Frédéric Caruso, MD (@caru_fred) header
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Anesthesiologist & ICU physician trained in 🇧🇪🇨🇦🇨🇵 #POCUS - 🍁

Joined October 2019
Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)Photo by Frédéric Caruso, MD (@caru_fred)
Very interesting / exciting book to recommend to beginners and experienced ultrasound specialists about cardiopulmonary care👌 @NephroP @pocus_today @POCUSJournal @HoosierPocus
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Frédéric Caruso, MD retweeted
The swan vs. echo debate is such a false dichotomy, great article/post below 👇 Swan complements echo assessment. Now, if I only have 1 option, I would choose echo as you can get anatomy + some hemodynamic measurements, but for sick deteriorating shock patients, having both is valuable. Much easier to try a hemodynamic intervention and repeat thermodilution on swan to get a new CI than it is to repeat a VTI on echo. So depends on how many sick patients you are managing at once!
Echo tells you the heart is struggling. The PAC tells you why: pump failure, vasoplegia, low preload, or a failing RV. Don’t fly blind. 🎩 tip to the authors. eddyjoemd.com/foamed
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🫀Hemodynamic stability does not necessarily mean adequate tissue perfusion. A patient with septic shock reaches a MAP of 65 mmHg, cardiac output improves, and vasopressor requirements decrease. Yet capillary refill remains prolonged, lactate is elevated, and organ dysfunction persists. Has resuscitation succeeded? Dr. Carlos Sanchez-Escalante and Xavier Monnet propose a fundamental shift: perfusion assessment should focus on physiological coherence rather than normalization of isolated numbers. The central problem is that macrocirculatory recovery does not guarantee microcirculatory recovery. CRT provides a practical starting point. It is inexpensive, rapidly responsive, and supported by clinical evidence. However, temperature, sympathetic activity, edema, and measurement technique influence its interpretation. Lactate remains valuable for risk assessment, but hyperlactatemia does not necessarily indicate persistent tissue hypoxia. Adrenergic stimulation, altered metabolism, and impaired clearance may sustain elevated concentrations after perfusion improves. Treating every persistent lactate elevation with additional fluids or vasopressors risks producing congestion rather than restoring perfusion. Venous oxygen saturation and the venoarterial CO₂ gap offer complementary information. SvO₂ reflects the relationship between oxygen delivery and consumption, but normal values cannot exclude impaired extraction or microcirculatory shunting. The Pv-aCO₂ gap helps assess whether blood flow is sufficient relative to metabolic CO₂ production. Neither measurement directly demonstrates microcirculatory recovery. Peripheral perfusion index, obtained through photoplethysmography, provides continuous information about peripheral circulatory changes. Its interpretation requires attention to temperature, vascular tone, and vasopressor exposure. When uncertainty persists, advanced assessment may incorporate cardiac output, tissue oxygenation, microcirculatory imaging, and venous congestion. An especially relevant concept is effective tissue perfusion pressure. MAP alone does not determine regional blood flow. Critical closing pressure, vascular tone, extravascular compression, and venous outflow influence the pressure gradient available for tissue perfusion. Consequently, increasing arterial pressure may not improve organ perfusion, particularly when vascular resistance or venous congestion is elevated. The authors propose a progressive approach: begin with clinical examination and basic markers, integrate complementary measurements when signals disagree, and escalate monitoring according to unresolved uncertainty and patient risk. The objective of resuscitation is not to normalize every variable. It is to restore effective tissue perfusion without creating additional injury through unnecessary interventions. Reference 📚 Sanchez-Escalante C, Monnet X. 2026. Critical Care Medicine. doi.org/10.1097/CCM.00000000…
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Frédéric Caruso, MD retweeted
The Surviving Sepsis Campaign has shaped sepsis care for decades. But do some of its core recommendations now lag behind the physiology and the evidence? Rory Spiegel @TheEMNerd led this new dissenting opinion, which I was very pleased to contribute to. We challenge: • fixed 30 mL/kg fluid loading • chasing lactate with fluid • fluid responsiveness as a sufficient reason to give fluid • pressure-centric resuscitation • the omission of POCUS from modern haemodynamic assessment • rigid bundle-driven care The argument is not for less treatment. It is for more individualised, physiology-driven treatment of shock. authors.elsevier.com/c/1npdk… The 2026 Surviving Sepsis Campaign Guidelines: The dissenting opinion Spiegel et al. AJEM, just published.
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Happy to share the publication of my new invited review article: Cardiopulmonary Point of Care Ultrasound in Critical Care published at the Clinical Medicine Journal of @RCPhysicians which demonstrates our proposed model for acute echo haemodynamics (The POCUS PYRAMID). Open access link here: sciencedirect.com/science/ar… #EACVI #echofirst #POCUS @EACVIPresident @RBandH @KingsCollegeLon #POCUS #MedEd #cardiotwitter
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Frédéric Caruso, MD retweeted
Dear friends, I love this paper. It was written with passion and summarizes with a conceptual perspective what we have learnt in 25 years of septic shock resuscitation (from EGDT to AS2). With close friends. Happy to share! rdcu.be/fwUIV
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🚀 CW Doppler interrogation in valvular heart disease. Pearls and pitfalls. Read our new document. 1st of series of our new consortium Reviving Echo Doppler (RED) with @argulian @echo_batman Open access link 🔗 academic.oup.com/ehjimp/arti… #echofirst #EACVI @EACVIPresident @DanXAugustine @dr_benoy_n_shah @denisamuraru @VDelgadoGarcia @EACVIPresident @alessia_gimelli
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Frédéric Caruso, MD retweeted
Interested in the major trials in critical care? We have summarised and critiqued 250 of the most important randomised controlled trials stretching back over the past 25 years. criticalcarereviews.com/coll…
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Frédéric Caruso, MD retweeted
🤓🫀We keep asking: “What’s the cardiac output?” But maybe the better question is: “How efficiently is the heart working?” In septic shock, we often focus on: Preload Cardiac output MAP But we forget something fundamental: 👉 The heart doesn’t work alone. 👉 It works against the arterial system. 1. The missing concept: Ventriculo–arterial coupling (LVAC) LVAC = interaction between: Ees → contractility Ea → arterial load 👉 Expressed as Ea / Ees This ratio reflects: How efficiently the heart converts energy into forward flow 2. What is “normal”? LVAC ≈ 0.5 → optimal efficiency LVAC ≈ 1 → maximal stroke work LVAC > 1 → uncoupling (inefficient system) But here’s the twist: 👉 In septic shock, LVAC is often >1 👉 Not just due to vasodilation—but also myocardial dysfunction 3. Why this matters clinically Two patients can have: Same MAP Same CO But completely different physiology: ✔ One → efficient coupling ❌ One → energy wasted, poor flow generation 4. The key insight Septic shock is NOT just: ❌ “low preload” ❌ “vasodilation” It is: 👉 A mismatch between heart and arterial system 5. Therapy changes the balance Fluids → may improve coupling (↓ LVAC) Norepinephrine → can improve OR worsen coupling Inotropes → target Ees Important: 👉 Increasing MAP ≠ improving flow 👉 Increasing pressure can worsen afterload 6. The most interesting part From the data: LVAC >1 can predict response to norepinephrine But improving LVAC ≠ guaranteed tissue perfusion and outcomes follow a U-shaped curve 👉 Both too high AND too low LVAC can be harmful 7. The limitation we must respect Even if you “optimize” LVAC: 👉 Microcirculation may still be impaired 👉 Lactate may still rise 👉 Shock may persist Because: Macro ≠ micro 🤓Final message We need to move from: ❌ “Fix the blood pressure” To: ✅ “Optimize the interaction between heart and vessels” LVAC doesn’t replace hemodynamics. It completes it. 📃Reference Caicedo Ruiz JD et al. Journal of Critical Care, 2026. doi.org/10.1016/j.jcrc.2026.…
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Frédéric Caruso, MD retweeted
🫀Modulation of the Vasopressin System in Distributive and Cardiogenic Shock *We are overusing catecholamines And we know it More Arrhythmias More Myocardial toxicity More Immunosuppression Yet we keep pushing norepinephrine higher *The real shift: decatecholaminization This paper reframes shock management Not more dose increase, but smarter combinations for sing non-adrenergic pathways 🫀 Clinical implication Shock is not a single pathway problem Why treat it with a single drug? *Vasopressin is not “second line”...it is a different system Adrenergic system → catecholamines Vasopressin system → independent pathway RAAS → angiotensin 🫀 Clinical implication Multimodal vasopressor therapy = physiology-driven care *The key concept: vasopressin deficiency In septic shock Phase 1 → high AVP Phase 2 → depletion Up to one-third of patients develop relative deficiency 🫀 Clinical implication You are not just treating hypotension You are replacing a missing hormone *Renal protection: the underestimated benefit Unlike norepinephrine Vasopressin: • Constricts efferent arteriole • Preserves GFR • Reduces RRT need 🫀 Clinical implication It is not just a pressor It is a renal strategy! *Mortality paradox No clear overall mortality benefit But: • Less RRT • Less catecholamine exposure • Less arrhythmias 🫀 Clinical implication We may be measuring the wrong endpoints *Terlipressin and selepressin: promise vs reality Terlipressin • Longer acting • Higher ischemia risk Selepressin • Pure V1a • Less edema But No clear superiority 🫀 Clinical implication Pharmacology ≠ clinical outcome *Cardiogenic shock: the emerging frontier Early data suggest: • Lower mortality in high-dose vasopressor patients • Better MAP with less norepinephrine 🫀 Clinical implication Especially useful in: • RV failure • Vasoplegic-CS phenotype • Arrhythmia-prone patients *The danger we ignore Vasopressin is powerful Too much → ischemia Too fast withdrawal → collapse 🫀 Clinical implication Never stop vasopressin first⚠️ *Future: precision vasopressor therapy Not “MAP < 65 → add drug” But: • Biomarkers (copeptin) • Vasopressor load • AI-guided titration 🫀 Clinical implication The future is individualized shock physiology 🤓Final reflection Shock management is evolving From: One drug → higher dose To: Multiple systems → lower toxicity Because The goal is not pressure The goal is perfusion⚠️ 📚 Mauriello A et al. J. Clin. Med. 2026, 15, 1953 doi.org/10.3390/jcm15051953
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Our new work just published in Hearts: “Why and How to Measure Left Ventriculo-Arterial Coupling in Rapidly Altered Hemodynamic States.” VAC (Ea/Ees) links ventricular contractility and arterial load, helping explain why BP, EF or CO alone often mislead in shock. A step toward mechanism-guided haemodynamic management. 🔗 mdpi.com/2673-3846/7/1/10 #CriticalCare #EchoFirst #POCUS #Hemodynamics
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Following many requests from colleagues worldwide for access to my recorded webinars, I’ve reactivated my dormant YouTube channel where you’ll find a dedicated playlist with 20+ full-length lectures from previous open-access sessions — all freely available — and I’ll continue adding more. Explore here: youtube.com/@EchoSoliman Hoping these resources continue to support global learning and collaboration in critical care echocardiography & POCUS. #EchoFirst #POCUS #EACVI
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Frédéric Caruso, MD retweeted
Perfect Happy New Year! @NEJM @CHassager
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Prof. Pinsky, such a legend 👏
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Delighted to share our latest article with @Manu_Malbrain and Prashant Nasa @Fluid_Academy Cardiovascular Effects of Intra-abdominal Hypertension: Current Perspectives. 🔗 Open access ait-journal.com/Cardiovascul… #cardiotwitter #MedEd
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Frédéric Caruso, MD retweeted
Replying to @EMNews
@EMNews @PendellM @PMcardioApp @ECGcases @josenalencar Emergency Medicine News just announced 2025's Most Popular Articles. This is number 1, and it is about our JACC Advances article on the new OMI NOMI Paradigm journals.lww.com/em-news/ful…
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Frédéric Caruso, MD retweeted
A great great article by our dear friend and researcher Ricardo Castro! Deep physiology as deep as it cans get. rdcu.be/eRvcE
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