCO3, AnGap, PO2, lytes, and preferably an albumin level), looking at each value independently and the panel as a whole.
    The ICU Rounds podcast has an excellent lecture on ABG interpretation.
    Last edit by PetERNurse on Jan 5, '12 : Reason: typo
    fiveofpeep likes this.


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