Current guidelines regarding diuretic use in HF patients
Different mechanism of action of different diuretic agents
Using diuretics in real clinical practice
When to switch to mechanical fluid removal
Define future needs for new diuretic agents
Key points are actually interesting
1) measuring UNa+ @ 2 hours if no UOP >100 cc/hr. UNa+ has to be > 50 mEq/ L to make sure you actually achieve "natriuresis" ( poor fellow running around all night checking Una + levels !)
2) A rise in creatinine is to be expected in many cases and should not lead to backing off from diuresis. I think we see as soon as creatinine goes up MDs back off on diuresis , which is the exact wrong thing to if congestive symptoms are still present
3) Inotropes are discouraged , unless the patient has "true" low output symptoms...and dopamine is not on this list, milrinone is preferred. Any inotrope in the acute setting is associated with increased mortality and purely provides symptomatic relief.
You are probably getting extremely tired seeing one cardiologyarticle after an other . However ,this JACC State-of-the-Art Review on Arrhythmia -Induced Cardiomyopathy, I thought was very important as it is a diagnosis seen not just in the CCU but also the MICU. The concept of a cardiomyopathy causing ventricular arrhythmia is nothing new. The reverse pathophysiology is actually very interesting. If you see a patient with atrial fibrillation with chronically uncontrolled rate mostly due to noncompliance or a patient with very frequent ventricular extrasystole, you have to think HFrEF. Below you will find the Central Figure, Abstract and links to the MP3 summary and actual article.
• Tachycardias, AF, and PVCs are known to trigger a reversible dilated CM.
• AiCM should be highly suspected in patients without an obvious etiology.
• Ambulatory ECG monitors are key to screen and properly diagnose AiCM.
• Reversal of CM by elimination of arrhythmia not only confirms the diagnosis but may significantly improve outcomes.
Most people we see with acute decompensated heart failure with congestion are secondary to HFpEF ( 50% vs HFrEF)
Unfortunately, 90% of the echoes are read wrong in either direction .
I posted this clip to show some of the measurements that go into it . Even when the parameters are obtained a correct diagnosis is still a challenge .
A pearl here is that patients with a normal size LA by CT scan or ECHO rarely have acute decompensated CHF unless acute MR from flail leaflet for example ( myxomatous valve) , or ischemic MR as two examples . There are others off course .
If their LA is very large they probably do have elevated LA pressure and the diagnosis of ADHF with congestion.
For example grade III DD is impossible with a nomal size LA . I rarely believe DD with elevated LAP unless I can look at CT and ECHO myself or the clinical scenario is compatible with this diagnosis.
You see from the slide show no busy cardiologist will look at this and the the tech has to set wall and gain filters just perfect .
Give the current environment of increased regulation on outpatient non - cancerous drug pain management and OUD, I am listing some very helpful; sites and books and a recent NEJM article on Opioid in Critical Illness.
If you want to become a true opioid expert , learn to dose methadone in the inpatient setting safely and also adjust opioid for cross tolerance when rotating drugs to avoid opioid hyperalgesia this is the book that has it all:
Demystifying Opioid Conversion Calculations- A Guide for Effective dosing by Mary Lynn McPherson . I still have the first edition from 2009 , but the 2nd edition published in 2018 is vastly improved , with multiple patient examples and clinical pearls.
A good website with also an Apple/Android app is https://www.crediblemeds.org/ as it ranks drugs form low to high risk when patient are on methadone and I think we see a lot of them admitted on methadone to the ICU.
Finally, the NEJM article on Opiods in Critical Illness is very helpful, particularly the online appendix with patient examples . I can definitely relate to this and the first example was the multi modal therapy they used on me including nerve blocks ( it would have been better if the darn epidurals would have stayed stay in place !!) , and certainly was very grateful for this after my MVA.
Dr Fisher saw one of these on her nightshift. Its a well known complication of BAV and TAVR. When a patient develops hours later cardiogenic shock post procedure , this is one of the complications to think off.
The link to this case report actually gives a good explanation how the outflow tract obstruction occurs. I have wondered if a preprocedure Brockenbrough sign could predict this complication during initial diagnostic catheterization.
Thanks to Dr Beth Fisher for bringing this case to my attention.
