USMLE Step 1 Question Breakdown (Cough. Cough.)
- Sep 04, 2018
Back by popular demand – USMLE Step 1 Question Breakdown. A tricky question and a stepwise approach to get you not only to the right answer, but smarter along the way. Break it down now!
A 67-year old man presents to the Emergency Department with a 2-day history of progressively worsening cough. He has a history of poorly-controlled hypertension, 30 pack-year smoking history, well-controlled diabetes, and a STEMI 4 years prior. He complains of mild sharp chest pain while coughing, some shortness of breath while walking around his apartment, and lightheadedness when standing up. Vital signs on arrival are HR 114, BP 100/55, RR 26, T 101.9 â„‰, SpO2 86% on 4 L nasal cannula. Physical exam is significant for general ill appearance, decreased breath sounds in the right lower chest, tachypnea, tachycardia, and use of accessory muscles of breathing. His is somewhat alert and oriented only to person and place. ABG shows pH 7.29/pCO2 60/pO2 69. EKG shows Q-waves in the inferior leads.
Which of the following is most likely to improve the patientâ€™s clinical status?
- Vancomycin and Piperacillin-Tazobactam
- Aspirin and Hepari
How to approach such a question? Weâ€™ve got a sick older gentlemen who is certainly on the decline. We will start with the way we approach any question – by forming a differential diagnosis.
Older man, smoking history as well as cardiac history, who is coming in with a cough. Letâ€™s start right there – what can cause a cough? It can be something as innocuous as an unnamed viral infection, or a particular virus like coronavirus or adenovirus. In a patient who is a lifetime smoker, we certainly need to be concerned for COPD and subsequent COPD exacerbation.. Given his history of MI, there is a chance that heâ€™s got scarred myocardium, and a bit of heart failure secondary to his dead chunk of heart (remember MI = infarction = dead, scarred, non-pumping, non-conducting heart tissue). Could he have lung cancer? A pleural effusion? Even the lowly GERD can cause cough, though thatâ€™s usually more chronic and indolent.
Most often, in an older patient with comorbidities, especially a sicker one like weâ€™ve got here, cough is driven by a cardiopulmonary process. In the real world, a patient like this would have a pretty in-depth workup, involving cardiac enzymes, chest X-ray, CBC, BMP, ABG, BNP, blood cultures, sputum cultures, etc. But, as is the case with USMLE questions, we donâ€™t have such luxury.
As we read further we notice that the patient has chest pain. Chest pain usually screams â€œcardiac natureâ€ at us, but not all chest pain is driven by the heart. Is this chest pain ischemic in nature?
Probably not, as it is more pleuritic in nature, worse with breathing, as opposed to being substernal pressure driven by activity. At this point, we are making a better case for a pneumonia, but cardiac etiologies certainly arenâ€™t off the table, and cannot afford to be missed. Other considerations with pleuritic chest pain are pleural effusion, pulmonary embolism, pneumothorax, and connective tissue diseases.
We are likely dealing with two main contenders for our pathology. This could be a COPD exacerbation driven by infection, or a heart failure exacerbation. Things arguing for COPD exacerbation include smoking history, decreased breath sounds, hypoxia, tachypnea, and progressive cough. On the acute decompensated heart failure side, weâ€™ve got worsening cough (due to pulmonary edema), decreased breath sounds, tachypnea, tachycardia, history of MI, and history of poorly controlled hypertension (which leads to stiffening of the left ventricle, impaired relaxation, and increase in pulmonary pressures/capillary leakage).
His vitals: Tachypneic, tachycardic, hypoxic, hypotensive, and febrile. All of a sudden, we are making a great case for an infectious etiology. In fact, if we are ready to chalk this presentation up to infection, we are meeting criteria for sepsis (elevated temp, tachycardia, tachypnea). Sick indeed. He is also meeting criteria for end-organ dysfunction, as lack of cerebral perfusion (or lack of oxygen in the blood that is reaching his brain) is starting to contribute to some mental status changes.
While COPD exacerbation (probably driven by a pneumonia in this case) and acute decompensated heart failure can appear very similar clinically, and patients suffering from both often have such similar histories, the finer points can help differentiate between the two. In real life, we have the luxury of lab testing and imaging to help further guide our management, but in this case, we have to get there with less information. A chest X-Ray would certainly help point us in one direction. If the right lower lobe is whited out, weâ€™ve got our pneumonia, plain and simple. If we see diffuse infiltrates, cephalization of pulmonary vessels, and bilateral pleural effusions at the lung bases, pulmonary edema secondary to heart failure is the winner.
Weâ€™ve made our diagnosis, something that is necessary in almost every USMLE question, even if it doesnâ€™t ask â€œWhat is the most likely diagnosis?â€ Whether we need treatment strategies, histologic/pathologic findings, or natural course of disease/prognosis, a diagnosis must be made.
With the diagnosis of Sepsis secondary to COPD exacerbation secondary to pneumonia, what will we do for this gentleman? The clear answer is broad-spectrum antibiotics, at least until some culture data guides our therapy, or the patient improves enough to make the switch to a PO regimen. For posterity, letâ€™s examine the other answer choices.
A. Dobutamine – This would be our therapy for cardiogenic shock. If we believed that his poor respiratory status and systemic hypotension was driven by a left ventricle thatâ€™s simply not pumping (something not uncommon for patients with previous MIs), then inotropic support with this beta agonist would help promote forward flow. Through its ð›ƒ2 agonism, dobutamine lowers SVR to take down the afterload that a failing heart must pump against.
B. Furosemide – A great choice for decompensated heart failure, as it will help the fluid overload through diuresis, and also serves as a venodilator, creating a larger reservoir for the increased intravascular volume to take some stress off of the heart.
C. Doxycycline – For a more gentle COPD exacerbation, doxycycline can be a fine choice of antibiotic. For instance, a patient with a low-grade fever and increased sputum production who visits his primary care doctor feeling slightly under the weather could benefit from an oral antibiotic, and be sent home with instructions to report to the ED if he gets much worse. In a septic patient like this, a PO antibiotic is not an appropriate first-line choice.
E. Pleurocentesis – The most invasive choice here could be employed at some point during his hospitalization if a pleural effusion is the leading culprit of his hypoxia. However, we would never start needling a patientâ€™s thorax in a non-emergent situation without obtaining some imaging first. Also, before performing an invasive procedure, we would begin with medical therapy, and see if the patientâ€™s clinical status (and any pleural effusion that might be driven by his pneumonia) improves first.
F. Aspirin and Heparin – If you were thinking acute coronary syndrome, this would be a great place to start. However, the patientâ€™s chest pain didnâ€™t seem very ischemic, and his EKG showed only Q-waves, which are consistent with previous MI and subsequent scarring.
Take home lessons:
As in any question, or any patient who you are working up, form a differential, and narrow as you incorporate information along the way. For nearly every USMLE question, you must make a diagnosis. Lastly, if asked, think about what you would do to fix the problem!
Questions about this question? Let us know below.