Eduardo R Argaiz Profile picture
Nov 22 12 tweets 7 min read
#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

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with Eduardo R Argaiz

Eduardo R Argaiz Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

More from @ArgaizR

Sep 17
Pt seen in ambulatory clinic with worsening kidney function

While the patient is sitting down (90 degrees), you notice neck pulsations!

Are they arterial or venous??

1/4 🧵
It is single peak (but not sharp)

The most striking feature is the inward movement

The breath of movement is diffuse

These are signs of venous pulsations!

Very helpful table from @AndreMansoor 👇



2/4
Thankfully we have #POCUS in clinic! I believe #POCUS can really help you improve your classic physical exam skills as it gives you immediate feedback!

Quick #VExUS reveals plethoric IVC, reverse S wave on Hepatic Vein, >100% portal vein pulsatility and mono-phasic IRVD!

3/4
Read 4 tweets
Aug 20
Young pt ➡️ 🏥 worsening shortness of breath

PMH: ESRD. Only 1 HD session/week. However, residual urine volume has now decreased substantially

On exam: BP 134/94, 2L O2,🧠✅, elevated JVP, decreased 🫁 sounds at bases, No murmurs, very mild edema. Functional left BC AVF

1/13
Careful examination of neck veins reveals no pulsations, even with pt sitting up 🤔

What could explain the absence of venous pulse? 2/13
Answer is all of the above. JVP examination can be complicated in pts with ESRD.

In the absence of pulsations, I find #POCUS much helpful. Let's enhance our physical examination of congestion:

3/13
Read 13 tweets
Jul 10
#AKIConsultSeries Middle-aged male ➡️🏥 for painful knee and fever. Now in shock 🚨

📂Chart review: PMH EtOH Cirrhosis, right knee arthroplasty.

It is always a good practice review previous PACS images🩻: Nodular liver, colateral vessels and prosthetic right knee

1/11
On exam: BP 72/48, HR 82, O2Sat 95%.
CRT 7 sec, 🧠somnolent, confused. No edema, no obvious ascites.

Warm, swollen and erythematous knee: Tap with obvious purulent fluid🧫

Cr 2.8 mg/dl (baseline 0.5), K 6.7, Urine 🔬: hyaline casts, some urothelial cells

2/11
Loos like hemodynamic AKI (AKA Pre-renal)

Usual causes in Cirrhosis:

🔷Distributive: Septic, "Hepatorenal physiology" 🔷Hypovolemic: Laxatives, vomiting, large volume paracentesis
🔷Congestive: Porto-pulmonary HTN, Co-existing cardiomyopathy

3/11
Read 11 tweets
Dec 23, 2021
Patient with flank pain, hematuria and significant leg edema

#POCUS 🧵

1/10
Lung Ultrasound #LUS 2/10
#IVC long axis 3/10
Read 10 tweets
Dec 8, 2021
A tale of two hearts: Physiological observations on AV shunts and congestion 🧵

These are 2 patients on IHD I saw in the outpatient clinic

🔷 Both with severe venous congestion (#VExUS = 3)
🔷 Both with tortuous brachiocephalic AV fístula

1/11
What I found remarkable was the diametrically opposed effects of manual AVF compression on JVP! 🤯

🔴 Patient A: AVF Compression improves venous congestion
🔵 Patient B: AVF Compression worsens venous congestion

2/11
🔴 Patient A: SLE + Lupus Nefritis ➡️ ESRD in HD

#echofirst: Plethoric IVC, good LVEF, paradoxical septal motion, ventricular interdependence, severe RV/RA dilation, torrential TR

3/11
Read 13 tweets
Nov 28, 2021
Pt with advanced Cirrhosis

AKI, Oliguria + Encephalopathy

Initial treatment = Albumin + Lactulose enemas

🧂Na is now 158 (From Lactulose induced free water loss)

#POCUS ninja @tumleal noticed something was wrong! He got his probe and texted me

📱 #WhatsAppAKIConsult 1/5
#POCUS: Plethoric non collapsible IVC

Based on the clinical scenario, IVC, heart rate and Pulse Pressure...

What is the likely underlying pathophysiology? 2/5
@tumleal went ahead and confirmed his suspicion:

He 📲texted me this:

LVOT VTI = 38!

Some 🔢:

VTI of 38, assuming a LVOT diameter of 20 mm: Stroke Volume = 119 ml

119 ml x HR (93 bpm) = 11.1 L/min of CO!

This is High Output Heart Failure (Very common in Cirrhosis) 3/5
Read 5 tweets

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us on Twitter!

:(