Synopsis
Recognise tissue hypoperfusion from cardiac failure, separate LV, RV and mechanical phenotypes and restore the cause and perfusion without delaying definitive intervention.
- Shock is inadequate tissue perfusion, not a blood-pressure number alone: look for altered mentation, cool/mottled skin, oliguria, narrow pulse pressure, rising lactate and metabolic acidosis.
- Common causes are acute MI, decompensated HFrEF, fulminant myocarditis, severe tachy/bradyarrhythmia, acute valve or post-MI mechanical complication and acute RV failure.
- Bedside echo must rapidly distinguish LV failure, RV failure, tamponade, acute MR, VSD and major valve disease; a single estimated EF does not define the whole shock state.
- In ACS shock, urgent culprit-vessel revascularisation is central; routine immediate non-culprit multivessel PCI is not the default.
- Give fluid only when hypovolaemia or clear preload deficiency is present; repeated empirical boluses worsen pulmonary oedema and RV/LV congestion.
- Use noradrenaline for hypotension and add an inotrope such as dobutamine when low output persists; doses are continuously titrated in critical care, not prescribed as fixed ward doses.
- Vasoactive support is a bridge to cause control, recovery, temporary mechanical support or advanced therapy—not a definitive plan.
- NICE 2026 restricts catheter-based LV microaxial flow pumps to designated PPCI centres with on-site intensive-care expertise and evidence-generation/governance arrangements.