So, Im going to go out on a limb and be the contrarian on this case. I don't think this was sepsis. I think this was volume depletion from gastroenteritis, but I dont think this gentleman had this syndrome for 3 days and suddenly became septic. He is afebrile, he is mentating, he is not tachycardic and he is not really hypothermic. I think if he was septic with that blood pressure, you would have been dealing with a much sicker patient than you present.
Instead, I would suggest there were possibly two processes going on here. This sounds like run-of-the-mill gastroenteritis to me. But I wonder if this guy had undiagnosed aortic stenosis. First, you say he was of Indian descent. If he had been in the states his whole life, it makes my diagnosis a little less likely. However, outside of first-world countries, rheumatic fever remains prevalent and is the number one cause of aortic valve disease.
Because of the stenotic valve, these patients have fixed cardiac output. They are exquisitely sensitive to volume depletion and when depleted experience hypotension and subsequently syncope. They can increase their peripheral resistance to a point, but without the ability to increase cardiac output, there is a ceiling to their ability to compensate and once that is reached, hypotension ensues.
You mention he had a non-productive cough and you heard noisy breath sounds. I would suggest that what you found was actually the effect of mild pulmonary edema. A heart rate in the high 80's may actually be a relative tachycardia for this man. Because the valve is stenotic, the heart is not able to empty with each systole since the HR has increased (decreased ejection time through a tight valve = incomplete ejection). This causes backup of blood into the pulmonary circulation and leads to the pulmonary edema. And because the heart doesnt have time to empty with each ejection, the cardiac output is actually decreased despite the increase in heart rate. This, combined with the hypotension probably decreased his coronary perfusion pressure and may be the cause of your EKG changes. These patients are exquisitely sensitive to decreases in their coronary perfusion pressures.
Most patients with aortic stenosis have what is called pulsus parvus et tardus. This means that the carotid pulsation is both weaker and slower than it would be in most patients. However, in the face of a blood pressure like this, it may be the only pulse you can palpate because the carotids come off the aortic arch. By the time the slow and weak pulse wave reaches the periphery, it is probably dampened enough to be non-palpable.
If this was the case, you saved this man's life. Fluids are most certainly the answer, despite the possible pulmonary edema. By restoring the patient's volume, you will increase the systemic blood pressure and thus perfuse the coronaries. This will likely slow the heart rate and allow the heart more time to eject blood through that stenotic valve, and likely resolve the pulmonary edema by relieving the backup into the pulmonary circulation.. Vasoconstrictors such as phenylephrine or vasopressin would also be options, though it may seem counterintuitive to raise the afterload on a stenotic valve. But, volume and coronary perfusion pressure are the key factors in treating patients with aortic stenosis. The worst thing you can do to these folks is put them on positive chronotropic drugs. Dopamine may very well have made this patient much worse.
All supposition, but food for thought.
