Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social

558 posts

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Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social

Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social

@RazvanAzamfirei

critical care | delirium | old man yelling at a cloud | tweets mine (the good ones) | @pennanesthesia | @HopkinsMedicine | @Yale

Philadelphia, PA Katılım Eylül 2015
554 Takip Edilen397 Takipçiler
Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social
The absolute worst thing about the proliferation of 'AI' is being forced to stop using em dashes. I love them, but I've started editing them out to avoid any doubts as to the provenance of my text.
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Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social
Increasing a pressure gradient does reliably increase flow if everything else is held constant, which is not always true in real life. By definition: - Spatial pressure gradients give a net force (−∇p). - Pressure “pushes” on boundaries (it’s the fluid’s normal stress).
Ashley Miller@icmteaching

12/ If gradients were causes, then simply increasing a gradient would reliably increase flow. But in physiology: • gradients often rise while flow falls • congestion can coexist with poor perfusion • pressure can be high when throughput is low That alone tells you gradients are reports, not drivers.

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Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social retweetledi
Ross Prager
Ross Prager@ross_prager·
(2/3) First, critical to recognize that if unaddressed this patient WILL die. Not may. WILL. They have severe microcirculatory dysfunction and macro-circulatory collapse being compensated with high doses of pressors. Why despite thrombolysis? Once a patient with a PE is thrombolysed, RV failure may be in its own cascading death spiral. Also, the PA pressures do not decrease immediately (these can take hours or even days) due to residual clot AND pulmonary constrictive mediators. Thrombolysis is the START of management for massive PE but certainly not the end. This is my general approach and then I will go through the logistics. 1) Defend MAP (MAP >65 for RV perfusion) 2) If in arrythmia, try to fix (e.g. Afib). If slow, speed up (HR 90-110 ideal) 3) Add inotropes. If hypotensive, I like epinephrine > milrinone/dobutamine given less vasodilation 4) Add a pulmonary vasodilator (e.g. NO/prostacyclins/inhaled milrinone). If not intubated, I use inhaled milrinone (5mg neb Q4-6h) 5) Consider and activate MCS EARLY. There is a >50% chance that the patient described above requires MCS despite everything, don't wait until they are arresting. For this patient I tried 20mcg of epinephrine as a push and saw an excellent hemodynamic response. Immediately started coming down on norepinephrine and started a epinephrine drip at 10mcg/min. With this, the cap refill didn't improve much. Next, while waiting for inhaled NO we nebulized 5mg of inhaled Milrinone through the vent. Finally, the patient had been going in/out of Afib with dorpping pressure in Afib so gave a bolus of amiodarone and started and infusion. We had a honeymoon period for 2-3 hours while the patient seemed to recover... cap refill 3-4 seconds... mottling improved... lactate steady however, called over to the bedside for "junctional rhythm". Heart rate was now 60. Huge takehome is that bradycardia (or normocardia) in acute RV failure is a patient about to arrest. We quickly called back the cardiac surgeons (they were already aware) and cannulated the patient for VA-ECMO. The best part about VA-ECMO For massive PE is that it immediately decompresses the RV and in typically is only required for a short period of time (24-48 hours). We decannulated 36 hours later, extubated the next day, and the patient made a full recovery. (take homes below 👇)
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Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social retweetledi
JerryRigEverything
JerryRigEverything@ZacksJerryRig·
So... I'm actually pretty fine with my tax dollars saving the life of someone who's bleeding out on the emergency room floor. I think that's a good idea.
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Razvan Azamfirei 🦋 @razvanazamfirei.bsky.social
Sometimes the reason for the upgrade is not purely the underlying pathology, but a mismatch between the current resources (e.g., nursing ratios, patient location) and the patient acuity. See the patient and give your colleagues the benefit of the doubt.
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Ashley Miller
Ashley Miller@icmteaching·
13/ In non cardiac shock, the opposite happens: Pms is too low. Either • Volume is depleted or • Elastance is low (vasodilatation) → Passive filling fails → Output drops Even with a healthy heart
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