I'm fully down the rabbit hole tonight - thinking about ventricular-arterial interactions in HF (HFrEF vs HFpEF). A quick thread (based off this 2012 JACC paper from Barry Borlaug and colleagues @MayoClinicCV)...

sciencedirect.com/science/articl…
- Changes in BP & SV with Δ in ventricular loading are predictable based on ventricular-arterial coupling.
- BP ⬇️ while the SV ⬆️ with vasodilation; the extent of Δ is dictated by slope and intercept of the end-systolic pressure volume relationship: end-systolic elastance (Ees)

Part II of the Basics of PV loops: preload, coupling, afterload, ventricular dysfunction, and valvular disorders.

Big thanks to the team who helped put this together: @jayamj94 & @PSullivan000, with guest editor @RyanTedfordMD.
If you missed Part I, check it out ⬇️

https://twitter.com/AHajduczok/status/1583429179915132935

- Preload is the stretching of cardiac myocytes prior to contraction (related to sarcomere length); it's measurable surrogate: ventricular end-diastolic pressure/volume.
- Δ in preload affect SV (width of PV loop), by the Frank-Starling mechanism. As preload ⬆️, SV (EDV-ESV) ⬆️.

Patient admitted for a COPD exacerbation. You see the patient in the ED an hour after admission and look at tele and see this…what do you do next? You examine the patient and realize they have cold extremities. Are you concerned about the patient?

Do you ❤️ hemodynamics? How about PV loops?

Here is Part I of our journey to to help YOU better understand PV loops and make them a little less daunting. Couldn't have done this without ⭐ @TJUHospital resident @jayamj94, and edits from @PSullivan000. Stay tuned for Part 2! Part 1: The Basics

What is a pressure-volume (PV) loop?

A PV loop is a visual representation of the LV pressure (on the y-axis) and LV volume (on the x-axis) throughout a single cardiac cycle. (Great resource: cvphysiology.com/Cardiac%20Func…)

Q: Why do we use a stethoscope?
A: For many reasons, and here’s one of them that I will argue is undervalued. And is still at the heart (hint hint) of some ongoing research… First described by Potain in 1880, the gallop rhythm refers to the presence and cadence of abnormal diastolic cardiac sounds, namely S3 and S4.

Things escalated again on nights last night:

Check out this 1984 paper (Am J Cardiol) on predictors of 1-yr mortality in dilated CMO

Only one prognostic factor based on physical exam - S3

36 years later; we have an ongoing study measuring electronic S3.
clinicaltrials.gov/ct2/show/NCT04… I actually stumbled across this while reading about something else (tweetorial pending, cc @DoctorVig), but I digress.

First, although this was a small study (69 patients), it elegantly used univariate/multivariate analysis to predict mortality. (I'm a big fan of regression)

1/ A few weeks ago while on service, I couldn't for the life of me remember the RCT evidence behind the use of beta-blockers in acute MI

According to the 2013 ACC/AHA STEMI guidelines it is a Class I recommendation (Level of Evidence: A) to start BB acutely, or within a few days 2/ Also, those with moderate or severe LV failure should receive beta-blocker therapy (Class I, Level of Evidence: B)

Furthermore the 2014 NSTEMI guidelines recommend starting BB within 24 hrs...