| Mechanism |
| Mechanism | Vasodilatory state from infection — capillary leak + vasopressor deficiency | Pump failure (MI, myocarditis, arrhythmia, valve) | Mechanical obstruction of filling or output (PE, tamponade, tension pneumothorax) | Intravascular volume loss (hemorrhage, GI/renal losses) |
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| Assessment |
| Preload | Low–normal (capillary leak) | Often elevated (congested); can be low | High (obstructed filling) | Low |
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| Cardiac output | Normal or high early; may fall late | Low | Low | Low |
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| SVR | Low | High (compensatory) | High | High |
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| CVP | Low | High | High — tamponade: blunted y descent | Low |
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| SvO₂ / ScvO₂ | High (impaired extraction) | Low | Low–variable | Low until late |
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| Skin / perfusion | Warm early; cool in late/decompensated phase | Cool, mottled | Cool | Cool, pale |
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| POCUS | Hyperdynamic LV, collapsing IVC; hunt the source | Reduced EF, dilated chambers, B-profile lungs | See obstructive trio comparison | Flat IVC, small hyperkinetic LV; free-fluid sweep |
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| Management |
| First priorities | Cultures → broad antimicrobials urgently; balanced crystalloid for hypoperfusion; norepinephrine to MAP ≥65; early source control | Support pump (inotrope), treat the cause urgently (revascularization, rate/rhythm, valve) — avoid reflexive fluid stacking | Relieve the obstruction: reperfusion / pericardiocentesis / decompression | Stop the loss + restore volume — blood early if hemorrhagic |
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| Traps & pitfalls |
| Common traps | Warm skin ≠ stability; delaying source control; ignoring rising lactate | Treating ACS cardiogenic shock that 'looks like sepsis' with more fluid | Fluid-loading tamponade or a failing RV — worsens both | Crystalloid-for-blood substitution in hemorrhagic shock |
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