#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!!!
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)
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)
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
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!