I believe the problem with HFpEF is lack of a standardized definition.
Typical case: a 70yo with HTN, DM, BMI of 40, bilateral knee arthritis, has been basically sitting in a chair for 5 yrs presents with SOB, 3+ dependent edema, underpenetrated CXR read as pulmonary congestion, BNP of 200, gets labeled HFpEF.
The problem is obesity and deconditioning. The morbidity and mortality are high, but heart failure meds are not going to make that better.
Thank you for he HFpEF discussion. The concept of “Diastolic Dysfunction” as a cause for clinical CHF was introduced to me in the late 80’s. I appreciate the fact that, after 40 years there are those still struggling with the same contradictions I saw.
As an Intensivist who was interested in getting my poor patient off the ventilator, oxygenation, not I/O was my goal. Yet some could not be weaned until there was significant diuresis which often resulted in a the spine chilling sudden and rapid increases in BUN out of proportion to Creatinine.
The difference I also saw in between these patients (pEF v dEF) overall was a relative lack or decrease in peripheral edema in the preserved ones.
How many times was I referred someone diagnosed as “Viral Pneumonia” who had no inflammatory markers, no orthopnea or edema and form who I diuresed 10Liters with clearing of the CXR?
Has anyone given thought to the idea that the “preserved” patient population is a heterogeneous population? I’m retired now and couldn’t even think about how that would look?
I also like the idea of rate contributing to increased pressure. It’s always been hammered into us “allow time for filling”. I never thought in terms of “too much filling”. I also recall, WAY back then, putting PA Catheters in these (poor) people with full knowledge of the EF (that’s how old I am) and seeing these sky-high pressures that never changed despite azotemia-inducing diuresis. More than one ended up on RRT and STILL requiring mechanical ventilation.
What disease was THAT??
All in all, one thing was I recall seeing back then was that the “Diastolic” were all Hypertensive, and many with elevated BMI, and metabolic disease (that’s not what it was commonly know as back then).
Thanks for exercising what remains of this old Intensivist’s wits!!!!
"Special diet" may be a ridiculous concept, but it is only logical that a diet high in sugar and processed food and low plant consumption, etc., would lead to poorer outcomes - with "outcome" linked to genetic predispositions. Lifestyle is also a bit too encompassing to limit the focus to dietary choices - over a lifetime. Exposures to environmental toxins, physical activity levels, intellectual exercise, social interactions, diet....and the gut microbiome...play a role in long term health, but since all facets are difficult to quantify and randomize, we come down to.....essentially great-grandma's logic. I am continually frustrated and heart-broken watching loved ones (especially my elderly dad, a retired MD) who eat a pretty normal "Standard American Diet" filled with additives, inflammatory oils and foods that spike blood glucose levels, end up with chronic health issues that are treated with pharmaceuticals with their side effects, interactions and limited efficacy.
I will continue to beg for an autotranscription of all of these podcasts. Many, many of us are missing really valuable content because we cannot read it. Autotranscribers are free/cheap and plenty good enough to vastly broaden your audience for this excellent content. Many other sites have started doing this to great effect. Beg. Beg. Beg.
I believe the problem with HFpEF is lack of a standardized definition.
Typical case: a 70yo with HTN, DM, BMI of 40, bilateral knee arthritis, has been basically sitting in a chair for 5 yrs presents with SOB, 3+ dependent edema, underpenetrated CXR read as pulmonary congestion, BNP of 200, gets labeled HFpEF.
The problem is obesity and deconditioning. The morbidity and mortality are high, but heart failure meds are not going to make that better.
Thank you for he HFpEF discussion. The concept of “Diastolic Dysfunction” as a cause for clinical CHF was introduced to me in the late 80’s. I appreciate the fact that, after 40 years there are those still struggling with the same contradictions I saw.
As an Intensivist who was interested in getting my poor patient off the ventilator, oxygenation, not I/O was my goal. Yet some could not be weaned until there was significant diuresis which often resulted in a the spine chilling sudden and rapid increases in BUN out of proportion to Creatinine.
The difference I also saw in between these patients (pEF v dEF) overall was a relative lack or decrease in peripheral edema in the preserved ones.
How many times was I referred someone diagnosed as “Viral Pneumonia” who had no inflammatory markers, no orthopnea or edema and form who I diuresed 10Liters with clearing of the CXR?
Has anyone given thought to the idea that the “preserved” patient population is a heterogeneous population? I’m retired now and couldn’t even think about how that would look?
I also like the idea of rate contributing to increased pressure. It’s always been hammered into us “allow time for filling”. I never thought in terms of “too much filling”. I also recall, WAY back then, putting PA Catheters in these (poor) people with full knowledge of the EF (that’s how old I am) and seeing these sky-high pressures that never changed despite azotemia-inducing diuresis. More than one ended up on RRT and STILL requiring mechanical ventilation.
What disease was THAT??
All in all, one thing was I recall seeing back then was that the “Diastolic” were all Hypertensive, and many with elevated BMI, and metabolic disease (that’s not what it was commonly know as back then).
Thanks for exercising what remains of this old Intensivist’s wits!!!!
Ann Hansen
24 min ago
"Special diet" may be a ridiculous concept, but it is only logical that a diet high in sugar and processed food and low plant consumption, etc., would lead to poorer outcomes - with "outcome" linked to genetic predispositions. Lifestyle is also a bit too encompassing to limit the focus to dietary choices - over a lifetime. Exposures to environmental toxins, physical activity levels, intellectual exercise, social interactions, diet....and the gut microbiome...play a role in long term health, but since all facets are difficult to quantify and randomize, we come down to.....essentially great-grandma's logic. I am continually frustrated and heart-broken watching loved ones (especially my elderly dad, a retired MD) who eat a pretty normal "Standard American Diet" filled with additives, inflammatory oils and foods that spike blood glucose levels, end up with chronic health issues that are treated with pharmaceuticals with their side effects, interactions and limited efficacy.
I will continue to beg for an autotranscription of all of these podcasts. Many, many of us are missing really valuable content because we cannot read it. Autotranscribers are free/cheap and plenty good enough to vastly broaden your audience for this excellent content. Many other sites have started doing this to great effect. Beg. Beg. Beg.