Central VA-ECMO #3: ECMO Initiation and Maintenance

1. Introduction

Initiation of central venoarterial extracorporeal membrane oxygenation (VA-ECMO) is a controlled transition from native cardiopulmonary circulation to partial or predominantly mechanical circulatory support. The objective is not simply to reach the highest achievable circuit flow, but to restore adequate systemic oxygen delivery while minimizing adverse ventricular loading and preserving appropriate native cardiac ejection whenever possible.

A practical initiation sequence is to start ECMO at low flow, increase support progressively according to systemic perfusion requirements, and continuously assess native cardiac output through arterial pulsatility and echocardiographic aortic-valve opening.

Importantly, the available literature does not establish a validated postcardiotomy-specific protocol defining the exact starting flow, rate of escalation, or universal “100% flow” target for central VA-ECMO. Flow must therefore be individualized according to systemic perfusion, oxygen delivery, residual cardiac function, vascular resistance, and ventricular loading conditions.

2. Start at Low Flow and Increase Gradually

Once the venous and arterial cannulas have been secured, de-aired, and connected to the circuit, ECMO should be initiated at relatively low flow and increased progressively.

Gradual escalation allows the surgical, perfusion, anesthesia, and intensive-care teams to assess simultaneously:

• Adequacy of venous drainage
• Stability and position of the arterial return cannula
• Systemic arterial pressure
• Native arterial pulsatility
• Ventricular size and function
• Aortic-valve opening
• Pulmonary venous congestion
• Surgical bleeding
• Circuit pressures and oxygenator performance

This approach is particularly important immediately after cardiopulmonary bypass, when myocardial contractility, circulating volume, systemic vascular resistance, pulmonary vascular resistance, and vasoplegia may change rapidly.

Although the teaching concept of progressing toward “full” or approximately 100% ECMO flow is useful, full flow should be interpreted physiologically rather than as a predetermined pump setting. The appropriate circuit flow is the amount of support required to restore systemic oxygen delivery while avoiding unnecessary increases in ventricular afterload or other complications.

3. Native Cardiac Output and ECMO Flow Are Interdependent

During VA-ECMO, systemic blood flow consists of two interacting components:

Native cardiac output + ECMO-generated systemic flow

However, these components are not independent. Increasing ECMO flow changes the loading conditions of the heart and can therefore reduce native cardiac output.

Greater venous drainage decreases systemic venous blood entering the right heart. This reduces right ventricular preload, pulmonary blood flow, pulmonary venous return, and ultimately LV preload. Conversely, inadequate venous drainage or excessive volume administration can increase cardiac filling and contribute to ventricular distension.

At the same time, arterial ECMO return increases systemic arterial pressure and therefore the pressure against which the LV must eject. Experimental and modeling studies demonstrate that increasing arterial pressure during VA-ECMO can increase LV volume when myocardial contractility is severely impaired, while increased afterload can reduce stroke volume and native ejection [1,2].

Much of the literature describes this phenomenon in peripheral VA-ECMO, where arterial flow travels retrogradely through the aorta. Central VA-ECMO differs because oxygenated blood is returned directly into the ascending aorta in an antegrade direction. Nevertheless, central arterial return can still increase aortic pressure and therefore LV afterload. The interaction among ECMO flow, venous drainage, preload, aortic pressure, and native contractility must therefore be considered together rather than treating pump flow as an isolated variable [2,3].

4. Titrate Flow According to Systemic Perfusion

The initial objective of VA-ECMO is restoration of effective systemic perfusion and oxygen delivery.

Circuit flow should therefore be increased only as necessary to achieve appropriate physiologic endpoints. Important parameters include:

Mean arterial pressure

MAP provides an immediate measure of systemic perfusion pressure but does not independently establish adequate blood flow.

Low MAP despite high ECMO flow may indicate vasoplegia, inadequate circulating volume, poor venous drainage, bleeding, or excessive systemic runoff. Conversely, excessive MAP may indicate increased systemic vascular resistance and can aggravate LV afterload.

Lactate

Serial lactate is useful for assessing the response to restoration of systemic oxygen delivery. A falling lactate generally supports improving tissue perfusion.

Persistent or rising lactate despite apparently satisfactory circuit flow should prompt assessment for inadequate effective systemic blood flow, anemia, regional ischemia, excessive systemic vasoconstriction, residual cardiovascular lesions, or increased metabolic demand.

Near-infrared spectroscopy

Cerebral and somatic NIRS provide continuous regional information and are particularly useful in neonatal and pediatric cardiac patients. Trends should be interpreted together with systemic hemodynamics rather than as isolated numerical targets.

Urine output and end-organ function

Urine output provides additional information regarding renal perfusion, although oliguria may persist after prolonged pre-ECMO shock despite restoration of circulation.

No single measurement reliably defines adequate ECMO support. MAP, lactate trajectory, NIRS, urine output, venous oxygen saturation when available, acid-base balance, capillary refill, temperature, and overall organ function should be integrated.

5. Continuously Assess Native Cardiac Ejection

As ECMO flow increases, native cardiac output frequently decreases because venous drainage reduces ventricular preload while arterial return may increase effective LV afterload.

Two particularly useful indicators of residual native ejection are:

1. Arterial-line pulsatility
2. Aortic-valve opening on echocardiography

Pulse pressure provides a readily available bedside indicator of native stroke volume. Progressive loss of pulsatility may reflect reduced preload, deteriorating myocardial function, excessive afterload, or increasing dependence on ECMO.

Echocardiography provides more direct information. Assessment should include:

• Frequency and extent of aortic-valve opening
• LV end-diastolic and end-systolic dimensions
• Global and regional LV function
• Mitral-valve opening
• Left atrial size
• Ventricular septal position
• Spontaneous echo contrast
• Intracardiac thrombus
• Pericardial effusion or tamponade
• Cannula-related mechanical abnormalities

Persistent absence of aortic-valve opening is particularly important because it indicates minimal or absent forward LV ejection and may predispose to progressive LV distension and intracardiac stasis [3,4].

6. Why Aortic-Valve Opening Matters

Residual native ejection is valuable for several reasons.

First, aortic-valve opening provides LV and aortic-root washout. When the valve remains closed for prolonged periods, stagnant blood can accumulate in the LV cavity and aortic root, increasing the risk of spontaneous echo contrast and thrombus formation.

Second, forward ejection indicates that the LV can generate sufficient pressure to overcome aortic pressure and eject at least part of its filling volume.

Third, changes in pulsatility and valve opening may provide early evidence of myocardial recovery.

However, preservation of pulsatility is not itself the primary therapeutic goal. A patient with profound myocardial failure may temporarily require near-complete circulatory support. ECMO flow should not be reduced simply to generate a pulse if doing so compromises systemic oxygen delivery.

The clinically relevant question is whether the LV remains adequately decompressed and free of harmful pressure or volume accumulation.

7. VA-ECMO and LV Distension

LV distension develops when blood entering the left heart cannot be adequately ejected.

The fundamental sequence is:

Increased effective LV afterload → reduced native stroke volume → reduced or absent aortic-valve opening → increased residual LV volume and pressure → increased left atrial and pulmonary venous pressure → pulmonary congestion

VA-ECMO-associated LV overload can increase myocardial wall stress and oxygen consumption and may delay myocardial recovery. Severe cases may produce pulmonary edema, refractory ventricular arrhythmias, intracardiac blood stasis, and thrombus formation [2,3].

Potential warning signs include:

• Low or progressively decreasing pulse pressure
• Persistent aortic-valve closure
• Progressive LV enlargement
• Elevated left-sided filling pressures
• Increasing pulmonary artery or pulmonary capillary wedge pressure when measured
• Pulmonary edema or hemorrhage
• Worsening pulmonary opacification on chest radiography
• Spontaneous echo contrast
• LV, left atrial, or aortic-root thrombus
• Refractory ventricular arrhythmia

Published studies demonstrate substantial variability in the criteria used to trigger mechanical LV unloading. No universally validated threshold for pulse pressure, LV dimension, pulmonary capillary wedge pressure, or duration of aortic-valve closure has been established [4,5].

8. Responding to Loss of Native Ejection

Loss of pulsatility or aortic-valve opening should trigger systematic assessment rather than an automatic reduction in ECMO flow.

First, determine whether current ECMO flow is necessary to maintain adequate systemic perfusion. If organ oxygen delivery remains marginal, reducing circuit support solely to restore pulsatility may be harmful.

Potentially reversible contributors should then be addressed:

• Excessive systemic vascular resistance or hypertension
• Excessive vasoconstrictor therapy
• Inadequate or excessive preload
• Suboptimal venous drainage
• Severe myocardial depression
• Residual intracardiac or extracardiac lesions
• Pericardial tamponade
• Significant valve regurgitation
• Mechanical cannula problems

When systemic perfusion permits, modest reduction of ECMO flow may decrease aortic pressure and improve native ejection. Inotropic support may increase ventricular contractility and facilitate aortic-valve opening. Vasodilator therapy may reduce systemic vascular resistance and LV afterload.

These adjustments must be individualized because reducing circuit flow may simultaneously decrease systemic perfusion.

9. When LV Unloading Is Required

Mechanical LV unloading should be considered when clinically significant LV distension or pulmonary congestion persists despite optimization of ECMO flow, preload, afterload, and myocardial support.

Reported indications include persistent aortic-valve closure, progressive LV distension, pulmonary edema, elevated filling pressures, very low pulse pressure, poor LV ejection, ventricular arrhythmia, and evidence of intracardiac stasis [4,5].

Unloading strategies include:

• Inotropic optimization
• Intra-aortic balloon pump
• Transaortic microaxial flow pumps such as Impella in anatomically and size-appropriate patients
• Transseptal or atrial decompression
• Left atrial venting
• Pulmonary venous venting
• Direct LV venting

Central postcardiotomy VA-ECMO provides a particular advantage in this setting because direct surgical access to the heart can permit efficient left atrial, pulmonary venous, or ventricular decompression [7,8].

A network meta-analysis of 16 studies including 3,930 patients found that LV unloading during VA-ECMO was associated with lower mortality than no unloading, with an overall odds ratio of 0.54 (95% CI 0.42–0.70) [6]. However, the available studies were predominantly observational and heterogeneous. These findings therefore support the importance of unloading in appropriately selected patients but do not establish a universal unloading strategy, timing threshold, or ECMO flow target.

10. Central VA-ECMO Requires Continuous Surgical Surveillance

During initial flow escalation, central cannulation requires direct attention to mechanical and surgical factors.

The team should confirm:

• Stable right atrial venous cannula position
• Effective systemic venous drainage
• Stable ascending aortic cannula position
• Absence of cannula kinking or obstruction
• Appropriate venous line pressure
• Adequate circuit filling
• Absence of air
• Acceptable surgical hemostasis

Increasing ECMO flow and restoring systemic pressure may reveal surgical bleeding that was less apparent during profound shock or immediately after cardiopulmonary bypass.

In congenital heart disease, circuit performance must also be interpreted in relation to the reconstructed anatomy. Residual intracardiac shunts, systemic-to-pulmonary shunts, aortopulmonary collateral vessels, patent ductal flow, pulmonary venous obstruction, arch obstruction, or significant valve regurgitation can substantially alter the relationship between measured circuit flow and effective systemic perfusion.

11. Maintenance Is Continuous Rebalancing

After initial stabilization, ECMO flow should not remain fixed simply because a particular flow was required during initiation.

The optimal balance changes with myocardial recovery, vascular tone, temperature, sedation, hemoglobin concentration, fluid status, pulmonary function, bleeding, renal replacement therapy, infection, and evolving residual-lesion physiology.

Management should repeatedly address three questions:

Is systemic perfusion adequate?

Assess MAP, lactate trend, NIRS, oxygen delivery, urine output, and end-organ function.

Is the native heart appropriately loaded and ejecting?

Assess arterial pulsatility, aortic-valve opening, ventricular dimensions, pulmonary congestion, and evidence of intracardiac stasis.

Is the ECMO circuit functioning safely?

Assess drainage, cannula position, circuit pressures, oxygenator performance, anticoagulation, bleeding, and thrombotic complications.

The appropriate flow is therefore not necessarily the maximum achievable flow. It is the flow that provides sufficient systemic support while maintaining acceptable ventricular loading and minimizing complications.

12. Practical Physiologic Framework

Central VA-ECMO initiation and maintenance can be summarized as:

Start low → increase gradually → restore systemic perfusion → reassess native ejection → assess LV loading → optimize preload, afterload, and contractility → unload the LV when necessary → reassess continuously.

At one extreme, inadequate ECMO flow permits persistent shock and progressive end-organ injury.

At the other extreme, unnecessarily high support may reduce native preload and increase effective LV afterload sufficiently to abolish aortic-valve opening and promote ventricular distension, pulmonary edema, and intracardiac stasis.

The fundamental objective is therefore not simply “100% ECMO flow.” It is adequate systemic oxygen delivery with appropriate cardiac decompression.

The current evidence supports cautious, physiology-guided flow titration and early recognition of LV overload, but it does not define a validated central postcardiotomy VA-ECMO initiation protocol or universal quantitative flow target.

References

[1] Dickstein ML. A Simple Formula for Predicting Ventricular Distension With Venoarterial Extracorporeal Membrane Oxygenation. ASAIO J. 2023. doi:10.1097/MAT.0000000000002045.

[2] Otake M, Morita H, Sato K, Saku K. Impact of Venoarterial Extracorporeal Membrane Oxygenation on Hemodynamics and Cardiac Mechanics: Insights From Pressure-Volume Loop Analysis. Int J Heart Fail. 2025. doi:10.36628/ijhf.2025.0005.

[3] Lim Y, Kim MC, Jeong IS. Left ventricle unloading during veno-arterial extracorporeal membrane oxygenation: review with updated evidence. Acute Crit Care. 2024. doi:10.4266/acc.2024.00801.

[4] Saeed O, Nunez JI, Jorde UP. Pulmonary Protection from Left Ventricular Distension During Venoarterial Extracorporeal Membrane Oxygenation: Review and Management Algorithm. Lung. 2023. doi:10.1007/s00408-023-00616-8.

[5] Calhoun A, Lee MH, Pisano DV, Karavas A, Ortoleva J. Variability in triggers for mechanical left ventricular unloading in VA-ECMO: A literature search. J Extra Corpor Technol. 2024. doi:10.1051/ject/2024031.

[6] Baldetti L, Gramegna M, Beneduce A, Melillo F, Moroni F, Calvo F, et al. Strategies of left ventricular unloading during VA-ECMO support: a network meta-analysis. Int J Cardiol. 2020. doi:10.1016/j.ijcard.2020.02.004.

[7] Pappalardo F, Ruggeri L. LV distention on VA-ECMO, what to do? Qatar Med J. 2017. doi:10.5339/qmj.2017.swacelso.23.

[8] Ricarte Bratti JP, Cavayas Y, Noly P, Serri K, Lamarche Y. Modalities of Left Ventricle Decompression during VA-ECMO Therapy. Membranes (Basel). 2021;11(3):209. doi:10.3390/membranes11030209.