U(UtI) ==> sepsis ==>ARDS==>INCREASE alveolar capillary permeability ==> hypoxemia ==> hyperventilation ==>hypocapnia
Did anyone else wonder WHAT "PULMONARY SYMPTOMS" is the question referring to?? There is literally not a single symptom mentioned in the whole vignette. No "crackles heard over both lung fields" are not symptoms. They are signs found by the physician.
Seriously doubting the whole NBME board test writers right now. Do they adequately revise their work? This is not the first technical mistake I realize on the new forms.
I see people are having problem with the “pulmonary symptom” part, but they way I thought about it is: what symptom?
She’s tachypneic because the CO2 is low, which I’m sure she could have noticed before she passed out. Everything else is a sign. So what makes a patient tachypneic? Well, your lungs filling up with crap can do it, which it says in the question since she has diffuse bilateral infiltrates.
So what causes your lungs to have infiltrates? Well, she has a kidney infection that’s turned into septic shock with gram negative bacteremia, so it’s going to be all the inflammatory mediators we produce in response to all of that bacterial LPS in the bloodstream causing pulmonary capillary leakage and ARDS.
How do you know her pulmonary symptoms are due to pulmonary capillary leakage and not hypoventilation? Is pulmonary capillary leakage just another way of saying pulmonary edema?
The pt is having a severe case of pneumonia/sepsis (ARDS?), as that’s why her PO2 is low at 64. So in pneumonia there is increased capillary leakage leading to pulmonary edema.
From AAFP:
"Acute respiratory distress syndrome is a manifestation of acute injury to the lung, commonly resulting from sepsis, trauma, and severe pulmonary infections. Clinically, it is characterized by dyspnea, profound hypoxemia, decreased lung compliance, and diffuse bilateral infiltrates on chest radiography...
In ARDS, the injured lung is believed to go through three phases: exudative, proliferative, and fibrotic, but the course of each phase and the overall disease progression is variable. In the exudative phase, damage to the alveolar epithelium and vascular endothelium produces leakage of water, protein, and inflammatory and red blood cells into the interstitium and alveolar lumen. These changes are induced by a complex interplay of proinflammatory and anti-inflammatory mediators."
https://www.aafp.org/afp/2003/0115/p315.html
they mentioned blood culture. blood culture= sepsis = ards > cxr infiltrates
This is septic shock leading to pulmonary edema aka “symptoms”. The leakage is caused by LPS leading to IL-1, IL-6, TNF-alpha which increases vascular permeability! The question and answers tries to trick you into thinking it’s something else but you know she had gram neg infections and the presentation is just sequelae of septic shock!
submitted by ∗neonem(629)
This patient isn't hypoventilating, they're HYPERventilating, hence the PCO2 < 40 mm Hg.
Let's walk it backwards: They are hyperventilating to compensate for the metabolic acidosis caused by widespread hypoxia. Hyperventilating allows you to blow off more CO2.
Why are they hypoxic? The person is hypoxic due to inflammation and acute respiratory distress syndrome from the pneumonia. All the cytokines from the inflammatory cells cause increased pulmonary capillary leakage, which blocks up the alveolar membrane so that O2 can't get through to the blood.
Why do they have metabolic acidosis in the first place? No oxygen --> no electron transport chain and no TCA --> lactic acidosis.