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Contemporary Comprehensive Monitoring of Veno-arterial Extracorporeal Membrane Oxygenation Patients
Journal Pre-proof Contemporary Comprehensive Monitoring Of The Veno-Arterial Extracorporeal Membrane Oxygenation Patient Meena Bhatia, MD, Jason N. Katz, MD, MHS PII:
S0828-282X(19)31384-4
DOI:
https://doi.org/10.1016/j.cjca.2019.10.031
Reference:
CJCA 3497
To appear in:
Canadian Journal of Cardiology
Received Date: 30 August 2019 Revised Date:
17 October 2019
Accepted Date: 30 October 2019
Please cite this article as: Bhatia M, Katz JN, Contemporary Comprehensive Monitoring Of The VenoArterial Extracorporeal Membrane Oxygenation Patient, Canadian Journal of Cardiology (2019), doi: https://doi.org/10.1016/j.cjca.2019.10.031. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society.
CONTEMPORARY COMPREHENSIVE MONITORING OF THE VENO-ARTERIAL EXTRACORPOREAL MEMBRANE OXYGENATION PATIENT Meena Bhatia, MD1 and Jason N. Katz, MD, MHS2
1
Department of Anesthesiology, Division of Critical Care Medicine, University of North Carolina, Chapel Hill, NC; email: [email protected]
2
Department of Medicine and Surgery, Division of Cardiovascular Medicine, University of North Carolina, Chapel Hill, NC; email: [email protected] Address for Correspondence: Jason N. Katz, MD, MHS 160 Dental Circle, CB#7075 6th Floor Burnett-Womack Building Chapel Hill, NC 27599-7075 Tel: (919) 843-0447 Email: [email protected]
Disclosures – The authors have nothing to disclose relevant to this manuscript.
ABSTRACT WORD COUNT: 225 DOCUMENT WORD COUNT (INCLUDING REFERENCES): 6598
ABSTRACT The use of veno-arterial extracorporeal membrane oxygenation (VA ECMO) has increased substantially over the last few decades. Today’s clinicians now have a powerful means with which to salvage a growing population of patients at risk for cardiopulmonary collapse. At the same time, patients supported with VA ECMO have become increasingly more complex. The successful use of VA ECMO depends not only upon choosing the right individual to support, but also being able to effectively navigate a potential torrent of device and patient-related complications until ECMO is no longer needed. A multitude of monitoring tools are now available to help the treatment team determine the adequacy of care, to detect problems, and to anticipate recovery. Monitoring with devices such as the Swan-Ganz catheter, transthoracic and transesophageal echocardiography, chest radiography, and near-infrared spectroscopy can all provide useful information to complement routine clinical care. Leveraging data derived from the ECMO circuit itself can also be instrumental in both evaluating the sufficiency of support and in troubleshooting complications. Each of these tools, however, has their own unique sets of limitations and liabilities. A thorough understanding of these risks and benefits is now critical to the contemporary care of the individual managed with VA ECMO. Additionally, more research is needed in order to establish optimal, evidence-based care pathways and best practice principles which incorporate these devices to improve patient outcomes.
ELECTRONIC TABLE OF CONTENTS SUMMARY (75 Words) Veno-Arterial Extracorporeal Membrane Oxygenation (VA ECMO) is used as an emergent support tool for patients with cardiogenic shock or cardiac arrest. Though it has great potential to reverse end-organ dysfunction and to re-establish adequate cardiopulmonary function, numerous complications may ensue. There are a myriad of monitoring tools – each with its unique set of benefits and liabilities –available to assist the treating physician. A comprehensive understanding of these monitoring modalities is now essential to contemporary care.
Extracorporeal membrane oxygenation (ECMO), in its veno-arterial (VA) configuration, is being increasingly utilized to mechanically support patients with severely compromised cardiopulmonary function.1 For patients with cardiogenic shock or cardiac arrest, whose conditions were once considered futile, ECMO can now be leveraged as an emergent bridge to recovery, to durable mechanical circulatory support (MCS), or to transplantation. Recent data would suggest that provider experience is perhaps the most important determinant of patient outcome.2 Today’s clinicians must not only be familiar with the various components of these devices but must also be comfortable with assessing the adequacy of support. At the same time, providers must vigilantly monitor for and be prepared to contend with the myriad of potential complications attributable to VA ECMO. These include device and patient thrombosis, progressive hemodynamic instability, bleeding, global and regional hypoxemia, neurologic injury, and limb ischemia. Numerous monitoring technologies are now available for the treating clinician, and can help guide care and aid in troubleshooting. The following review will focus on the benefits, liabilities, and evidence informing the use of these tools, and outline their potential role in complementing the routine clinical management of today’s VA ECMO patient.
Monitoring Tools
When utilizing circulatory support strategies for critically ill patients with shock, a clear understanding of the goals of care is crucial to patient success. VA ECMO is most often used to promptly restore and then maintain the following three clinical conditions: 1) adequate balance between systemic oxygen delivery and consumption, 2) adequate tissue and end-organ perfusion, and 3) adequate systemic gas exchange (i.e. oxygenation and ventilation). In conjunction with serial clinical examinations, a variety of monitoring modalities can help the provider continuously assess the adequacy of support and confirm that the aforementioned conditions are being met. Additionally, these monitoring tools can be used to assess and troubleshoot acute changes to patient and device stability, and can provide highly valuable and often real-time diagnostic information necessary to identify and treat a variety of potential complications.
The ECMO Circuit
Most ECMO circuits have a display monitor that provides real-time data that can be reviewed. Figure 1 illustrates several common features of a contemporary VA ECMO monitor. While specific ECMO flow targets have been poorly elucidated, and should be individualized based upon patient need and the desired degree of mechanical assistance, it has been suggested that flows between 50-70 mL/kg/min may be a reasonable initial goal.3 VA ECMO flows that vary considerably despite a stable ECMO speed may indicate a device or patient problem and requires prompt investigation. Sudden and sustained alterations in both venous (inflow) and arterial (outflow) circuit pressures may suggest problems with cannula positioning, device obstruction, or acute changes in cardiac loading conditions.4 Additionally, measures of premembrane oxygen saturation – or mixed venous oxygen saturation – are usually displayed on contemporary VA ECMO circuits. A decrease in pre-membrane oxygen saturation is often correlated with a decrease in systemic oxygen delivery and an increase in tissue extraction ratio. This should prompt the treating clinician to consider efforts to either optimize delivery or reduce oxygen consumption.
Laboratory Studies
Serial review of laboratory studies may also help one to determine both the adequacy and stability of VA ECMO support for a critically ill patient. Maintaining reasonable end-organ perfusion is vital, and serum markers of organ function can be readily obtained. Blood urea nitrogen (BUN) and creatinine should be frequently monitored measures of renal function and recovery. Improvements in serum electrolytes should parallel optimization in renal, hepatic, and generalized tissue perfusion. Liver function studies should be used to monitor hepatic stability, and repeated assessments of plasma lactate can inform clinicians about the persistence or resolution of a patient’s shock state.5 Persistent lactic acidosis, despite sufficient resuscitation and seemingly adequate support, could be indicative of a concealed complication;
examples include bowel ischemia, limb ischemia, and the abdominal compartment syndrome, to name a few. Regardless of the cause, immediate investigation of unrelenting acidosis is vital.
Invasive Hemodynamics - Arterial Lines and Pulmonary Artery Catheters
Monitoring invasive blood pressure, acid-base balance, and systemic gas exchange are all vital components linked to the successful management of VA ECMO patients. An arterial line, ideally placed in the right arm, is an important indicator of the adequacy of circulatory support. While a target mean arterial pressure (MAP) is debatable, data extrapolated from other critical care cohorts would suggest a goal of between 65-80 mmHg is reasonable.6 This would presumably provide good systemic perfusion while avoiding the potentially deleterious impact of high left ventricular afterload. Much like serial measurements of serum lactate, the presence and persistence of metabolic acidosis can suggest inadequate tissue perfusion and should lead to alterations in ECMO support. Likewise, problems with gas exchange may warrant intensification of ECMO flow, modification of complementary ventilatory therapy, or alterations to oxygenation or sweep rates within the ECMO circuit.
The pulmonary artery catheter (PAC) can also be a useful adjunct to the monitoring armamentarium used by clinicians who manage patients on VA ECMO. Invasive cardiac filling pressures can indicate the degree and adequacy of ventricular unloading, particularly if clinical decompensation is present. Additionally, variations in pulmonary arterial saturation – like changes in ECMO pre-membrane venous saturation – can alert the treatment team to changes in systemic oxygen delivery and consumption. While cardiac pressures and oxygen saturations are directly measured, it is important to note that cardiac output measurements derived from thermodilution methods are assumed to be less reliable.7 Mixing of blood in the right heart and variations in venous drainage will frequently threaten to confound measurements of temperature changes over time.
Changes in both systemic and pulmonary arterial pulse pressure, or pulsatility, can also be observed during VA ECMO support. Absent or very low pulsatility suggests severe cardiac contractile dysfunction and/or markedly reduced ventricular ejection. Interventions to reduce blood stasis and to attenuate resulting thrombotic risk may therefore be indicated. Increasing pulsatility, on the other hand, may be indicative of a recovering heart and improved native heart function. Monitoring the morphology of the pulse waveforms can therefore assist clinicians in assessing the adequacy of and need for ongoing MCS. Given the breadth of information that can be derived from invasive hemodynamic monitoring, the authors recommend the routine placement of arterial lines and pulmonary artery catheters in all VA ECMO patients unless a clinical contraindication exists.
Echocardiography and Chest Radiography
The echocardiogram, and in particular the use of serial echocardiography, is also a pivotal component of ECMO management. A transthoracic echocardiogram (TTE) can provide vital information about cardiac chamber size (as a surrogate for ventricular decompression), aortic valve excursion, the presence or absence of intracardiac and aortic root thrombus, valvular competency, pericardial disease (effusion and tamponade), and contractility.8 Additionally, TTE can confirm appropriate cannula positioning and can identify certain causes of circuit obstruction (including cannula thrombosis and kinking). In some cases, TTE may fail to provide adequate enough spatial resolution.9 In these instances, transesophageal echocardiography (TEE) should be considered. In instances where echo quality remains poor due to the presence of chest tubes, ventilator interference, or restricted patient positioning, intra-cavitary opacification with echo contrast has been employed. At this time, however, there is insufficient data to support the safety of this approach. Reports of contrast material activating the integrated bubble detector on some devices have been published, and this can lead to temporary cessation of ECMO flow and resulting patient instability.10 Until formally tested in a prospective manner, the ideal frequency of echocardiographic monitoring will remain unclear. Anecdotally, however, many believe that daily imaging should be part of a standard ECMO
monitoring protocol. Table 1 outlines the valuable information that can be derived specifically from echocardiography during ECMO support.
Radiographic imaging of the chest is also a useful monitoring tool. In particular, the presence of pulmonary edema can be an indirect clue that the left heart is being inadequately unloaded and that left-sided cardiac filling pressures are elevated. Additionally, the chest x-ray can be used to assess the stability of invasive catheters and ECMO cannulas, as well as to evaluate for concomitant pulmonary pathologies (e.g. alveolar hemorrhage, pleural effusions, pneumonia). An enlarging cardiac silhouette on plain film may indicate the development of a pericardial fluid collection or may be a sign of suboptimal cardiac decompression. While there is little evidence to establish the optimal frequency of radiographic monitoring, the authors currently advise daily chest x-rays to complement clinical care.
Near-Infrared Spectroscopy and Neurovascular Monitoring
Near-Infrared Spectroscopy (NIRS) is a non-invasive tool that leverages near-infrared wavelengths of light to provide continuous measurements of regional tissue oxygen saturation (rSO2).11 It has been used to determine the relative balance between oxygen delivery and demand in ECMO patients. More specifically, when placed on a patient’s scalp, NIRS can measure cerebral oximetry in both the left and right frontal regions (Figure 2). Cerebral desaturation has been associated with poor outcomes among adult patients supported with VA ECMO and may predict acute cerebral complications.12,13 Very high cerebral rSO2 values have also been associated with poor neurologic outcomes.14 While the potential merit of this tool in evaluating neurologic function in ECMO patients whose clinical exams may be confounded by the use of sedatives, analgesics, and neuromuscular blockers seems obvious, no well-validated NIRS protocols currently exist. The evidence base, instead, is limited to small case series and expert opinion documents. Additionally, it is important to acknowledge that this technology can only be used to assess regional cerebral oxygen saturations; deeper, subcortical and global pathologies may be missed.13
NIRS has also been used to monitor for distal limb ischemia – a potential complication of peripheral ECMO cannulation that develops in greater than 20% of patients and has substantial morbidity and mortality liability.15,16 The clinical examination and Doppler pulse evaluation of an ECMO patient are notoriously unreliable, especially for detecting early limb compromise.17 A sustained drop in lower extremity rSO2 has been observed in the majority of patients with lower extremity ischemia and can often improve with acute interventions such as the placement of a distal perfusion catheter.17 Additional prospective evaluation is needed to better define the role of NIRS for ECMO patient monitoring, but this technology appears to hold great promise.
NIRS monitoring, however, should not replace routine clinical examinations. Frequent neurologic exams with daily sedation interruptions remain vital to the care of the VA ECMO patient and should be performed regularly when possible. Any acute changes in exam findings must be noted and investigated. Routine serial neurological imaging, on the other hand, is neither required nor supported by the current evidence-base, and brain imaging should instead be used only if a change in the patient’s neurologic exam requires additional investigation. Certainly if a patient is arousable, demonstrates no focal neurological deficits, and can follow simple commands while on VA ECMO, it is reasonable to assume that cerebral function and perfusion is stable.
Monitoring for Specific Complications
Bleeding and Clotting
Despite the advances and evolution of VA ECMO techniques for cardiopulmonary support, survival remains low.18 Complications are commonplace and often lead to severe morbidity. By far the most common complication, regardless of cannulation strategy, is bleeding, with a reported incidence as high as 80%.19 Bleeding is a side effect not only of vessel injury from
cannula placement, but also due to the need for systemic anticoagulation (necessary to prevent device thrombosis and thromboembolism). Bleeding can be monitored by closely following the patient’s anticoagulation status with either activated clotting time (ACT) measurements or partial thromboplastin time (aPTT) values. Generally, maintaining ACT levels between 180-220 or aPTT levels 1.5 to 2.5 times baseline are acceptable goals.20 Unfractionated heparin is by far the most commonly used agent; however, in cases of heparin intolerance or allergy, argatroban or other direct thrombin inhibitors have been used. Institution-specific protocols, usually leveraging aPTT monitoring, should be developed specifically to help titrate these agents.
Typically, if the ECMO flows are high then clotting is uncommon. The smaller the cannulas and the lower the flows, the greater the risk for thrombotic complications. Monitoring for potential clotting can be done by physical inspection of the cannulas and oxygenator daily. Small deposition of fibrin is commonly found at these sites and, unless the clot burden becomes large, these will usually be of little clinical significance. In rare circumstances however, a circuit can partially or completely thrombose. In these cases, ECMO flows will dramatically decline and the patient will likely need emergent resuscitation. Depending upon clot location, inflow or outflow circuit pressures may change from baseline, alerting the clinician to flow perturbations. If the oxygenator, on the other hand, slowly accumulates thrombus, the blood passing through it will be less efficiently oxygenated. This can easily be monitored by checking a pre- and postoxygenator blood gas to examine the effectiveness of oxygenation and gas exchange. In a situation in which the oxygenator is no longer effective, it may be replaced. Replacement should be performed with the help of experienced providers in order to limit disruptions to blood flow and the sudden perturbations in patient hemodynamics that may ensue.
Left Ventricular Distension and Its Sequelae
A well-documented problem associated with VA ECMO is left ventricular distension. Inadequate unloading of the left ventricle (LV) is a variable but highly undesirable complication, seen roughly 10-70% of the time, particularly when using peripheral support.21,22 Peripheral VA
ECMO cannulation most often involves the placement of a venous cannula in the femoral vein that extends into the right atrium and an arterial cannula placed in the femoral artery extending retrograde into the descending aorta. LV distention occurs when the venous cannula is unable to completely empty the right heart, leaving residual blood to travel its normal course through the heart and lung’s native circulation. This, in addition to blood that already drains into the left heart from the bronchial circulation and Thebesian veins, will need to be ejected from the LV. At the same time, LV afterload will be increased as a result of the enhanced aortic pressures generated from the ECMO outflow limb. If LV contractile function is compromised enough then ventricular distension my ensue, resulting in a number of potential complications. This includes increased myocardial oxygen demand, ischemia, malignant arrhythmias, and impaired cardiac recovery. Additionally, inadequate unloading of the left heart can also lead to blood stasis and thrombus formation (Figure 3). The incidence of LV thrombus is unknown, but may complicate up to 10% of VA ECMO cases and can lead to pulmonary hemorrhage, systemic thromboembolism, and even death if not quickly addressed.23,24
There are several ways in which LV distention can be monitored. Periodic bedside echocardiography, using either TTE or TEE, can often very easily identify a left heart that is inadequately decompressed. It can often also aid in the recognition of stagnant blood and thrombus formation. Showing serial increases in a patient’s LV end-diastolic diameter (LVEDD) is one commonly used marker of worsening distention. Suboptimal aortic leaflet excursion, elevated Doppler-derived left heart pressures, and worsening aortic or mitral valve insufficiency can also be seen during echocardiographic evaluation of a distended LV.
Invasive hemodynamic data from a PAC can likewise be illustrative when monitoring for LV distention associated with VA ECMO. A distended left heart will often demonstrate rising LV and pulmonary arterial pressures – most notably an increase in pulmonary capillary wedge pressure (PCWP) as a surrogate for LV end-diastolic pressure (LVEDP). Truby et al recently described a sophisticated diagnostic criterion for LV distention based upon the pulmonary artery diastolic blood pressure (PADBP). In this study, patients with an elevated PADBP
underwent direct decompression though a variety of means including atrial septostomy, percutaneous left ventricular assist device (LVAD) placement, or via central LV vent implantation. These investigators followed trends in PADBP over time and noted that PADBP after a successful unloading maneuver could then replicate those values seen in patients without any distention from the start.21
Another complication that can result from worsening LV distention is the development of pulmonary edema. An elevated LVEDP from inadequate unloading can cause fluid to rapidly move out of the pulmonary capillaries and into lung’s interstitial space. This will lead to worsening edema (Figure 4, B). Ways to monitor for this complication include checking daily chest radiographs while patients are on VA ECMO and by looking for deteriorations in lung compliance reported on the ventilator circuit. Increasing oxygen requirements or increasing peak or plateau airway pressures on the ventilator may also indicate the development of worsening pulmonary edema or the presence of other pulmonary pathologies (including pneumonia, pneumothorax, or acute lung injury).
There are several options for addressing LV distension and its sequelae. Medical management may include the employment of specific lung-protective ventilator strategies, the use of diuretic therapies, tailored adjustments to ECMO flows, or the intensification of systemic anticoagulation. By far the most effective means for decompressing the left heart, however, is through the placement of an LV vent. LV vents can be placed percutaneously with a transseptal cannula via the femoral vein that drains the left atrium (LA) directly, or by using other percutaneous modalities such as an intra-aortic balloon pump or the axial-flow Impella platform of devices to help unload the LV.25-27 In many cases these interventions will be guided by echocardiographic monitoring. In a proof of concept study, Eliet et al assessed the impact of the Impella device on changes in LVEDD. Among their 11 patients with peripheral VA ECMO who had an Impella placed as a venting strategy, the LVEDD consistently decreased and pulmonary blood flow substantially increased with escalating Impella support.28 It should be noted, however, that the Impella may have its own set of complications which require
monitoring; this includes but is not limited to the development of hemolysis, limb ischemia, and device migration. Despite this, there is mounting evidence to suggest that it can be an effective adjunct for ventricular unloading.29
Limb Ischemia
Femoral arterial cannulation can impede blood flow to the distal extremity. Depending upon cannula size, vessel size, and the presence or absence of underlying peripheral vascular disease, patients may be at considerable risk for limb ischemia. The literature suggests that the incidence of limb ischemia while on VA ECMO may range from 13-25%.19 It is prudent, therefore, to monitor patients closely with frequent neurovascular examinations looking for clinical signs of limb ischemia including the loss of palpable pulses or Doppler signals, the presence of cold extremities, pain, tense or taught anatomical compartments. It should be noted however that physical examination may be challenging and even unreliable in patients on VA ECMO. To mitigate this complication, a distal reperfusion catheter can be placed in the superficial femoral artery that will allow blood flow to the distal extremity, generally at a rate of 0.5-1 L/min.30,31 Many institutions place these catheters on all peripherally cannulated VA ECMO patients as a matter of routine prophylaxis. Others may instead elect to wait until clinical signs of limb hyperperfusion develop. Still others have begun to rely on complementary NIRS monitoring (as previously described). Early identification is paramount – when ischemia compromises tissue integrity and results in compartment syndrome, patients my require emergent fasciotomy or even limb amputation.
Harlequin Syndrome
Even with full VA ECMO support and optimal unloading conditions, there will always be residual blood in the right heart that travels through the lungs, fills the LV, and may be ejected into the systemic circulation. In the setting of concomitant respiratory failure, the blood being ejected from the LV may be poorly oxygenated. Cerebral and coronary perfusion during peripheral VA
ECMO is dependent upon the premise that highly oxygenated blood from the femoral arterial cannula can travel retrograde.32 However, as the LV recovers and begins to eject, deoxygenated blood returned from the compromised lungs will begin to merge with oxygenated blood from the ECMO circuit at a site known as the mixing point. Resulting regional or differential hypoxemia can then occur, and the more distal the mixing point is the greater the risk for cerebral hypoxemia. This theory is supported by several animal models in which upper extremity hypoxemia worsens in the setting of persistent respiratory failure but progressive LV recovery.33,34 If regional hypoxemia becomes severe, hypoxic brain injury can ensue. Several monikers have been used for this clinical condition including Harlequin Syndrome or NorthSouth Syndrome.
Multiple methods for monitoring may be effective in identifying the Harlequin Syndrome. Checking arterial blood gases from the right radial artery (a site assumed to be most distal from the mixing point) is suggested. If the partial pressure of oxygen is adequate from the right radial artery, it can be inferred that cerebral oxygenation is likewise reasonable. Patients should also have daily neurological exams and scheduled sedation interruptions so that changes in mental status or the development of focal neurologic deficits can be tracked. If the Harlequin Syndrome is present, several acute interventions can be considered; this includes increasing the FiO2 on the ECMO circuit, increasing both the FiO2 and positive end-expiratory pressure (PEEP) on the ventilator, and increasing ECMO flows. If these maneuvers are insufficient, cannula adjustments may be required. Hou et al, for instance, recreated differential hypoxemia and then advanced the venous drainage cannula from the inferior vena cava more distally into the superior vena cava. This intervention alone resulted in improved drainage of deoxygenated blood and improvements in systemic oxygen saturation in many cases.35 In an analogous manner, the placement of a second venous drainage cannula in the superior vena cava, to augment right atrial decompression, may reduce the amount of deoxygenated blood returning to the left heart and therefore reduce its contribution to systemic oxygenation. LV venting can also be leveraged to reduce the contribution of poorly oxygenated LV blood to total systemic blood flow, and perhaps limit regional hypoxemia. For cases in which severe differential
hypoxemia persists, conversion to Veno-Arterial-Veno ECMO (VAV ECMO) can be considered. In this situation, oxygenated blood is delivered not only to the femoral arterial cannula but also to a venous drainage cannula. This allows for more oxygenated blood to travel through the native circulation and eject from the LV. If none of these interventions are successful, conversion to central VA ECMO may ultimately be required to overcome the deleterious impact of the Harlequin Syndrome.
Other Device Considerations
Often the ECMO circuit itself requires monitoring and potential troubleshooting. Both preload and afterload can impact blood flow through the device. Increases in afterload can diminish flow and cause high line pressures in the arterial cannula. Vasodilators are often used in this scenario to facilitate afterload reduction. Decreases in preload can lead to a rise in negative pressures within the venous cannula and can reduce ECMO flows. Following trends in central venous pressures can help to establish the reason for decreased preload. If low, this would suggest that intravascular volume administration may help to improve ECMO flows. Inadequate venous drainage can also occur in the setting of cardiac tamponade or due to mal-positioning of the venous cannula; in these cases, central venous pressures will usually be quite elevated. Daily chest radiography can confirm correct cannula positioning and assist in re-positioning if necessary (Figure 4, A). It is recommended that either an ECMO specialist or a perfusionist closely monitor the circuit and assist with troubleshooting. The circuit should be routinely checked for fibrin deposition as discussed previously. Air in the circuit can be catastrophic and should be both closely monitored and immediately addressed. Some of the newer devices have automated “bubble detection” algorithms in place that will promptly de-activate the device if air or abrupt changes in blood viscosity are identified. Limiting unnecessary access to the ECMO circuit can help to mitigate this complication.
Monitoring for Patient Recovery
Successful weaning of a patient from VA ECMO can be challenging. Among the myriad of conditions that may lead to ECMO use, post-cardiotomy cardiogenic shock patients have historically had the highest rates of successful weaning from mechanical support.19 Weaning from VA ECMO is a stepwise process that requires a multi-disciplinary team of nurses, intensivists, perfusionists, and surgeons (Figure 5). Before a patient can be assessed for recovery, end-organ dysfunction should be reversed. Experts from the Extracorporeal Life Support Organization (ELSO) suggest that prior to weaning, improvement in hepatic function is one of the most pivotal considerations.36 We believe that neurological recovery is also important to establish.
A number of studies have described predictors for successful VA ECMO weaning. Several have suggested that improved systemic arterial pulsatility (confirmed by an arterial line and reflective of increasing ejection of blood from the left ventricle) may be among the most useful markers.37,38 While specific cutoff values for arterial pulse pressure have not been validated, the return of pulsatility appears to be a useful tool for establishing recovery. Similarly, improvements in right ventricular function can be monitored by trending hemodynamics from a PAC. In particular, improved pulmonary arterial pulsatility may signify right ventricular recovery and a readiness to wean from mechanical support.
Another monitoring tool that can help to establish recovery is the echocardiogram. As previously mentioned, both TTE and TEE allow providers to assess LV and RV function, and can be a useful component of the decision tree when weaning is considered. Huang and colleagues used three-dimensional volumetric analysis and determined that if patients had an RV ejection fraction > 24.6% that they had a higher chance of successful weaning from VA ECMO and a lower 30-day mortality.39 Aissaoui et al have suggested that several other echocardiographic parameters may be helpful in determining weaning success; among these were the aortic velocity-time integral and the lateral mitral annulus peak systolic velocity.37 Echocardiography not only helps to determine a patient’s readiness for weaning but is also integral to the weaning process itself. Once a patient is deemed ready for de-escalation of mechanical support, initial
steps often include dropping the ECMO flows in 0.5-1.0 L/min intervals under real-time echocardiographic guidance. Contractile function, chamber size, and valvular integrity should all be closely monitored during progressive cardiac loading. Invasive hemodynamic parameters during the weaning process should also be closely monitored. Reassuring values that might suggest a successful wean include: cardiac index >2.4 L/min/m2, mean arterial blood pressure >60 mmHg, pulmonary capillary wedge pressure <18 mm Hg and central venous pressure <18 mmHg.40 If at any point during the weaning trial a patient decompensates, the ECMO flows should be immediately intensified to establish more robust cardiopulmonary support.
When considering weaning and decannulation from VA ECMO, it is also necessary to make sure patients are adequately supported with invasive mechanical ventilation. Patients should ideally be placed on lung protective ventilation settings. During the weaning trial, oxygen saturations should be closely observed. It is important to maintain a low FiO2 and low sweep gas flow rates through the ECMO circuit in order to leverage the ventilator as the primary means for pulmonary support. Pulmonary function that is consistent with successful weaning can be determined by several parameters, including a PaO2/ FiO2 ratio greater than 200 and an oxygen saturation above 90% at non-toxic supplemental FiO2 levels (i.e. less than 60%).
Once the patient is stable from a respiratory standpoint, the ECMO weaning trial can continue. Flows can be systematically decreased to a goal rate of 1-1.5 L/min as the patient’s hemodynamics, ventricular function and size, and volume status are assessed. Low dose vasoactive medications can be used as an adjunct during the weaning trial. It is important to note that low flows can lead to clot formation and propagation, so it is imperative that patients be adequately anticoagulated during this process if at all possible. If a patient tolerates minimal ECMO support, de-cannulation can be considered. De-cannulation can occur at the bedside for patients on peripheral ECMO, however most are taken to the operating room for safety reasons. Failure to wean from VA ECMO support should be evaluated. A more durable mechanical support option (i.e. LVAD), transplantation, or comfort care might be considered.
Engaging a multidisciplinary team of care providers to assist in this decision-making can often be most fruitful.
Monitoring Futility During VA ECMO
While outside the scope of this review, clinicians use monitoring tools not only to determine adequacy of support, eligibility for definitive therapies, and potential for recovery, but also to derive key information related to overall prognosis. What is less well-defined is the concept of futility and how monitoring technologies can assist with futility and withdrawal decisions. No doubt this is a challenging concept and can lead to ethical dilemmas and even disputes between providers and families or surrogates.41 Severe neurological injury, identified by either clinical exam or neuro-imaging may be one example of a futile clinical scenario. Unrelenting multisystem organ failure, including refractory hepatic failure, metabolic acidosis, sepsis, or hemodynamic instability are other conditions which may warrant futility discussions. Whether or not monitoring can be used to better understand futility in ECMO care remains to be determined, but should be a fertile area for future investigation.
Conclusion
The use of VA ECMO for cardiopulmonary support has escalated substantially over the past several years. Employing a multidisciplinary team of care providers – including surgeons, intensivists, nurses, perfusionists and others – to help make decisions is often best. Those clinicians who care for patients on VA ECMO can now capitalize on a myriad of monitoring tools that can help to establish adequacy of circulatory support, to monitor for complications, and to aid in the recovery and weaning process (Figure 6). It is also imperative that these clinicians understand both the strengths and limitations of each of these monitoring instruments. Finally, there is a compelling need to design and execute more robust, prospective clinical research studies and randomized trials to better inform the practice of ECMO patient monitoring.
Figure & Table Legend Figure 1:
Some typical features of a commercial ECMO monitor. Speed, flow, inflow (or venous) pressure, outflow (or arterial) pressure, and mixed venous oxygen saturation (SvO2) can be used to assess adequacy of support and to assist in ECMO and patient troubleshooting.
Figure 2:
A typical NIRS monitor will display oxygen saturations from both the left and right frontal regions of the brain. The monitor will alert clinicians if there is an acute change in observed saturations (e.g., the left NIRS has decreased 11% (A) and the right NIRS has decreased 12% (B)).
Figure 3:
Transesophageal echocardiogram showing LV distention and spontaneous echo contrast consistent with the development of stasis and thrombus.
Figure 4:
Chest radiograph showing a patient on VA ECMO confirming placement of the venous cannula in the right atrium (A) and showing evidence of pulmonary edema in bilateral lung fields (B).
Figure 5:
Typical pathway of weaning from VA ECMO. If the patient remains hemodynamically stable, the patient can likely proceed to decannulation.
Figure 6:
Overview of monitoring tools and their potential role in complementing the routine clinical care of a patient on VA ECMO.
Table 1:
Principles of Echocardiographic Monitoring During VA ECMO Support
TABLE 1 Monitoring Parameter
Goal(s) of Assessment
Chamber Size
Enlarged chamber size may suggest inadequate decompression Small chamber size may suggest excessive decompression and/or suboptimal preload Lack of leaflet excursion may indicate poor left ventricular contractile function and/or excessive left ventricular afterload All valves (especially aortic) can be evaluated for the presence/absence of severe insufficiency that may compromise the adequacy of ECMO support and optimal ventricular unloading All cardiac chambers and the aortic root can be interrogated for the presence/absence of thrombus or spontaneous echo contrast as a marker of blood stasis The presence/absence of pericardial effusion or cardiac tamponade can be assessed Cannula positioning and the presence/absence of cannula “kinking” or obstruction can be determined
Aortic Valve Excursion
Valvular Competency
Thrombus
Pericardium Venous Drainage Cannula
REFERENCES 1. Gerke AK, Tang F, Cavanaugh JE, et al. Increased trend in extracorporeal membrane oxygenation use by adults in the United States since 2007. BMC Res Notes 2015; 8:6869. 2. Barbaro RP, Odetolo 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. 3. Keebler ME, Haddad EV, Choi CW, et al. Venoarterial extracorporeal membrane oxygenation in cardiogenic shock. J Am Coll Cardiol HF 2018;6:503-16. 4. Rao P, Khalpey Z, Smith R, et al. Venoarterial extracorporeal membrane oxygenation for cardiogenic shock and cardiac arrest. Cardinal considerations for initiation and management. Circ Heart Fail 2018;11:1-17. 5. Vincent JL, Quintairos E, Silva A, et al. The value of blood lactate kinetics in critically ill patients: a systematic review. Crit Care 2016:20:257-70. 6. Werdan K, Russ M, Buerke M, et al. Cardiogenic shock due to myocardial infarction: diagnosis, monitoring and treatment. A German-Austrian S3 guideline. Dtsch Arztebl Int 2012;109:343-51. 7. Douflé G, Ferguson ND. Monitoring during extracorporeal membrane oxygenation. Curr Opin Crit Care 2016;22:230-8. 8. Douflé G, Roscoe A, Billia F, et al. Echocardiography for adult patients supported with extracorporeal membrane oxygenation. Crit Care 2015;19:326-35. 9. 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;25:131-41. 10. Bennett CE, Tweet MS, Michelena HI, et al. Safety and feasibility of contrast echocardiography for ECMO evaluation. JACC Cardiovasc Imag 2017;10:603-4. 11. Krishnan S, Schmidt GA. Hemodynamic monitoring in the extracorporeal membrane oxygenation patient. Curr Opin Crit Care 2019;25:285-91.
12. Pozzebon S, Blandino Ortiz A, Franchi F, et al. Cerebral near-infrared spectroscopy in adult patients undergoing veno-arterial extracorporeal membrane oxygenation. Neurocrit Care 2018;29:94-104. 13. Khan I, Rehan M, Parikh G, et al. Regional cerebral oximetry as an indicator of acute brain injury in adults undergoing veno-arterial extracorporeal membrane oxygenation – a prospective pilot study. Front Neurol 2018;9:993-1011. 14. Bickler P, Feiner J, Rollins M, et al. Tissue oximetry and clinical outcomes. Anesth Analg 2017;124:72-82. 15. Foley PJ, Morris RJ, Woo EY, et al. Limb ischemia during femoral cannulation for cardiopulmonary support. J Vasc Surg 2010;52:850-3. 16. Smedira NG, Moazami N, Golding CM, et al. Clinical experience with 202 adults receiving extracorporeal membrane oxygenation for cardiac failure: survival at five years. J Thorac Cardiovasc Surg 2001;122:92-102. 17. Kim DJ, Cho YJ, Park SH, et al. Near-infrared spectroscopy monitoring for early detection of limb ischemia in patients on veno-arterial extracorporeal membrane oxygenation. ASAIO J 2017;63:613-7. 18. Makdisi G, Wang I. Extracorporeal membrane oxygenation (ECMO) review of a lifesaving technology. J Thorac Dis 2015;7(7):E166-E176. 19. Lafçı G, Budak AB, Yener AU, et al. Use of extracorporeal membrane oxygenation in adults. Heart Lung Circ 2014;23:10-23. 20. Muntean W. Coagulation and anticoagulation in extracorporeal membrane oxygenation. Artif Organs 1999;23(11):979-83. 21. Truby LK, Takeda K, Mauro C, et al. Incidence and implications of left ventricular distention during venoarterial extracorporeal membrane oxygenation support. ASAIO J 2017;63:257-65. 22. Soleimani B, Pae WE. Management of left ventricular distention during peripheral extracorporeal membrane oxygenation for cardiogenic shock. Perfusion 2012;274(4):326-31.
23. Hireche-Chikaou H, Grubler MR, Bloch A, et al. Nonejecting hearts on femoral venoarterial extracorporeal membrane oxygenation: aortic root blood stasis and thrombus formation. Crit Care Med 2018;46:459-64. 24. Williams B, Bernstein W. Review of venoarterial extracorporeal membrane oxygenation and development of intracardiac thrombosis in adult cardiothoracic patients. J Extra Corpor Technol 2016; 48:162–67. 25. Meani P, Gelsomino S, Natour E, et al. Modalities and effects of left ventricle unloading on extracorporeal life support: a review of the current literature. Eur J Heart Fail 2017;19Suppl 2:84-91. 26. Dulnuan K, Guglin M, Zwischenberger J, et al. Left atrial veno-arterial extracorporeal membrane oxygenation: percutaneous bi-atrial drainage to avoid pulmonary edema in patients with left ventricular systolic dysfunction. JACC 2018;71(11):supplement. 27. Pappalardo F, Schulte C, Pieri M, et al. Concomitant implantation of Impella on top of veno-arterial extracorporeal membrane oxygenation may improve survival of patients with cardiogenic shock. Eur J Heart Fail 2017;19:404-12. 28. Eliet J, Gaudard P, Zeroual N, et al. Effect of Impella during veno-arterial extracorporeal membrane oxygenation on pulmonary artery flow as assessed by end-tidal carbon dioxide. ASAIO J 2018;64(4):502-7. 29. Koeckert MS, Jorde UP, Naka Y, et al. Impella LP 2.5 for left ventricular unloading during venoarterial extracorporeal membrane oxygenation support. Journal of Cardiac Surgery 2011;26(6):666-84. 30. Foley PJ, Morris RJ, Woo EY, et al. Limb ischemia during femoral cannulation for cardiopulmonary support. J Vasc Surg 2010;52:850-3. 31. Russo CF, Cannata A, Vitali E, et al. Prevention of limb ischemia and edema during peripheral venoarterial extracorporeal membrane oxygenation in adults. J Card Surg 2009;24:185-7. 32. Avgerinos DV, DeBois W, Voevidko L, et al. Regional variation in arterial saturation and oxygen delivery during venoarterial extracorporeal membrane oxygenation. 2013; 45(3): 183–86.
33. Kamimura T, Sakamoto H, Misumi K. Regional blood flow distribution from the proximal arterial cannula during veno-arterial extracorporeal membrane oxygenation in neonatal dog. J Vet Med Sci 1999;61:311–15. 34. Kato J, Seo T, Ando H, et al. Coronary arterial perfusion during venoarterial extracorporeal oxygenation. J Thorac Cardiovasc Surg 1996;111:630–636. 35. Hou X, Yang X, Du Z, et al. Superior vena cava drainage improves upper body oxygenation during veno-arterial extracorporeal membrane oxygenation in sheep. Crit Care 2015;19:68. 36. Aissaoui N, El-Banayosy A, Combes A. How to wean a patient from veno-arterial extracorporeal membrane oxygenation. Intensive Care Med 2015;41:902-5. 37. 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;37:1738-45. 38. Pappalardo F, Pieri M, Arnaez Corada B, et al. Timing and strategy for weaning From Venoarterial ECMO are Complex Issues. JCVA 2015;29:906-11. 39. Huang KC, Lin LY, Chen YS, et al. Three-dimensional echocardiography-derived right ventricular ejection fraction correlates with success of decannulation and prognosis in patients stabilized by venoarterial extracorporeal life support. J Am Soc Echocardiogr 2018;31:169-79. 40. Aziz TA, Singh G, Popjes E, et al. Initial experience with CentriMag extracorporeal membrane oxygenation for support of critically ill patients with refractory cardiogenic shock. J Heart Lung Transplant 2010;29:66-71. 41. Meltzer EC, Ivascu NS, Stark M, et al. A survey of physician attitudes toward decisionmaking authority for initiating and withdrawing VA-ECMO: results and ethical implications for shared decision-making. J Clin Ethics 2016;27:281-9.
ECMO Circuit •
Adequacy of Support
• •
Maintenance of flows between 50-70 mL/kg Stable inflow/outflow pressures Adequate mixed venous O2 sat
Invasive Hemodynamics
Laboratory Values • • • •
Stable acid/base status Lactate normalizes Improved BUN, creatinine, LFTs Markers of anticoagulation at target (ACT, aPTT)
• • •
Normalization of intracardiac filling pressures Adequate mixed venous O2 sat Target MAP (65-80 mmHg) achieved
TTE and TEE Imaging • •
Monitor for adequate ventricular unloading Identify optimal cannula positioning
NIRS and Other Imaging • •
Stable NIRS cerebral oxygenation Resolution of pulmonary edema on CXR
Complications •
Bleeding
•
•
Clotting
• •
May see reduced inflow circuit pressures May see decreased mixed venous O2 saturation Depending upon location within ECMO circuit, may see acute changes in inflow or outflow pressures May see reduced ECMO flows May see clot in oxygenator or circuit and suboptimal postoxygenator gas exchange
• •
•
Will see a decline in serum Hgb May see rise in serum lactate if compromising systemic perfusion
May see markers of hemolysis (elevated LDH, reduced haptoglobin, elevated plasma-free Hgb)
• • •
•
• •
LV Distension
Reduced cardiac filling pressures Hypotension and reduced arterial pulsatility Reduced mixed venous O2 sat
May see rising intracardiac filling pressures and reduced mixed venous O2 sat depending upon clot location and impact on ECMO flows
Minimal arterial pulsatility Elevated PCWP
• •
•
•
• •
Look for potential causes – cannula mal-positioning, pericardial effusion
Inadequate ventricular unloading may suggest suboptimal ECMO support due to thrombosis May visualize intra-cardiac clot
Enlarged LV chamber size Limited aortic valve leaflet excursion
•
•
May see pulmonary edema on CXR as a consequence of inadequate ECMO support
•
Pulmonary edema on CXR
•
May see acute or unilateral decrease in cerebral oxygen saturations
•
Persistent pulmonary edema or co-existing pulmonary pathology (e.g. pneumonia/pneumonitis,
Neurologic Injury Limb Ischemia
•
May see rise in serum lactate, creatine kinase
•
Regional Hypoxemia
If intra-cranial bleeding, may see reduction in regional cerebral oxygen saturation on ipsilateral side Alveolar infiltrates on CXR if pulmonary hemorrhage
Reduced PaO2 or O2 saturation in right radial artery
•
May identify improved cardiac function causing differential systemic
S0828-282X(19)31384-4
DOI:
https://doi.org/10.1016/j.cjca.2019.10.031
Reference:
CJCA 3497
To appear in:
Canadian Journal of Cardiology
Received Date: 30 August 2019 Revised Date:
17 October 2019
Accepted Date: 30 October 2019
Please cite this article as: Bhatia M, Katz JN, Contemporary Comprehensive Monitoring Of The VenoArterial Extracorporeal Membrane Oxygenation Patient, Canadian Journal of Cardiology (2019), doi: https://doi.org/10.1016/j.cjca.2019.10.031. This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. © 2019 Published by Elsevier Inc. on behalf of the Canadian Cardiovascular Society.
CONTEMPORARY COMPREHENSIVE MONITORING OF THE VENO-ARTERIAL EXTRACORPOREAL MEMBRANE OXYGENATION PATIENT Meena Bhatia, MD1 and Jason N. Katz, MD, MHS2
1
Department of Anesthesiology, Division of Critical Care Medicine, University of North Carolina, Chapel Hill, NC; email: [email protected]
2
Department of Medicine and Surgery, Division of Cardiovascular Medicine, University of North Carolina, Chapel Hill, NC; email: [email protected] Address for Correspondence: Jason N. Katz, MD, MHS 160 Dental Circle, CB#7075 6th Floor Burnett-Womack Building Chapel Hill, NC 27599-7075 Tel: (919) 843-0447 Email: [email protected]
Disclosures – The authors have nothing to disclose relevant to this manuscript.
ABSTRACT WORD COUNT: 225 DOCUMENT WORD COUNT (INCLUDING REFERENCES): 6598
ABSTRACT The use of veno-arterial extracorporeal membrane oxygenation (VA ECMO) has increased substantially over the last few decades. Today’s clinicians now have a powerful means with which to salvage a growing population of patients at risk for cardiopulmonary collapse. At the same time, patients supported with VA ECMO have become increasingly more complex. The successful use of VA ECMO depends not only upon choosing the right individual to support, but also being able to effectively navigate a potential torrent of device and patient-related complications until ECMO is no longer needed. A multitude of monitoring tools are now available to help the treatment team determine the adequacy of care, to detect problems, and to anticipate recovery. Monitoring with devices such as the Swan-Ganz catheter, transthoracic and transesophageal echocardiography, chest radiography, and near-infrared spectroscopy can all provide useful information to complement routine clinical care. Leveraging data derived from the ECMO circuit itself can also be instrumental in both evaluating the sufficiency of support and in troubleshooting complications. Each of these tools, however, has their own unique sets of limitations and liabilities. A thorough understanding of these risks and benefits is now critical to the contemporary care of the individual managed with VA ECMO. Additionally, more research is needed in order to establish optimal, evidence-based care pathways and best practice principles which incorporate these devices to improve patient outcomes.
ELECTRONIC TABLE OF CONTENTS SUMMARY (75 Words) Veno-Arterial Extracorporeal Membrane Oxygenation (VA ECMO) is used as an emergent support tool for patients with cardiogenic shock or cardiac arrest. Though it has great potential to reverse end-organ dysfunction and to re-establish adequate cardiopulmonary function, numerous complications may ensue. There are a myriad of monitoring tools – each with its unique set of benefits and liabilities –available to assist the treating physician. A comprehensive understanding of these monitoring modalities is now essential to contemporary care.
Extracorporeal membrane oxygenation (ECMO), in its veno-arterial (VA) configuration, is being increasingly utilized to mechanically support patients with severely compromised cardiopulmonary function.1 For patients with cardiogenic shock or cardiac arrest, whose conditions were once considered futile, ECMO can now be leveraged as an emergent bridge to recovery, to durable mechanical circulatory support (MCS), or to transplantation. Recent data would suggest that provider experience is perhaps the most important determinant of patient outcome.2 Today’s clinicians must not only be familiar with the various components of these devices but must also be comfortable with assessing the adequacy of support. At the same time, providers must vigilantly monitor for and be prepared to contend with the myriad of potential complications attributable to VA ECMO. These include device and patient thrombosis, progressive hemodynamic instability, bleeding, global and regional hypoxemia, neurologic injury, and limb ischemia. Numerous monitoring technologies are now available for the treating clinician, and can help guide care and aid in troubleshooting. The following review will focus on the benefits, liabilities, and evidence informing the use of these tools, and outline their potential role in complementing the routine clinical management of today’s VA ECMO patient.
Monitoring Tools
When utilizing circulatory support strategies for critically ill patients with shock, a clear understanding of the goals of care is crucial to patient success. VA ECMO is most often used to promptly restore and then maintain the following three clinical conditions: 1) adequate balance between systemic oxygen delivery and consumption, 2) adequate tissue and end-organ perfusion, and 3) adequate systemic gas exchange (i.e. oxygenation and ventilation). In conjunction with serial clinical examinations, a variety of monitoring modalities can help the provider continuously assess the adequacy of support and confirm that the aforementioned conditions are being met. Additionally, these monitoring tools can be used to assess and troubleshoot acute changes to patient and device stability, and can provide highly valuable and often real-time diagnostic information necessary to identify and treat a variety of potential complications.
The ECMO Circuit
Most ECMO circuits have a display monitor that provides real-time data that can be reviewed. Figure 1 illustrates several common features of a contemporary VA ECMO monitor. While specific ECMO flow targets have been poorly elucidated, and should be individualized based upon patient need and the desired degree of mechanical assistance, it has been suggested that flows between 50-70 mL/kg/min may be a reasonable initial goal.3 VA ECMO flows that vary considerably despite a stable ECMO speed may indicate a device or patient problem and requires prompt investigation. Sudden and sustained alterations in both venous (inflow) and arterial (outflow) circuit pressures may suggest problems with cannula positioning, device obstruction, or acute changes in cardiac loading conditions.4 Additionally, measures of premembrane oxygen saturation – or mixed venous oxygen saturation – are usually displayed on contemporary VA ECMO circuits. A decrease in pre-membrane oxygen saturation is often correlated with a decrease in systemic oxygen delivery and an increase in tissue extraction ratio. This should prompt the treating clinician to consider efforts to either optimize delivery or reduce oxygen consumption.
Laboratory Studies
Serial review of laboratory studies may also help one to determine both the adequacy and stability of VA ECMO support for a critically ill patient. Maintaining reasonable end-organ perfusion is vital, and serum markers of organ function can be readily obtained. Blood urea nitrogen (BUN) and creatinine should be frequently monitored measures of renal function and recovery. Improvements in serum electrolytes should parallel optimization in renal, hepatic, and generalized tissue perfusion. Liver function studies should be used to monitor hepatic stability, and repeated assessments of plasma lactate can inform clinicians about the persistence or resolution of a patient’s shock state.5 Persistent lactic acidosis, despite sufficient resuscitation and seemingly adequate support, could be indicative of a concealed complication;
examples include bowel ischemia, limb ischemia, and the abdominal compartment syndrome, to name a few. Regardless of the cause, immediate investigation of unrelenting acidosis is vital.
Invasive Hemodynamics - Arterial Lines and Pulmonary Artery Catheters
Monitoring invasive blood pressure, acid-base balance, and systemic gas exchange are all vital components linked to the successful management of VA ECMO patients. An arterial line, ideally placed in the right arm, is an important indicator of the adequacy of circulatory support. While a target mean arterial pressure (MAP) is debatable, data extrapolated from other critical care cohorts would suggest a goal of between 65-80 mmHg is reasonable.6 This would presumably provide good systemic perfusion while avoiding the potentially deleterious impact of high left ventricular afterload. Much like serial measurements of serum lactate, the presence and persistence of metabolic acidosis can suggest inadequate tissue perfusion and should lead to alterations in ECMO support. Likewise, problems with gas exchange may warrant intensification of ECMO flow, modification of complementary ventilatory therapy, or alterations to oxygenation or sweep rates within the ECMO circuit.
The pulmonary artery catheter (PAC) can also be a useful adjunct to the monitoring armamentarium used by clinicians who manage patients on VA ECMO. Invasive cardiac filling pressures can indicate the degree and adequacy of ventricular unloading, particularly if clinical decompensation is present. Additionally, variations in pulmonary arterial saturation – like changes in ECMO pre-membrane venous saturation – can alert the treatment team to changes in systemic oxygen delivery and consumption. While cardiac pressures and oxygen saturations are directly measured, it is important to note that cardiac output measurements derived from thermodilution methods are assumed to be less reliable.7 Mixing of blood in the right heart and variations in venous drainage will frequently threaten to confound measurements of temperature changes over time.
Changes in both systemic and pulmonary arterial pulse pressure, or pulsatility, can also be observed during VA ECMO support. Absent or very low pulsatility suggests severe cardiac contractile dysfunction and/or markedly reduced ventricular ejection. Interventions to reduce blood stasis and to attenuate resulting thrombotic risk may therefore be indicated. Increasing pulsatility, on the other hand, may be indicative of a recovering heart and improved native heart function. Monitoring the morphology of the pulse waveforms can therefore assist clinicians in assessing the adequacy of and need for ongoing MCS. Given the breadth of information that can be derived from invasive hemodynamic monitoring, the authors recommend the routine placement of arterial lines and pulmonary artery catheters in all VA ECMO patients unless a clinical contraindication exists.
Echocardiography and Chest Radiography
The echocardiogram, and in particular the use of serial echocardiography, is also a pivotal component of ECMO management. A transthoracic echocardiogram (TTE) can provide vital information about cardiac chamber size (as a surrogate for ventricular decompression), aortic valve excursion, the presence or absence of intracardiac and aortic root thrombus, valvular competency, pericardial disease (effusion and tamponade), and contractility.8 Additionally, TTE can confirm appropriate cannula positioning and can identify certain causes of circuit obstruction (including cannula thrombosis and kinking). In some cases, TTE may fail to provide adequate enough spatial resolution.9 In these instances, transesophageal echocardiography (TEE) should be considered. In instances where echo quality remains poor due to the presence of chest tubes, ventilator interference, or restricted patient positioning, intra-cavitary opacification with echo contrast has been employed. At this time, however, there is insufficient data to support the safety of this approach. Reports of contrast material activating the integrated bubble detector on some devices have been published, and this can lead to temporary cessation of ECMO flow and resulting patient instability.10 Until formally tested in a prospective manner, the ideal frequency of echocardiographic monitoring will remain unclear. Anecdotally, however, many believe that daily imaging should be part of a standard ECMO
monitoring protocol. Table 1 outlines the valuable information that can be derived specifically from echocardiography during ECMO support.
Radiographic imaging of the chest is also a useful monitoring tool. In particular, the presence of pulmonary edema can be an indirect clue that the left heart is being inadequately unloaded and that left-sided cardiac filling pressures are elevated. Additionally, the chest x-ray can be used to assess the stability of invasive catheters and ECMO cannulas, as well as to evaluate for concomitant pulmonary pathologies (e.g. alveolar hemorrhage, pleural effusions, pneumonia). An enlarging cardiac silhouette on plain film may indicate the development of a pericardial fluid collection or may be a sign of suboptimal cardiac decompression. While there is little evidence to establish the optimal frequency of radiographic monitoring, the authors currently advise daily chest x-rays to complement clinical care.
Near-Infrared Spectroscopy and Neurovascular Monitoring
Near-Infrared Spectroscopy (NIRS) is a non-invasive tool that leverages near-infrared wavelengths of light to provide continuous measurements of regional tissue oxygen saturation (rSO2).11 It has been used to determine the relative balance between oxygen delivery and demand in ECMO patients. More specifically, when placed on a patient’s scalp, NIRS can measure cerebral oximetry in both the left and right frontal regions (Figure 2). Cerebral desaturation has been associated with poor outcomes among adult patients supported with VA ECMO and may predict acute cerebral complications.12,13 Very high cerebral rSO2 values have also been associated with poor neurologic outcomes.14 While the potential merit of this tool in evaluating neurologic function in ECMO patients whose clinical exams may be confounded by the use of sedatives, analgesics, and neuromuscular blockers seems obvious, no well-validated NIRS protocols currently exist. The evidence base, instead, is limited to small case series and expert opinion documents. Additionally, it is important to acknowledge that this technology can only be used to assess regional cerebral oxygen saturations; deeper, subcortical and global pathologies may be missed.13
NIRS has also been used to monitor for distal limb ischemia – a potential complication of peripheral ECMO cannulation that develops in greater than 20% of patients and has substantial morbidity and mortality liability.15,16 The clinical examination and Doppler pulse evaluation of an ECMO patient are notoriously unreliable, especially for detecting early limb compromise.17 A sustained drop in lower extremity rSO2 has been observed in the majority of patients with lower extremity ischemia and can often improve with acute interventions such as the placement of a distal perfusion catheter.17 Additional prospective evaluation is needed to better define the role of NIRS for ECMO patient monitoring, but this technology appears to hold great promise.
NIRS monitoring, however, should not replace routine clinical examinations. Frequent neurologic exams with daily sedation interruptions remain vital to the care of the VA ECMO patient and should be performed regularly when possible. Any acute changes in exam findings must be noted and investigated. Routine serial neurological imaging, on the other hand, is neither required nor supported by the current evidence-base, and brain imaging should instead be used only if a change in the patient’s neurologic exam requires additional investigation. Certainly if a patient is arousable, demonstrates no focal neurological deficits, and can follow simple commands while on VA ECMO, it is reasonable to assume that cerebral function and perfusion is stable.
Monitoring for Specific Complications
Bleeding and Clotting
Despite the advances and evolution of VA ECMO techniques for cardiopulmonary support, survival remains low.18 Complications are commonplace and often lead to severe morbidity. By far the most common complication, regardless of cannulation strategy, is bleeding, with a reported incidence as high as 80%.19 Bleeding is a side effect not only of vessel injury from
cannula placement, but also due to the need for systemic anticoagulation (necessary to prevent device thrombosis and thromboembolism). Bleeding can be monitored by closely following the patient’s anticoagulation status with either activated clotting time (ACT) measurements or partial thromboplastin time (aPTT) values. Generally, maintaining ACT levels between 180-220 or aPTT levels 1.5 to 2.5 times baseline are acceptable goals.20 Unfractionated heparin is by far the most commonly used agent; however, in cases of heparin intolerance or allergy, argatroban or other direct thrombin inhibitors have been used. Institution-specific protocols, usually leveraging aPTT monitoring, should be developed specifically to help titrate these agents.
Typically, if the ECMO flows are high then clotting is uncommon. The smaller the cannulas and the lower the flows, the greater the risk for thrombotic complications. Monitoring for potential clotting can be done by physical inspection of the cannulas and oxygenator daily. Small deposition of fibrin is commonly found at these sites and, unless the clot burden becomes large, these will usually be of little clinical significance. In rare circumstances however, a circuit can partially or completely thrombose. In these cases, ECMO flows will dramatically decline and the patient will likely need emergent resuscitation. Depending upon clot location, inflow or outflow circuit pressures may change from baseline, alerting the clinician to flow perturbations. If the oxygenator, on the other hand, slowly accumulates thrombus, the blood passing through it will be less efficiently oxygenated. This can easily be monitored by checking a pre- and postoxygenator blood gas to examine the effectiveness of oxygenation and gas exchange. In a situation in which the oxygenator is no longer effective, it may be replaced. Replacement should be performed with the help of experienced providers in order to limit disruptions to blood flow and the sudden perturbations in patient hemodynamics that may ensue.
Left Ventricular Distension and Its Sequelae
A well-documented problem associated with VA ECMO is left ventricular distension. Inadequate unloading of the left ventricle (LV) is a variable but highly undesirable complication, seen roughly 10-70% of the time, particularly when using peripheral support.21,22 Peripheral VA
ECMO cannulation most often involves the placement of a venous cannula in the femoral vein that extends into the right atrium and an arterial cannula placed in the femoral artery extending retrograde into the descending aorta. LV distention occurs when the venous cannula is unable to completely empty the right heart, leaving residual blood to travel its normal course through the heart and lung’s native circulation. This, in addition to blood that already drains into the left heart from the bronchial circulation and Thebesian veins, will need to be ejected from the LV. At the same time, LV afterload will be increased as a result of the enhanced aortic pressures generated from the ECMO outflow limb. If LV contractile function is compromised enough then ventricular distension my ensue, resulting in a number of potential complications. This includes increased myocardial oxygen demand, ischemia, malignant arrhythmias, and impaired cardiac recovery. Additionally, inadequate unloading of the left heart can also lead to blood stasis and thrombus formation (Figure 3). The incidence of LV thrombus is unknown, but may complicate up to 10% of VA ECMO cases and can lead to pulmonary hemorrhage, systemic thromboembolism, and even death if not quickly addressed.23,24
There are several ways in which LV distention can be monitored. Periodic bedside echocardiography, using either TTE or TEE, can often very easily identify a left heart that is inadequately decompressed. It can often also aid in the recognition of stagnant blood and thrombus formation. Showing serial increases in a patient’s LV end-diastolic diameter (LVEDD) is one commonly used marker of worsening distention. Suboptimal aortic leaflet excursion, elevated Doppler-derived left heart pressures, and worsening aortic or mitral valve insufficiency can also be seen during echocardiographic evaluation of a distended LV.
Invasive hemodynamic data from a PAC can likewise be illustrative when monitoring for LV distention associated with VA ECMO. A distended left heart will often demonstrate rising LV and pulmonary arterial pressures – most notably an increase in pulmonary capillary wedge pressure (PCWP) as a surrogate for LV end-diastolic pressure (LVEDP). Truby et al recently described a sophisticated diagnostic criterion for LV distention based upon the pulmonary artery diastolic blood pressure (PADBP). In this study, patients with an elevated PADBP
underwent direct decompression though a variety of means including atrial septostomy, percutaneous left ventricular assist device (LVAD) placement, or via central LV vent implantation. These investigators followed trends in PADBP over time and noted that PADBP after a successful unloading maneuver could then replicate those values seen in patients without any distention from the start.21
Another complication that can result from worsening LV distention is the development of pulmonary edema. An elevated LVEDP from inadequate unloading can cause fluid to rapidly move out of the pulmonary capillaries and into lung’s interstitial space. This will lead to worsening edema (Figure 4, B). Ways to monitor for this complication include checking daily chest radiographs while patients are on VA ECMO and by looking for deteriorations in lung compliance reported on the ventilator circuit. Increasing oxygen requirements or increasing peak or plateau airway pressures on the ventilator may also indicate the development of worsening pulmonary edema or the presence of other pulmonary pathologies (including pneumonia, pneumothorax, or acute lung injury).
There are several options for addressing LV distension and its sequelae. Medical management may include the employment of specific lung-protective ventilator strategies, the use of diuretic therapies, tailored adjustments to ECMO flows, or the intensification of systemic anticoagulation. By far the most effective means for decompressing the left heart, however, is through the placement of an LV vent. LV vents can be placed percutaneously with a transseptal cannula via the femoral vein that drains the left atrium (LA) directly, or by using other percutaneous modalities such as an intra-aortic balloon pump or the axial-flow Impella platform of devices to help unload the LV.25-27 In many cases these interventions will be guided by echocardiographic monitoring. In a proof of concept study, Eliet et al assessed the impact of the Impella device on changes in LVEDD. Among their 11 patients with peripheral VA ECMO who had an Impella placed as a venting strategy, the LVEDD consistently decreased and pulmonary blood flow substantially increased with escalating Impella support.28 It should be noted, however, that the Impella may have its own set of complications which require
monitoring; this includes but is not limited to the development of hemolysis, limb ischemia, and device migration. Despite this, there is mounting evidence to suggest that it can be an effective adjunct for ventricular unloading.29
Limb Ischemia
Femoral arterial cannulation can impede blood flow to the distal extremity. Depending upon cannula size, vessel size, and the presence or absence of underlying peripheral vascular disease, patients may be at considerable risk for limb ischemia. The literature suggests that the incidence of limb ischemia while on VA ECMO may range from 13-25%.19 It is prudent, therefore, to monitor patients closely with frequent neurovascular examinations looking for clinical signs of limb ischemia including the loss of palpable pulses or Doppler signals, the presence of cold extremities, pain, tense or taught anatomical compartments. It should be noted however that physical examination may be challenging and even unreliable in patients on VA ECMO. To mitigate this complication, a distal reperfusion catheter can be placed in the superficial femoral artery that will allow blood flow to the distal extremity, generally at a rate of 0.5-1 L/min.30,31 Many institutions place these catheters on all peripherally cannulated VA ECMO patients as a matter of routine prophylaxis. Others may instead elect to wait until clinical signs of limb hyperperfusion develop. Still others have begun to rely on complementary NIRS monitoring (as previously described). Early identification is paramount – when ischemia compromises tissue integrity and results in compartment syndrome, patients my require emergent fasciotomy or even limb amputation.
Harlequin Syndrome
Even with full VA ECMO support and optimal unloading conditions, there will always be residual blood in the right heart that travels through the lungs, fills the LV, and may be ejected into the systemic circulation. In the setting of concomitant respiratory failure, the blood being ejected from the LV may be poorly oxygenated. Cerebral and coronary perfusion during peripheral VA
ECMO is dependent upon the premise that highly oxygenated blood from the femoral arterial cannula can travel retrograde.32 However, as the LV recovers and begins to eject, deoxygenated blood returned from the compromised lungs will begin to merge with oxygenated blood from the ECMO circuit at a site known as the mixing point. Resulting regional or differential hypoxemia can then occur, and the more distal the mixing point is the greater the risk for cerebral hypoxemia. This theory is supported by several animal models in which upper extremity hypoxemia worsens in the setting of persistent respiratory failure but progressive LV recovery.33,34 If regional hypoxemia becomes severe, hypoxic brain injury can ensue. Several monikers have been used for this clinical condition including Harlequin Syndrome or NorthSouth Syndrome.
Multiple methods for monitoring may be effective in identifying the Harlequin Syndrome. Checking arterial blood gases from the right radial artery (a site assumed to be most distal from the mixing point) is suggested. If the partial pressure of oxygen is adequate from the right radial artery, it can be inferred that cerebral oxygenation is likewise reasonable. Patients should also have daily neurological exams and scheduled sedation interruptions so that changes in mental status or the development of focal neurologic deficits can be tracked. If the Harlequin Syndrome is present, several acute interventions can be considered; this includes increasing the FiO2 on the ECMO circuit, increasing both the FiO2 and positive end-expiratory pressure (PEEP) on the ventilator, and increasing ECMO flows. If these maneuvers are insufficient, cannula adjustments may be required. Hou et al, for instance, recreated differential hypoxemia and then advanced the venous drainage cannula from the inferior vena cava more distally into the superior vena cava. This intervention alone resulted in improved drainage of deoxygenated blood and improvements in systemic oxygen saturation in many cases.35 In an analogous manner, the placement of a second venous drainage cannula in the superior vena cava, to augment right atrial decompression, may reduce the amount of deoxygenated blood returning to the left heart and therefore reduce its contribution to systemic oxygenation. LV venting can also be leveraged to reduce the contribution of poorly oxygenated LV blood to total systemic blood flow, and perhaps limit regional hypoxemia. For cases in which severe differential
hypoxemia persists, conversion to Veno-Arterial-Veno ECMO (VAV ECMO) can be considered. In this situation, oxygenated blood is delivered not only to the femoral arterial cannula but also to a venous drainage cannula. This allows for more oxygenated blood to travel through the native circulation and eject from the LV. If none of these interventions are successful, conversion to central VA ECMO may ultimately be required to overcome the deleterious impact of the Harlequin Syndrome.
Other Device Considerations
Often the ECMO circuit itself requires monitoring and potential troubleshooting. Both preload and afterload can impact blood flow through the device. Increases in afterload can diminish flow and cause high line pressures in the arterial cannula. Vasodilators are often used in this scenario to facilitate afterload reduction. Decreases in preload can lead to a rise in negative pressures within the venous cannula and can reduce ECMO flows. Following trends in central venous pressures can help to establish the reason for decreased preload. If low, this would suggest that intravascular volume administration may help to improve ECMO flows. Inadequate venous drainage can also occur in the setting of cardiac tamponade or due to mal-positioning of the venous cannula; in these cases, central venous pressures will usually be quite elevated. Daily chest radiography can confirm correct cannula positioning and assist in re-positioning if necessary (Figure 4, A). It is recommended that either an ECMO specialist or a perfusionist closely monitor the circuit and assist with troubleshooting. The circuit should be routinely checked for fibrin deposition as discussed previously. Air in the circuit can be catastrophic and should be both closely monitored and immediately addressed. Some of the newer devices have automated “bubble detection” algorithms in place that will promptly de-activate the device if air or abrupt changes in blood viscosity are identified. Limiting unnecessary access to the ECMO circuit can help to mitigate this complication.
Monitoring for Patient Recovery
Successful weaning of a patient from VA ECMO can be challenging. Among the myriad of conditions that may lead to ECMO use, post-cardiotomy cardiogenic shock patients have historically had the highest rates of successful weaning from mechanical support.19 Weaning from VA ECMO is a stepwise process that requires a multi-disciplinary team of nurses, intensivists, perfusionists, and surgeons (Figure 5). Before a patient can be assessed for recovery, end-organ dysfunction should be reversed. Experts from the Extracorporeal Life Support Organization (ELSO) suggest that prior to weaning, improvement in hepatic function is one of the most pivotal considerations.36 We believe that neurological recovery is also important to establish.
A number of studies have described predictors for successful VA ECMO weaning. Several have suggested that improved systemic arterial pulsatility (confirmed by an arterial line and reflective of increasing ejection of blood from the left ventricle) may be among the most useful markers.37,38 While specific cutoff values for arterial pulse pressure have not been validated, the return of pulsatility appears to be a useful tool for establishing recovery. Similarly, improvements in right ventricular function can be monitored by trending hemodynamics from a PAC. In particular, improved pulmonary arterial pulsatility may signify right ventricular recovery and a readiness to wean from mechanical support.
Another monitoring tool that can help to establish recovery is the echocardiogram. As previously mentioned, both TTE and TEE allow providers to assess LV and RV function, and can be a useful component of the decision tree when weaning is considered. Huang and colleagues used three-dimensional volumetric analysis and determined that if patients had an RV ejection fraction > 24.6% that they had a higher chance of successful weaning from VA ECMO and a lower 30-day mortality.39 Aissaoui et al have suggested that several other echocardiographic parameters may be helpful in determining weaning success; among these were the aortic velocity-time integral and the lateral mitral annulus peak systolic velocity.37 Echocardiography not only helps to determine a patient’s readiness for weaning but is also integral to the weaning process itself. Once a patient is deemed ready for de-escalation of mechanical support, initial
steps often include dropping the ECMO flows in 0.5-1.0 L/min intervals under real-time echocardiographic guidance. Contractile function, chamber size, and valvular integrity should all be closely monitored during progressive cardiac loading. Invasive hemodynamic parameters during the weaning process should also be closely monitored. Reassuring values that might suggest a successful wean include: cardiac index >2.4 L/min/m2, mean arterial blood pressure >60 mmHg, pulmonary capillary wedge pressure <18 mm Hg and central venous pressure <18 mmHg.40 If at any point during the weaning trial a patient decompensates, the ECMO flows should be immediately intensified to establish more robust cardiopulmonary support.
When considering weaning and decannulation from VA ECMO, it is also necessary to make sure patients are adequately supported with invasive mechanical ventilation. Patients should ideally be placed on lung protective ventilation settings. During the weaning trial, oxygen saturations should be closely observed. It is important to maintain a low FiO2 and low sweep gas flow rates through the ECMO circuit in order to leverage the ventilator as the primary means for pulmonary support. Pulmonary function that is consistent with successful weaning can be determined by several parameters, including a PaO2/ FiO2 ratio greater than 200 and an oxygen saturation above 90% at non-toxic supplemental FiO2 levels (i.e. less than 60%).
Once the patient is stable from a respiratory standpoint, the ECMO weaning trial can continue. Flows can be systematically decreased to a goal rate of 1-1.5 L/min as the patient’s hemodynamics, ventricular function and size, and volume status are assessed. Low dose vasoactive medications can be used as an adjunct during the weaning trial. It is important to note that low flows can lead to clot formation and propagation, so it is imperative that patients be adequately anticoagulated during this process if at all possible. If a patient tolerates minimal ECMO support, de-cannulation can be considered. De-cannulation can occur at the bedside for patients on peripheral ECMO, however most are taken to the operating room for safety reasons. Failure to wean from VA ECMO support should be evaluated. A more durable mechanical support option (i.e. LVAD), transplantation, or comfort care might be considered.
Engaging a multidisciplinary team of care providers to assist in this decision-making can often be most fruitful.
Monitoring Futility During VA ECMO
While outside the scope of this review, clinicians use monitoring tools not only to determine adequacy of support, eligibility for definitive therapies, and potential for recovery, but also to derive key information related to overall prognosis. What is less well-defined is the concept of futility and how monitoring technologies can assist with futility and withdrawal decisions. No doubt this is a challenging concept and can lead to ethical dilemmas and even disputes between providers and families or surrogates.41 Severe neurological injury, identified by either clinical exam or neuro-imaging may be one example of a futile clinical scenario. Unrelenting multisystem organ failure, including refractory hepatic failure, metabolic acidosis, sepsis, or hemodynamic instability are other conditions which may warrant futility discussions. Whether or not monitoring can be used to better understand futility in ECMO care remains to be determined, but should be a fertile area for future investigation.
Conclusion
The use of VA ECMO for cardiopulmonary support has escalated substantially over the past several years. Employing a multidisciplinary team of care providers – including surgeons, intensivists, nurses, perfusionists and others – to help make decisions is often best. Those clinicians who care for patients on VA ECMO can now capitalize on a myriad of monitoring tools that can help to establish adequacy of circulatory support, to monitor for complications, and to aid in the recovery and weaning process (Figure 6). It is also imperative that these clinicians understand both the strengths and limitations of each of these monitoring instruments. Finally, there is a compelling need to design and execute more robust, prospective clinical research studies and randomized trials to better inform the practice of ECMO patient monitoring.
Figure & Table Legend Figure 1:
Some typical features of a commercial ECMO monitor. Speed, flow, inflow (or venous) pressure, outflow (or arterial) pressure, and mixed venous oxygen saturation (SvO2) can be used to assess adequacy of support and to assist in ECMO and patient troubleshooting.
Figure 2:
A typical NIRS monitor will display oxygen saturations from both the left and right frontal regions of the brain. The monitor will alert clinicians if there is an acute change in observed saturations (e.g., the left NIRS has decreased 11% (A) and the right NIRS has decreased 12% (B)).
Figure 3:
Transesophageal echocardiogram showing LV distention and spontaneous echo contrast consistent with the development of stasis and thrombus.
Figure 4:
Chest radiograph showing a patient on VA ECMO confirming placement of the venous cannula in the right atrium (A) and showing evidence of pulmonary edema in bilateral lung fields (B).
Figure 5:
Typical pathway of weaning from VA ECMO. If the patient remains hemodynamically stable, the patient can likely proceed to decannulation.
Figure 6:
Overview of monitoring tools and their potential role in complementing the routine clinical care of a patient on VA ECMO.
Table 1:
Principles of Echocardiographic Monitoring During VA ECMO Support
TABLE 1 Monitoring Parameter
Goal(s) of Assessment
Chamber Size
Enlarged chamber size may suggest inadequate decompression Small chamber size may suggest excessive decompression and/or suboptimal preload Lack of leaflet excursion may indicate poor left ventricular contractile function and/or excessive left ventricular afterload All valves (especially aortic) can be evaluated for the presence/absence of severe insufficiency that may compromise the adequacy of ECMO support and optimal ventricular unloading All cardiac chambers and the aortic root can be interrogated for the presence/absence of thrombus or spontaneous echo contrast as a marker of blood stasis The presence/absence of pericardial effusion or cardiac tamponade can be assessed Cannula positioning and the presence/absence of cannula “kinking” or obstruction can be determined
Aortic Valve Excursion
Valvular Competency
Thrombus
Pericardium Venous Drainage Cannula
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ECMO Circuit •
Adequacy of Support
• •
Maintenance of flows between 50-70 mL/kg Stable inflow/outflow pressures Adequate mixed venous O2 sat
Invasive Hemodynamics
Laboratory Values • • • •
Stable acid/base status Lactate normalizes Improved BUN, creatinine, LFTs Markers of anticoagulation at target (ACT, aPTT)
• • •
Normalization of intracardiac filling pressures Adequate mixed venous O2 sat Target MAP (65-80 mmHg) achieved
TTE and TEE Imaging • •
Monitor for adequate ventricular unloading Identify optimal cannula positioning
NIRS and Other Imaging • •
Stable NIRS cerebral oxygenation Resolution of pulmonary edema on CXR
Complications •
Bleeding
•
•
Clotting
• •
May see reduced inflow circuit pressures May see decreased mixed venous O2 saturation Depending upon location within ECMO circuit, may see acute changes in inflow or outflow pressures May see reduced ECMO flows May see clot in oxygenator or circuit and suboptimal postoxygenator gas exchange
• •
•
Will see a decline in serum Hgb May see rise in serum lactate if compromising systemic perfusion
May see markers of hemolysis (elevated LDH, reduced haptoglobin, elevated plasma-free Hgb)
• • •
•
• •
LV Distension
Reduced cardiac filling pressures Hypotension and reduced arterial pulsatility Reduced mixed venous O2 sat
May see rising intracardiac filling pressures and reduced mixed venous O2 sat depending upon clot location and impact on ECMO flows
Minimal arterial pulsatility Elevated PCWP
• •
•
•
• •
Look for potential causes – cannula mal-positioning, pericardial effusion
Inadequate ventricular unloading may suggest suboptimal ECMO support due to thrombosis May visualize intra-cardiac clot
Enlarged LV chamber size Limited aortic valve leaflet excursion
•
•
May see pulmonary edema on CXR as a consequence of inadequate ECMO support
•
Pulmonary edema on CXR
•
May see acute or unilateral decrease in cerebral oxygen saturations
•
Persistent pulmonary edema or co-existing pulmonary pathology (e.g. pneumonia/pneumonitis,
Neurologic Injury Limb Ischemia
•
May see rise in serum lactate, creatine kinase
•
Regional Hypoxemia
If intra-cranial bleeding, may see reduction in regional cerebral oxygen saturation on ipsilateral side Alveolar infiltrates on CXR if pulmonary hemorrhage
Reduced PaO2 or O2 saturation in right radial artery
•
May identify improved cardiac function causing differential systemic