Preamble. I am a physician in acute internal medicine based in London, UK. Recently I managed a case that brought up a clinical scenario I face time and time again and am unsure regarding the correct approach.
On the shop floor on our level 1 acute medical unit was an 84 year old female previously independent in ADL and IADLS with a past medical history significant for osteoporosis, renovascular CKD stage 1, treated arterial hypertension, degenerative lumbar spondylosis with spinal stenosis. She was admitted 24 hours prior with a short history of new generalized abdominal discomfort, vomiting, subjective fevers and altered mental status. Examination was significant for SIRS (tachycardia 150, T 38.8, RR 24, other parameters within normal limits) a positive Murphy's sign without focal peritonism and hypoactive delirium. The patient was in hypoxaemic respiratory failure with RR 24, FiO2 0.40 with bilateral basilar rales. Laboratory studies revealed lactate 2.2 (without acidemia) CRP 200, WCC 18,000 (neutrophil predominant with left shift and toxic granulation), moderete cholestatic hepatitis with normal bilirubin. ECG was AF with RVR and erect chest radiograph demonstrated bilateral perihilar haze with interstitial opacities. USS of hepatobiliary tree revealed features consistent with cholecystitis. POC echocardiogram was not performed.
Prior to my attendance the patient was managed with empiric antibiotics for intra-abdominal sepsis and commenced on furosemide 40mg IV BID while awaiting surgical consult. When I evaluated BP was 120 systolic and rate 130-150/min with expected lability characteristic of AF. UO per urometer was 40ml/hr. FiO2 was 0.40 with SpO2 93% and RR 28. ABG revealed hypoxaemia without hypercapnia. Serial hsTnT were 35 and 33ng/L respectively. I instituted two treatments and the patient's clinical status and parameters improved significantly.
My question relates to how to best manage acute cardiogenic pulmonary oedema in the context of the sepsis syndrome. I am particularly interested in the approach of any intensivists/cardiologists amongst us. The reason I asked is that my treatment regimen in this case was contested by a colleague and I realised I don't have a significant evidence base for most of my acute interventions aside from personal experience.
Tl:dr How to manage sepsis related AF with RVR and consequent acute cardiogenic pulmonary oedema
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