🫀Before calling septic shock “refractory,” look again. A patient remains hypoperfused. Norepinephrine requirements continue to rise. Additional vasopressors are being considered. It is tempting to conclude that we are dealing with refractory septic shock, but high vasopressor requirements do not necessarily mean true refractoriness. Melo et al propose a framework for distinguishing an apparent refractory trajectory from established refractory septic shock. The question at the bedside therefore becomes: What potentially reversible mechanism is still sustaining hypoperfusion or increasing vasopressor requirements? The authors describe these mechanisms as the “usual suspects.” First comes the foundation: adequate antimicrobial therapy and source control. Without control of the infectious stimulus, optimization of fluids and vasoactive drugs cannot eliminate the underlying inflammatory and vasoplegic drive. Then comes fluid status, but with an important evolution beyond simply asking whether the patient is “fluid responsive.” We should evaluate three different concepts ALWAYS fluid Responsiveness, Tolerance, cardiac efficiency. A patient can therefore be fluid responsive but fluid intolerant, and even an initial hemodynamic response may disappear rapidly. Fluid responsiveness alone is not an indication for fluid administration. Persistent vasoplegia should also trigger evaluation of potentially reversible endocrine, metabolic and iatrogenic contributors. Corticosteroid insufficiency, relative vasopressin deficiency, severe acidemia and excessive sedation may all increase apparent catecholamine resistance. Importantly, sedation itself can reduce venous tone, venous return, myocardial contractility and vascular tone, potentially increasing preload dependence and vasopressor requirements. Sepsis induced myocardial dysfunction may involve LV systolic or diastolic dysfunction, RV dysfunction or hyperdynamic phenotypes. The authors also emphasize VAC. Increasing arterial pressure by increasing effective arterial elastance may improve pressure and flow when ventricular reserve is adequate, but in another patient it may create afterload mismatch: MAP rises while stroke volume and tissue perfusion deteriorate. Dynamic LVOT obstruction represents another easily missed mechanism. Low preload, low afterload and hypercontractility can generate obstruction and paradoxically reduce stroke volume despite an apparently excellent ejection fraction. More catecholamine stimulation can make the problem worse. Reference 📚 Melo, P., Wendel-Garcia, P. D., Leone, M., Khanna, A. K., Morales, S., Ospina-Tascón, G. A., Castro, R., Hernández, G., & Kattan, E. (2026). The usual suspects: A pragmatic framework to identify and address reversible contributors in apparent refractory septic shock. Critical Care, 30, 378. doi.org/10.1186/s13054-026-0…

#ACVC 2026: Mixed shock: the reality behind cardiogenic shock An outstanding session by Dr. David Morrow. Morrow highlighting a critical and often under-recognized concept: 👉 Pure cardiogenic shock is rare. Mixed shock is common. 🔍 Key messages: SVR is not always elevated in cardiogenic shock → Wide variability, often with vasoplegia (SIRS component) Mixed shock = low CO + inappropriately low SVR → A combination of cardiac failure + vasodilatory physiology 📊 Epidemiology (SHARC data): .Cardiogenic shock (isolated): ~65% .Mixed shock: ~17% .Mortality highest in mixed shock (~48%) 🧠 Common phenotypes: -Cardiogenic shock → secondary vasoplegia -Cardiac arrest → stunned myocardium + vasodilation -Sepsis + cardiac dysfunction -Toxic cardiomyopathy (e.g., Ca-blockers, BBs) -Post-cardiotomy vasoplegia ⚙️ Pathophysiology: Inflammation (SIRS) plays a central role Microcirculatory dysfunction + iNOS activation Loss of vascular tone despite vasopressors ⚠️ Clinical implication: 👉 Hemodynamics must be interpreted dynamically, not assumed 👉 SVR ≠ always high → avoid “one-size-fits-all” approach 🛠️ Management principles: Phenotype-guided therapy Combine: Vasopressors (norepinephrine first-line) Inotropes when needed Careful fluid strategy Consider: .Methylene blue / hydroxocobalamin in refractory vasoplegia .CIRCI (steroids) in selected patients 📌 Take-home message: Cardiogenic shock is not purely cardiac. Recognizing the vasoplegic component is key to survival. #ACVC26 #CardiogenicShock #MixedShock #CriticalCare #Hemodynamics #ShockManagement