#HFpEF pearl of the day: HFpEF patients can have cardiac and extracardiac causes of volume overload. Abnormal LV GLS, reduced TDI velocities, and/or ⬆️⬆️ECG QRST angle (R axis – T axis) are clues to a more cardiac predominant phenotype. 
RE: ⬆️QRST angle and abnormal cardiac structure/function in HFpEF: check out this paper by one of my stellar mentees @senthil_selv: ncbi.nlm.nih.gov/pmc/articles/P…
Here’s an example case: 62-year-old man with cirrhosis due to EtOH presents to HFpEF clinic confused, SOB, volume overloaded. Meds: bumetanide, spironolactone, lactulose, rifaximin. JVP 16 cm, ascites, 3+ leg edema. LVEF 57%. GLS -12.3%. What would you do next?
Answer: I increased diuretics, started carvedilol, and uptitrated it to 25 mg po bid. Confusion, dyspnea, and fluid overload resolved. LV longitudinal strain improved dramatically. Diagnosis = EtOH cardiomyopathy with LVEF higher than expected due to cirrhosis.
Can't prove the Dx, but there was no evidence of ischemia or CAD and no other obvious cause of cardiomyopathy (he refused cardiac MRI). HF was exacerbating liver failure so treating it improved mental status. I used carvedilol (non-selective BB) to avoid exacerbating portal HTN.
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