(RV) dysfunction veno-venous ECMO will not provide any hemodynamic support.

Veno-venous ECMO allows physicians to separately titrate oxygenation and carbon dioxide clearance.Oxygenationdependsmainlyontheratio of blood flow through the ECMO circuit relative to the patient’s cardiac output (CO), whereas carbon dioxide elimination depends on flow of gas through the oxygenator, referred to as sweep gas flow [10]. Other factors can influence oxygen transfer through the membrane to a more limited extent, including inspired fraction of oxygen in the gas flow through the membrane, membrane lung properties, time of exposure of blood in the membrane, hemoglobin concentration, and gradient of gases across the membrane. The combination of those factors determines the rated flow or maximal oxygen delivery, which is the amount of desaturated blood that can be fully saturated per minute [11].

To allow optimal oxygenation, ECMO flows must represent a significant proportion of the patient’s CO. This can be achieved by increasing ECMO flows in an attempt to match patient’s CO or by decreasing the patient’s CO [12]. It has been shown that flows equating 60% of the patient’s CO were usually sufficient to maintain arterial oxygen saturation above 90% [10]. Carbon dioxide clearance is more effective than oxygenation because of the higher solubility and diffusivity of carbon dioxide, and can be titrated by increasing or decreasing the sweep gas flow. Shortly after ECMO initiation, respiratory system compliance is often extremely low and the patient’s native pulmonary function is almost negligible. During that phase, all gas exchange is supported with ECMO. Recommendations of ventilatory strategies on ECMO suggest ventilatory settings allowing lung rest [11,13]. In the recovery phase, respiratory compliance improves and the patient’s pulmonary function also contributes to arterial oxygenation and carbon dioxide clearance.

MONITORING OF BLOOD GASES

Arterial blood gases

Monitoring of arterial oxygen saturation on venovenous ECMO does not differ from any other patient.Apulse oximeter canbe placedinterchangeably on both arms and arterial blood gases drawn from either side. As the blood is traveling using the normal pathway, there should not be any substantialdifferencebetweensides.Arterialpartialpressure of oxygen is determined bymixed venoussaturation (SvO₂) and intrapulmonary shunt. Thus in the early phase, when lung function may be almost nonexistent (shunt fraction being equal to 100%), partial pressure of oxygen is very close to SvO₂ [14]. Arterial oxygensaturationabove85%isacceptableaslongas oxygen delivery is adequate. Oxygen delivery/oxygen consumption ratio (DO ₂/VO₂) should be maintained above 3 to avoid tissue hypoxia [11,13,14]. Some centers tolerate even lower levels of saturation, whereas targeting a higher hemoglobin level (12g/dl) to optimize oxygen delivery, which is still the target recommended in the ELSO guidelines [15]. One may advocate against this higher threshold as transfusion in the critical care population has been shown to worsen outcome. In addition, lower levels of 2,3 diphosphoglycerate in transfused blood and subsequent increase of hemoglobin affinity for oxygen may limit oxygen uptake. In our center, we tolerate saturations as low as 85% while aiming for a hemoglobin level above 8g/dl. There is no published study comparing these approaches,although arecentlypublished report on blood conservation protocol on ECMO showed similar outcome [16^&&]. In this study, they tolerated hemoglobin levels as low as 7g/dl in combination with saturation above 92% (Table 1).

In the recovery phase, pulmonary shunt and dead space must be accounted for to obtain arterial saturation and arterial pressure of carbon dioxide level. Estimation of the shunt fraction remains cumbersome and requires a pulmonary catheter. Some authors recommend daily monitoring of the shunt fraction, although this is not something we do in routine clinical practice [17].

Venous blood gases

In normal conditions, measurements of central or mixed venous saturation allow physicians to assess adequacy of oxygen delivery in relationship to oxygen demand. However, on veno-venous ECMO venous saturation as measured in the RA or pulmonary artery does not represent the true venous saturation. Thus, venous saturation may not be suitable to assess (DO₂/VO₂) adequacy. Indeed a variable portion of the blood is reinfused from the ECMO circuit, and therefore contains highly oxygenated blood. Venous saturation on ECMO represents a mixture of blood coming from systemic venous return and from the ECMO circuit.One can estimate the resulting venous saturation by knowing the oxygen content of the venous blood, the oxygen content of the blood coming from the ECMO, and the respective proportion of ECMO blood to venous return [2^&&]. Some centers use the blood from the drainage line of the ECMO circuit (premembrane blood gases or inlet blood gases) as a surrogate for mixed venoussaturation.Inabsenceofrecirculation premembrane blood gases remain a good reflection of central/mixed venous saturation, and levels above 75% indicate adequacy of oxygen delivery/ consumption. Some centers use continuous monitoring of mixed venous saturation to calculate systemic VO₂ and DO₂ in addition to ECMO VO₂ and follow them over time to assess recovery [17]. Others continuously monitor inlet and outlet blood gas saturation and calculate oxygen transport and oxygen consumption via ECMO [3,15].

Nevertheless, since the blood is drained and reinfused in the same chamber there is potential for recirculation. Recirculation represents the fraction of blood reinjected into the RA and immediately suctioned back into the drainage cannula [18^&&]. This recirculation fraction is not available for systemic oxygenation and may contribute to ineffective ECMO and hypoxemia. Gross recirculation can be diagnosed by observing a sudden change ofcolorinthedrainage cannulaalternatingbetween oxygenated and deoxygenated blood. Macroscopic recirculation occurs when drainage and reinjection cannulae are too close to one another, ECMO drainage suction is too high or alternatively when CO is critically low. ECMO flows should be decreased or attempt to increase CO initiated. Double lumen catheters present less potential for recirculation

[18^&&].

Recirculation fraction can be estimated with a formula integrating premembrane, post membrane, and mixed venous saturations:

Recirculation fraction: (S_preO₂SvO₂)/(S_post O₂SvO₂)100

This equation requires a true SvO₂, only obtainable when the sweep gas is totally interrupted, which may not be tolerated in the early phase of ECMO support [18^&&,19–22]. Other methods use blood from the superior vena cava (SVC) or the inferior vena cava (IVC) as a surrogate, rendering the calculation less accurate. Therefore, other mathematical models have been developed in vitro to try to estimate recirculation fraction [19]. Ultrasound dilution technique has also been described to quantify amount of recirculation. This technique allows calculation of recirculation fraction without SvO₂. It is based on ultrasound velocity properties and dilution of blood. It requires two sensors, one placed on the drainage limb of the circuit, one on the reinjection. Dilution of blood will change the ultrasound velocity [22]. After injection of saline, changes in velocity will be detected by the sensors and generate a dilution curve for each limb of the circuit. The ratio of the area under the curve will represent the recirculation fraction. If there is no changeinvelocityinthedrainagelimb,thenthereis no recirculation. Those techniques have not gained widespread use. Most centers still use increased oxygen saturation and its trend over time in the premembrane blood gases as a marker for recirculation.

Postmembrane or outlet blood gases

The membrane lung is also subject to shunt and dead space fractions, which will worsen with time, as progressive thrombosis and fibrin formation will deposit in the membrane [23]. This will be associated with progressive decline in oxygen and carbon dioxide transfer over time. Proper function of the membrane usually allows to obtain outlet pressure of oxygen above 300mmHg [11]. Postmembrane pressure of oxygen should be monitored regularly as significant deterioration in membrane performance may cause hypoxemia and warrant a change of the membrane. Carbon dioxide clearance is usually maintained but may require higher sweep gas flow.

Although, routinely used in some centers the place of the pulmonary artery catheter in venovenous ECMO patients remains in our opinion, questionable [17,24]. Firstly, SVO₂ is influenced not only by the oxygen delivery/consumption ratio but also by ECMO flows. Additionally, it is unclear on how flows to and from the RA impact calculation of CO with the thermodilution technique. As vascular resistance is also derived from measurement of CO and cardiac pressure, it is debatable if those calculations remain accurate.

Echocardiographic monitoring

As previously mentioned, veno-venous ECMO does not directly affect cardiac function. Therefore, normal or subnormal cardiac function is usually present in most patients. Indications for echocardiography to monitor cardiac function itself are guided by clinical context, as deemed necessary by the attending physician.

However, echocardiography in patients supported with veno-venous ECMO presents specific indications [6^&&,25–28]. Optimal cannula positioning is crucial for adequate oxygenation. It is recommended that the cannula’s tip sits in the RA (just beyond the IVC/RA junction, ensuring a safe distance from the interatrial septum and tricuspid valve). If the drainage cannula is too distant from the IVC RA junction, appropriate flows may not be obtained because of collapse of the vein around the cannula, especially in case of decreased intravascular volume, or when patients initiate spontaneous breathing. As a consequence, it may hinder maintenance of restrictive fluid strategy, as fluid may need to be administered to restore adequate flows [29]. On the other hand, if the cannulae are too close, recirculation may become an issue. Thus, appropriate cannula position should be ascertained not only with chest radiograph but also with echocardiography, as chest radiography does not allow visualization of the distance between the tip of the cannula and IVC/RA junction [30].

Inadequate flows may also be because of thrombusformationwithinthecannula,whichcanalsobe identified with echocardiography [31].

In addition, presence of pericardial and pleural effusion should be noted, and monitored as anticoagulation may potentially worsen them.

Double lumen catheters present specific challenges inherent to their design. The lumen dedicated for blood drainage displays two sites: proximal, which should be positioned in the SVC, while the distal tip should be in the IVC. The second lumen containing the oxygenated blood terminates via an orifice sitting in the RA. Optimal position of the reinjection orifice is the mid-RA, facing the tricuspid valve [32]. Double lumen catheters are prone to dislodgment with potential deleterious consequences on oxygenation [22]. When the cannula migrates too deep intotheIVC,reinjectionmaybeinthehepaticvein. Conversely, if the cannula is too far out, reinjection flow will be within the SVC. Additionally, if the flow is directed toward the interatrial septum, oxygenation may become suboptimal. In all cases, oxygenation may be compromised. Chest radiograph is not sufficient to ascertain proper position of the cannula as it does not allow to identify the different portions of the cannula and their relative position to cardiac structures. Echocardiography is best suited to identify the precise positioning of each portion of the cannula [33,34]. Therefore, in presenceofpersistenthypoxemia,lowECMOflows, thecannula’slocationshouldbeverifiedwithechocardiography. Transthoracic views are usually adequate, but transesophageal echocardiography may be warranted. Both tip and reinjection orifice are usually easily identified, either on the subcostal and parasternal views (RV inflow and inflow outflow view on transthoracic echocardiography) or in the mid esophageal bicaval view (transesophageal echocardiography). Cannula repositioning under echo guidance should be considered in case of malpositioning and impaired oxygenation. To betterguidethepositioning, echocardiography should be performed by an operator accustomed to performing echocardiography in ECMO patients, as some alternative views may be required to properly visualize all portions of the cannula [35]. Additionally, color flow Doppler may help identify the appropriatedirectionofthereinjectionflowtoward the tricuspid valve.

During the weaning phase, unless hypoxemia and hypercarbia precipitate RV dysfunction, there should not be any change in cardiac function, thus indications for echocardiography are guided by clinical and hemodynamic status.

MONITORING ON VENO-ARTERIAL

EXTRACORPOREAL MEMBRANE OXYGENATION

Physiology of veno-arterial extracorporeal membrane oxygenation

Veno-arterial ECMO provides both cardiac and pulmonary support. Blood is also drained from the venous system but reinjected in the arterial system either centrally (reinjection cannula in the ascending aorta in adults) or peripherally via the femoral artery (Fig. 1). On peripheral veno-arterial ECMO, when the patient’s cardiac function is severely depressed, high ECMO flows will ensure complete cardiac and pulmonary support. Blood reinfused by the ECMO reaches the ascending aorta and perfuses all the organs in a retrograde fashion. As blood travels from iliac artery to the ascending aorta oxygen uptake along the aorta results in a progressive decrease in arterial partial pressure of oxygen. If left ventricular function is not completely depressed, and the left ventricle (LV) still manages to eject a significant stroke volume, there will be mixing of blood within the aorta. The exact location of the mixing is unpredictable and depends on ECMO flows, vascular resistance, and the patient’s intrinsic ventricular function. If respiratory function is preserved and in absence of pulmonary edema, this phenomenon has little consequence. On the other hand, if pulmonary function is impaired, it can result in poor oxygenation of the most proximal branches of the aorta, namely coronary arteries and head vessels (Fig. 3) [36]. This can potentially expose the patient to coronary and cerebral hypoxia. The extreme manifestation of this phenomenon is described as ‘Harlequin syndrome’ with clinically identifiable differential oxygenation: concomitant cyanosis of the upper body with normal oxygenation of the lower body. Some authors reported the use of near infrared spectroscopy to monitor cerebral function on ECMO. Any decrease in cerebral oxygenation prompted implementation of therapeutic measures, including reposition of patient or cannula, titration of ECMO flows to optimize oxygen delivery, and neuroimaging if persisting cerebral hypoxia. In their cohort, all patients who exhibited refractory alteration in cerebral tracings had confirmed cerebral events on imaging [36].

MONITORING OF BLOOD GASES

Arterial blood gases

On peripheral veno-arterial ECMO, it is crucial to monitor oxygenation as far as possible from the reinjection site. An arterial line should ideally be placed on the right arm, and blood gases taken from the right side. Arterial blood gases drawn on the left side or worse on a femoral artery could be completely discrepant from oxygenation at the level of coronary, innominate, and left common carotid arteries (Table 1).

When an arterial line cannot be placed on the right side at least a pulse oximeter should be placed on the right side, though this can also be a challenge if intrinsic CO is very low as the ECMO flow is nonpulsatile.

The underlying disease will dictate the appropriatemanagementinpresenceofsignificantdifferential oxygenation.Pulmonaryedemasecondarytoleftventricular distension may subside by venting of the left atrium[37–40].Addingaveno-venouscomponentfor aveno-venousarterialconfigurationmaybeindicated in case of concomitant pulmonary disease.

The aforementioned phenomenon is not an issue with central cannulation as proximity of reinjection from the coronaries and anterograde direction of blood flow do not usually cause significant competition.

Venous blood gases

Unlikeonveno-venousECMO,venoussaturationon veno-arterial ECMO is a true reflection of venous oxygen content. Indeed, there is no recirculation on veno-arterial ECMO since there is no communicationbetween drainageandreinjection sites. Therefore, venous saturation, measured either from a central line or premembrane blood gases is highly valuableto ensure thatoxygen deliveryis adequately matched to oxygen consumption. Continuous in-line venous saturation monitors incorporated in the circuit are available and may help guide management, allowing instantaneous readjustment of therapy. A low venous saturation should be addressed as for any critically ill patient. In presence of concomitant hyperlactatemia and signs of endorgan hypoperfusion, the first step should usually be to increaseECMO flowstooptimize oxygen delivery. Ifpersistentlylow,optimizationofvolumestatusand possibly transfusion may be warranted.

Pulmonary artery catheter/cardiac output measurement

Similar to veno-venous ECMO, it is unknown how veno-arterialECMO affects degreeoftricuspid regurgitationandCOmeasurementwiththermodilution. However, pulmonary artery occlusion pressure and mixed venous saturation are not affected by venoarterial ECMO. Pulse pressure contour analysis methods may be limited by decreased pulsatility. There are, to our knowledge, no reported studies of pulse contour analysis technique in ECMO patients.

Echocardiography on veno-arterial extracorporeal membrane oxygenation

Echocardiographic monitoring on veno-arterial ECMO is paramount [6^&&,35]. Each study performed should be reported with mention of hemodynamic parameters, dose of vasoactive drugs and ongoing flows,asthis willserveasreferenceto assess recovery if and when it occurs. In addition, assessment of size and function of both ventricles is greatly affected by ECMO flows. Appropriate unloading of the right ventricle should be ensured, by checking cannula position and RV size. It is difficult to know how veno-arterial ECMO may influence the degree of tricuspid regurgitation and estimation of pulmonary artery pressure. Left ventricular size should also be assessed as progressive distension may induce pulmonary edema.

As in veno-venous ECMO, proper cannula positionshouldbeascertained,andintracannulathrombus and pericardial effusion ruled out. Diagnosis of pericardial tamponade can be difficult in ECMO patients and should remain a clinical diagnosis. For instance,presenceofpericardial effusionwithpartial chamber collapse on veno-arterial ECMO may be delicate to interpret under high flows.

Additionally, opening of the aortic valve should be documented using echocardiography. It usually coincideswithpulsatilityonarteriallinetracing,but echocardiography allows a direct visualization of the valve. Presence of spontaneous echo contrast or thrombi in the LV or aorta can also be seen on echocardiography [41–43]. Whether presence or absenceofpulsatilityislinkedtooutcomeisunclear. Nevertheless, when the aortic valve remains closed, there is higher risk for thrombosis [41–43]. Therefore, therapies are usually implemented to allow opening of the valve. Reducing vascular resistance or ECMO flows may allow more consistent opening of the valve. Some authors have suggested the concomitant use of intra-aortic balloon pump or microaxial pump to decrease the LV afterload [44–49]. When severe pulmonary edema is present, left atrial venting has been proven effective to alleviate pulmonary congestion [37–40,45,50].

Presence and severity of aortic and mitral regurgitation should be noted. Increased afterload can aggravate aortic regurgitation and subsequently worsen LV distension, with potential subendocardial ischemia hindering recovery [51–53]. Mitral regurgitation will worsen pulmonary edema.

When signs of cardiac recovery are present, (i.e., higher pulsatility and maintained hemodynamics with decremental flows) quantification of cardiac function whereas lowering flows allow assessment of recovery. Some authors have used aortic velocity integral and tissue Doppler at the mitral annulus to predict successful weaning [54^&,55,56]. To test if the patient can be weaned off ECMO, flows are decreased transiently to approximately 1l/min, while assessing size and function of both ventricles.

Flows are usually not decreased further in fear of circuit thrombosis. If biventricular function and hemodynamics are maintained despite low flows, the patient is deemed weanable. Specific attention should be paid to RV size and function, as even a low flow can mask dysfunction.

CONCLUSION

In summary, cardiopulmonary monitoring of patients on ECMO is unachievable without proper understanding of the type of ECMO configuration. Even blood gases measurements can be misleading if not integrated in clinical context. Echocardiography is an invaluable tool in managing patients on ECMO, but does also require proper knowledge of the patient’s configuration and should be integrated within clinical context.

Acknowledgements

The authors would like to thank Dr Alberto Goffi for his contribution with the figures.

Financial support and sponsorship None.

Conflicts of interest

There are no conflicts of interest.

REFERENCES AND RECOMMENDED

READING

Papers of particular interest, published within the annual period of review, have been highlighted as: ^& of special interest

^&& of outstanding interest

1. Barbaro RP, Odetola FO, Kidwell KM, et al. Association of hospital-level volume of extracorporeal membrane oxygenation cases and mortality. Analysis of the extracorporeal life support organization registry. Am J Respir Crit Care Med 2015; 191:894–901.

2. Brain MJ, Butt WW, MacLaren G. Physiology of extracorporeal life support.

^&& In: Schmidt GA, editor. Extracorporeal life support for adults. Springer Science, NY: Humana Press; 2016.

The chapter contains a comprehensive review on physiology of ECMO.

3. Bartlett R. Physiology of extracorporeal life support. In: Annich GM, MacLaren G, editors. ECMO-extracorporeal cardiopulmonary support in critical care. Ann Arbor, Michigan: ELSO; 2012. pp. 11–31.

4. Abrams D, Combes A, Brodie D. Extracorporeal membrane oxygenation in cardiopulmonary disease in adults. J Am Coll Cardiol 2014; 63:2769–2778.

5. Sidebotham D, Allen SJ, McGeorge A, et al. Venovenous extracorporeal membrane oxygenation in adults: practical aspects of circuits, cannulae, and procedures. J Cardiothorac Vasc Anesth 2012; 26:893–909.

6. Doufle? G, Roscoe A, Billia F, Fan E. Echocardiography for adult patients

^&& supported with extracorporeal membrane oxygenation. Crit Care 2015; 19:326.

The review contains supplementary online material, including echocardiography clips, illustrating concepts discussed in the present article.

7. Bouferrache K, Vieillard-Baron A. Acute respiratory distress syndrome, mechanical ventilation, and right ventricular function. Curr Opin Crit Care 2011; 17:30–35.

8. Gue?rin C, Matthay MA. Acute cor pulmonale and the acute respiratory distress syndrome. Intensive Care Med 2016. [Epub ahead of print]

9. Miranda DR, Brodie D, Bakker J. Right ventricular unloading after initiation of VV ECMO. Am J Respir Crit Care Med 2015; 191:346–347.

10. Schmidt M, Tachon G, Devilliers C, et al. Blood oxygenation and decarboxylation determinants during venovenous ECMO for respiratory failure in adults.

Intensive Care Med 2013; 39:838–846.

11. ELSO. ELSO Guidelines for Cardiopulmonary Extracorporeal Life Support version1.3: ELSO, Ann Arbor, MI, USA; 2013. Available from: http://www.elsonet.org. [Accessed 24 March 2016]

12. Guarracino F, Zangrillo A, Ruggeri L, et al. Beta-blockers to optimize peripheral oxygenation during extracorporeal membrane oxygenation: a case series. J Cardiothorac Vasc Anesth 2012; 26:58–63.

13. Bartlett R, Zwischenberger JB. Management of blood flow and gas exchange during ECLS. In: Annich GM, Lynch W, MacLaren G, Wilson JM, Bartlett R, editors. ECMO-extracorporeal cardiopulmonary support in critical care: extracorporeal life support organization. Ann Arbor, Michigan: ECMO; 2012. pp. 149–156.

14. ELSO Guidelines for adult respiratory failure version 1.3: ELSO, Ann Arbor, MI. USA; 2013. Available from: http://www.elsonet.org. [Accessed 24 March 2016]

15. Holzgraefe B, Broome? M, Kalze?n H, et al. Extracorporeal membrane oxygenation for pandemic H1N1 2009 respiratory failure. Minerva Anestesiol 2010; 76:1043–1051.

16. Agerstrand CL, Burkart KM, Abrams DC, et al. Blood conservation in extra^&& corporeal membrane oxygenation for acute respiratory distress syndrome.

Ann Thorac Surg 2015; 99:590–595.

In this study, they report a blood conservative strategy for ECMO patients.

17. Zanella A, Mojoli F, Castagna L, Patroniti N. Respiratory monitoring of the ECMO patient. In: Sangalli F, editor. ECMO-extracorporeal life support in adults. Milan, Italy: Springer-Verlag Italia; 2014. pp. 249–263.

18. Abrams D, Bacchetta M, Brodie D. Recirculation in venovenous extracorpor^&& eal membrane oxygenation. ASAIO J 2015; 61:115–121. The study reviews the mechanism of recirculation and different methods of assessment.

19. Walker JL, Gelfond J, Zarzabal LA, Darling E. Calculating mixed venous saturation during veno-venous extracorporeal membrane oxygenation. Perfusion 2009; 24:333–339.

20. Darling EM, Crowell T, Searles BE. Use of dilutional ultrasound monitoring to detect changes in recirculation during venovenous extracorporeal membrane oxygenation in swine. ASAIO J 2006; 52:522–524.

21. Van Heijst AF, Van Der Staak FH, De Haan A, et al. Recirculation in double lumen catheter veno-venous extracorporeal membrane oxygenation measured by an ultrasound dilution technique. ASAIO J 2001; 47:372–376.

22. Korver EP, Ganushchak YM, Simons AP, et al. Quantification of recirculation as an adjuvant to transthoracic echocardiography for optimization of duallumen extracorporeal life support. Intensive Care Med 2012; 38:906–909.

23. Isgro` S, Mojoli F, Avalli L. Monitoring of the ECMO patient: the extracorporeal circuit. In: Sangalli F, editor. ECMO-extracorporeal life support in adults. Milan, Italy: Springer-Verlag Italia; 2014.

24. Guarracino F, Baldassarri R. Haemodynamic monitoring. In: Sangalli F, editor. ECMO-extracorporeal life support in adults. Milan, Italy: Springer-Verlag Italia; 2014.

25. Peris A, Lazzeri C, Cianchi G, et al. Clinical significance of echocardiography in patients supported by venous-venous extracorporeal membrane oxygenation. J Artif Organs 2015; 18:99–105.

26. Platts DG, Sedgwick JF, Burstow DJ, et al. The role of echocardiography in the management of patients supported by extracorporeal membrane oxygenation. J Am Soc Echocardiogr 2012; 25:131–141.

27. Combes A, Brodie D, Bartlett R, et al. Position paper for the organization of extracorporeal membrane oxygenation programs for acute respiratory failure in adult patients. Am J Respir Crit Care Med 2014; 190:488–496.

28. Bianco N, Avalli L, Sangalli F. Echocardiography in venoarterial and venovenous ECMO. In: ECMO: extracorporeal life support in adults. Milan, Italy: Springer-Verlag Italia; 2014. pp. 361–374.

29. Schmidt M, Bailey M, Kelly J, et al. Impact of fluid balance on outcome of adult patients treated with extracorporeal membrane oxygenation. Intensive Care Med 2014; 40:1256–1266.

30. Thomas TH, Price R, Ramaciotti C, et al. Echocardiography, not chest radiography, for evaluation of cannula placement during pediatric extracorporeal membrane oxygenation. Pediatr Crit Care Med 2009; 10:56–59.

31. Ranasinghe AM, Peek GJ, Roberts N, et al. The use of transesophageal echocardiography to demonstrate obstruction of venous drainage cannula during ECMO. ASAIO J 2004; 50:619–620.

32. Dolch ME, Frey L, Buerkle MA, et al. Transesophageal echocardiographyguided technique for extracorporeal membrane oxygenation dual-lumen catheter placement. ASAIO J 2011; 57:341–343.

33. Tabak B, Elliott CL, Mahnke CB, et al. Transthoracic echocardiography visualization of bicaval dual lumen catheters for veno-venous extracorporeal membrane oxygenation. J Clin Ultrasound 2012; 40:183–186.

34. Javidfar J, Wang D, Zwischenberger JB, et al. Insertion of bicaval dual lumen extracorporeal membrane oxygenation catheter with image guidance. ASAIO J 2011; 57:203–205.

35. Taylor MA, Taylor BS. Cardiac ultrasound and extracorporeal life support: the two go together. J Am Soc Echocardiogr 2015; 28:A18–A19.

36. Wong JK, Smith TN, Pitcher HT, et al. Cerebral and lower limb near-infrared spectroscopy in adults on extracorporeal membrane oxygenation. Artif Organs 2012; 36:659–667.

37. Hacking DF, Best D, d’Udekem Y, et al. Elective decompression of the left ventricle in pediatric patients may reduce the duration of venoarterial extracorporeal membrane oxygenation. Artif Organs 2015; 39:319–326.

38. Kotani Y, Chetan D, Rodrigues W, et al. Left atrial decompression during venoarterial extracorporeal membrane oxygenation for left ventricular failure in children: current strategy and clinical outcomes. Artif Organs 2013; 37:29– 36.

39. Rupprecht L, Florchinger B, Schopka S, et al. Cardiac decompression on extracorporeal life support: a review and discussion of the literature. ASAIO J 2013; 59:547–553.

40. Soleimani B, Pae WE. Management of left ventricular distension during peripheral extracorporeal membrane oxygenation for cardiogenic shock. Perfusion 2012; 27:326–331.

41. Ramjee V, Shreenivas S, Rame JE, et al. Complete spontaneous left heart and aortic thromboses on extracorporeal membrane oxygenation support. Echocardiography 2013; 30:E342–E343.

42. Moubarak C, Weiss N, Leprince P, Luyt C. Massive intraventricular thrombus complicating ECMO support. Can J Cardiol 2008; 24:e1.

43. Madershahian N, Weber C, Scherner M, et al. Thrombosis of the aortic root and ascending aorta during extracorporeal membrane oxygenation. Intensive Care Med 2014; 40:432–433.

44. Petroni T, Harrois A, Amour J, et al. Intra-aortic balloon pump effects on macrocirculation and microcirculation in cardiogenic shock patients supported by venoarterial extracorporeal membrane oxygenation. Crit Care Med 2014; 42:2075–2082.

45. Vlasselaers D, Desmet M, Desmet L, et al. Ventricular unloading with a miniature axial flow pump in combination with extracorporeal membrane oxygenation. Intensive Care Med 2006; 32:329–333.

46. Madershahian N, Liakopoulos OJ, Wippermann J, et al. The impact of intraaortic balloon counterpulsation on bypass graft flow in patients with peripheral ECMO. J Card Surg 2009; 24:265–268.

47. Madershahian N, Wippermann J, Liakopoulos OJ, et al. The acute effect of IABP-induced pulsatility on coronary vascular resistance and graft flow in critical ill patients during ECMO. J Cardiovasc Surg 2011; 52:411–418.

48. Hu W, Liu C, Chen L, et al. Combined intraaortic balloon counterpulsation and extracorporeal membrane oxygenation in 2 patients with fulminant myocarditis. Am J Emerg Med 2015; 33:736.

49. Cheng A, Swartz MF, Massey HT. Impella to unload the left ventricle during peripheral extracorporeal membrane oxygenation. ASAIO J 2013; 59:533– 536.

50. Avalli L, Maggioni E, Sangalli F, et al. Percutaneous left-heart decompression during extracorporeal membrane oxygenation: an alternative to surgical and transeptal venting in adult patients. ASAIO J 2011; 57:38–40.

51. Lucas SK, Schaff HV, Flaherty JT, et al. The harmful effects of ventricular distention during postischemic reperfusion. Ann Thorac Surg 1981; 32:486– 494.

52. Mills SA, Hansen K, Vinten-Johansen J, et al. Enhanced functional recovery with venting during cardioplegic arrest in chronically damaged hearts. Ann Thorac Surg 1985; 40:566–573.

53. Kanter KR, Schaff HV, Gott VL, Gardner TJ. Reduced oxygen consumption with effective left ventricular venting during postischemic reperfusion. Circulation 1982; 66:I50–I54.

54. Aissaoui N, El-Banayosy A, Combes A. How to wean a patient from veno-

^& arterial extracorporeal membrane oxygenation. Intensive Care Med 2015; 41:902–905.

The commentary contains an algorithm on how to wean patients from veno-arterial ECMO.

55. Aissaoui N, Guerot E, Combes A, et al. Two-dimensional strain rate and Doppler tissue myocardial velocities: analysis by echocardiography of hemodynamic and functional changes of the failed left ventricle during different degrees of extracorporeal life support. J Am Soc Echocardiogr 2012; 25:632–640.

56. Aissaoui N, Luyt CE, Leprince P, et al. Predictors of successful extracorporeal membrane oxygenation (ECMO) weaning after assistance for refractory cardiogenic shock. Intensive Care Med 2011; 37:1738–1745.