What is your take on #vasodilators in acute #HeartFailure? The upcoming November issue of #EHJACVC will bring you a PRO/CON "Vasodilator therapy in acute heart failure revisited"
As our PRO paper was published in advanced access, a sneak preview Tweetorial below...
First some background...
Current @escardio guidelines state (IIb, B): "In patients with AHF and a systolic blood pressure (SBP) >110 mmHg, intravenous vasodilators may be considered as an initial therapy to improve symptoms and reduce congestion."
Only 1 flowchart has them in...
So far, I consider this a fair recommendation... In hyper/normotensive pulmonary oedema, they might be helpful in some cases, with their main benefit a reduced need for (non-)invasive ventilation!
Our PRO viewpoint however is more a critique of this flowchart. Personally, I am really annoyed by this updated version in the guidelines, which carries the risk of increasing the already inappropriately high use of #inotropes or even worse #vasopressors...
Great effort by @SVanhentenrijk to write this piece, discussing pathophysiology & reasons for vasodilators in AHF, explaining why we need trials in the RIGHT population (low cardiac output w increased systemic vascular resistance).
First, know your drugs, not all #vasodilators are alike...
Organic nitrates: mainly preload reduction, afterload at higher dose
Hydralazine: pure afterload reduction
Nitroprusside: balanced preload/afterload reduction (my favorite in AHF)
If You remember 1 thing from our paper, let it be: "SBP = awful marker of #afterload or ventriculo-arterial coupling, making it pretty useless in decision to employ #vasodilators"
Why is this? Need pressure-volume loops in here:
In preserved CO/SV (steep Ees~contractility), reducing afterload (Ea) has little impact on stroke volume (SV), which is already high. However, marked impact on BP (preload dependency!)
In low CO/SV (more flat Ees) however, despite lower SBP to start from, impact of reducing afterload (Ea) on BP is minimal, because lower vascular tonus is compensated by a massive increase in SV (afterload dependency!)
Thus, as the Great Guyton has teached us:
Blood pressure is not the same as #Perfusion
So we need to employ vasodilators in patients who are very vasoconstricted with low #CardiacOutput, typically w low SBP, low #PulsePressure & preserved MAP
90/70 mmHg means MAP=77 mmHg!!!
If you have understood this well, who gets vasodilator therapy from you?
Let's give it some time to reflect... Will come up with the answer tomorrow!
We finish this perspective w indications for which vasodilators seem as good as their alternatives (diuretics, inotropes, vasopressors mechanical support) for which the line of evidence is thin as well.
✅Optimise renal perfusion to enhance decongestion
✅Improve perfusion to prevent end-organ damage
✅Enabling early optimization of disease-modifying treatments (switch from IV nitroprusside to oral sac/val!)
✅Reduce surgical risk by reducing lung water & optimized hemodynamics
The CON party, will undoubtedly point towards failing trials with vasodilators in AHF, but look who they recruited, this is no low output #Heartfailure!
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Extremely proud that our journal offers a platform to 3 great clinicians & Twitter educators. I always learn from them...
A strong argument is made to switch mainstream thinking in #AKI away from the fallacious concept of fluid responsiveness in all to a primary assessment of fluid tolerance.
Probably the most important thing I have learned on Twitter: #VExUS
Why do I like #VExUS so much? Because it really changed my everyday practice... Portal vein became part of my standard #echocardiography assessment.
And that's what we want to achieve with this review, offer something directly applicable at your bedside!
For those who can't get enough from #ADVOR, below the promised Tweetorial!
Acetazolamide in acute #HeartFailure w volume overload on background high-dose loop diuretics:
👍Increases diuresis & natriuresis
👍More euvolemia after 3 days & discharge
👍⬇️LOS #ESCCongress#Cardiology
First, the unsung hero's of this trial, done with a little bit over 2 million €, bargain for largest diuretic #RCT ever! @KatrienTartagl2 & her team, with only 3FTE, they ran the most successful trial in #AHF @PieterMartensMD & @JeroenDauw who did most fieldwork
👏
How did we come up with the idea? Actually, cause we all love #physiology. Credits go to Prof. Em. Paul Steels who teached us all how kidneys work. @GLW_UHasselt
65% of sodium is reabsorbed in the proximal tubules, can be up to 85% in #HeartFailure
Do You keep slamming Your face because You missed the 1st #HFA@escardio Clinical Practice Update Course on #HeartFailure, orchestrated masterfully by MC Mullens?
I'll release just a teaser under the form of a clinical case below. You might call on my partners in crime @Ph_Bertrand & @petranijst to do the same...
How is diuretic efficiency changing with severity of #CKD? What is its prognostic relevance?
Read our new paper in CardioRenal Medicine!
@WilsonTangMD@BammensBert
Also thanks to Jeff Testani, Pieter Martens & Dirk Kuypers for their help with the paper...
We used 3 metrics of diuretic efficiency, based on urine output, natriuresis & chloruresis.
Irrespectively of metric, loop diuretic efficiency decreased significantly from KDIGO class IV, while remaining relatively preserved in less advanced CKD.
Patterns were similar for furosemide versus bumetanide (very little patients were on torsemide, which is hardly used in Belgium). Yet, baseline characteristics were strikingly different with bumetanide users older with higher cardiovascular risk.
Key points: 1. Spironolactone = most cost-effective drug in #HFrEF 2. Considering modest diuretic effects with 25-50mg, likely due to pleiotropic effects (Figure) 3. Natriuretic effects increase with dosing up to 600 mg (cirrhosis) 4. Average TOPCAT ~ RALES dose
5. Current study shows marginal (<1%) & short-term (first 8 months) effect on weight loss in TOPCAT Americas.
Spiro patients gradually had lower diuretic need and RAS blockers more frequently withdrawn. 6. Beneficial effects of spironolactone independent of these trends
Why #kidney function does not equal #GFR (and certainly not Cr), making it an elusive target in clinical practice & the latter a poor surrogate outcome, despite its robust correlation with prognosis. Caring for kidneys versus improving Cr/GFR. A thread below:
The kidneys in essence have 3 functions: 1. Glomerular function = Clearance 2. Tubular function = Homeostasis 3. Neurohumoral function
GFR mainly reflects 1. So why do we take GFR (or its estimate Cr) as a surrogate for renal function?
Look at GFR determinants (=N x snGFR).
In stable circumstances, GFR mainly reflects the number of functional nephrons.
Starting from 1 million per kidney at birth, one loses 5,000-10,000 per year with aging: age-related GFR decline <1 mL/min/1.73m²/y