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Septic shock is commonly taught as a warm, vasodilated state, but the cold, low‐output phenotype, in which the underlying process is still sepsis but cardiac output is low and vascular resistance high, is under‐recognised. Escalating vasopressors alone in these patients support the blood pressure while leaving the low output untreated. I describe how I separate low from high cardiac output shock at the bedside using peripheries, pulse pressure and central venous oxygen saturation and where cold septic shock and its mechanisms sit within this framework. The phenotype is recognised at the bedside, whereas identifying the underlying mechanism usually requires echocardiography. The central principle is to treat the haemodynamic phenotype, not the label.
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Priyanka Maan (2026) studied this question.
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