Stage it (SCAI A-E), find the cause (usually acute MI), revascularise the culprit lesion early, support with noradrenaline ± inotrope, and involve a shock team early for mechanical support in selected patients.
At the bedside
Timed steps- 1
Recognise
0-10 minSBP < 90 mmHg (or vasopressor needed) with hypoperfusion (cold, oliguria, confusion, lactate > 2) and a cardiac cause.
- 2
ECG, echo, troponin
0-10 minSTEMI or equivalent? Mechanical complication (VSR, papillary muscle rupture, free wall rupture)? RV infarct? Tamponade? Arrhythmia?
- 3
Stage
0-30 minSCAI A (at risk) → B (beginning: hypotension or tachycardia without hypoperfusion) → C (classic) → D (deteriorating) → E (extremis, CPR or ECMO).
- 4
Revascularise
0-90 minImmediate coronary angiography and culprit-only PCI in MI with shock (CULPRIT-SHOCK). If PCI cannot be done promptly, thrombolysis for STEMI and transfer.
- 5
Pressors and inotropes
SupportNoradrenaline to MAP ≥ 65; add dobutamine if low output persists. Avoid dopamine. Cautious fluid only if no congestion (RV infarct may need preload).
- 6
Oxygen and PEEP
VentilationNIV or intubation for pulmonary oedema; PEEP reduces LV afterload but can drop BP during induction (use low-dose drugs, pressor ready).
- 7
Mechanical circulatory support
EscalateShock team discussion for SCAI C-D despite therapy. Routine IABP is not recommended (IABP-SHOCK II); routine VA-ECMO did not help (ECLS-SHOCK); microaxial pump reduced mortality in selected STEMI-CS (DanGer Shock) with more complications. See module 14.
SCAI SHOCK stages (simplified)
| Stage | Description | Typical findings |
|---|---|---|
| A: At risk | Large MI, decompensated HF, no shock | Normal BP and perfusion |
| B: Beginning | Relative hypotension or tachycardia without hypoperfusion | SBP < 90 or MAP < 60, lactate < 2 |
| C: Classic | Hypoperfusion needing one vasoactive or MCS | Lactate ≥ 2, cold, oliguria |
| D: Deteriorating | Failing to respond to initial support | Escalating drugs or adding MCS; rising lactate |
| E: Extremis | Refractory shock, CPR, or ECMO | Multiple high-dose drugs, pH < 7.2, lactate > 8 |
References
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Cardiogenic shock pathway
Step 1 of ~7
ECG, echo, troponin, lactate; O2; arterial line
Based on Byrne RA, Rossello X, Coughlan JJ, et al; Naidu SS, Baran DA, Jentzer JC, et al. Educational use; follow local protocol.
Pathophysiology
Reduced contractility lowers stroke volume and coronary perfusion, causing more ischaemia (a downward spiral). Systemic inflammation after large MI adds vasodilatation in up to a fifth of patients (mixed shock).
Evidence
- CULPRIT-SHOCK (2017): culprit-only PCI reduced 30-day death or RRT compared with immediate multivessel PCI.
- IABP-SHOCK II (2012): IABP did not reduce 30-day mortality.
- ECLS-SHOCK (2023): early VA-ECMO did not reduce 30-day mortality and increased bleeding.
- DanGer Shock (2024): microaxial flow pump reduced 180-day mortality in STEMI with cardiogenic shock (excluding comatose OHCA), with more bleeding, limb ischaemia and RRT.
- ESC ACS 2023: immediate angiography and PCI of the IRA for cardiogenic shock; routine IABP not recommended.
Controversies
- Choice of first vasoactive agent beyond noradrenaline and timing of MCS.
🇮🇳 India notes
- Primary PCI is concentrated in urban centres; pharmaco-invasive strategy (tenecteplase then transfer) is common. Many districts lack cath labs.
- Impella and VA-ECMO are available in few Indian centres and cost is high; IABP remains common but is not supported for routine use.
References
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Test yourself
Module quiz · score 70% to complete the module
Educational reference for trained clinicians. Check doses against your hospital protocol and the patient in front of you.