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
**this may be a stretch but...If we look closer and asume the antegrade wave is systolic there might even be an S1 and an S2 wave (The notch between S1 and S2 representing tricuspid valve closure or "c" wave on CVP). Here are several tracings I obtained: 4/7
Without ECG, Is it impossible to know if the antegrade wave = S wave? I don't think so! This antegrade wave should be visible on intra-renal venous doppler which has a simultaneous arterial waveform. Looking at this, it seems the antegrade venous wave happens in systole! 5/7
Lastly, if this analysis is wrong, then there is S wave reversal and we would expect severe TR to be the underlying pathology. Here is the heart! Patient had all the signs of tamponade physiology (Trans-Mitral variation, RV collapse) and no significant TR. 6/7
Classically expiratory D wave reversal has been well described in tamponade. Oddly in this patient it occured all throughout the respiratory cycle. However I think everything points to D wave reversal. But hey this whole thread is pure speculation! 7/7
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 💪
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:
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)
“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
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)
"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)