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Chapter 11 — VA ECMO: Indications and Patient Selection

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Chapter question: Who should be put on VA ECMO — and on what basis, now that four randomised trials have failed to show benefit?

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Evidence search date: 6 September 2026. This chapter opens Part III, and unlike Part II it rests on a randomised evidence base — one that is almost entirely negative. Primary sources: ECMO-CS (2022), ECLS-SHOCK (2023), the Zeymer individual-patient-data meta-analysis (2023) and the Thiele mechanical-circulatory-support individual-patient-data meta-analysis with 6-month follow-up (2024), supplemented by ELSO Red Book Ch 27, the ISCCM Manual and ECPR and Resuscitative ECMO.

What this chapter covers — and what it does not

This chapter owns

Deferred to

What the randomised evidence actually shows and what it did not test; ECMO-responsive versus ECMO-unresponsive shock; SCAI staging as a selection tool; the indication list organised by reversibility; contraindications; prognostic markers at initiation; the questions to answer before cannulating

Cannulation technique → Chapter 12 VA haemodynamics, afterload and mixing → Chapter 13 Initial VA management → Chapter 14 LV distension and unloading → Chapter 15 Differential hypoxaemia → Chapter 16 Limb ischaemia and vascular complications → Chapter 17 VA weaning and decannulation → Chapter 18 ECPR principles and ECPR patient selection → Chapters 19–20 Ethics, futility and withdrawal → Part XI

11.1 Why this chapter is different from Chapter 4

Chapter 4 asked who should receive VV ECMO. It could draw on CESAR and EOLIA — trials that, whatever their limitations, pointed towards benefit in selected patients and which underpin guideline thresholds still in use.

Part III opens on different ground. Four randomised trials and two individual-patient-data meta-analyses have now tested VA ECMO in infarct-related cardiogenic shock, and none has shown a mortality benefit. Every one of them has shown substantial harm from bleeding and vascular complications.

This creates an obligation. A chapter on VA ECMO indications written as though that literature did not exist would help clinicians make worse decisions. But a chapter concluding "VA ECMO does not work" would be an equally serious error, because the trials tested a narrow question in a narrow population, and much of what VA ECMO is actually used for was never studied.

The task is to hold both facts at once: the strategy of early, unselective VA ECMO in infarct-related cardiogenic shock has been tested and does not improve survival — and this tells us remarkably little about the myocarditis patient, the poisoned patient, or the patient with a massive pulmonary embolism in front of you tonight.

11.2 The randomised evidence

Study	Population and design	Primary result	Harms
ECMO-CS (2022) Ostadal et al., Circulation	122 randomised (58 versus 59 in the ITT analysis) across four Czech tertiary ICUs, 2014–2022. Severe or rapidly deteriorating cardiogenic shock, SCAI stage D or E. Immediate VA ECMO versus an early conservative strategy that permitted downstream ECMO	Composite of death, resuscitated cardiac arrest or another mechanical circulatory support at 30 days: 63.8% versus 71.2%, risk difference −7.4% (95% CI −24.3 to 9.5) — not significant. No difference in 30-day all-cause mortality	No significant difference in clinically significant bleeding, leg ischaemia, pneumonia or sepsis
ECLS-SHOCK (2023) Thiele et al., NEJM	417 in the ITT analysis. Acute myocardial infarction with cardiogenic shock undergoing revascularisation. Early VA ECMO plus usual care versus usual care alone	30-day all-cause mortality 48% versus 49%, relative risk 0.98 (95% CI 0.80 to 1.19), p = 0.81. No difference in poor neurological outcome, renal replacement therapy, repeat revascularisation, time to stabilisation, or ICU or hospital stay	Limb ischaemia requiring intervention 11% versus 4%; moderate or severe bleeding 23% versus 10%
Zeymer IPD meta-analysis (2023) Lancet	Four randomised trials, 567 patients (284 VA ECMO, 283 control), infarct-related cardiogenic shock	30-day death: OR 0.93 (95% CI 0.66 to 1.29). Prespecified subgroups consistent, with no benefit in any (p for interaction 0.079 or greater)	Major bleeding OR 2.44 (1.55–3.84); peripheral ischaemic vascular complications OR 3.53 (1.70–7.34)
Thiele MCS IPD meta-analysis, 6-month follow-up (2024) Lancet	Nine randomised trials, 1,114 patients, infarct-related cardiogenic shock, temporary mechanical circulatory support of all types	6-month mortality overall HR 0.87 (0.74–1.03), p = 0.10. Unloading devices HR 0.80 (0.62–1.02); loading devices HR 0.93 (0.75–1.17). One subgroup did show benefit: STEMI without risk of hypoxic brain injury, HR 0.77 (0.61–0.97), p = 0.024	Major bleeding increased 2.64-fold; vascular complications increased 4.43-fold

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Evidence — what this body of work establishes

The conclusions of the two meta-analyses are worth quoting as written. Zeymer and colleagues: "These data do not justify unselected use of VA-ECMO in patients with cardiogenic shock." Thiele and colleagues, a year later and with 6-month follow-up: "MCS use should only be reserved for selected patients, i.e., patients with STEMI and CS without risk of hypoxic brain injury."

Certainty: high that early unselective VA ECMO does not reduce mortality in infarct-related cardiogenic shock. High that it increases major bleeding and peripheral vascular complications, by roughly two- to four-fold. Low for the STEMI-without-hypoxic-brain-injury subgroup signal — a subgroup finding from a pooled analysis, hypothesis-generating rather than practice-defining.

Note the direction of travel. The point estimates are not dramatically adverse: they cluster near unity with confidence intervals that do not exclude a modest benefit. What this evidence excludes is the large benefit that the physiological argument for VA ECMO has always implied.

11.3 What the trials did not test — and why it matters enormously

This section determines whether the evidence above is used well or badly.

11.3.1 The population was narrow

ECLS-SHOCK enrolled patients with acute myocardial infarction complicated by cardiogenic shock, with planned revascularisation. Its explicit exclusions are as informative as its inclusions: more than 45 minutes of CPR before enrolment; mechanical or non-cardiac causes of shock; shock onset more than 12 hours earlier; severe peripheral vascular disease; age over 80; life-limiting illness.

So the trials say nothing about the patients for whom many experienced clinicians consider VA ECMO most defensible:

Not tested	Why the reasoning may differ
Fulminant myocarditis	Typically a young patient with a genuinely self-limiting insult and a high probability of complete myocardial recovery — the paradigm of a reversible bridge
Drug overdose or poisoning with cardiac depression	The toxin is cleared or metabolised on a knowable timescale; the heart is otherwise normal
Massive pulmonary embolism	An obstructive, mechanically reversible lesion; support buys time for thrombolysis, embolectomy or clot resolution
Refractory arrhythmic storm	Inotropes worsen the arrhythmia and antiarrhythmics worsen contractility — a bind that circulatory support resolves directly
Post-cardiotomy failure to wean from bypass	Anticipated, often transient myocardial stunning, in a fully monitored setting
Primary graft failure after transplantation	Frequently recovers; the alternative is loss of the graft
Accidental hypothermia with arrest	Rewarming on the circuit is itself the definitive treatment, with well-described good outcomes
Bridge to transplantation or durable device	The destination is not myocardial recovery at all, so a trial measuring recovery-mediated survival cannot assess it

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Danger — do not read "no benefit in infarct-related shock" as "no benefit"

Generalising these trials to fulminant myocarditis, or to a 30-year-old with beta-blocker overdose, is an error of the same kind as generalising EOLIA to every hypoxaemic patient. The populations differ in the one variable that matters most: the probability and timescale of reversibility.

The honest statement is narrower and more useful: in infarct-related cardiogenic shock, adding VA ECMO early and unselectively does not improve survival and does cause bleeding and limb ischaemia. Everything outside that sentence remains a zone in which physiological reasoning, reversibility and an exit strategy must carry the decision — and in which the absence of evidence should make you more careful, not more confident.

11.3.2 The comparison was a strategy, not a device

This is the most commonly missed point about all of these trials. Neither ECMO-CS nor ECLS-SHOCK compared ECMO with no ECMO. They compared early ECMO against conservative management that permitted rescue ECMO on deterioration.

In ECMO-CS, 39% of the control arm crossed over to VA ECMO; of those, 52.2% died.
In ECLS-SHOCK, 28 control patients crossed over to VA ECMO.

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Trial design — what crossover does to the question

With crossover of this magnitude, the trials answer: "is it better to cannulate everyone early, or to wait and cannulate those who declare themselves?" They cannot answer: "does ECMO save the life of a patient who would otherwise die?" — because the patients most likely to be saved by it received it in both arms.

The result is therefore compatible with two very different truths: that ECMO helps nobody, or that ECMO helps a specific subgroup who can be identified as they deteriorate, and that identifying them by waiting works as well as treating everyone. These trials cannot distinguish between those, and honest practice has to say so.

What they do establish decisively is the cost side: cannulating everybody early buys a great deal of bleeding and limb ischaemia, and does not pay for it in survival.

11.3.3 The resulting stance

VA ECMO should be a considered, selective decision about an individual patient with a reversible or bridgeable problem — not a protocolised early response to a shock syndrome. The burden of proof sits with initiation, and the question "what is this a bridge to?" must have an answer before cannulation, not after.

11.4 Is this shock ECMO-responsive?

Before staging severity, establish mechanism. The ECPR literature frames this well: the practitioner should be looking for three ECMO-responsive shock aetiologies — cardiogenic shock, rhythm instability, and massive pulmonary embolism. All three produce a low cardiac output state that a pump can rescue.

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Danger — vasodilatory shock is not ECMO-responsive

The source is explicit: patients with distributive shock from sepsis "have far less to gain and possibly experience significant harm from ECMO initiation." Resuscitative VA ECMO is described as not beneficial in vasodilatory shock.

The physiology is straightforward. VA ECMO substitutes for a failing pump. In vasodilatory shock the pump is not the problem — cardiac output is normal or high and systemic vascular resistance has collapsed. Adding a pump to a circuit whose resistance is the failure point does not correct the lesion, and it imposes every one of ECMO's costs.

The exception that proves the rule is sepsis with profound myocardial depression — a genuinely low-output state that happens to be caused by sepsis. That is cardiogenic shock in mechanism, and it is on the indication list below. Distinguishing the two is an echocardiographic and cardiac-output question, not a syndromic one.

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Clinical pearl — echocardiography is the selection instrument

The ECPR text puts echocardiography at the centre of this decision: "Shock states can mimic each other, and inaccurate determination can be to the detriment of the patient." A formal study may not be possible in the time available, and a bedside study by a competent non-cardiologist is described as sufficient — studies have shown that bedside echocardiography yields accurate assessment of low ejection fraction in non-cardiology practitioners.

Add a measure of cardiac output where possible. The most accessible is central venous oxygen saturation from an upper-body central line — low ScvO₂ with a low-output picture supports an ECMO-responsive state; high ScvO₂ with vasoplegia argues against it.

11.5 SCAI staging — how sick, and is that the reason to cannulate?

The Society for Cardiovascular Angiography and Interventions consensus stratifies cardiogenic shock from A to E, and validation studies show worsening outcomes with more profound shock.

Stage	Features	In-hospital mortality
A — At risk	No signs or symptoms of shock; normal laboratory values, blood pressure and cardiac output	3%
B — Beginning	Hypotension (systolic under 90 mmHg) or tachycardia (over 100/min), without hypoperfusion; normal lactate and cardiac output	7.1%
C — Classic	Hypoperfusion requiring inotropes or vasopressors; cool, dusky or mottled extremities; raised lactate, raised transaminases, or creatinine twice baseline; cardiac index below 2.2 despite pharmacological therapy	12.4%
D — Deteriorating	Stage C features persisting beyond 30 minutes and requiring additional inotropes, vasopressors or mechanical support to maintain perfusion	40.4%
E — Extremis	Cardiac arrest, refractory ventricular arrhythmias, or hypotension despite maximal support	67%

Source: SCAI stages as reproduced in ECPR and Resuscitative ECMO, Table 1. Mechanical support is most commonly indicated in stages C, D and E.

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Pitfall — a severity score is not an indication

SCAI staging tells you how likely this patient is to die. It does not tell you whether ECMO will change that. These are different questions, and conflating them is the central selection error in VA ECMO.

Note what the trials did here. ECMO-CS enrolled exactly the sick end — SCAI D and E — and found no benefit. The Thiele meta-analysis found its only positive signal in a subgroup defined not by severity but by substrate: STEMI without risk of hypoxic brain injury. Severity earned nothing; reversibility and an intact brain earned something.

Use SCAI to describe the patient, to communicate with colleagues, and to trigger the conversation. Do not use it as the reason.

11.6 The indication list, organised by what you are bridging to

The ISCCM manual's indication list is reproduced below, reorganised around the question that actually governs the decision.

Bridge to what?	Indications
Bridge to recovery — the insult is self-limiting or treatable, and the myocardium is expected to recover	Myocarditis; drug overdose or toxicity with profound cardiac depression; sepsis with profound cardiac depression; acute anaphylaxis; cardiac dysrhythmic storm refractory to other measures; isolated cardiac trauma; post-cardiotomy inability to wean from cardiopulmonary bypass; primary graft failure after heart or heart–lung transplantation
Bridge to a procedure — support spans a definitive intervention	Acute coronary syndrome (spanning revascularisation); pulmonary embolism (spanning thrombolysis, embolectomy or clot resolution); periprocedural support for high-risk percutaneous cardiac intervention
Bridge to a longer-term device or transplant	Chronic cardiomyopathy as a bridge to durable ventricular assist device support; bridge to transplantation
Bridge to decision — the destination is genuinely not yet known	Chronic cardiomyopathy where candidacy for advanced therapies is unresolved

Indication list from the ISCCM Manual of RRT and ECMO in ICU; the bridge-based organisation is this book's.

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Danger — "bridge to decision" is the category that gets abused

It is a legitimate indication, and it is also the one under which patients drift into the position Chapter 8 warned about: a bridge to nowhere, reached gradually across a fortnight of individually reasonable daily decisions.

The ISCCM manual is unusually candid about this: "basic principles of reversibility and exit strategies should never be forgotten," and "as you do more cases, you will realize that you can never be too careful." It names what follows when selection fails — hypoxic ischaemic encephalopathy, fear of a vegetative state, and an emotional and resource burden borne by the family and the team.

If you cannot name the decision, the person who will make it, and the date by which it will be made, you do not have a bridge to decision. You have a bridge to nowhere with better branding.

11.7 Contraindications

Contraindications to ECLS initiation for cardiac failure in adults

Cardiac recovery unlikely and no indication for heart transplant or durable LV assist device

Poor life expectancy — end-stage peripheral organ disease, malignant tumour, massive pulmonary emboli in cancer patients, chemotherapy-induced chronic cardiomyopathy

Severe aortic valve regurgitation

Severe vascular disease with extensive aortic and peripheral vessel involvement (calcification, stenosis, occlusion), including the axillary arteries

Acute type A or type B aortic dissection with extensive aortic branch involvement (ascending, supra-aortic and femoral), pre-operatively

Severe neurological impairment — for example prolonged anoxic brain damage, extensive trauma and bleeding

Severe immunological disease with marked blood and coagulation disorders

Liver cirrhosis, Child–Pugh class B and C

Source: ELSO Red Book 6th ed., Table 27-1, adapted there from Lorusso et al.

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Physiology — why severe aortic regurgitation is on that list

It is the one entry that looks out of place to anyone who has not thought about VA physiology, and it is worth understanding rather than memorising.

Peripheral VA ECMO returns blood retrogradely up the descending aorta, pressurising the aortic root against a left ventricle that is already failing. With a competent aortic valve, this raises LV afterload — the mechanism behind LV distension (Chapter 15). With an incompetent valve, the retrograde flow regurgitates straight back into the left ventricle. The circuit then fills the ventricle it is supposed to be supporting, and forward flow across the valve falls further.

The consequence is rapid ventricular distension, pulmonary oedema and pulmonary haemorrhage. This is the reason the ELSO Red Book states that aortic regurgitation should be addressed at the escalation stage rather than discovered afterwards — and the reason echocardiography before cannulation is not optional.

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Evidence — a prognostic marker at initiation

The Red Book reports that arterial lactate of 10 mmol/L or more at ECLS initiation, and its delayed clearance over the first 12–24 hours, identifies patients with poor outcomes.

Read this as a prognostic marker, not a contraindication threshold. A lactate of 11 mmol/L in a hypothermic drowning victim or a poisoned patient does not mean the same thing as a lactate of 11 mmol/L in a 78-year-old with an infarct and a failed revascularisation. Certainty: low — an observational association, cited by the Red Book to references not retrieved here.

For context on what the therapy achieves overall: the ELSO Registry reports that 44% of patients receiving ECMO for cardiac support are discharged from hospital alive.

11.8 Five questions to answer before cannulating

Chapter 4 closed with three questions for VV. VA requires five, because the failure modes are worse and the evidence is weaker.

Is this shock ECMO-responsive? A low-output state from cardiogenic shock, rhythm instability or massive pulmonary embolism — confirmed on echocardiography, not inferred from the syndrome. If it is vasoplegia, the answer is no.
What is the bridge to, and by when? Recovery, procedure, durable device, transplant, or a named decision with a named decision-maker and a date. "We will see how they go" is not an answer.
Is there a contraindication? Aortic regurgitation, aortic dissection, severe peripheral vascular disease, established anoxic brain injury, and the absence of both recovery potential and advanced-therapy candidacy.
Would this patient have been eligible for the trials — and if so, does their result apply? If this is infarct-related cardiogenic shock in a patient who resembles the ECLS-SHOCK population, the honest position is that early cannulation has been tested and does not improve survival. That should raise the threshold, not be ignored.
Can this centre deliver it? Cannulation, 24-hour circuit expertise, vascular surgical backup, transfusion support, and the ability to run the difficult conversation in a week's time if none of this works.

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Clinical pearl — the timing tension is real and unresolved

Two true statements sit in opposition. The ECPR text observes that outcomes for ECMO started for cardiogenic shock differ significantly from ECMO started during cardiac arrest, so the timing of support in the decompensating patient is critical — an argument for acting before arrest. Against that, the randomised evidence shows early unselective cannulation does not help and does harm.

The resolution is not a time threshold. It is that early is better than late for patients who should receive ECMO at all, and the trials' failure is a failure of selection, not of speed. Decide who, carefully; then move quickly.

11.9 Controversies

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Controversy 1 — Should VA ECMO still be offered in infarct-related cardiogenic shock at all?

The question. Four randomised trials and two individual-patient-data meta-analyses show no mortality benefit and consistent harm. Is continued use in this specific population defensible?

The case for stopping. This is not a single underpowered trial but a coherent body of randomised evidence with concordant point estimates, consistent subgroups, and quantified harm — bleeding roughly 2.4 to 2.6-fold, vascular complications 3.5 to 4.4-fold. In most areas of medicine this would end the practice. Continuing to offer an expensive, invasive, harmful therapy on physiological reasoning after it has failed randomised testing is precisely the pattern that has repeatedly embarrassed critical care.

The case for continuing, selectively. The trials tested a strategy of early unselective use against conservative care with rescue ECMO available — and 39% of ECMO-CS controls and 28 ECLS-SHOCK controls crossed over. A trial in which a large fraction of controls receive the intervention cannot demonstrate that the intervention is useless; it can only show that giving it to everyone early is no better than giving it to those who declare themselves. Some patients in both arms plainly survived because of it.

What the evidence actually shows. No benefit from early unselective use; real and quantified harm; one hypothesis-generating subgroup (STEMI without risk of hypoxic brain injury, HR 0.77, 0.61–0.97). Certainty: high for the primary conclusion, low for the subgroup.

Where practice actually sits. Most experienced centres have not abandoned VA ECMO in this population but have raised the threshold, moved away from protocolised early cannulation, and now use it as rescue in patients deteriorating despite optimal care — which is, notably, close to what the control arms of these trials actually did.

What would resolve it. A trial of ECMO versus genuinely no ECMO would answer the question and is not ethically feasible. The realistic path is trials targeting the subgroups the pooled analysis identified, and better real-time markers of who is deteriorating irreversibly.

This book's position. Continue to offer it in this population, but as a rescue decision in a selected, deteriorating patient, never as a protocolised early response — and tell families the truth about what the randomised evidence shows.

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Controversy 2 — Is severity or substrate the right basis for selection?

The question. Should the decision be driven by how sick the patient is (SCAI stage, lactate, vasoactive requirement) or by what is wrong with them (the reversibility of the underlying lesion)?

The case for severity. It is measurable, reproducible, communicable, and mortality rises steeply across SCAI stages — from 12.4% at stage C to 67% at stage E. Severity identifies who will die without something changing, which is a necessary condition for benefit.

The case for substrate. Necessary is not sufficient. A patient dying of an unrecoverable myocardium is not helped by a pump, however sick they are; a patient dying of a clearing toxin is helped enormously. Substrate determines whether the bridge has a far bank.

What the evidence actually shows. This is the striking thing. ECMO-CS selected on severity — SCAI D and E — and found nothing. The 2024 pooled analysis found its only positive signal in a subgroup defined by substrate and neurological integrity: STEMI without risk of hypoxic brain injury. Severity-based selection has been tested and failed; substrate-based selection has never been formally tested at all. Certainty: moderate that severity alone is insufficient; very low on any specific substrate-based rule.

Where practice actually sits. Most centres use both, informally and without a framework: severity to trigger the conversation, substrate and comorbidity to decide. The framework in §11.8 makes that explicit.

What would resolve it. Trials enrolling by aetiology rather than by shock severity — myocarditis, poisoning, pulmonary embolism. These are small populations and such trials are hard, which is why the evidence-free zone in §11.3.1 is likely to persist.

The transferable lesson. Severity tells you the patient may die. Only substrate tells you whether ECMO changes that. Prognosis is not indication.

11.10 The errors that recur in VA selection

Error	Correction
Cannulating because the patient is very sick	Severity is not indication. Ask what the bridge is to (§11.8)
Treating the negative trials as proof that VA ECMO does not work	They tested early unselective use in infarct-related shock, with heavy crossover. Most VA indications were never studied
Treating the negative trials as irrelevant because "our patients are different"	If the patient resembles the trial population, the result applies and should raise your threshold
Cannulating vasodilatory shock	A pump does not fix a resistance problem. Echocardiography and ScvO₂ distinguish them
Not looking for aortic regurgitation before cannulation	Retrograde flow regurgitates into the ventricle it is meant to support — rapid distension and pulmonary oedema
Using "bridge to decision" without a decision, a decision-maker or a date	That is a bridge to nowhere. Name all three at the outset
Quoting the STEMI subgroup as justification	It is one subgroup in a pooled analysis — hypothesis-generating, not practice-defining

11.11 Key points

Four randomised trials and two pooled analyses show no mortality benefit from early unselective VA ECMO in infarct-related cardiogenic shock, with major bleeding raised roughly 2.4–2.6-fold and vascular complications 3.5–4.4-fold.
The trials compared strategies, not devices. Heavy crossover (39% in ECMO-CS) means they cannot show that ECMO saves no one — only that treating everyone early is no better than rescuing those who declare themselves.
Most VA indications were never tested: myocarditis, poisoning, pulmonary embolism, arrhythmic storm, post-cardiotomy failure, graft failure, hypothermia, and bridging to transplant or durable device.
Establish mechanism before severity. Cardiogenic shock, rhythm instability and massive pulmonary embolism are ECMO-responsive; vasodilatory shock is not, and may be harmed.
Echocardiography is the selection instrument, and a competent bedside study is sufficient when time is short. Add ScvO₂ from an upper-body line.
SCAI staging describes prognosis, not indication. Selection on severity has been tested and failed; the one positive subgroup was defined by substrate and neurological integrity.
Severe aortic regurgitation is a contraindication because retrograde return regurgitates into the failing ventricle. Look for it before cannulating, not after.
Lactate of 10 mmol/L or more at initiation, with delayed clearance, marks poor outcome — prognostic information, interpreted against the substrate.
The ELSO Registry reports 44% survival to hospital discharge for cardiac ECMO overall.
Name the bridge before you cannulate. If you cannot name the destination, the decision-maker and the date, you do not have an indication.
The failure in these trials was selection, not speed. Decide who carefully; then move quickly.

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[VERIFICATION REQUIRED] — open items in this chapter

ECLS-SHOCK, ECMO-CS and both meta-analyses were read through secondary summaries (The Bottom Line and the American College of Cardiology journal scans), not from the primary articles, because NEJM, Lancet, Circulation and ScienceDirect are all inaccessible from this environment. Every number quoted is reproduced as those summaries state it. The DOIs given are as reported there.
ECLS-SHOCK: the full author list beyond the first author, the exact volume and page numbers, and the precise definitions of the bleeding and limb-ischaemia endpoints have not been verified.
ECMO-CS: the 1-year follow-up publication exists and has not been retrieved; its results are not reflected here.
Zeymer 2023: the four constituent trials are not individually named in the summary read, so the trial list is not stated here. Volume, pages and DOI unverified.
Thiele 2024: the nine constituent trials, and the exact device categorisation behind the "loading" and "unloading" split, were not verified. The summary's description of the 611/503 split and its statement that IABP and microaxial pumps were not specifically compared appear internally inconsistent with a nine-trial pooled analysis, so the device breakdown should be checked against the primary before being quoted elsewhere. The headline hazard ratios are reproduced as given.
SCAI stage mortality figures (3%, 7.1%, 12.4%, 40.4%, 67%) are reproduced from the ECPR text's table, which cites its own sources; those were not retrieved, and no population or era is stated.
The lactate 10 mmol/L marker and the 44% ELSO Registry cardiac survival figure are both cited by their textbooks to references not retrieved; the registry figure has no stated year.
No VA instalment of the ANZ GRADE guideline series was found on searching. ELSO's adult cardiac guidance dates from August 2021 and therefore predates every trial in §11.2 — it cannot be relied on for this question.
The Formica haemodynamic criteria for diagnosing cardiogenic shock appear in the ISCCM manual and were reviewed but not used in this chapter, as the trials' own inclusion criteria are more current and better specified.

Cross-references

Chapter 3 — ECMO Configurations: VA configurations, the aortic mixing zone, and V-VA hybrids
Chapter 4 — VV ECMO: Indications and Patient Selection: the parallel chapter for respiratory failure, and the contrast in evidence quality
Chapter 12 — VA ECMO Cannulation
Chapter 13 — VA ECMO Haemodynamics: afterload, the mixing point, and why the pump changes loading conditions
Chapter 15 — LV Distension and LV Unloading: the consequence of the afterload physiology introduced in §11.7
Chapter 16 — Differential Hypoxaemia / Harlequin Syndrome
Chapter 17 — Limb Ischaemia and Vascular Complications: the harm quantified in §11.2
Chapter 18 — VA ECMO Weaning and Decannulation: and the warning that the sweep gas off trial of Chapter 10 must never be used here
Chapters 19–20 — ECPR: patient selection where the presentation is arrest rather than shock
Part XI — Ethics and Palliative Care: the bridge to nowhere, and the conversation that §11.6 makes unavoidable

References

Ostadal P, et al. Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock: Results of the ECMO-CS Randomized Clinical Trial. Circulation. 2022. DOI: 10.1161/CIRCULATIONAHA.122.062949. [VERIFICATION REQUIRED] — read via secondary summary; full author list, volume and pages unverified.
Thiele H, et al. Extracorporeal Life Support in Infarct-Related Cardiogenic Shock (ECLS-SHOCK). N Engl J Med. 2023. DOI: 10.1056/NEJMoa2307227. [VERIFICATION REQUIRED] — read via secondary summary; full author list, volume and pages unverified.
Zeymer U, Freund A, Hochadel M, et al. Venoarterial extracorporeal membrane oxygenation in patients with infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials. Lancet. 2023. [VERIFICATION REQUIRED] — read via secondary summary; volume, pages and DOI unverified; constituent trials not named.
Thiele H, Møller JE, Henriques JP, et al., on behalf of the MCS Collaborator Scientific Group. Temporary mechanical circulatory support in infarct-related cardiogenic shock: an individual patient data meta-analysis of randomised trials with 6-month follow-up. Lancet. 2024. [VERIFICATION REQUIRED] — read via secondary summary; volume, pages and DOI unverified; constituent trials and device categorisation not verified.
Extracorporeal Life Support: The ELSO Red Book, 6th edition, Chapter 27, Initiating Extracorporeal Life Support for Adult Cardiac Failure (including Table 27-1, contraindications, adapted there from Lorusso et al.) and Chapter 44 (escalation criteria). Contraindications; lactate at initiation; escalation reasoning; aortic regurgitation to be addressed at escalation.
Shinar Z, Badulak J, eds. ECPR and Resuscitative ECMO, Chapter 13. ECMO-responsive versus unresponsive shock states; the role of echocardiography and ScvO₂; SCAI staging table with in-hospital mortality; ELSO Registry cardiac survival; timing of support.
ISCCM Manual of RRT and ECMO in ICU. Indian Society of Critical Care Medicine. VA ECMO indication list; contraindications; reversibility and exit strategy as governing principles. [VERIFICATION REQUIRED] — edition, editors, year and page numbers not confirmed.

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Chapter status

Drafted and audited 6 September 2026. Ten-pass quality control completed: clinical, physiology, evidence, citation, numerical, safety, contradiction, redundancy, bedside utility and literature-currency passes.

This chapter opens Part III — VA ECMO. Unusually for this book, its central evidence is randomised and negative, and the chapter's main work is to state that accurately while resisting two opposite misreadings. All four trials were read through secondary summaries because the primary journals are inaccessible from this environment; that limitation is declared above rather than concealed, and every figure is reproduced as the summary stated it. No citation, threshold or effect estimate has been reconstructed from memory.