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

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

So we have:

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

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

You can see many liver Arteriovenous malformations on CT scan!

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

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".

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?

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!!!

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!

⬆️ 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!

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

Sustained ⬇️ SVR can be caused by:

1⃣ Shunts

2⃣ Increased Metabolic Demands

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!

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

Also a similar case of mine:

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!

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!

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!

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!


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More from @ArgaizR

13 Jul

👴 w Advanced Cirrhosis, hemorrhagic portal hypertension and hx of a heart block (w pacemaker).

Came to the ED w diarrhea 2/2 severe C. Diff.

Now in shock...

Initial resus with Norepinephrine 0.3 ug/kg/min, Crystalloid and albumin. Cr 3.8

18 hrs later, no renal improvement + oliguria.

MABP 70, CRT 2 seconds. 🧠 confused, + asterixis. No ascites or edema

Workup: hemodynamic AKI (⬆️SG, ⬇️UNa, ⬆️BUN/Cr, bland sediment)

Team wants to continue fluids, albumin and antibiotics... Dr. Harris, do you concur?

Obviously you are here for the #POCUS so here we go:

IVC: Plethoric (No subX window 2/2 intestinal air)
LV, RV: Relatively preserved systolic fx
Pacemaker lead seen causing important Tricuspid Regurgitation!

Read 7 tweets
3 May
AKI Consult: 👵 ➡️ ED with severe DKA. CT Abdomen and Chest to look for infectious trigger: negative. Tx with IV insulin and balanced crystalloid + 6 L with obvious improvement. Cr was 2.7

Remained oliguric, now in sudden shock with increasing NE dose (0.5 ucg/kg/min) 🚨 1/12
#POCUS Very hyper-dynamic🫀 with increased contractility and no RV dysfunction.

🔎 Look carefully at color of flow exiting the LV:

Aliasing (green color): This means ultrasound system is trying to image an event that is occurring faster than the sample rate

This means flow is fast. But how fast? Choose the CW doppler setting and find out!

In this case acceleration was almost 6 m/s!

Flow acceleration occurs in the setting of obstruction (similar to putting your finger on the hose exit)

So what is causing the obstruction? 3/12
Read 12 tweets
16 Feb
Pt w advanced liver cirrhosis. 🏥 Comes w worsening ascites. No fever🤒, no bleeding🩸. 🧠 ok, no asterixis. BP 91/50. Labs📈: AKI (Cr 3.0 mg/dl), UNa 7 mEq/L, bland sediment. #POCUS 👉small cirrhotic liver with significant ascites. Paracentesis ruled out PBE. 📊Poll below👇 1/11
What would your initial treatment be? 2/11
Don't treat reflexively. A thorough physical exam ♥️🩺revealed a systolic murmur at left lower sternal border. Neck exam 👇

Sitting Down (90º) /// Supine (45º) 3/11
Read 11 tweets
10 Feb
📞 Nurse: Patient has a blood pressure of 226/118 mmHg!
📞 Resident: Nifedipine 30 mg STAT!
📞 Me: About that last call, please hold Nifedipine until we assess the patient

A 🧵of some cases of Inpatient Hypertension 👇 1/15
🔎🖥️..This was a pt w ARDS on IMV. Other vitals 🆗. Previous BP= normal, no recent change in sedation, vent 🆗, no asynchronies. UOP = 0 for 2 hrs 🤔. Exam: Distended bladder!

After foley catheter change, BP normalised 😎

Why do we have this reflex to treat acute high BP? 2/15
A big component is the perceived expectation that we must do something! (In our minds, Are we trying to prevent organ injury?)

A great example can be seen here 👇 3/15

Read 15 tweets
16 Oct 20
Elderly ♂️, PMH of T2DM and CKD.

Suspected COVID-19 because of shortness of breath. Sent to the COVID-19 ED service.

No fever, no cough. No chest pain. Physical exam with patient sitting up (almost 90°):

¿Is this neck pulse arterial or venous? 1/8
Pulse is diffuse and the most striking feature is inward movement. I borrowed this table from @AndreMansoor's must-see lecture on Jugular Venous Pulse **Curiously, notice that there is a single peak instead of the expected double peak 🤔 2/8
I had to get my probe! #POCUS showed severely reduced EF with anterior wall motion abnormality and normal RV function.

EKG showed anterior ST segment changes. This was ACS! Cath lab was activated

Read 8 tweets
6 Oct 20
A case for hepatic vein Doppler lovers:

ECG tracing not abvailable on the ultrasound machine (I tried, I swear)

Can we still interpret this HV waveform without ECG?

I speculate we can!

I'll try to do it step by step: 1/7
What can we tell?

For one, there are 2 retrograde waves and 1 antegrade wave.

Given the patient was in sinus rhythm, then one of the retrograde waves MUST be an A wave! 2/7
Given HV waveform sequence should always be A-S-D, AND A wave is always retrograde:

Then this leaves only 2 possibilities: There could either be S wave reversal or D wave reversal 3/7
Read 8 tweets

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