Eduardo R Argaiz Profile picture
Internist | Nephrology Fellow @incmnszmx | #DiuresisJedi #POCUS #VExUS
Dr. Jhonny Enrique G Profile picture Julio C. Sauza-Sosa Profile picture paco sarmiento Profile picture 4 added to My Authors
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

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
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

3/8
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
5 Oct 20
Back on COVID-19 service this month

Went to see this patient with "increased respiratory drive despite high dose sedation and NMB". This is the vent: 1/4
Looking at the patient's monitor, the respiratory curve seems oddly coincident with heart rate: 2/4
Inspiratory pause reveals NO respiratory drive and several cardiogenic oscillations! 3/4
Read 4 tweets
14 May 20
🧵 AKI and #COVID19

68 yo ♂️ PMH obesity, HTN, CAD w stent, OSA, T2DM
➡️ ED w SOB + fever 39.9°C. Poor oral intake

RR 40, Sat 94% Room Air, BP 157/74 HR 124. Alert. Bibasilar crackles

Labs: Cr 1.3 (baseline 0.8), WBC 10, K 5.4, HCO3 17, CK 184. UA and CXR👇 (case from @NEJM)
How would you manage this AKI initially? What is the likely cause of AKI in patients with #COVID19? (this last question discussed in thread 🧵)
No easy answer except to say that FENa is very unlikely to be useful. It is not unreasonable to try fluids for AKI in the setting of perceived hypovolemia. However, this gets complicated when the potential for worsening ARDS exists. I'll try to tackle the answers one by one 💪
Read 17 tweets
11 May 20
Which of these patients has a more severe degree of venous congestion? #VExUS Thread 🧵 about the Portal Vein (1/17)
Video above shows IVC in short axis, long axis and diameter (from left to right)

Which of these patients has a more severe degree of venous congestion? (2/17)
Abdominal IVC size depends on the difference between CVP and IAP. At a constant IAP, IVC size will increase proportionally to CVP until it reaches the flat part of it's compliance curve. (Great thread by @Thind888 here: ) (3/17)
Read 18 tweets
28 Apr 20
Dr. Gattinoni or: How I Learned to Stop Worrying about P-SILI and Love Furosemide

WEIRD THREAD 🧵 About the blood-gas barrier and #COVID19 (1/9)
Clinical Case: A 4 year old Thoroughbred Horse with a history of recurrent racing-associated epistaxis comes to your office complaining of decreased track performance. He wants to know if there is anyway to prevent this from happening (2/9)
What treatment would you recommend? (3/9)
Read 10 tweets
22 Apr 20
“If you think an awake patient having normal mental status and a basic metabolic panel is available needs a blood gas, you’re wrong. You need the blood gas done on yourself because you may be brain dead.” quote from Dr. Corey Slovis (1/7)
A few days ago I ran this poll. Most of you chose not to get an ABG. This is in fact what I did (and disappointed the consulting team) Pt had no comorbidities, and HCO3 was normal. (2/7)
Pt not on opioids and no COPD should have a preserved respiratory drive, thus hypercapnia should NOT occur unless exhaustion. Instead, I monitored my pt closely and that same evening O2sat much better. A few days later pt was discharged home. Not a single ABG was drawn. (3/7)
Read 7 tweets
18 Apr 20
"Dry (#COVID19) lungs are happy lungs." This is the last line of this thoughtful piece on @MGHMedicine's FLARE: us19.campaign-archive.com/?u=ef98149bee3… Well balanced concerns with fluid loading vs aggressive diuresis. I'd like to add some thoughts.... (1/13)
Goal is euvolemia (Duh?). Easy to say but, WTH is euvolemia anyway?. Let's be honest, fluid therapy has always been about keeping the kidneys happy. Two examples of this #nephrocentric approach to fluids (one from FLARE, one from @jlvincen) (2/13)
Non of this is wrong. Definitely hypovolemic patients (vomiting, diarrhea, and poor oral intake) will benefit from fluids. However, the emphasis of fluid therapy tailored to creatinine ignores that most Sepsis-induced AKI is NOT VOLUME RELATED! (3/13)
Read 14 tweets
16 Apr 20
#COVID19 Early vs delayed intubation. IMV has many known adverse effects and complications. Why would anyone want to intubate early? Two proposed reasons: 1) Prolonged hypoxemia might be harmful 2) Severely increased work of breathing might actually increase lung damage. (1)
1⃣Should we tolerate hypoxemia? Physiology 1st: If nothing else changes, even a 40% sat would still mean a DO2 of about 2x VO2 (normally 5x greater). Increased CO can improve this a lot. A young, previously healthy and hemodynamically stable pt should tolerate 80% just fine (2)
In the words of Dr Martin J. Tobin: Evidence of end-organ damage is difficult to demonstrate in patients with PaO2 above 40 mmHg (equivalent to oxygen saturation of approximately 75%). doi.org/10.1164/rccm.2… (3)
Read 18 tweets
15 Apr 20
Common Physiological Misconceptions: (thread)
🌊
🔹Fluid responsiveness predicts clinical benefit from fluid administration
🔹High lactate = under-resuscitated
🔹Venous Congestion effects on organs (e.g Renosarca) are different according to cause (CHF vs Pulm HTN)
🎈
🔹Significant hypoxemia from alveolar disease should cause dyspnea
🔹PEEP tirtration benefit comes from improvement in hypoxemia
🔹There is an absolute plateau pressure number that causes VILI regardless of driving pressure
🧂
🔹Harm with rapid sodium correction is symmetrical (from either hypo or hypernatremia)
🔹Insulin therapy goal in DKA is to lower glucose
🔹Ringers Lactate exacerbates hyperkalemia
🔹Metabolic alkalosis = overdiuresis
Read 4 tweets
11 Apr 20
Genius is providing simple solutions. Vasopressor challenge in sepsis: Does the patient remain hypotensive after early vasopressor/ initial resus (CENSER Trial)? Is a 65 MAP enough? (1/5)
(ANDROMEDA) 1) look at CRT, if abnormal ➡️ 2) look at Diastolic BP. Two phenotypes “D” and “P”: D) Diastolic Predominant hypotension/ Normal pulse pressure; P) Low pulse pressure/ Normal DBP. (2/5)
Treatment (early vasopressor always): D) Increase vasopressor (this is vasoplegia); P) Confirm low stroke volume (LVOT VTI/ PICCO) and perform #EchoFirst, if abnormal LV/RV fix it; if normal LV/RV THEN, and ONLY then do a fluid challenge (3/5)
Read 6 tweets
10 Apr 20
Case of mine: Young patient, O2sat <50% room air; 80% on 15 L NRM. Completely normal mental status, no shortness of breath, no increased WOB, no tachypnea. Pt feeling ok and looked happy. (1/4)
I was perplexed by the lack of symptoms. Very low PaO2 confirmed by ABG. I even ruled out R-L shunt by #POCUS (agitated saline). Diffuse B-Lines seen. CT Scan showed diffuse ground glass opacities. Hypoxemia persisted, patient treated with NIV on CPAP and improved! (2/4)
Final diagnosis was influenza. This was 2 yeas ago. This is when I learned about happy hypoxemia. Remembering this now makes me wonder why are we so surprised this is happening now with COVID? I certainly was perplexed then (enough to look for intracardiac shunt 🤣). (3/4)
Read 8 tweets
1 Mar 20
AKI consult: 60 y f w Diabetic Nephropathy G2A3 and ischemic cardiomyopathy LVEF 30%, no PH. Hospitalised 5 days ago for ADHF and mild foot cellulitis. Tx: IV Lasix + Zosyn. Admission Cr 0.8 mg/dl, now 3.4 mg/dl. Cumulative fluid balance -4 L. Last 24 hrs UOP: 400 ml. (1/11) Image
HR 82, BP 130/85, T 37.1 No leg edema. Normal CRT (1 sec), lactate 1.1. Neck Veins at 30 degrees shown (with consent). UA: Specific Gravity 1.027, Protein ++ (unchanged from baseline), WBC 21-30, RBC 21-30. Sediment no casts seen. (2/11)
With this data only, What is the most likely etiology for this Cr rise? (3/11)
Read 17 tweets
13 Feb 20
A brief reflection into the mechanism of Hyperdiuresis (3% saline + Lasix) in patients with with acute decompensated heart failure sparked by this excellent review by @PulmCrit emcrit.org/pulmcrit/pulmc… and emcrit.org/pulmcrit/hyper… #DiuresisJedi (1/13)
Here are the possible mechanisms that explain the effect:

1⃣Reversal of Hypochloremia
2⃣Pull fluid into the intravascular space
3⃣Reducing neurohormonal sodium retention (e.g. renin/angiotensin/aldosterone and sympathetic nervous system stimulation)

(2/13)
1⃣ Certainly hypochloremia causes diuretic resistance, and Cl supplementation (lysine chloride) augments diuretic efficacy (read @PulmCrit blog). What is the mechanism behind hypochloremia induced diuretic resistance? (3/13)
Read 13 tweets
11 Jan 20
Pt w Child B cirrhosis and portal HTN (varices). Comes w UTI and Cr of 5.8 mg/dl (baseline 1.1 mg/dl). BP 70/50. Lactate 5. Initially tx w crystalloid UOP 0.3 ml/kg/hr for 14 hrs. Norepinephrine and albumin were started with improved UOP 0.7 ml/kg/hr. CT scan on admission: Image
On day 3, Cr improved to 2.6 mg/dl (pt received single dose Lasix 60 mg on day 2 because of positive fluid balance of 1.6 L). On day 4 i met this patient. Lactate 1, BP 90/60. Looking at admission CT scan I was intrigued by the intra-hepatic IVC size. Gotta #POCUS ➡️ #IVC 2.2 cm
Full #VExUS #VenousExcessUScore Normal Hepatic, Portal and Splenic Vein. However IRVD = Biphasic ImageImageImageImage
Read 13 tweets
2 Dec 19
Brief Tweetorial on Hepatic Vein Doppler in patients with Tricuspid Regurgitation. Two days ago I asked this question, most answered "B" which is what you would usually expect on severe TR (1/13)
Normal HV doppler has 3 (or 4) waves. 1) S wave: during systole, corresponds to x descent of RAP; 2) V wave: late systole (not always seen) 3) D wave: during diastole, (y descent of RAP) 4) A wave: during atrial contraction. S and D are antegrade. A and V are retrograde (2/13)
Large TR causes a large V wave on RAP and thus the Hepatic Vein shows reversal of the systolic wave. **Antegrade flow (from liver to heart) is shown below the baseline while retrograde flow (heart to liver) is show above the baseline. Example from some of my patients: (3/13)
Read 14 tweets
28 Jul 19
#POCUS #VenousEXcessUScore guided diuresis in ❤️renal sx. Pt w T2DM and CKDG4A3 with HFpEF. After multi-agent diuresis (targeted to normalize venous flow patterns) pt lost 14 kg and returned to basal kidney function. ¿Should we pursue "decongestion" goals in these pts? (1/13)
It's interesting that the recent statement from @American_Heart spends a great deal discussing Bioelectrical impedance Vector Analysis (BIVA) as an aid to guide discharge and diuresis goals (2/13)
There is some evidence that "Hidration Status" (by BIVA) at discharge predicts CV events better than BNP. However for some reason this study used admission BNP while it is most likely that discharge BNP is the one that matters (3/13)
Read 14 tweets