Eduardo R Argaiz Profile picture
Nov 22, 2022 12 tweets 7 min read Read on X
#AKIConsultSeries:👨w T2DM➡️🏥 for fever, dysuria and CVA tenderness. On arrival: ⬇️BP, ⬆️Glucose, ⬆️AGMA. Dx UTI + DKA. Tx: Abx + Insulin Pump + 4 L Crystalloid + NE

After resus, pt still oliguric, Cr 3.2. NE 0.7 ug/kg/min,🧠confused, BP 85/62, HR 123, 2L O2. CRT 4 sec

1/12
Given DKA, giving additional fluids is tempting. But before we do this, its easy to do a quick assessment of fluid tolerance #POCUS

#LUS shows some B-lines (bilat)
#IVC plethoric w no respiratory collapse
#VExUS shows very pulsatile portal vein 🚨🤔

2/12
Pulse pressure is low (23!): This suggest a low cardiac output state!

Also, there are signs of fluid intolerance!

#EchoFirst: Window is suboptimal, but we see a Hyper-dynamic LV w small cavity and a turbulent flow (green color). There was no systolic RV failure

3/12
The combination of sepsis, hyper-dynamic LV, small LV cavity w turbulent flow and LOW Pulse Pressure suggests the possibility of LV obstruction!

How to assess this?

Obstruction leads to increased blood velocity (think of thumb on a hose)...

4/12
CW Doppler allows us to assess flow velocity and look for signs of obstruction

CW Doppler was performed with gate at LVOT and mid-cavity: Flow velocity > 5 m/s! (Velocity > 2.7 m/s is considered significantly elevated)

¿What could be causing this obstruction?

5/12
In a hyper-dynamic state, decreased LV filling can lead to systolic anterior motion of the mitral valve (SAM) and obstruct the outflow tract, there may also be mid-cavitary obliteration.

Sepsis and very high NE doses can create the ideal conditions for this to happen!

6/12
In this case, such a high velocity (>5 m/s) suggests I might be sampling a component of mitral regurgitation, so SAM might be happening here!

Since catecholamines worsen obstruction, a reasonable strategy is to switch to a vasopressor with no inotropism/chronotropism

7/12
In this case we did not give any additional fluid. Stopped NE and started High Dose Vasopressin (0.2 U/min). On reassessment 2 hrs later this worked!

HR down to 111, and most significantly Pulse Pressure now 67!!!

Increased PP strongly suggests improved stroke volume!

8/12
Also intra-ventricular gradient significantly improved and portal vein showed decongestion! (probably from improved cardiac output)!

**Shape suggests mid-ventricular gradient is still present (but definitely better than before)

9/12
48 hours later, as sepsis improved, pt was off pressors.

Both LVOT and Mid-Ventricular gradients disappeared (Velocity = 1 m/s) and Portal Vein was completely normal!

10/12
I found this case really interesting as this patient was likely fluid responsive even though he was NOT fluid tolerant!

More on Fluid Tolerance assessment here:

doi.org/10.1093/ehjacc…

11/12
A similar case that goes into more detail into the physiology of LV obstruction here:

12/12

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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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