Mechanical circulatory support: IABP, Impella, and ECMO for cardiogenic shock · ICU Topics

In one line

MCS for refractory cardiogenic shock spans a spectrum of escalating invasiveness and support: IABP (counterpulsation, ~0.5–1.0 L/min augmentation — IABP-SHOCK II: NO mortality benefit, use selectively for bridge-to-surgery/mechanical complications); Impella (trans-aortic axial micro-pump actively unloading the LV, 2.5–5.5 L/min — DanGer-SHOCK 2024: IMPROVED 180-day survival in AMI-CS, but IMPRESS negative in severe shock); VA-ECMO (full cardiopulmonary bypass 4–6 L/min + oxygenation — ECLS-SHOCK 2023: no 30-day benefit; strongest support, for biventricular/lung failure, ECPR); TandemHeart (LA→femoral arterial, ~3–4 L/min) and ProtekDuo (RA→PA dual-lumen, RV support). Escalate by SCAI stage (A→E) and reserve for refractory shock before irreversible end-organ injury. Complications: bleeding, thrombosis, limb ischaemia (use distal perfusion cannula), haemolysis, LV distension (VA-ECMO), Harlequin syndrome, stroke, infection.

[1]

MCS devices array: IABP, Impella axial pump, VA-ECMO circuit in ICU — FigureMCS spectrum — match device to SCAI stage and failure mode before irreversible end-organ injury.

Cardiogenic shock spiral of low output, vasoconstriction, and multi-organ hypoperfusion — FigureShock spiral — escalating vasoactives without unloading worsens myocardial O2 demand and lactate.

Device selection algorithm by LV vs biventricular vs cardiopulmonary failure — FigureSelect Impella for isolated LV AMI-CS (DanGer-Shock era); VA-ECMO for biventricular/arrest; IABP alone rarely sufficient.

SCAI shock stages: when to escalate [1]

The Society for Cardiovascular Angiography and Interventions (SCAI) classification stratifies shock severity from a pre-shock "at risk" state through extremis, and is the framework used to time MCS initiation.[6]

SCAI shock stages (A–E) and the role of MCS

Stage	Definition	Haemodynamics	Typical MCS role
A — At risk	Risk factors for shock (large MI, ADHF); not yet shocked	Normal, warm, well perfused	None — optimise guideline therapy
B — Beginning shock	Early/presumed shock; clinical concern	Warm, mildly hypoperfused; lactate rising	None — inotropes/vasopressors, close monitoring
C — Classic shock	Hypoperfusion + hypotension requiring inotropes/vasopressors	Cold, hypoperfused; SBP <90 / MAP <60 despite drugs	Consider IABP/Impella — bridge to decision/recovery
D — Deteriorating	Rapidly worsening despite escalating pharmacological support	Falling MAP, rising lactate, organ dysfunction	Definite MCS — Impella or VA-ECMO (early, before organ failure)
E — Extremis	Collapse, refractory arrest, near-circulatory standstill	Cardiac arrest / PEA / profound bradyasystole	ECPR (VA-ECMO during CPR); consider futility screen

[1]

Key principle: MCS should be contemplated at Stage C and instituted by Stage D, before irreversible end-organ injury. Waiting for Stage E carries the highest mortality; the goal is "bridge to decision" — stabilise haemodynamics, unload the ventricle, and define a definitive plan (recovery, durable LVAD, transplant, or palliation).[7]

Escalation algorithm for refractory cardiogenic shock

Confirm shock + aetiology: lactate >2 mmol/L with hypoperfusion (cold extremities, oliguria, altered mentation); echocardiography to define LV vs RV vs biventricular failure; exclude/treat reversible triggers (ischaemia → PCI, arrhythmia, tamponade, mechanical complication of MI)
Stage A/B (pharmacological): achieve euvolaemia (careful, lung US for B-lines), start inotrope (dobutamine 2.5–10 µg/kg/min OR milrinone 0.125–0.5 µg/kg/min) and/or vasopressor (noradrenaline first-line) targeting MAP >65 mmHg; serial lactate, urine output, mixed venous saturation
Stage C (refractory on single agent): add second inotrope/vasopressor; insert arterial line + consider PA catheter for cardiac index (CI) and pulmonary capillary wedge pressure (PCWP). If CI <2.2 L/min/m² despite drugs → plan MCS
Device selection by failure mode:
- Isolated LV failure (AMI-CS, myocarditis, decompensated HFrEF): Impella CP (preferred where AMI-CS, per DanGer-SHOCK) or IABP (selective — bridge to surgery)
- Biventricular or cardiopulmonary failure (concomitant hypoxaemia, massive PE, ARDS + shock): VA-ECMO
- RV failure (acute PE, RV infarct, post-LVAD): ProtekDuo + inotrope, or Impella RP
- Refractory arrest (Stage E): ECPR (VA-ECMO during ongoing CPR)
Vascular access: ultrasound-guided, percutaneous femoral for IABP/Impella/peripheral VA-ECMO; surgical cut-down or central sternotomy for central VA-ECMO. Mandatory distal perfusion cannula at index cannulation for femoro-femoral VA-ECMO to prevent limb ischaemia
Anticoagulation: unfractionated heparin infusion titrated to ACT 150–180 (IABP), 160–180 s (Impella), 180–220 s (VA-ECMO); monitor aPTT, anti-Xa, haemoglobin, platelets (watch for HIT)
Monitor while on support: arterial waveform, CI/PCWP (PA catheter), lactate trend, organ function (urine, liver), hourly limb perfusion, LDH/plasma-free haemoglobin (haemolysis), renal Dopplers, daily echocardiography for LV distension (VA-ECMO) and aortic regurgitation
Define endpoint: bridge to recovery (wean), bridge to decision (stabilise then plan), bridge to durable LVAD/transplant, or transition to comfort care if futile

[1]

IABP — intra-aortic balloon pump

Mechanism (counterpulsation)

The IABP is a 30–50 mL helium-filled polyurethane balloon percutaneously placed in the descending thoracic aorta (tip distal to left subclavian artery, proximal to renal arteries). It operates on counterpulsation: the balloon inflates in early diastole (immediately after aortic valve closure), timed to the dicrotic notch — this augments diastolic coronary and cerebral perfusion pressure; it deflates rapidly at end-diastole (just before systole), causing an abrupt fall in afterload → reduced LV stroke work, reduced myocardial oxygen demand (MVO₂), and a modest rise in cardiac output (~0.5–1.0 L/min). Triggering is from the ECG R-wave (preferred) or arterial pressure waveform; with intrinsic heart rates <40 bpm or >150 bpm, triggering becomes unreliable.[1]

Indications

Bridge to definitive therapy in cardiogenic shock: mechanical complications of MI (acute MR, VSR) awaiting surgery; high-risk PCI support; refractory ischaemia/arrhythmia
Cardiogenic shock complicating acute MI (selective use — NOT routine, per IABP-SHOCK II)
Weaning from cardiopulmonary bypass, intractable ventricular failure post-cardiotomy
Intractable angina as a bridge to revascularisation

Contraindications

Absolute	Relative
Moderate–severe aortic regurgitation (balloon augments regurgitant volume → worsens LV distension)	Severe peripheral vascular disease (cannot pass sheath)
Aortic dissection or thoracic aortic aneurysm	Active bleeding / coagulopathy
Sepsis (uncontrolled — relative contraindication)	Uncontrolled tachyarrhythmia (poor triggering)
	Sheathless/severe iliofemoral disease

The IABP-SHOCK II trial

Thiele et al. (NEJM 2012) randomised 600 patients with AMI-CS planned for early revascularisation to IABP vs no IABP. No difference in 30-day mortality (39.7% vs 41.3%, RR 0.96, p=0.69), 12-month mortality, or 6-year all-cause mortality (Thiele, Circulation 2019). Routine IABP in AMI-CS is not recommended (ESC Class III, AHA Class IIb). Selective use remains reasonable for mechanical complications of MI, bridge to surgery, and refractory ischaemia.[1][2]

Impella — trans-aortic axial-flow micro-pump

Mechanism (active LV unloading)

Impella is a catheter-mounted axial-flow (Archimedes screw) pump advanced retrogradely across the aortic valve so the inlet sits in the left ventricle and the outlet in the ascending aorta. It continuously aspirates blood from the LV and ejects it into the aorta, actively unloading the LV — reducing LV end-diastolic pressure, wall stress, and MVO₂ — while delivering forward systemic flow independent of the cardiac cycle. Unlike IABP, it does not require intrinsic systole or ECG triggering.[9]

Device variants and flow

Device	Max flow	Insertion	Typical use
Impella 2.5	2.5 L/min	12 Fr femoral	High-risk PCI support, moderate shock
Impella CP	3.5–4.0 L/min	14 Fr femoral	AMI-CS (used in DanGer-SHOCK, IMPRESS)
Impella 5.0 / 5.5	5.0–5.5 L/min	21–25 Fr (surgical/axillary)	Deep shock, bridge to durable LVAD
Impella RP / RP Flex	4.0+ L/min (RV)	23 Fr femoral/ij — across PV	Acute RV failure (PE, RV infarct, post-LVAD)

Indications

Acute MI cardiogenic shock (AMI-CS) — DanGer-SHOCK supports use in STEMI-CS with reduced LVEF (≤40%) and early (<6 h) intubation/high-dose inotrope
High-risk PCI haemodynamic support
Decompensated chronic heart failure as bridge to decision/LVAD
Myocarditis, peri-partum cardiomyopathy with refractory LV failure

Contraindications

Absolute	Relative
Moderate–severe aortic regurgitation (pump output regurgitates back into LV)	Severe aortic stenosis (cannot cross valve) — relative; can be used post-AVR
Mechanical aortic valve (cannot cross)	Severe peripheral arterial disease
Left ventricular thrombus (risk of systemic embolisation)	Active bleeding requiring anticoagulation
Ventricular septal rupture (VSR) with significant L→R shunt	Hepatic failure/coagulopathy
Severe aortic stenosis (pre-cross)	Pregnancy (relative)

DanGer-SHOCK (Møller 2024, NEJM) — the practice-changing positive trial

Randomised 360 patients with STEMI-CS (LVEF ≤40%, early after PCI) to Impella CP + standard care vs standard care alone. Primary endpoint (all-cause death at 180 days): 45.8% (Impella) vs 58.5% (control), HR 0.74 (95% CI 0.55–0.99), p=0.04 — significant mortality reduction. Trade-off: higher device-related complications (composite safety endpoint 24.0% vs 6.2% — severe bleeding, limb ischaemia, haemolysis, need for renal replacement therapy). This is the first RCT to show survival benefit of a micro-axial pump in AMI-CS and has shifted practice toward earlier Impella in STEMI-CS with reduced EF.[3]

Contrast with IMPRESS in severe shock (Ouweneel 2017, JACC): 48 patients with severe AMI-CS (lactate >8, often post-arrest) randomised to Impella CP vs IABP — no mortality difference (66% vs 47%, p=0.27) at 30 days, with higher complications in the Impella arm. Likely reflect that in extremis (Stage E), unloading alone is too late — supporting earlier (Stage C–D) deployment.[4]

VA-ECMO — venoarterial extracorporeal membrane oxygenation

Mechanism (full cardiopulmonary bypass)

VA-ECMO drains deoxygenated venous blood via a large cannula, passes it through an external centrifugal pump + membrane oxygenator (gas exchange + decarboxylation), and returns oxygenated blood under pressure to the arterial tree — providing both circulatory support (4–6 L/min) and oxygenation independent of heart and lung. This is the strongest temporary MCS available.[8]

Peripheral vs central VA-ECMO

Peripheral vs central VA-ECMO cannulation

Feature	Peripheral (femoro-femoral)	Central (ascending aorta / RA)
Access	Percutaneous, bedside possible	Surgical — sternotomy, theatre/ICU
Cannulation	Femoral vein (drainage) + femoral artery (return)	RA appendage (drainage) + ascending aorta (return)
Speed	Rapid (minutes) — preferred for arrest/ECPR	Slower — planned, post-cardiotomy
Oxygenation distribution	Lower body only (see Harlequin)	Whole body (aortic root first) — better coronary/cerebral oxygenation
LV afterload	↑↑ (closed arterial system, retrograde flow) — risk LV distension	Less afterload increase
Bleeding	Cannulation-site, groin	Larger surgical wound — higher bleeding
Mobility / tracheostomy	Limited (groin cannulae)	Easier mobilisation
Typical use	ECPR, acute shock, bridge to decision	Post-cardiotomy failure, post-VAD, chronic support

Distal perfusion cannula (DPC) — mandatory limb protection

Femoral arterial return (15–25 Fr) occludes ipsilateral limb perfusion → critical limb ischaemia in up to 10–30% without protection. A distal perfusion cannula (6–8 Fr antegrade sheath in the superficial femoral artery, or retrograde posterior tibial) back-perfuses the limb from the ECMO circuit. Current best practice: place the DPC at index cannulation (prophylactic) rather than reactively. Monitor hourly: colour, temperature, dorsalis pedis/posterior tibial Doppler, capillary refill, and consider near-infrared spectroscopy (NIRS) on both calves.[8]

LV venting — preventing LV distension

VA-ECMO increases LV afterload (retrograde arterial flow against a failing LV) → LV distension, raised LVEDP, pulmonary oedema, subendocardial ischaemia, and stasis thrombus. Signs on echo: dilated, under-contractile LV with closed aortic valve (no ejection). LV venting strategies:

Impella as an LV vent in combination with VA-ECMO ("ECPELLA") — unloads LV while ECMO supports systemic flow
Intra-aortic balloon pump (IABP) — modest afterload reduction
Pulmonary artery vent (percutaneous, via PV) — drains LV output into circuit
Atrial septostomy (TANRP / left atrial vent)
Direct LV apical vent (surgical) Signs that venting is needed: rising PCWP, pulmonary oedema, LV stasis, subendocardial ischaemia on ECG, aortic root stasis thrombus on echo.[7]

ECLS-SHOCK (Thiele 2023, NEJM)

Randomised 420 patients with AMI-CS to early VA-ECMO + standard care vs standard care alone. Primary endpoint (30-day all-cause mortality): 47.8% (ECMO) vs 49.0% (control), RR 0.98 (95% CI 0.75–1.13), p=0.70 — NO significant difference. Higher rates of bleeding (ventilator/sedation and transfusion), vascular complications, and renal replacement therapy in ECMO arm. Importantly, ECLS-SHOCK enrolled a heterogeneous AMI-CS population (not restricted to reduced EF, many milder shock) and did not require protocolised LV venting — both may have diluted any benefit. Practice has not abandoned VA-ECMO, but the trial underscores that ECMO is not a reflex in all AMI-CS: it is reserved for biventricular failure, hypoxaemia, ECPR, and refractory (Stage D–E) shock where its full cardiopulmonary support is required.[5]

TandemHeart and ProtekDuo

TandemHeart (percutaneous LA-to-femoral arterial support)

A centrifugal pump (TandemLife) drains oxygenated blood from the left atrium via a trans-septal 21 Fr cannula (femoral vein → RA → across interatrial septum → LA) and returns it to a femoral artery (15–17 Fr), bypassing the LV. Provides ~3–5 L/min of systemic flow with effective LV unloading (drains LA → lowers LV preload). Advantages over Impella: does not cross the aortic valve (useful in severe AS or mechanical AVR). Disadvantages: requires trans-septal puncture expertise; higher bleeding; no RV support.[8]

Indications: refractory LV shock when Impella is contraindicated (severe AS, mechanical AVR); bridge to recovery/decision
Contraindications: severe PAD, unable to anticoagulate, LA thrombus, VSR

ProtekDuo (dual-lumen RA-to-PA cannula for RV support)

A single 29–31 Fr dual-lumen cannula inserted via the right internal jugular vein drains deoxygenated blood from the RA and reinfuses it into the main pulmonary artery after passing through the TandemLife pump and oxygenator — providing RV support (up to 4–5 L/min) and, when an oxygenator is inline, oxygenation (useful for RV failure + ARDS or massive PE). Advantages: single-site (RIJ) access, no femoral cannulation, patient can mobilise; oxygenator can be added/removed.

Indications: acute RV failure (massive/submassive PE, RV infarct, post-LVAD RV failure, post-cardiotomy, decompensated pulmonary hypertension); ARDS with RV failure
Contraindications: severe tricuspid regurgitation (relative), IJ thrombosis, unable to anticoagulate, PFO with right-to-left shunt

Indications and contraindications across MCS devices

Device	Strong indications	Key contraindications
IABP	Mechanical complication of MI (bridge to surgery), refractory ischaemia, weaning from CPB, high-risk PCI	Moderate-severe AR, aortic dissection, severe PAD
Impella	AMI-CS with reduced EF (DanGer-SHOCK), high-risk PCI, myocarditis, decompensated HFrEF	Moderate-severe AR, mechanical AVR, LV thrombus, VSR, severe AS
VA-ECMO	Biventricular failure, AMI-CS with hypoxaemia/ARDS, massive PE, ECPR, refractory arrest	Moderate-severe AR (unvented), irreversible brain injury, futility, severe PAD (consider central)
TandemHeart	LV shock when Impella contraindicated (severe AS, mechanical AVR)	Severe PAD, LA thrombus, VSR, unable to anticoagulate
ProtekDuo	RV failure (PE, RV infarct, post-LVAD), RV failure + ARDS	TR (relative), IJ thrombosis, unable to anticoagulate
Impella RP	RV failure (PE, RV infarct) — alternative to ProtekDuo	Mechanical PV, severe TR, RV thrombus, severe PAD

[1]

Comparison of temporary MCS devices — haemodynamics and logistics

Feature	IABP	Impella (CP/5.0)	VA-ECMO	TandemHeart	ProtekDuo
Mechanism	Counterpulsation (diastolic inflation)	Axial pump across AV	External pump + oxygenator	LA→artery centrifugal pump	RA→PA centrifugal pump
Max flow	0.5–1.0 L/min (augment)	2.5–5.5 L/min	4–6 L/min	3–5 L/min	4–5 L/min
Ventricle supported	LV (afterload)	LV (active unloading)	Both (biventricular) + lung	LV (bypasses LV)	RV (bypasses RV)
Oxygenation	No	No	Yes	No	Optional (add oxygenator)
Insertion	7–8 Fr femoral art	12–25 Fr femoral art	19–25 Fr art + 21–25 Fr vein	Trans-septal + femoral art	29–31 Fr RIJ
Anticoagulation (ACT)	150–180 s	160–180 s	180–220 s	Moderate-high	Moderate-high
Pulsatility / afterload	Preserves pulsatility; ↓ afterload	Non-pulsatile; ↓ LV afterload	Non-pulsatile; ↑↑ afterload (LV distension)	Non-pulsatile	Non-pulsatile
Key complications	Limb ischaemia, infection, gas embolus	Haemolysis, limb ischaemia, AR	Limb ischaemia, bleeding, Harlequin, LV distension	Bleeding (trans-septal), limb	Bleeding, RIJ thrombosis
Evidence (RCT)	IABP-SHOCK II: NO benefit	DanGer-SHOCK: POSITIVE (AMI-CS); IMPRESS: negative (severe)	ECLS-SHOCK: NO benefit at 30 d	Observational only	Observational only
When to use	Bridge to surgery, selective	AMI-CS, high-risk PCI	Biventricular/lung failure, ECPR	LV shock + contraindicated Impella	RV failure ± ARDS

[1]

Approach to mechanical circulatory support in cardiogenic shock

Optimise conventional therapy FIRST: inotropes (dobutamine, milrinone), vasopressors (noradrenaline), correct volume status, treat arrhythmia, revascularise (if ischaemic). Define SCAI stage and shock phenotype (LV vs RV vs biventricular ± lung)
If refractory (rising lactate, worsening organ failure, high inotrope/vasopressor doses, Stage C–D) → escalate to MCS before irreversible organ damage
Assess suitability: reversible cause? (bridge to recovery/transplant). Contraindications? (severe AR for IABP, severe AS/mechanical AVR/LV thrombus for Impella, severe PAD, active bleeding, multi-organ failure, futility)
Device selection: (a) IABP — selective (mechanical complications of MI, bridge to surgery). (b) Impella — AMI-CS with reduced EF (DanGer-SHOCK positive), bridge to decision. (c) VA-ECMO — biventricular failure, hypoxaemia, ECPR, bridge to transplant/VAD. (d) TandemHeart/ProtekDuo for niche LV/RV indications
Insertion: percutaneous (femoral access) where possible. Ultrasound-guided. Arterial line monitoring. Distal perfusion cannula at index cannulation for VA-ECMO (prevent limb ischaemia)
Anticoagulation: heparin (unfractionated) — titrate to device-specific ACT. Monitor for bleeding; watch for HIT (falling platelets after day 5)
Monitor: haemodynamics (arterial line, cardiac output, PA catheter CI/PCWP), hourly limb perfusion, haemolysis (LDH, plasma-free haemoglobin), renal/hepatic function, daily echo (LV distension for VA-ECMO), signs of infection, organ recovery
Prevent and recognise device-specific complications: LV distension/Harlequin (VA-ECMO), haemolysis/thrombosis (Impella), limb ischaemia (all femoral), bleeding (all)
Wean: as native heart function recovers (rising native cardiac output, falling lactate, reducing inotropes, stable echo). Trial of lower support. Decannulate when stable — achieve haemostasis, repair vessel

[1]

Exam practice — SAQs

SAQ — IABP in post-infarction cardiogenic shock with a mechanical complication

10 minutes · 10 marks

A 68-year-old man is admitted 6 hours after an anterior STEMI complicated by out-of-hospital cardiac arrest (ROSC after 12 minutes). Primary PCI to the proximal LAD was technically successful. On ICU arrival he is intubated and sedated: MAP 58 on noradrenaline 0.4 mcg/kg/min, HR 118 (sinus), SpO2 94% on FiO2 0.6. A new loud pansystolic murmur is audible at the apex. Lactate 5.8 mmol/L, urine output 0.2 mL/kg/h. Bedside PA catheter: CI 1.7 L/min/m2, PCWP 28 mmHg with a large V-wave. Focused echo: flail anterior mitral leaflet with severe MR, LVEF ~35%, no aortic regurgitation. The cardiology team propose inserting an intra-aortic balloon pump (IABP).

[1]

SAQ — Impella vs VA-ECMO selection in refractory AMI cardiogenic shock

10 minutes · 10 marks

A 55-year-old woman presents 4 hours after an infero-lateral STEMI. Primary PCI to a dominant RCA was complicated by repetitive VT and pulmonary oedema. On arrival in ICU she is intubated, MAP 55 on noradrenaline 0.6 mcg/kg/min and adrenaline 0.2 mcg/kg/min, HR 130 (sinus), SpO2 88% on FiO2 1.0 and PEEP 12. Lactate 7.4 mmol/L, urine 0.1 mL/kg/h. Echo: LVEF ~25%, no aortic regurgitation, RV mildly impaired. The team must choose between an Impella CP and peripheral VA-ECMO.

[1]

Clinical pearls

High-yield MCS points for CICM/FFICM exam

IABP-SHOCK II: IABP does NOT improve mortality in MI-related cardiogenic shock. Thiele 2012 (NEJM): 600 patients with AMI cardiogenic shock, IABP vs no IABP. No difference in 30-day mortality (39.7% vs 41.3%). IABP routine use NOT recommended (ESC Class III). Use selectively (bridge to surgery, mechanical complications of MI, refractory ischaemia). 6-year follow-up confirms no late benefit.[1][2]
IABP provides MODEST support (0.5–1.0 L/min augmentation). Mechanism: balloon inflates in DIASTOLE (coronary perfusion augmented), deflates in SYSTOLE (reduced afterload → improved cardiac output). Contraindications: aortic regurgitation (worsens), aortic dissection, severe peripheral vascular disease, bleeding. Trigger timing is critical — must synchronise with the cardiac cycle (ECG R-wave or arterial pressure dicrotic notch).[1]
Impella provides STRONGER support (2.5–5.5 L/min) and ACTIVELY UNLOADS the LV. Axial-flow pump placed across the aortic valve (inlet in LV, outlet in ascending aorta). Reduces LV wall stress and MVO₂ while delivering forward flow independent of the cardiac cycle. Impella CP (3.5–4.0 L/min) for AMI-CS; Impella 5.0/5.5 for deeper shock/bridge-to-LVAD; Impella RP for RV failure.[9]
DanGer-SHOCK (Møller 2024, NEJM): the FIRST positive RCT for Impella in AMI-CS. 360 STEMI-CS patients (LVEF ≤40%) randomised to Impella CP + standard care vs standard care. 180-day all-cause mortality 45.8% vs 58.5% (HR 0.74, p=0.04) — significant. Caveat: higher complications (bleeding, limb ischaemia, haemolysis, RRT). This has shifted practice toward earlier Impella in STEMI-CS with reduced EF.[3]
IMPRESS in severe shock (Ouweneel 2017): Impella CP vs IABP showed NO benefit in severe AMI-CS. 48 patients with very severe shock (lactate >8, often post-arrest). 30-day mortality 66% (Impella) vs 47% (IABP), p=0.27 — no difference, more complications. Lesson: in extremis (Stage E), unloading alone is too late — supports earlier (Stage C–D) deployment.[4]
VA-ECMO provides FULL cardiopulmonary support (4–6 L/min + oxygenation). Indications: refractory cardiogenic shock (heart AND/OR lung failure), massive PE, ECPR (refractory cardiac arrest). Femoral vein (drainage) + femoral artery (return) for peripheral; RA + ascending aorta for central. Oxygenator adds gas exchange. Strongest support available.[8]
ECLS-SHOCK (Thiele 2023, NEJM): VA-ECMO did NOT improve 30-day mortality in AMI-CS. 420 patients, ECMO + standard care vs standard care. 30-day mortality 47.8% vs 49.0% (p=0.70) — no difference; more bleeding/vascular/RRT complications. Does NOT contraindicate ECMO — reserved for biventricular failure, hypoxaemia, ECPR, refractory Stage D–E shock. Heterogeneous population and lack of protocolised LV venting may have diluted benefit.[5]
ECPR (extracorporeal CPR) for refractory cardiac arrest. If conventional CPR failing (no ROSC after 10–15 min of high-quality CPR), consider ECPR (cannulate during CPR). Rationale: provides circulation + oxygenation while reversible cause addressed (PE, hypothermia, drug toxicity). Best outcomes: witnessed arrest, early cannulation (<30 min), reversible cause. Cochrane 2023 found low-certainty evidence of benefit; selection bias in observational series remains a concern.[11]
Timing matters — early MCS before irreversible organ damage. Prolonged shock → end-organ injury (renal, hepatic, gut) → multi-organ failure → MCS won't help. Early MCS (within hours of refractory shock, SCAI Stage C–D) → better outcomes. 'Bridge to decision' (Impella or ECMO) → stabilise → definitive plan (recovery, transplant, VAD, palliation).[7]
Limb ischaemia is a MAJOR complication (Impella, VA-ECMO). Large-bore arterial cannula → reduced distal flow → limb ischaemia (pain, pallor, pulseless, paraesthesia, paralysis). Prevention: prophylactic distal perfusion cannula at index cannulation (best practice). Monitor hourly: colour, temperature, pulses (dorsalis pedis/posterior tibial), capillary refill, Doppler; consider calf NIRS. If ischaemia → insert DPC (if not already), or relocate cannula.[8]
Bleeding is the MOST COMMON complication (all MCS). Anticoagulation required (prevent thrombosis in circuit/device). Bleeding sites: cannulation site, GI, intracranial. Balance: thrombosis (device failure, stroke) vs bleeding. Monitor: ACT (activated clotting time), aPTT, anti-Xa, haemoglobin, platelets. Maintain ACT 150–180 (IABP), 160–180 (Impella), 180–220 (VA-ECMO). Reduce anticoagulation if bleeding; watch for HIT (falling platelets, day 5–14).[8]
Haemolysis is common with Impella and ECMO. Mechanical shear stress on red cells → haemolysis (elevated LDH, plasma-free haemoglobin, dark/tea-coloured urine, falling haemoglobin). Monitor daily: LDH, plasma-free haemoglobin, haemoglobin, urine colour, haptoglobin. Management: optimise device position, reduce flow (if possible), transfusion; if severe/persistent, device repositioning or exchange may be needed.[9]
Weaning MCS requires native heart recovery. Criteria: (1) Rising native cardiac output (pump flow reduced, CO maintained). (2) Stable haemodynamics (MAP, lactate falling). (3) Reducing inotropes/vasopressors. (4) Improving organ function (urine output, liver). (5) Improving LV/RV function on echo (aortic valve opening, VTI). Trial: reduce support gradually (e.g., ECMO 4 L/min → 2 L/min → 1.5 L/min over hours–days), monitor for deterioration. If stable at low flow → clamp trial → decannulate with surgical repair.[7]
IABP contraindications: (1) Aortic regurgitation (moderate-severe) — balloon augments regurgitant flow → worsens. (2) Aortic dissection. (3) Severe peripheral vascular disease (cannot pass catheter). (4) Active bleeding. (5) Sepsis (relative). Trigger timing is critical — must synchronise with cardiac cycle (ECG or arterial pressure trigger).[1]
Impella contraindications: (1) Severe aortic stenosis (cannot cross valve — unless post-AVR). (2) Moderate-severe aortic regurgitation (pump output returns to LV). (3) Mechanical aortic valve (cannot cross). (4) Left ventricular thrombus (embolisation risk). (5) Severe peripheral vascular disease. (6) Active bleeding (anticoagulation). (7) Ventricular septal rupture (L→R shunt worsens).[9]
VA-ECMO contraindications: (1) Aortic regurgitation (moderate-severe — ECMO return flow regurgitates into LV → LV distension, unless vented). (2) Severe peripheral vascular disease (consider central). (3) Active bleeding (anticoagulation needed). (4) Multi-organ failure (futility). (5) Irreversible brain injury (post-cardiac arrest anoxic). (6) Non-compliance/limited social support (for prolonged support). (7) Age/frailty (relative).[8]
Harlequin syndrome (differential hypoxaemia / north-south syndrome) in peripheral VA-ECMO. When lungs are poorly functioning (e.g., ARDS) AND native heart ejects → deoxygenated LV output perfuses the upper body (coronaries, brain, right arm via arch branches) while well-oxygenated ECMO return (retrograde up descending aorta) perfuses the lower body. Result: differential cyanosis — hypoxaemia in coronary/cerebral circulation with pink lower body. Detect: monitor right radial SaO₂ and cerebral NIRS. Solution: improve lung oxygenation, increase native CO (risk of LV distension), switch to central ECMO, or convert to V-AV ECMO (add venous return oxygenating upper body).[8]
LV distension is the silent killer of VA-ECMO. Retrograde ECMO flow raises LV afterload → failing LV cannot eject → LV distension → raised LVEDP, pulmonary oedema, subendocardial ischaemia, aortic root stasis with thrombus formation (risk of coronary embolisation). Echo signs: dilated thin-walled LV, aortic valve not opening, smoke/stasis in LV. Fix: LV venting — Impella (ECPELLA), IABP, PA vent, atrial septostomy, or surgical LV apical vent. Any VA-ECMO patient with a closed AV or rising PCWP needs venting.[7]
TandemHeart bypasses the LV entirely (LA→femoral artery). Useful when LV support is needed but Impella is contraindicated (severe AS, mechanical AVR). Requires trans-septal puncture skill. Flow ~3–5 L/min. Major risk: bleeding from trans-septal puncture and large femoral sheath; cannot support the RV.[8]
ProtekDuo is the percutaneous RV support of choice in many centres. Dual-lumen RIJ cannula (RA→PA) with TandemLife pump; add oxygenator for RV failure + hypoxaemia (massive PE, ARDS). Advantages: single-site RIJ access (patient can mobilise, sit up), no femoral cannulation, oxygenator modular. Contraindications: severe TR (relative), IJ thrombosis, unable to anticoagulate.[8]
SCAI shock stages guide escalation. Stage A (at risk) → B (beginning, warm) → C (classic shock, needs drugs) → D (deteriorating despite drugs) → E (extremis/arrest). Contemplate MCS at C, institute by D. Higher stages carry exponentially higher mortality; the goal of MCS is to prevent progression to irreversible end-organ injury. Each step up roughly doubles mortality risk.[6]
The cardiac index / PCWP pair drives MCS decisions. Aim for CI >2.2 L/min/m² and PCWP <18 mmHg. A PA catheter (or PiCCO) is invaluable in shock — distinguishes LV (high PCWP, low CI) from RV (high RA, low PCWP) failure and guides weaning. Vasopressors raise SVR and PCWP; inotropes raise CI but may worsen arrhythmia/ischaemia — escalating doses are themselves a trigger for MCS.[10]
ECPELLA (VA-ECMO + Impella) for profound biventricular failure with LV distension. Combines full systemic flow + oxygenation (ECMO) with active LV unloading (Impella). Indicated when VA-ECMO alone causes LV distension/pulmonary oedema. Observational data suggest better unloading and trend to improved survival vs ECMO alone — no RCT yet. Requires dual femoral access and dual anticoagulation vigilance.[7]
Anticoagulation monitoring and HIT. All MCS devices require systemic anticoagulation (typically UFH). Target ACT: IABP 150–180 s, Impella 160–180 s, VA-ECMO 180–220 s. HIT (heparin-induced thrombocytopenia) occurs in 2–5% — monitor platelets every 2–3 days; if >50% fall, switch to direct thrombin inhibitor (bivalirudin, argatroban). Bleeding remains the leading cause of device-related morbidity.[8]
Neurological complications are devastating and under-recognised. Ischaemic stroke (thromboembolism from circuit/LV stasis), intracranial haemorrhage (anticoagulation + reperfusion), and seizures. Daily neurological exam; if sedated, consider continuous EEG. Any sudden rise in inotrope/vasopressor need or unexplained lactate rise → think thrombosis (pump thrombosis, circuit clot) vs bleeding.[8]
Recognise pump thrombosis and circuit clot early. Signs: rising haemolysis (LDH, plasma-free Hb), falling device flow, rising lactate despite stable flow, visible clot in circuit/oxygenator, rising anticoagulation requirement. Management: increase anticoagulation, exchange circuit/device; exclude LV stasis thrombus on echo. Prophylaxis: therapeutic anticoagulation, avoid flow interruptions.[9]
Bridge-to-decision is the most common strategy in modern practice. Most MCS is temporary — the goal is to buy time: (a) Bridge to recovery (myocarditis, stunning) — wean; (b) Bridge to durable LVAD or transplant; (c) Bridge to decision — stabilise, then assess candidacy. Up to 30–50% of refractory shock patients survive to discharge with timely MCS; futility (irreversible brain injury, multi-organ failure, non-candidacy for definitive therapy) should be openly assessed with palliative care involvement.[7]

Red flags

Critical MCS red flags — recognise and act

Refractory shock despite escalating inotropes/vasopressors (SCAI C–D) → early MCS (before irreversible organ damage); do not wait for Stage E.[7]
Cold, mottled, painful limb with absent Doppler signals (Impella/VA-ECMO) → ischaemia — insert/check distal perfusion cannula immediately, vascular surgery review.[8]
Sudden bleeding or falling haemoglobin (anticoagulation) → balance thrombosis vs bleeding; reduce heparin, transfuse, search source (groin, GI, intracranial).[8]
IABP/Impella in moderate-severe aortic regurgitation → CONTRAINDICATED (worsens regurgitation / LV distension).[1][9]
Rising PCWP + pulmonary oedema + closed aortic valve on echo during VA-ECMO → LV distension — urgent LV venting (Impella, IABP, PA vent).[7]
Differential cyanosis (desaturated right radial / cerebral NIRS, pink lower body) on peripheral VA-ECMO → Harlequin syndrome — improve lung oxygenation, switch to central or V-AV ECMO.[8]
Tea-coloured urine + rising LDH/plasma-free Hb → haemolysis (Impella/ECMO) — check device position, optimise flow, transfuse; consider exchange.[9]
Falling device flow + rising lactate + visible clot → pump/circuit thrombosis — escalate anticoagulation, exchange circuit/device.[9]
Sudden neurological change or unexplained rise in vasopressors → stroke (ischaemic or haemorrhagic) or thrombosis — CT brain, image circuit.[8]
ECPR for refractory arrest — best outcomes if witnessed, <30 min low-flow, reversible cause; early cannulation during ongoing CPR.[11]
Gross haematuria/urea rising without other cause on VA-ECMO → renal vein congestion from high CVP/LV distension, or renal hypoperfusion from differential hypoxaemia.[8]

Prognosis and key trials

IABP-SHOCK II (Thiele 2012, NEJM) + 6-year follow-up (Circulation 2019)

RCT: 600 patients with acute MI + cardiogenic shock (planned early revascularisation). IABP vs no IABP.

30-day mortality: IABP 39.7% vs no IABP 41.3% (RR 0.96, p=0.69 — NO significant difference)
12-month mortality: IABP 52% vs no IABP 51% (no difference)
6-year all-cause mortality: ~57% both arms (no late emergence of benefit)
Secondary outcomes: no difference in complications, ICU stay, quality of life
CONCLUSION: Routine IABP does NOT improve outcomes in AMI cardiogenic shock (ESC Class III). Use selectively — mechanical complications of MI, bridge to surgery, refractory ischaemia.[1][2]

DanGer-SHOCK (Møller 2024, NEJM) — FIRST positive RCT for Impella

RCT: 360 patients with STEMI complicated by cardiogenic shock (LVEF ≤40%), randomised to Impella CP + standard care vs standard care alone.

Primary endpoint — all-cause mortality at 180 days: 45.8% (Impella) vs 58.5% (control), HR 0.74 (95% CI 0.55–0.99), p=0.04 — significant
Composite safety endpoint (severe bleeding, limb ischaemia, haemolysis, device failure, worsening AR, need for RRT): 24.0% (Impella) vs 6.2% (control) — more complications
CONCLUSION: Routine early Impella CP in STEMI-CS with reduced EF improved 180-day survival. The benefit must be weighed against higher device-related complication rates. Practice-changing for STEMI-CS with low EF; less applicable to non-ischaemic or very severe (Stage E) shock.[3]

ECLS-SHOCK (Thiele 2023, NEJM) — VA-ECMO negative in AMI-CS

RCT: 420 patients with AMI-CS, randomised to early VA-ECMO + standard care vs standard care alone.

Primary endpoint — 30-day all-cause mortality: 47.8% (ECMO) vs 49.0% (control), RR 0.98 (95% CI 0.75–1.13), p=0.70 — NO significant difference
Complications: more moderate/severe bleeding (23.4% vs 9.6%), more vascular complications requiring surgery (11.0% vs 3.6%), more RRT (29.7% vs 21.4%) in ECMO arm
CONCLUSION: Routine early VA-ECMO did not improve 30-day mortality in AMI-CS. Caveats: heterogeneous shock severity (many milder), no protocolised LV venting, crossover 4%. ECMO remains indicated for biventricular failure, hypoxaemia, ECPR, and refractory Stage D–E shock — not a reflex for all AMI-CS.[5]

IMPRESS in severe shock (Ouweneel 2017, JACC)

RCT: 48 patients with severe AMI-CS (lactate >8 mmol/L, often post-arrest), Impella CP vs IABP.

30-day mortality: 66% (Impella) vs 47% (IABP), p=0.27 — no significant difference
CONCLUSION: No benefit (and non-significant harm signal) of Impella in very severe AMI-CS. Likely reflects that unloading alone is insufficient in extremis — supports earlier (Stage C–D) deployment rather than waiting for Stage E. Small sample limits conclusions.[4]

Overall outcomes by device (observational + trial data):

IABP: no mortality benefit in AMI-CS (IABP-SHOCK II); useful selectively.
Impella: DanGer-SHOCK shows survival benefit in STEMI-CS with reduced EF when used early; IMPRESS negative in severe shock — timing matters.
VA-ECMO: ECLS-SHOCK negative in broad AMI-CS; observational survival to discharge 30–50% in refractory cardiogenic shock (higher if early, reversible cause, single-organ failure).
ECPR: 20–30% survival to discharge in refractory cardiac arrest (Cochrane 2023 — low-certainty evidence; selection bias concerns); best if witnessed, early cannulation, reversible cause.
Bridge to durable therapy: up to 30–50% of refractory shock patients survive to discharge with timely MCS; durable LVAD/transplant candidacy must be assessed early.[7][10][11]

References

[1]Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock N Engl J Med, 2012.PMID 22920912
[2]Thiele H, Akin I, Sandri M, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial Circulation, 2019.PMID 30586721
[3]Møller JE, Engstrøm T, Jensen LO, et al. Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock N Engl J Med, 2024.PMID 38587239
[4]Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction J Am Coll Cardiol, 2017.PMID 27810347
[5]Thiele H, Zeymer U, Akin I, et al. Extracorporeal Life Support in Infarct-Related Cardiogenic Shock N Engl J Med, 2023.PMID 37634145
[6]Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019 Catheter Cardiovasc Interv, 2019.PMID 31104355
[7]Lüsebrink E, Binzenhöfer L, Adamo M, et al. Cardiogenic shock Lancet, 2024.PMID 39550175
[8]Nakata J, Yamamoto T, Saku K, et al. Mechanical circulatory support in cardiogenic shock J Intensive Care, 2023.PMID 38115065
[9]Masiero G, Arturi F, Panza A, et al. Mechanical Circulatory Support with Impella: Principles, Evidence, and Daily Practice J Clin Med, 2024.PMID 39200728
[10]Sarma D, Jentzer JC. Cardiogenic Shock: Pathogenesis, Classification, and Management Crit Care Clin, 2024.PMID 37973356
[11]Burrell A, Kim J, Alliegro P, et al. Extracorporeal membrane oxygenation for critically ill adults Cochrane Database Syst Rev, 2023.PMID 37750499

In one line

[1]

SCAI shock stages: when to escalate [1]

SCAI shock stages (A–E) and the role of MCS

Stage	Definition	Haemodynamics	Typical MCS role
A — At risk	Risk factors for shock (large MI, ADHF); not yet shocked	Normal, warm, well perfused	None — optimise guideline therapy
B — Beginning shock	Early/presumed shock; clinical concern	Warm, mildly hypoperfused; lactate rising	None — inotropes/vasopressors, close monitoring
C — Classic shock	Hypoperfusion + hypotension requiring inotropes/vasopressors	Cold, hypoperfused; SBP <90 / MAP <60 despite drugs	Consider IABP/Impella — bridge to decision/recovery
D — Deteriorating	Rapidly worsening despite escalating pharmacological support	Falling MAP, rising lactate, organ dysfunction	Definite MCS — Impella or VA-ECMO (early, before organ failure)
E — Extremis	Collapse, refractory arrest, near-circulatory standstill	Cardiac arrest / PEA / profound bradyasystole	ECPR (VA-ECMO during CPR); consider futility screen

[1]

Escalation algorithm for refractory cardiogenic shock

Confirm shock + aetiology: lactate >2 mmol/L with hypoperfusion (cold extremities, oliguria, altered mentation); echocardiography to define LV vs RV vs biventricular failure; exclude/treat reversible triggers (ischaemia → PCI, arrhythmia, tamponade, mechanical complication of MI)
Stage A/B (pharmacological): achieve euvolaemia (careful, lung US for B-lines), start inotrope (dobutamine 2.5–10 µg/kg/min OR milrinone 0.125–0.5 µg/kg/min) and/or vasopressor (noradrenaline first-line) targeting MAP >65 mmHg; serial lactate, urine output, mixed venous saturation
Stage C (refractory on single agent): add second inotrope/vasopressor; insert arterial line + consider PA catheter for cardiac index (CI) and pulmonary capillary wedge pressure (PCWP). If CI <2.2 L/min/m² despite drugs → plan MCS
Device selection by failure mode:
- Isolated LV failure (AMI-CS, myocarditis, decompensated HFrEF): Impella CP (preferred where AMI-CS, per DanGer-SHOCK) or IABP (selective — bridge to surgery)
- Biventricular or cardiopulmonary failure (concomitant hypoxaemia, massive PE, ARDS + shock): VA-ECMO
- RV failure (acute PE, RV infarct, post-LVAD): ProtekDuo + inotrope, or Impella RP
- Refractory arrest (Stage E): ECPR (VA-ECMO during ongoing CPR)
Vascular access: ultrasound-guided, percutaneous femoral for IABP/Impella/peripheral VA-ECMO; surgical cut-down or central sternotomy for central VA-ECMO. Mandatory distal perfusion cannula at index cannulation for femoro-femoral VA-ECMO to prevent limb ischaemia
Anticoagulation: unfractionated heparin infusion titrated to ACT 150–180 (IABP), 160–180 s (Impella), 180–220 s (VA-ECMO); monitor aPTT, anti-Xa, haemoglobin, platelets (watch for HIT)
Monitor while on support: arterial waveform, CI/PCWP (PA catheter), lactate trend, organ function (urine, liver), hourly limb perfusion, LDH/plasma-free haemoglobin (haemolysis), renal Dopplers, daily echocardiography for LV distension (VA-ECMO) and aortic regurgitation
Define endpoint: bridge to recovery (wean), bridge to decision (stabilise then plan), bridge to durable LVAD/transplant, or transition to comfort care if futile

[1]

IABP — intra-aortic balloon pump

Mechanism (counterpulsation)

Indications

Bridge to definitive therapy in cardiogenic shock: mechanical complications of MI (acute MR, VSR) awaiting surgery; high-risk PCI support; refractory ischaemia/arrhythmia
Cardiogenic shock complicating acute MI (selective use — NOT routine, per IABP-SHOCK II)
Weaning from cardiopulmonary bypass, intractable ventricular failure post-cardiotomy
Intractable angina as a bridge to revascularisation

Contraindications

Absolute	Relative
Moderate–severe aortic regurgitation (balloon augments regurgitant volume → worsens LV distension)	Severe peripheral vascular disease (cannot pass sheath)
Aortic dissection or thoracic aortic aneurysm	Active bleeding / coagulopathy
Sepsis (uncontrolled — relative contraindication)	Uncontrolled tachyarrhythmia (poor triggering)
	Sheathless/severe iliofemoral disease

The IABP-SHOCK II trial

Impella — trans-aortic axial-flow micro-pump

Mechanism (active LV unloading)

Device variants and flow

Device	Max flow	Insertion	Typical use
Impella 2.5	2.5 L/min	12 Fr femoral	High-risk PCI support, moderate shock
Impella CP	3.5–4.0 L/min	14 Fr femoral	AMI-CS (used in DanGer-SHOCK, IMPRESS)
Impella 5.0 / 5.5	5.0–5.5 L/min	21–25 Fr (surgical/axillary)	Deep shock, bridge to durable LVAD
Impella RP / RP Flex	4.0+ L/min (RV)	23 Fr femoral/ij — across PV	Acute RV failure (PE, RV infarct, post-LVAD)

Indications

Acute MI cardiogenic shock (AMI-CS) — DanGer-SHOCK supports use in STEMI-CS with reduced LVEF (≤40%) and early (<6 h) intubation/high-dose inotrope
High-risk PCI haemodynamic support
Decompensated chronic heart failure as bridge to decision/LVAD
Myocarditis, peri-partum cardiomyopathy with refractory LV failure

Contraindications

Absolute	Relative
Moderate–severe aortic regurgitation (pump output regurgitates back into LV)	Severe aortic stenosis (cannot cross valve) — relative; can be used post-AVR
Mechanical aortic valve (cannot cross)	Severe peripheral arterial disease
Left ventricular thrombus (risk of systemic embolisation)	Active bleeding requiring anticoagulation
Ventricular septal rupture (VSR) with significant L→R shunt	Hepatic failure/coagulopathy
Severe aortic stenosis (pre-cross)	Pregnancy (relative)

DanGer-SHOCK (Møller 2024, NEJM) — the practice-changing positive trial

VA-ECMO — venoarterial extracorporeal membrane oxygenation

Mechanism (full cardiopulmonary bypass)

Peripheral vs central VA-ECMO

Peripheral vs central VA-ECMO cannulation

Feature	Peripheral (femoro-femoral)	Central (ascending aorta / RA)
Access	Percutaneous, bedside possible	Surgical — sternotomy, theatre/ICU
Cannulation	Femoral vein (drainage) + femoral artery (return)	RA appendage (drainage) + ascending aorta (return)
Speed	Rapid (minutes) — preferred for arrest/ECPR	Slower — planned, post-cardiotomy
Oxygenation distribution	Lower body only (see Harlequin)	Whole body (aortic root first) — better coronary/cerebral oxygenation
LV afterload	↑↑ (closed arterial system, retrograde flow) — risk LV distension	Less afterload increase
Bleeding	Cannulation-site, groin	Larger surgical wound — higher bleeding
Mobility / tracheostomy	Limited (groin cannulae)	Easier mobilisation
Typical use	ECPR, acute shock, bridge to decision	Post-cardiotomy failure, post-VAD, chronic support

Distal perfusion cannula (DPC) — mandatory limb protection

LV venting — preventing LV distension

Impella as an LV vent in combination with VA-ECMO ("ECPELLA") — unloads LV while ECMO supports systemic flow
Intra-aortic balloon pump (IABP) — modest afterload reduction
Pulmonary artery vent (percutaneous, via PV) — drains LV output into circuit
Atrial septostomy (TANRP / left atrial vent)
Direct LV apical vent (surgical) Signs that venting is needed: rising PCWP, pulmonary oedema, LV stasis, subendocardial ischaemia on ECG, aortic root stasis thrombus on echo.[7]

ECLS-SHOCK (Thiele 2023, NEJM)

TandemHeart and ProtekDuo

TandemHeart (percutaneous LA-to-femoral arterial support)

Indications: refractory LV shock when Impella is contraindicated (severe AS, mechanical AVR); bridge to recovery/decision
Contraindications: severe PAD, unable to anticoagulate, LA thrombus, VSR

ProtekDuo (dual-lumen RA-to-PA cannula for RV support)

Indications: acute RV failure (massive/submassive PE, RV infarct, post-LVAD RV failure, post-cardiotomy, decompensated pulmonary hypertension); ARDS with RV failure
Contraindications: severe tricuspid regurgitation (relative), IJ thrombosis, unable to anticoagulate, PFO with right-to-left shunt

Indications and contraindications across MCS devices

Device	Strong indications	Key contraindications
IABP	Mechanical complication of MI (bridge to surgery), refractory ischaemia, weaning from CPB, high-risk PCI	Moderate-severe AR, aortic dissection, severe PAD
Impella	AMI-CS with reduced EF (DanGer-SHOCK), high-risk PCI, myocarditis, decompensated HFrEF	Moderate-severe AR, mechanical AVR, LV thrombus, VSR, severe AS
VA-ECMO	Biventricular failure, AMI-CS with hypoxaemia/ARDS, massive PE, ECPR, refractory arrest	Moderate-severe AR (unvented), irreversible brain injury, futility, severe PAD (consider central)
TandemHeart	LV shock when Impella contraindicated (severe AS, mechanical AVR)	Severe PAD, LA thrombus, VSR, unable to anticoagulate
ProtekDuo	RV failure (PE, RV infarct, post-LVAD), RV failure + ARDS	TR (relative), IJ thrombosis, unable to anticoagulate
Impella RP	RV failure (PE, RV infarct) — alternative to ProtekDuo	Mechanical PV, severe TR, RV thrombus, severe PAD

[1]

Comparison of temporary MCS devices — haemodynamics and logistics

Feature	IABP	Impella (CP/5.0)	VA-ECMO	TandemHeart	ProtekDuo
Mechanism	Counterpulsation (diastolic inflation)	Axial pump across AV	External pump + oxygenator	LA→artery centrifugal pump	RA→PA centrifugal pump
Max flow	0.5–1.0 L/min (augment)	2.5–5.5 L/min	4–6 L/min	3–5 L/min	4–5 L/min
Ventricle supported	LV (afterload)	LV (active unloading)	Both (biventricular) + lung	LV (bypasses LV)	RV (bypasses RV)
Oxygenation	No	No	Yes	No	Optional (add oxygenator)
Insertion	7–8 Fr femoral art	12–25 Fr femoral art	19–25 Fr art + 21–25 Fr vein	Trans-septal + femoral art	29–31 Fr RIJ
Anticoagulation (ACT)	150–180 s	160–180 s	180–220 s	Moderate-high	Moderate-high
Pulsatility / afterload	Preserves pulsatility; ↓ afterload	Non-pulsatile; ↓ LV afterload	Non-pulsatile; ↑↑ afterload (LV distension)	Non-pulsatile	Non-pulsatile
Key complications	Limb ischaemia, infection, gas embolus	Haemolysis, limb ischaemia, AR	Limb ischaemia, bleeding, Harlequin, LV distension	Bleeding (trans-septal), limb	Bleeding, RIJ thrombosis
Evidence (RCT)	IABP-SHOCK II: NO benefit	DanGer-SHOCK: POSITIVE (AMI-CS); IMPRESS: negative (severe)	ECLS-SHOCK: NO benefit at 30 d	Observational only	Observational only
When to use	Bridge to surgery, selective	AMI-CS, high-risk PCI	Biventricular/lung failure, ECPR	LV shock + contraindicated Impella	RV failure ± ARDS

[1]

Approach to mechanical circulatory support in cardiogenic shock

Optimise conventional therapy FIRST: inotropes (dobutamine, milrinone), vasopressors (noradrenaline), correct volume status, treat arrhythmia, revascularise (if ischaemic). Define SCAI stage and shock phenotype (LV vs RV vs biventricular ± lung)
If refractory (rising lactate, worsening organ failure, high inotrope/vasopressor doses, Stage C–D) → escalate to MCS before irreversible organ damage
Assess suitability: reversible cause? (bridge to recovery/transplant). Contraindications? (severe AR for IABP, severe AS/mechanical AVR/LV thrombus for Impella, severe PAD, active bleeding, multi-organ failure, futility)
Device selection: (a) IABP — selective (mechanical complications of MI, bridge to surgery). (b) Impella — AMI-CS with reduced EF (DanGer-SHOCK positive), bridge to decision. (c) VA-ECMO — biventricular failure, hypoxaemia, ECPR, bridge to transplant/VAD. (d) TandemHeart/ProtekDuo for niche LV/RV indications
Insertion: percutaneous (femoral access) where possible. Ultrasound-guided. Arterial line monitoring. Distal perfusion cannula at index cannulation for VA-ECMO (prevent limb ischaemia)
Anticoagulation: heparin (unfractionated) — titrate to device-specific ACT. Monitor for bleeding; watch for HIT (falling platelets after day 5)
Monitor: haemodynamics (arterial line, cardiac output, PA catheter CI/PCWP), hourly limb perfusion, haemolysis (LDH, plasma-free haemoglobin), renal/hepatic function, daily echo (LV distension for VA-ECMO), signs of infection, organ recovery
Prevent and recognise device-specific complications: LV distension/Harlequin (VA-ECMO), haemolysis/thrombosis (Impella), limb ischaemia (all femoral), bleeding (all)
Wean: as native heart function recovers (rising native cardiac output, falling lactate, reducing inotropes, stable echo). Trial of lower support. Decannulate when stable — achieve haemostasis, repair vessel

[1]

Exam practice — SAQs

SAQ — IABP in post-infarction cardiogenic shock with a mechanical complication

10 minutes · 10 marks

[1]

SAQ — Impella vs VA-ECMO selection in refractory AMI cardiogenic shock

10 minutes · 10 marks

[1]

Clinical pearls

High-yield MCS points for CICM/FFICM exam

IABP-SHOCK II: IABP does NOT improve mortality in MI-related cardiogenic shock. Thiele 2012 (NEJM): 600 patients with AMI cardiogenic shock, IABP vs no IABP. No difference in 30-day mortality (39.7% vs 41.3%). IABP routine use NOT recommended (ESC Class III). Use selectively (bridge to surgery, mechanical complications of MI, refractory ischaemia). 6-year follow-up confirms no late benefit.[1][2]
IABP provides MODEST support (0.5–1.0 L/min augmentation). Mechanism: balloon inflates in DIASTOLE (coronary perfusion augmented), deflates in SYSTOLE (reduced afterload → improved cardiac output). Contraindications: aortic regurgitation (worsens), aortic dissection, severe peripheral vascular disease, bleeding. Trigger timing is critical — must synchronise with the cardiac cycle (ECG R-wave or arterial pressure dicrotic notch).[1]
Impella provides STRONGER support (2.5–5.5 L/min) and ACTIVELY UNLOADS the LV. Axial-flow pump placed across the aortic valve (inlet in LV, outlet in ascending aorta). Reduces LV wall stress and MVO₂ while delivering forward flow independent of the cardiac cycle. Impella CP (3.5–4.0 L/min) for AMI-CS; Impella 5.0/5.5 for deeper shock/bridge-to-LVAD; Impella RP for RV failure.[9]
DanGer-SHOCK (Møller 2024, NEJM): the FIRST positive RCT for Impella in AMI-CS. 360 STEMI-CS patients (LVEF ≤40%) randomised to Impella CP + standard care vs standard care. 180-day all-cause mortality 45.8% vs 58.5% (HR 0.74, p=0.04) — significant. Caveat: higher complications (bleeding, limb ischaemia, haemolysis, RRT). This has shifted practice toward earlier Impella in STEMI-CS with reduced EF.[3]
IMPRESS in severe shock (Ouweneel 2017): Impella CP vs IABP showed NO benefit in severe AMI-CS. 48 patients with very severe shock (lactate >8, often post-arrest). 30-day mortality 66% (Impella) vs 47% (IABP), p=0.27 — no difference, more complications. Lesson: in extremis (Stage E), unloading alone is too late — supports earlier (Stage C–D) deployment.[4]
VA-ECMO provides FULL cardiopulmonary support (4–6 L/min + oxygenation). Indications: refractory cardiogenic shock (heart AND/OR lung failure), massive PE, ECPR (refractory cardiac arrest). Femoral vein (drainage) + femoral artery (return) for peripheral; RA + ascending aorta for central. Oxygenator adds gas exchange. Strongest support available.[8]
ECLS-SHOCK (Thiele 2023, NEJM): VA-ECMO did NOT improve 30-day mortality in AMI-CS. 420 patients, ECMO + standard care vs standard care. 30-day mortality 47.8% vs 49.0% (p=0.70) — no difference; more bleeding/vascular/RRT complications. Does NOT contraindicate ECMO — reserved for biventricular failure, hypoxaemia, ECPR, refractory Stage D–E shock. Heterogeneous population and lack of protocolised LV venting may have diluted benefit.[5]
ECPR (extracorporeal CPR) for refractory cardiac arrest. If conventional CPR failing (no ROSC after 10–15 min of high-quality CPR), consider ECPR (cannulate during CPR). Rationale: provides circulation + oxygenation while reversible cause addressed (PE, hypothermia, drug toxicity). Best outcomes: witnessed arrest, early cannulation (<30 min), reversible cause. Cochrane 2023 found low-certainty evidence of benefit; selection bias in observational series remains a concern.[11]
Timing matters — early MCS before irreversible organ damage. Prolonged shock → end-organ injury (renal, hepatic, gut) → multi-organ failure → MCS won't help. Early MCS (within hours of refractory shock, SCAI Stage C–D) → better outcomes. 'Bridge to decision' (Impella or ECMO) → stabilise → definitive plan (recovery, transplant, VAD, palliation).[7]
Limb ischaemia is a MAJOR complication (Impella, VA-ECMO). Large-bore arterial cannula → reduced distal flow → limb ischaemia (pain, pallor, pulseless, paraesthesia, paralysis). Prevention: prophylactic distal perfusion cannula at index cannulation (best practice). Monitor hourly: colour, temperature, pulses (dorsalis pedis/posterior tibial), capillary refill, Doppler; consider calf NIRS. If ischaemia → insert DPC (if not already), or relocate cannula.[8]
Bleeding is the MOST COMMON complication (all MCS). Anticoagulation required (prevent thrombosis in circuit/device). Bleeding sites: cannulation site, GI, intracranial. Balance: thrombosis (device failure, stroke) vs bleeding. Monitor: ACT (activated clotting time), aPTT, anti-Xa, haemoglobin, platelets. Maintain ACT 150–180 (IABP), 160–180 (Impella), 180–220 (VA-ECMO). Reduce anticoagulation if bleeding; watch for HIT (falling platelets, day 5–14).[8]
Haemolysis is common with Impella and ECMO. Mechanical shear stress on red cells → haemolysis (elevated LDH, plasma-free haemoglobin, dark/tea-coloured urine, falling haemoglobin). Monitor daily: LDH, plasma-free haemoglobin, haemoglobin, urine colour, haptoglobin. Management: optimise device position, reduce flow (if possible), transfusion; if severe/persistent, device repositioning or exchange may be needed.[9]
Weaning MCS requires native heart recovery. Criteria: (1) Rising native cardiac output (pump flow reduced, CO maintained). (2) Stable haemodynamics (MAP, lactate falling). (3) Reducing inotropes/vasopressors. (4) Improving organ function (urine output, liver). (5) Improving LV/RV function on echo (aortic valve opening, VTI). Trial: reduce support gradually (e.g., ECMO 4 L/min → 2 L/min → 1.5 L/min over hours–days), monitor for deterioration. If stable at low flow → clamp trial → decannulate with surgical repair.[7]
IABP contraindications: (1) Aortic regurgitation (moderate-severe) — balloon augments regurgitant flow → worsens. (2) Aortic dissection. (3) Severe peripheral vascular disease (cannot pass catheter). (4) Active bleeding. (5) Sepsis (relative). Trigger timing is critical — must synchronise with cardiac cycle (ECG or arterial pressure trigger).[1]
Impella contraindications: (1) Severe aortic stenosis (cannot cross valve — unless post-AVR). (2) Moderate-severe aortic regurgitation (pump output returns to LV). (3) Mechanical aortic valve (cannot cross). (4) Left ventricular thrombus (embolisation risk). (5) Severe peripheral vascular disease. (6) Active bleeding (anticoagulation). (7) Ventricular septal rupture (L→R shunt worsens).[9]
VA-ECMO contraindications: (1) Aortic regurgitation (moderate-severe — ECMO return flow regurgitates into LV → LV distension, unless vented). (2) Severe peripheral vascular disease (consider central). (3) Active bleeding (anticoagulation needed). (4) Multi-organ failure (futility). (5) Irreversible brain injury (post-cardiac arrest anoxic). (6) Non-compliance/limited social support (for prolonged support). (7) Age/frailty (relative).[8]
Harlequin syndrome (differential hypoxaemia / north-south syndrome) in peripheral VA-ECMO. When lungs are poorly functioning (e.g., ARDS) AND native heart ejects → deoxygenated LV output perfuses the upper body (coronaries, brain, right arm via arch branches) while well-oxygenated ECMO return (retrograde up descending aorta) perfuses the lower body. Result: differential cyanosis — hypoxaemia in coronary/cerebral circulation with pink lower body. Detect: monitor right radial SaO₂ and cerebral NIRS. Solution: improve lung oxygenation, increase native CO (risk of LV distension), switch to central ECMO, or convert to V-AV ECMO (add venous return oxygenating upper body).[8]
LV distension is the silent killer of VA-ECMO. Retrograde ECMO flow raises LV afterload → failing LV cannot eject → LV distension → raised LVEDP, pulmonary oedema, subendocardial ischaemia, aortic root stasis with thrombus formation (risk of coronary embolisation). Echo signs: dilated thin-walled LV, aortic valve not opening, smoke/stasis in LV. Fix: LV venting — Impella (ECPELLA), IABP, PA vent, atrial septostomy, or surgical LV apical vent. Any VA-ECMO patient with a closed AV or rising PCWP needs venting.[7]
TandemHeart bypasses the LV entirely (LA→femoral artery). Useful when LV support is needed but Impella is contraindicated (severe AS, mechanical AVR). Requires trans-septal puncture skill. Flow ~3–5 L/min. Major risk: bleeding from trans-septal puncture and large femoral sheath; cannot support the RV.[8]
ProtekDuo is the percutaneous RV support of choice in many centres. Dual-lumen RIJ cannula (RA→PA) with TandemLife pump; add oxygenator for RV failure + hypoxaemia (massive PE, ARDS). Advantages: single-site RIJ access (patient can mobilise, sit up), no femoral cannulation, oxygenator modular. Contraindications: severe TR (relative), IJ thrombosis, unable to anticoagulate.[8]
SCAI shock stages guide escalation. Stage A (at risk) → B (beginning, warm) → C (classic shock, needs drugs) → D (deteriorating despite drugs) → E (extremis/arrest). Contemplate MCS at C, institute by D. Higher stages carry exponentially higher mortality; the goal of MCS is to prevent progression to irreversible end-organ injury. Each step up roughly doubles mortality risk.[6]
The cardiac index / PCWP pair drives MCS decisions. Aim for CI >2.2 L/min/m² and PCWP <18 mmHg. A PA catheter (or PiCCO) is invaluable in shock — distinguishes LV (high PCWP, low CI) from RV (high RA, low PCWP) failure and guides weaning. Vasopressors raise SVR and PCWP; inotropes raise CI but may worsen arrhythmia/ischaemia — escalating doses are themselves a trigger for MCS.[10]
ECPELLA (VA-ECMO + Impella) for profound biventricular failure with LV distension. Combines full systemic flow + oxygenation (ECMO) with active LV unloading (Impella). Indicated when VA-ECMO alone causes LV distension/pulmonary oedema. Observational data suggest better unloading and trend to improved survival vs ECMO alone — no RCT yet. Requires dual femoral access and dual anticoagulation vigilance.[7]
Anticoagulation monitoring and HIT. All MCS devices require systemic anticoagulation (typically UFH). Target ACT: IABP 150–180 s, Impella 160–180 s, VA-ECMO 180–220 s. HIT (heparin-induced thrombocytopenia) occurs in 2–5% — monitor platelets every 2–3 days; if >50% fall, switch to direct thrombin inhibitor (bivalirudin, argatroban). Bleeding remains the leading cause of device-related morbidity.[8]
Neurological complications are devastating and under-recognised. Ischaemic stroke (thromboembolism from circuit/LV stasis), intracranial haemorrhage (anticoagulation + reperfusion), and seizures. Daily neurological exam; if sedated, consider continuous EEG. Any sudden rise in inotrope/vasopressor need or unexplained lactate rise → think thrombosis (pump thrombosis, circuit clot) vs bleeding.[8]
Recognise pump thrombosis and circuit clot early. Signs: rising haemolysis (LDH, plasma-free Hb), falling device flow, rising lactate despite stable flow, visible clot in circuit/oxygenator, rising anticoagulation requirement. Management: increase anticoagulation, exchange circuit/device; exclude LV stasis thrombus on echo. Prophylaxis: therapeutic anticoagulation, avoid flow interruptions.[9]
Bridge-to-decision is the most common strategy in modern practice. Most MCS is temporary — the goal is to buy time: (a) Bridge to recovery (myocarditis, stunning) — wean; (b) Bridge to durable LVAD or transplant; (c) Bridge to decision — stabilise, then assess candidacy. Up to 30–50% of refractory shock patients survive to discharge with timely MCS; futility (irreversible brain injury, multi-organ failure, non-candidacy for definitive therapy) should be openly assessed with palliative care involvement.[7]

Red flags

Critical MCS red flags — recognise and act

Refractory shock despite escalating inotropes/vasopressors (SCAI C–D) → early MCS (before irreversible organ damage); do not wait for Stage E.[7]
Cold, mottled, painful limb with absent Doppler signals (Impella/VA-ECMO) → ischaemia — insert/check distal perfusion cannula immediately, vascular surgery review.[8]
Sudden bleeding or falling haemoglobin (anticoagulation) → balance thrombosis vs bleeding; reduce heparin, transfuse, search source (groin, GI, intracranial).[8]
IABP/Impella in moderate-severe aortic regurgitation → CONTRAINDICATED (worsens regurgitation / LV distension).[1][9]
Rising PCWP + pulmonary oedema + closed aortic valve on echo during VA-ECMO → LV distension — urgent LV venting (Impella, IABP, PA vent).[7]
Differential cyanosis (desaturated right radial / cerebral NIRS, pink lower body) on peripheral VA-ECMO → Harlequin syndrome — improve lung oxygenation, switch to central or V-AV ECMO.[8]
Tea-coloured urine + rising LDH/plasma-free Hb → haemolysis (Impella/ECMO) — check device position, optimise flow, transfuse; consider exchange.[9]
Falling device flow + rising lactate + visible clot → pump/circuit thrombosis — escalate anticoagulation, exchange circuit/device.[9]
Sudden neurological change or unexplained rise in vasopressors → stroke (ischaemic or haemorrhagic) or thrombosis — CT brain, image circuit.[8]
ECPR for refractory arrest — best outcomes if witnessed, <30 min low-flow, reversible cause; early cannulation during ongoing CPR.[11]
Gross haematuria/urea rising without other cause on VA-ECMO → renal vein congestion from high CVP/LV distension, or renal hypoperfusion from differential hypoxaemia.[8]

Prognosis and key trials

IABP-SHOCK II (Thiele 2012, NEJM) + 6-year follow-up (Circulation 2019)

RCT: 600 patients with acute MI + cardiogenic shock (planned early revascularisation). IABP vs no IABP.

30-day mortality: IABP 39.7% vs no IABP 41.3% (RR 0.96, p=0.69 — NO significant difference)
12-month mortality: IABP 52% vs no IABP 51% (no difference)
6-year all-cause mortality: ~57% both arms (no late emergence of benefit)
Secondary outcomes: no difference in complications, ICU stay, quality of life
CONCLUSION: Routine IABP does NOT improve outcomes in AMI cardiogenic shock (ESC Class III). Use selectively — mechanical complications of MI, bridge to surgery, refractory ischaemia.[1][2]

DanGer-SHOCK (Møller 2024, NEJM) — FIRST positive RCT for Impella

RCT: 360 patients with STEMI complicated by cardiogenic shock (LVEF ≤40%), randomised to Impella CP + standard care vs standard care alone.

Primary endpoint — all-cause mortality at 180 days: 45.8% (Impella) vs 58.5% (control), HR 0.74 (95% CI 0.55–0.99), p=0.04 — significant
Composite safety endpoint (severe bleeding, limb ischaemia, haemolysis, device failure, worsening AR, need for RRT): 24.0% (Impella) vs 6.2% (control) — more complications
CONCLUSION: Routine early Impella CP in STEMI-CS with reduced EF improved 180-day survival. The benefit must be weighed against higher device-related complication rates. Practice-changing for STEMI-CS with low EF; less applicable to non-ischaemic or very severe (Stage E) shock.[3]

ECLS-SHOCK (Thiele 2023, NEJM) — VA-ECMO negative in AMI-CS

RCT: 420 patients with AMI-CS, randomised to early VA-ECMO + standard care vs standard care alone.

Primary endpoint — 30-day all-cause mortality: 47.8% (ECMO) vs 49.0% (control), RR 0.98 (95% CI 0.75–1.13), p=0.70 — NO significant difference
Complications: more moderate/severe bleeding (23.4% vs 9.6%), more vascular complications requiring surgery (11.0% vs 3.6%), more RRT (29.7% vs 21.4%) in ECMO arm
CONCLUSION: Routine early VA-ECMO did not improve 30-day mortality in AMI-CS. Caveats: heterogeneous shock severity (many milder), no protocolised LV venting, crossover 4%. ECMO remains indicated for biventricular failure, hypoxaemia, ECPR, and refractory Stage D–E shock — not a reflex for all AMI-CS.[5]

IMPRESS in severe shock (Ouweneel 2017, JACC)

RCT: 48 patients with severe AMI-CS (lactate >8 mmol/L, often post-arrest), Impella CP vs IABP.

30-day mortality: 66% (Impella) vs 47% (IABP), p=0.27 — no significant difference
CONCLUSION: No benefit (and non-significant harm signal) of Impella in very severe AMI-CS. Likely reflects that unloading alone is insufficient in extremis — supports earlier (Stage C–D) deployment rather than waiting for Stage E. Small sample limits conclusions.[4]

Overall outcomes by device (observational + trial data):

IABP: no mortality benefit in AMI-CS (IABP-SHOCK II); useful selectively.
Impella: DanGer-SHOCK shows survival benefit in STEMI-CS with reduced EF when used early; IMPRESS negative in severe shock — timing matters.
VA-ECMO: ECLS-SHOCK negative in broad AMI-CS; observational survival to discharge 30–50% in refractory cardiogenic shock (higher if early, reversible cause, single-organ failure).
ECPR: 20–30% survival to discharge in refractory cardiac arrest (Cochrane 2023 — low-certainty evidence; selection bias concerns); best if witnessed, early cannulation, reversible cause.
Bridge to durable therapy: up to 30–50% of refractory shock patients survive to discharge with timely MCS; durable LVAD/transplant candidacy must be assessed early.[7][10][11]

References

[1]Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock N Engl J Med, 2012.PMID 22920912
[2]Thiele H, Akin I, Sandri M, et al. Intraaortic Balloon Pump in Cardiogenic Shock Complicating Acute Myocardial Infarction: Long-Term 6-Year Outcome of the Randomized IABP-SHOCK II Trial Circulation, 2019.PMID 30586721
[3]Møller JE, Engstrøm T, Jensen LO, et al. Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock N Engl J Med, 2024.PMID 38587239
[4]Ouweneel DM, Eriksen E, Sjauw KD, et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction J Am Coll Cardiol, 2017.PMID 27810347
[5]Thiele H, Zeymer U, Akin I, et al. Extracorporeal Life Support in Infarct-Related Cardiogenic Shock N Engl J Med, 2023.PMID 37634145
[6]Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock: This document was endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019 Catheter Cardiovasc Interv, 2019.PMID 31104355
[7]Lüsebrink E, Binzenhöfer L, Adamo M, et al. Cardiogenic shock Lancet, 2024.PMID 39550175
[8]Nakata J, Yamamoto T, Saku K, et al. Mechanical circulatory support in cardiogenic shock J Intensive Care, 2023.PMID 38115065
[9]Masiero G, Arturi F, Panza A, et al. Mechanical Circulatory Support with Impella: Principles, Evidence, and Daily Practice J Clin Med, 2024.PMID 39200728
[10]Sarma D, Jentzer JC. Cardiogenic Shock: Pathogenesis, Classification, and Management Crit Care Clin, 2024.PMID 37973356
[11]Burrell A, Kim J, Alliegro P, et al. Extracorporeal membrane oxygenation for critically ill adults Cochrane Database Syst Rev, 2023.PMID 37750499