Thread by @ArgaizR

One of my favorite and most intriguing causes of severe venous congestion (#VExUS = 3)

A 🧵on High Output Heart Failure (HOHF) 1/18

First, the index case:

Clip above shows hyperdynamic flow from the vena cava

#echofirst 👇: Very dilated and plethoric IVC, LV OK, Dilated RV, D sign

Overall: Increased Right heart filling pressures

2/18

IVC = 3.4 cm
Portal Vein = > 100% pulsatility
LVOT VTI = 26
TRVmax = 3.04 m/s

So we have:

Venous Congestion (IVC, Portal Vein)
High Cardiac Output (LVOT-VTI)
Pulmonary Hypertension (TRVmax)

3/18

This was a case of High Output Heart failure secondary to Hereditary hemorrhagic telangiectasia

You can see many liver Arteriovenous malformations on CT scan!

4/18

What is HOHF?

CO is usually normal or ⬇️ in patients with HF

A minority of pts present in a high-output state,
historically referred to as HOHF

The largest published cohort (PMID: 27470455) defined HOHF as:

elevated cardiac index (≥4 l/min/m2) + Clinical HF

5/18

There are 5 main causes 👇

Regardless of cause, hemodynamics look pretty similar:

🔷Post-capilary PH (Wedge pressure > 15 mm Hg)
🔷⬆️RH and PA pressures
🔷 Preserved LV Ejection Fraction

*This cohort excluded anemia and hyperthyroidism as "reversible causes".

6/18

What leads to HOHF?

As this is a state of ⬆️ CO + Venous Congestion, increased plasma volume looks like a likely culprit

And yes, there is definitely increased Plasma Volume in HOHF.

But is ⬆️ plasma volume the cause of this condition?

7/18

The answer is a strong: NO

⬆️ Plasma volume (whether caused by experimental saline loading or primary renal salt and water retention) does in fact initially lead to ⬆️CO

However this is NOT sustained!!!

8/18

Why is ⬆️CO not sustained?

⬆️CO will lead to tissue over-perfusion: Tissues do not like this!!

Tissues have the ability to regulate their flow by changing their resistance to flow

Regulation of flow has a higher priority than the regulation of pressure!

9/18

⬆️ Tissue perfusion ➡️ Increased resistance (vasoconstriction) ➡️ Systemic Hypertension

Hypertension is a necessary evil because it leads to "pressure natriuresis". This helps the body get rid of most of the extra plasma volume!

10/18

This means the only way to have a sustained ⬆️ in CO is to have a sustained decrease in total peripheral resistance!

ALL patients with HOHF have ⬇️ systemic vascular resistance (SVR) which happens to be the most important hemodynamic determinant of survival

11/18

Sustained ⬇️ SVR can be caused by:

1⃣ Shunts

2⃣ Increased Metabolic Demands

12/18

1⃣ Shunts:

AV fístula or AV malformation itself is the cause of ⬇️ SVR

In Cirrhosis: Sustained splanchnic vasodilation is the cause. This is likely why AKI in these patients respond so well to Norepinefrine (work from @VelezNephHepato). They don't need more fluid!

13/18

Here is a case of HOHF in Cirrhosis from my friend @Thind888:



Also a similar case of mine:



14/18

Besides splanchnic vasodilation, porto-systemic shunts (bypassing liver sinusoid resistance) can also contribute to HOHF

This is an awesome case of a congenital porto-systemic shunt WITHOUT cirrhosis leading to HOHF.

Shunt closure fixed this!

15/18

2⃣ Increased Metabolic Demands

⬆️ tissue metabolic demands will need ⬆️ blood flow for sustenance.

This will cause ⬇️ SVR and could end up causing HOHF!

This is the cause in Obesity.

This is also the cause of reversible pulmonary hypertension in Graves disease!

16/18

Here is one of my favorite cases of HOHF from @AndreMansoor resulting from increase metabolic demands 2/2 thiamine deficiency. This was diagnosed at the beside by examining the nails!



17/18

In summary:

🔷HOHF is caused by sustained Low SVR
🔷 Low SVR is caused by 1) Shunt or 2) Increased metabolic demands
🔷 These pts have preserved EF. If one ignores CO, one might confuse this as garden variety HFpEF
🔷 Measuring CO is easy with #POCUS. Look at LVOT VTI!

18/18