Eduardo R Argaiz Profile picture
May 3, 2021 12 tweets 7 min read Read on X
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

2/12
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
Aortic stenosis is one possibility, if you look at #POCUS 👆 aortic valve looks normal.

In the setting of a hyper-dynamic LV, Dynamic Obstruction of the Left Ventricular Outflow Tract (DOLVOT) should be the first thing that comes to mind!

4/12

journals.sagepub.com/doi/10.1177/03…
DOLVOT can occur suddenly whenever there is
🚨Decreased LV filling volume🚨

Predisposing mechanisms:

Asymmetric septal hypertrophy
Sigmoid septum
Motion wall abnormalities (including 🐙)
Systolic anterior motion of the mitral valve (SAM)

5/12

atsjournals.org/doi/10.1513/An…
Decreased LV filling is always secondary to any of this three variables:

⬇️ Preload: Hypovolemia, Obstruction (RV failure w interdependence)

⬆️ Contractility and Heart Rate: Beta agonist, Norepinephrine

⬇️ Afterload: Sepsis

6/12
As such, treatment should focus on:

⬆️ Preload: Fluids.

*sometimes this is enough if the cause is hypovolemia (attached case)

⬆️ Afterload: Alfa agonists with no inotropism

⬇️ Contractility and heart rate: Beta Blockers

7/12

In this case, even though cause was not clear, I started fluid bolus and stopped NE.

Then...the patient had abundant GI bleeding 🩸🩸🩸

We aggressively resuscitated with fluid and blood products. Patient improved immediately 8/12
However, one hour later we were back at square one:

Patient was in shock again!

Did patient need more fluid? I performed #LUS: Clear B-lines. Even thought patient is still fluid responsive. She is no longer fluid tolerant!!!

I was not keen on continuing fluids... 9/12
I ordered AngioCT to rule out active recurrent bleeding.

No bleeding.

However diverticulitis with abscess formation was diagnosed!!

Not previously seen because of lack of IV contrast 🤦‍♂️
10/12
We started antibiotics and vasopressin (⬆️ afterload with no inotropism). *IV beta-blocker was not available at the moment (public hospital shortage).

Fortunately, vasopressin did the trick and patient improved and oliguria resolved! Repeat #POCUS showed DLVOTO resolution 11/12
🔑
💎DLVOTO is easy to diagnose (CW Doppler)
💎Norepinephrine should be avoided at all costs
💎Although these patients improve rapidly with fluid,
THIS IS NOT A PERMANENT SOLUTION
💎Treat with Phenylephrine + IV BB

Bonus: Always use IV contrast even in AKI! @PulmCrit

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More from @ArgaizR

Sep 17, 2023
👩♀️ Past Medical History: SLE, Antiphospholipid syndrome, portal vein trombosis, ESKD on HD, 🫀Group 1 PH + Severe TR

Now with worsening ascites (Para: SAAG > 1.1, total protein 2.5 g/dL). Lowering dry weigh was attempted..

BP 90/60. No edema. On room air, ⬆️ JVP

#POCUS

1/8
Is this cardiac ascites? Should we lower dry weight even further?

2/8
🔷 Although IVC is plethoric, this is not reliable in severe TR

🔷 VExUS can't be performed here (Portal Vein Trombosis, ESRD very small kidneys)

How about HV Doppler and Femoral Vein Doppler? 👇

Is this severe congestion? I do not think so! They also reflect severe TR!

3/8
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Read 8 tweets
Aug 4, 2023
Hemodynamic Evaluation of Right-Sided Congestion With Doppler Ultrasonography in Pulmonary Hypertension @AmJCardio



50 days' free access link: https://t.co/ADD3F7NgEf

🧵of our findings 👇 (1/6) https://t.co/ORDsb9Nu4rdoi.org/10.1016/j.amjc…
authors.elsevier.com/a/1hXCqgQkyqNA

Image
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1⃣ Intra-Renal Doppler (IRVD) alterations are usually classified using morphological patterns (Continuous, Biphasic, Monophasic)

Looking at the relationship between Portal Vein Flow and IRVD you can notice the "Biphasic" pattern shows a very large spread of values! (2/6)
Image
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Switching to a classification based on interruption-time identified pts with a "Biphasic" pattern who were non-congested (short interruptions) or severely congested (long interruptions)

This classification has a much better agreement with Portal Vein Alterations! (3/6)


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Read 6 tweets
Jul 7, 2023
👴 w Cirrhosis ➡️🏥 with spontaneous bacterial peritonitis and septic shock

After fluid resuscitation, vasopressors and antibiotics shock resolved

However now with oliguria and ⬆️ Na (165 meq/L). Cr 1.0 mg/dl, BUN 30 mg/dl

1/10
BP is 155/63 (MAP 94), HR 77, O2 is 94 on O2 8 L/min.

🧠 Encephalopahy on tx w lactulose, edema +++, CRT 1 second, mild ascites.

#POCUS LV/RV OK, LVOT VTI 40 (CO 9.8 L/min), B-Lines, VExUS = 2 (Plethoric IVC + Biphasic Intra-renal Doppler) ➡️ High Output Heart Failure

2/10
1⃣¿Why is the pt Oliguric?

Is this hemodynamic AKI?

🔷Hypovolemic unlikely given congestion and ⬆️ CO

🔷Distributive? Although pt has Cirrhosis, MABP is 94 without vasopressors, also unlikely

🔷Congestive? Possible given VExUS 2

3/10
Read 11 tweets
Feb 27, 2023
HV Doppler from a pt with severe group 1 pulmonary hypertension 👇

Many of us don't have ECG when doing POCUS...

Is it posible to determine this waveform components?

The answer is yes! I'll show you how I did it here

A 🧵on HV Doppler in Pulmonary Hypertension

#VExUS 1/12 Image
Normal HV is a mirror image of normal CVP waveform.

It usually has 4 waves:

2 antegrade (flow from liver to 🫀) waves (S and D)

2 retrograde (flow from 🫀 to liver) waves (A and V)

2/12 ImageImage
A frequent alteration in pts w severe PH is Severe Tricuspid Regurgitation

In severe TR, there is retrograde flow from the RV to the RA in systole. If the right atrium is not compliant, this flow reaches the HV and gives a reverse S wave!

Example from another case 👇

3/12 Image
Read 12 tweets
Jan 29, 2023
Young ♀️ w CKD on HD, seen in Cardiorenal clinic

Pt had torrential tricuspid regurgitation due to CVC induced leaflet perforation ➡️ She underwent tricuspid valve replacement surgery 🫀🔪

However, 1 month after discharge she is still using a wheelchair 🤔

1/12🧵
#POCUS above shows plethroic, non-collapsible IVC and Hepatic Veins

Did surgery work?

Is there residual tricuspid regurgitation?

#Echofist (PLAx RV view + A4ch) color Doppler lets us see there is no or minimal TR

Prosthetic valve seems to be working

2/12
But there is still venous congestion. In fact congestion is significant, take a look at portal vein Doppler 👇

Pulsatility Fraction = 40%, this means there is significant venous congestion. Why?

Is this just volume overload? Should we probe a lower dry weight?

3/12
Read 13 tweets
Dec 28, 2022
Ambulatory Hemodialysis Unit Rounds:

Called to see a patient with hypotension: BP 76/40,🧠 OK, CRT 5 seconds

1st step ➡️🛑Ultrafiltration + 300 ml bolus. BP 90/60

Pt is a middle aged ♂️ w ESRD and T2DM

1/9 🧵
Now 3 kg above Dry Weight.

UF Volume so far: Only 600 ml

🔎📁 Previos HD sessions with no hypotensive episodes

1 week with URI symptoms, 2 days with dyspnea on exertion

On exam: No leg edema, Clear 🫁, JVP hard to assess (hx of multiple CVCs and central vein stenosis)

2/9
#POCUS:

Pericardial Effusion, Normal LV function, looks like there is some RV colapse

Plethoric IVC, Portal Pulsatility 39%.

A-Pattern on LUS, Small bilateral pleural effusions

🚨⬇️BP + Collapsing RV + Venous Congestion (IVC + Portal Pulsatility) suggests Tamponade!

3/9
Read 9 tweets

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