Question of the Week # 243

243) A 65 year old man with a long history of COPD and history of metastatic colon cancer presents with complaints of increasingly severe shortness of breath that occurred at rest today. He reports that his symptoms are much more severe than his usual baseline. On examination , he is afebrile and tachypneic. Blood pressure is normal. Chest exam reveals occassional rhonchii. EKG shows sinus tachycardia. Arterial blood gases are obtained on the room air and show Ph : 7.45 Po2 40 PCo2 50 and Bicarbonate of 36. Chest X-ray shows changes of emphysema. His home medications include ipratropium and albuterol inhalers. He is placed on 4 liters oxygen by nasal cannula.

Which of the following is the most appropriate next step?

A) Intravenos corticosteroids

B) Intubation

C) Spiral CT scan and empiric Low molecular weight heparin

D) Non invasive positive pressure ventilation

E) Bed-side Spirometry

17 Responses

  1. C is the answer

  2. pt may have PE, so cccccccc

  3. c

  4. Maybe my mind is not working but can PE explain the ABG findings… Ph : 7.45 Po2 40 PCo2 50 and Bicarbonate of 36.. looks like pa tient has metabolic alkalosis.. shouldnt the COPD cause acidosis.. I wanna go with C but something tells me the answer is B..

  5. same here , but intubating a pt with COPD ???

  6. C….
    Pulmonary embolism may cause a quarter of the exacerbations of chronic obstructive pulmonary disease (COPD) serious enough to warrant hospital admission

    Clinicians should consider pulmonary embolism when working up a patient with a severe exacerbation, especially if the etiology of the event is not clear

    Since a pulmonary embolism — like infection — can cause shortness of breath and cough, it’s possible that such clots could be the cause of a substantial number of exacerbations, they said. They noted that COPD patients are at higher risk of venous thromboembolism than the general population

    Blood gases in PE are…… low PaO2 (< 80 mm Hg), low PaCO2 ( 20 mm Hg]). In this pacient the hypoxia is severe (40), so PE has to be part of DDx. Why PCO2 high?…..A person with COPD may have an increased partial pressure of carbon dioxide because not enough carbon dioxide is being exchanged in the lungs. People with COPD may also display low levels of dissolved oxygen and oxygen saturation. But Why high HCO3? Chronic COPD with over ventilation

    With various combinations of the PaO2 of 80 mm Hg or more, the PaCO2 of 35 mm Hg or higher, and the P(A-a)O2 gradient of 20 mm Hg or less, PE could not be excluded in more than 30% of patients with no prior cardiopulmonary disease and PE could not be excluded in more than 14% of patients with prior cardiopulmonary disease. Blood gas levels, therefore, are of insufficient discriminant value to permit exclusion of the diagnosis of PE.

  7. ccc

  8. D:) Patient is hypoxic. Start with NIPPV but if not response with NIPPV, then we will go to intubation.
    this patient has respiratory acidosis with metabolic alkalosis. Cause of metabolic alkalosis???
    sudden onset of SOB in COPD: PE is one of the possibilities. but PE would not cause metabolic alkalosis.

  9. D) NIPPV, if no improvement then intubation … i agree

    This is severe case of severe COPD with metab alk as a compensation for chronic resp acidosis. Members of 50/50 club (both O2 and CO2 close to 50) and PH normal (normal PH is 7.35 – 7.45)

    this not PE because PE will give both hypoxia (perfusion defect) and hypocarbia (from increased RR). In this case PCO2 is higher than normal which is not typical of PE

  10. This is quite a challenging question on so many levels. Even tough for specialists!

    Here are the scenarios:

    1. The problem here is that we have cancer in the history, and it surely can cause PE. Lets look at the pretest probability for PE using Weils criteria:
    Cancer gets +1 point, We arent given RR, and no clinical signs of DVT/Hemoptysis. So Pre test score is only 1, and hence PE is unlikely.

    Another aspect against PE is the ABG findings. PE will give a hyperventilation response, and will have decreased pCO2. However, one could argue that lung function is compromised in COPD and you cannot hyperventilate to drop CO2 to that level….Not quite!
    You see, the pH is still maintained in the normal range. That means the lungs ARE ABLE TO COMPENSATE even now! I know this concept from UW of CK. There was a similar scenario, and they explained that the compensation ability of the lungs is NOT impaired in COPD. It still can compensate, though it does retain CO2. That is because of impaired central chemoreceptors.

    Therefore, 2 things against PE here. Low score and no decrease in pCO2.

    2. If it is COPD exacerbation, what should be the next step.
    Well, UW of CK says that all patients should be tried NPPV before you intubate. So, NIPPV does seem the next appropriate step.

    3. I don’t know why you all are ignoring steroids! Steroids are used to get the patient OUT of the exacerbation. Its the standard! The albuterol/inhalers only treat the symptoms, they don’t take you OUT of it.

    So now, I am confused between NIPPV and Steroids. Either could be the right answer.

    However, let me go one more step further. We have to do something quick and efficient for that low O2. We already gave nasal cannula so that addresses the low O2. But a nasal cannula isnt sufficient enough, and steroids take time to act. By that logic, it should be NIPPV

    Dr Red, your input will be highly appreciated, as this is a very confusing and difficult question. Please respond.

    • Hi Qamar, This question tests a simple concept of A-a gradient and difference between hypoxic and hypercapnic respiratory failure.
      PE causes hypoxic failure but COPD causes hypercapnic failure. Although you see that pCO2 is higher than normal, it does not automatically mean it is hypercapnic . The patient was hypercapnic at baseline from his COPD, now hyperventilated from getting a PE and ended up in post hypercapnic alkalosis. As you can see the bicarb is high and ph is 7.45 and this is post-hypercapnic alkalosis. In COPD exacerbation with acute CO2 retention, you should see respiratory acidosis with pH on lower side not on the higher side. So, this is not acute hypercapnia from COPD. This is hypoxic resp failure from PE. Patient has enough risk factors for PE . Start lovenox and get spiral CT. Hope this is clear. Best wishes

      • Thanks for the reply Dr. Red. Indeed, I see your point now.

        Amazing question, and it really is a tough one! I applied all the physiology I know, but I think sometimes its best just to stick to the simple rules of acid/base disorders, and not to overthink 😀

      • Thank you for the explanation .

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