review article monitoring of the adult patient on...

Review ArticleMonitoring of the Adult Patient on Venoarterial ExtracorporealMembrane Oxygenation

Mabel Chung,1 Ariel L. Shiloh,1 and Anthony Carlese1,2

1 Division of Critical Care Medicine—The Jay B. Langner Critical Care Service, Department of Medicine,Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA

2Cardiothoracic Intensive Care Unit, Moses Campus, USA

Correspondence should be addressed to Anthony Carlese; [email protected]

Received 11 October 2013; Accepted 27 November 2013; Published 3 April 2014

Academic Editors: W. W. Butt and H. Spapen

Copyright © 2014 Mabel Chung et al. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Venoarterial extracorporeal membrane oxygenation (VA ECMO) provides mechanical support to the patient with cardiac orcardiopulmonary failure. This paper reviews the physiology of VA ECMO including the determinants of ECMO flow and gasexchange.The efficacy of this therapy may be determined by assessing patient hemodynamics and device flow, overall gas exchangesupport, markers of adequate oxygen delivery, and pulsatility of the arterial blood pressure waveform.

1. Introduction

Cardiopulmonary bypass (CPB) was used successfully forthe first time in 1953 when Dr. John H. Gibbon repaired anatrial septal defect in an 18-year-old woman. Since then, tech-nological improvements in extracorporeal life support haveallowed for the development of a type of partial cardiopul-monary bypass called extracorporeal membrane oxygenation(ECMO). Not only has the technology of ECMO beenbrought out of the operating room into the bedside allowingclinicians to aid in the care of critically ill patients requiringpulmonary or cardiopulmonary support, but EMCO has alsobecome remarkably portable and has allowed for intra- andinterhospital transport of otherwise unstable patients. WhileECMO support can be venovenous (VV) or venoarterial(VA), this paper aims to focus on the functional mechanicsand the monitoring considerations in a patient with VAECMO.

2. Indications/Benefits

VA ECMO provides both respiratory and hemodynamicsupport, in contrast to VV ECMO, which provides onlyrespiratory support. VA ECMO is ideally placed in a patientwith a reversible pathological process and is commonlyplaced in those with cardiogenic shock as well as those

with other causes of hemodynamic instability refractory tomedical management (Table 1). In the case of a myocardialinfarction leading to cardiac arrest, peripheral VAECMOcanbe placed quickly and canprovide hemodynamic stabilizationuntil the neurologic status of the patient is determined— atherapeutic strategy called bridge to decision [1, 2]. If thepatient recovers neurologic function, VA ECMO supportcan be continued, allowing clinicians time to determinethe suitability of the patient for myocardial recovery or asa candidate for transplantation or placement of a durableventricular assist device. A decision tree for utilization ofVA ECMO in the setting of cardiac arrest and uncertainneurologic status is outlined in Figure 1.

3. Limitations/Contraindications

VA ECMO provides partial hemodynamic support and canprovide ventricular decompression, augmentation of per-fusion pressure, and oxygenation and removal of carbondioxide in the blood; however, it also increases the afterloadagainst which the left ventricle (LV) works. The balance ofthe beneficial effect of decompression against the detrimentaleffect of increased afterload depends on the level of supportand the state of the myocardium. Those on VA ECMOmust be anticoagulated, the requirement of which must

Hindawi Publishing Corporatione Scientific World JournalVolume 2014, Article ID 393258, 10 pageshttp://dx.doi.org/10.1155/2014/393258

2 The Scientific World Journal

Withdrawal of support

Cardiac arrest/acute refractory cardiogenic shockMultisystem organ failure

Uncertain neurologic status

VA ECMO or CentriMag support

End-organ functional recoveryNeurological recovery

Cardiac recoveryNeurological recoveryNo cardiac recovery

No neurological recoveryCardiac recovery

Bridge to transplantBridge to a bridge

Destination therapy

If disqualified from above: Bridge to nowhere

End-organ functional recovery End-organ functional recovery

Bridge to decision

Bridge to recovery

Figure 1: VA ECMO support after cardiac arrest provides hemodynamic stabilization, which allows time for therapeutic hypothermia andassessment of the neurologic status of the patient. If the patient achieves both neurologic and cardiac recovery, VA ECMO support will havefunctioned as a bridge to recovery and can subsequently be removed. If the patient does not recover neurologic function, VA ECMO supportis typically withdrawn. If the patient awakens but does not have recoverable myocardial function, candidacy for heart transplant (bridge totransplant) and temporary (bridge to a bridge) or permanent (destination therapy) implantation of a ventricular assist device can be assessed.The neurologically intact patient that is disqualified from a heart transplant or ventricular assist device presents a dilemma that may bedescribed as a bridge to nowhere. Figure adapted from [1].

be weighed against the risk of bleeding. In addition, VAECMO cannot bemaintained on a long-term basis. Althoughthere is no set time frame for device therapy, correction ofphysiologic derangements should occur within the first 24–48 hours. Recent studies have published durations of supportranging from 1.4 days to 11.5 days [2, 5–12]. VA ECMO iscontraindicated in a number of conditions (Table 2).

4. Types of Cannulations/Circuit

Cannulation for VA ECMO can be described as eitherperipheral or central (Figure 2) [3]. Peripheral cannulationcan be accomplished either percutaneously or by cut-down,and typically utilizes the femoral or internal jugular vein forthe venous (inflow) cannula and the femoral, axillary, or thecarotid artery for the arterial (outflow) cannula. Peripheralcannulation, especially with the femoral vein and femoralartery, can be done quickly and on an emergency basis atthe bedside. However, it often involves cannulas of smallerdiameter than those used in central cannulation. Central can-nulation, in contrast, requires a sternotomy or thoracotomy.It is frequently seen in the context of the inability to weanoff CPB after cardiac surgery, as the cannulas used for bypasscan be directly connected to the VA ECMO circuit. Central

cannulation typically involves a venous cannula from theright atrium and an arterial cannula into the ascending aorta.The larger diameter cannulas allow for greater flow due todecreased resistance.

The fundamental components of a VA ECMO circuitinclude a venous inflow cannula, a pump, a membraneoxygenator/lung, and an arterial outflow cannula.The venouscannula withdraws blood at the level of the right atrium/venacava. The blood is pumped through the membrane oxygena-tor allowing for oxygen uptake and carbon dioxide removal,and this arterialized blood is returned to the systemic cir-culation through an artery. Other components of the circuitmay include a saturation sensor on the venous cannula toassess the mixed venous saturation (SvO

2), a flow probe

that clips onto to the arterial cannula to directly assessflow in liters/minute, a pre- and postoxygenator pressuremonitor, a console whereby the speed of the pump canbe adjusted, various access ports through which medica-tions can be infused and blood samples withdrawn, a heatexchanger by which temperature can be controlled, anda bridge between the venous and arterial lines. Such abridge allows blood to continue to circulate through thecircuit after proximal clamping, which can be performed totest the effects of temporarily suspending ECMO support.

The Scientific World Journal 3

From patient

To patient

Deoxygenated bloodOxygenated bloodMixed oxygenated and deoxygenated blood

(a)

From patientTo patient

(b)

FromTo patient

patient

(c)

Figure 2: Illustrations of various VA ECMO cannulations. Diagram (a) depicts a femoral vein-femoral artery peripheral cannulation.Retrograde outflow from a femoral arterial cannula competes with anterograde cardiac output ejected from the left ventricle. In this situation,poor lung function results in the ejection of deoxygenated blood (blue) from the left ventricle, whichmixes with oxygenated blood (red) fromthe ECMOcircuit.Thepoint ofmixing (dark red) is located at the base of the aortic root, butwill vary depending on the patient’s heart functionand ECMO flow. Poor lung function and good myocardial function in the context of a femoral-femoral ECMO cannulation may result inupper body hypoxemia (see text). Diagram (c) shows central cannulation with venous inflow drawn from the right atrium and arterial outflowpumped into the ascending aorta.

Table 1: Indications for VA ECMO.

Refractory cardiogenic shockMyocardial infarctionMyocarditisPrimary graft failure following heart transplantationPostcardiotomy (failure to wean from CPB after cardiacsurgery)Drug overdose resulting in profound myocardial depressionSeptic cardiomyopathyPeripartum cardiomyopathy

Pulmonary embolismRecurrent dysrhythmias such as ventriculartachycardia/fibrillationSevere pulmonary hypertensionAnaphylactic shockTrauma to major vessels or myocardiumMassive hemoptysis or pulmonary hemorrhagePre- or postprocedure circulatory support for high riskinterventional procedures

The ability to circulate blood during clamping decreases therisk of stasis and thrombosis. An ECMO circuit may also

Table 2: Contraindications to VA ECMO.

Absolute contraindicationsUncontrolled, active bleeding or other contraindication toanticoagulationEnd-stage, irreversible processes from which patient is notexpected to recover (unless transplant candidate)

(i) Cardiac disease(ii) Respiratory disease(iii) Neurologic disease

Poor preexisting functional status or multisystem organ failureUnwitnessed cardiac arrest or prolonged cardiopulmonaryresuscitation (>60min)Aortic dissectionSevere aortic valve regurgitation

Other considerationsAdvanced ageRenal or liver failureActive malignancyMorbid obesitySignificant peripheral vascular diseaseHeparin-induced thrombocytopenia

include a venous reservoir or bladder located on the venousline prior to the pump to serve as an air bubble trap as


Table 3: Similarities and differences between VA ECMO oxygena-tion and ventilation.

Variable Affectsoxygenation

Affects CO2elimination

Diffusion gradient Yes YesMembrane surface area Yes YesFDO2 Yes NoBlood flow Yes NoFresh gas flow rate No Yes

well as a volume buffer. Centrifugal pumps (see followingsection) can generate substantial negative pressure at thevenous inlet; thus, the presence of a reservoir can provideextra preload reserve to prevent cavitation of the cannulatedvessel with resultant hemolysis. The bladder also allows fornoninvasive monitoring of venous inlet pressure, althoughcertain consoles may allow for pressure monitoring withoutthe presence of a reservoir. Venous inlet pressures should notexceed negative 50mmHg.

5. Functional Mechanics: Flow andGas Exchange

VA ECMO, as a form of partial cardiopulmonary bypass,provides 60–80% of the predicted resting cardiac output.The remaining 20–40% of venous return flows normallythrough the native pulmonary circulation.The cardiac outputprovided by the ECMO circuit (i.e., ECMO blood flow) isaccomplished with one of two types of pumps—centrifugalor roller. This paper will focus on centrifugal pumps, whichare more commonly used than roller pumps in the adultpopulation. Centrifugal pumps like the CentriMag (Thoratec,Pleasanton, CA) propel blood forward with a magneticallylevitated impeller that spins like a top.

The flow of blood through a VA ECMO circuit may bethought of as being governed by the modifiable variables ofpreload, afterload, and revolutions per minute (RPM) of theimpeller as well as by the static variables of cannula lengthand diameter. Centrifugal pumps are preload dependent andafterload sensitive.The preload dependency of the centrifugalpump manifests as decreased flows with significant hypo-volemia or with mechanical obstructive processes such astamponade or tension pneumothorax. The centrifugal pumpis also afterload sensitive. Decreased flows can occur withpostpump obstructions such as thrombus in the oxygenatoror kinks in the arterial cannula, as well as with excessivesystemic vascular resistance (SVR) or mean arterial pressure(MAP). A decrease in the RPMs decreases flow through thecircuit, while an increase in the RPMs, when not limitedby preload, afterload, or circuit components, should causean increase in the flow. Resistance to blood flow increasesdirectly with cannula length and inversely with cannuladiameter. Hence shorter and larger bore cannulas promotegreater flow, while longer and smaller bore cannulas tendto limit flow. Circuit components are chosen to allow forat least 50–75 cc/kg/min of flow in adults (compared with

80 cc/kg/min for pediatric patients and 100 cc/kg/min forneonates). Larger patients may require additional inflow oroutflow cannulas if adequate flows cannot be achieved with agiven set of circuit components.

Gas exchange occurs in the membrane oxygenator(Figure 3) [4]. Extracorporeal venous blood is exposed tofresh gas (or sweep gas) that oxygenates and removes carbondioxide. Both oxygen uptake and carbon dioxide removaldepend on the presence of a diffusion gradient as well as onthe available surface area of the semipermeable membrane.Oxygenation is affected by the fraction of delivered oxygen(FDO2) and the blood flow rate. A gas blender attachedto the oxygenator mixes air and oxygen and allows for arange of FDO2. Increases in FDO2 will increase the partialpressure of oxygen in the blood (PaO

2). In addition, increases

in blood flow will also increase oxygenation as a greatervolume of blood is exposed to the surface of the membrane.Augmentation of oxygenation only occurs up to a certainpoint after which the time for oxygen transfer becomes tooshort. Oxygenation is independent of sweep gas flow rate.In contrast to oxygenation, carbon dioxide elimination isdependent on sweep gas flow rate and is independent ofblood flow (Table 3). A flowmeter regulates gas flow to themembrane. An increase in the sweep gas flow rate resultsin a decreased concentration of carbon dioxide in the freshgas. This increases the diffusion gradient, promotes greatercarbon dioxide elimination, and causes a decrease in thepartial pressure of carbon dioxide in the blood (PaCO

2).

Carbon dioxide diffuses faster than oxygen because it ismore soluble. As a result, it transfers approximately 10 timesmore efficiently than oxygen, sometimes necessitating theuse of carbon dioxide enriched fresh gas in order to preventhypocarbia. A comparison between pre- and postoxygenatorblood samples should reveal an increase in PaO

2and a

decrease in PaCO2. If such a change is not seen, membrane

malfunction should be suspected.Together, the blood flow and gas exchange of VA ECMO

act as a surrogate heart and lung that supports end-organfunction.

6. Monitoring

VAECMOprovides circulatory, oxygenation, and ventilatorysupport for the purpose of aidingwith end-organ perfusion aswell as to, potentially, provide myocardial rest. ECMO flowsand the MAP should be monitored. The adequacy of gasexchange support must be verified by blood gases from anappropriately located arterial catheter. Markers of total bodyoxygenation—SvO

2and lactate—should be tracked to ensure

adequate perfusion and oxygen delivery to the end-organs.And finally, the hemodynamic effects of VA ECMO upon themyocardium—beneficial or detrimental—may be gauged byfollowing the pulsatility of the arterial waveform (Table 5).

6.1. ECMO Flows and MAP. VA ECMO flows should bemonitored for changes. In the setting of a stable RPM, adrop in flow in a circuit with a centrifugal pump may becaused by decreased preload or excessive afterload. Decreases


Arterial outflow

Venous inflow

Air Oxygen

Blender

OxygenatorGas

Membrane

Blood

Pump

O2

CO2

O2

O2

CO2

CO2

Figure 3: The oxygenator (also known as the membrane lung) is divided into a blood compartment and a gas compartment by asemipermeable membrane. The pump propels venous blood into the oxygenator and gas exchange occurs across the membrane as the bloodinteracts with fresh gas. After oxygenation and carbon dioxide removal, the arterialized blood is returned to the patient through an artery.A blender allows for adjustment of the fraction of delivered oxygen (FDO2). From [4]. Copyright © (2011) Massachusetts Medical Society.Reprinted with permission fromMassachusetts Medical Society.

in preloadmay be secondary to hypovolemia or bleeding.Thenegative pressure generated by the pump in the hypovolemicstate can cause hemolysis resulting in a rise in plasma freehemoglobin (significant if > 50mg/dL) as well as a rise inlactate dehydrogenase (LDH). Spillage of free hemoglobininto the urine may result in a pink tinge to the urine. Inaddition, hypovolemia may also result in chattering— a low-frequency jerking or shaking movement of the cannulas dueto a physical interaction between the inflow cannula andthe vessel from decreased space. Hemolysis and chatteringcan occur independently of hypovolemia due to patient orcannula positioning or from excessive centrifugal pumpsspeeds (>3000 RPM) [13]. Inadequate preload may also becaused by mechanical obstructive processes such as tampon-ade, tension pneumothorax, and abdominal compartmentsyndrome. These processes decrease preload by restrictingvenous return and are typically associated with a risingcentral venous pressure (CVP). Drops in flow may also becaused by kinking of the venous cannula. Excessive afterloaddue tomembrane oxygenator thrombus, a kink in the arterialcannula or a high SVR and MAP may also restrict flowthrough the VA ECMO circuit.

While maintenance of flows are crucial to the care of thepatient onVAECMO, attentionmust also be paid to themeanarterial pressure, as the end-organs require both a cardiacoutput as well as a perfusion pressure for optimal function.A goal MAP > 65mmHg may be used as a starting pointbut can be adjusted either lower or higher given individualcircumstances. MAP should not exceed 90mmHg in orderto limit afterload and to promote forward flow. Recall that

MAP = CO × SVR, (1)

where CO is cardiac output and SVR is systemic vascularresistance. In the hypotensive patient, MAPmay be increasedby manipulating either CO or SVR. The total cardiac outputof the body is composed of native cardiac output and VAECMOflows.Thus, hypotensionmay potentially be correctedby increasing VA ECMO flows and its contribution to totalCO. Assuming a centrifugal pump, this may be achievedby administering volume or by increasing the RPMs of thepump. If the problem is related to SVR, such as with septicshock, a vasoconstrictor may be needed to increase MAP,although this must be weighed against the effect of increasedafterload and the increase in pressurework of the left ventricle(described in “Pulsatility” below).

6.2. Gas Exchange Support. As a partial cardiopulmonarybypass circuit, VA ECMO creates a separate circulationsystemparallel to the native circulation by siphoning a certainportion of venous return and reinfusing it as a contributionto the overall cardiac output of the body. The body’s netoxygenation and ventilation depends on the interactionbetween the body’s own capacity to oxygenate, ventilate, andperfuse (native lung function and cardiac output) and thecontribution from VA ECMO in doing the same (membranelung function and flow).The accurate interrogation of net gasexchange support depends on where the two systems con-verge.The location of the arterial ECMO cannula determinesthe point of convergence and the suitability of a particulararterial site for blood sampling or monitoring of SpO

2.


Table 4 compares the different arterial cannulation sites withcomments on the appropriate location of a peripheral arterialcatheter for monitoring.

Cannulation of the right common carotid artery flusheswell-oxygenated and ventilated blood down the right upperextremity. Thus, blood gases drawn from the right radialarterywill not be reflective of net gas exchange support. Bloodgases obtained distal to the location of mixing (e.g., the leftradial artery) will bemore accurate. Right radial arterial gaseswill not be accurate in right axillary artery cannulation, aswell, due to its location relative to the ECMO cannulationsite. Similarly, left radial arterial gases should be avoided inpatients with left axillary artery cannulation. Direct aorticroot cannulation allows for accurate blood gas analysis fromany artery regardless of heart or lung function.

The preferred site of blood gas sampling with femoralartery cannulation is the right radial artery. When heartfunction is poor (with or without good lung function),retrograde ECMO flow should provide the vessels of theaortic arch with arterialized blood and allow good oxygendelivery to the coronary and cerebral circulations. Recoveryof myocardial function pushes the mixing point of the twocirculations more distally along the aorta causing nativecardiac output to take over perfusion of the coronary andcerebral circulations. With good lung function, the coronaryarteries, the innominate, and the right carotid artery willreceive well-oxygenated blood. However, poor lung functionin the setting of good myocardial function may cause thesecirculations to receive poorly oxygenated blood. In extremecases, the patient’s head may appear blue, while the lowerextremities appear pink. Placement of a right radial arte-rial catheter, which interrogates oxygenation to the heartand brain, will allow for the detection of coronary andcerebral hypoxemia. This phenomenon is known by severaldescriptors including upper body hypoxemia, North-SouthSyndrome and Harlequin Syndrome.

Upper body hypoxemiamay be addressed in several ways.The oxygen content of pulmonary venous blood may beaugmented by adjusting ventilator settings, such as increasingthe fraction of inspired oxygen (FIO

2) and/or positive end-

expiratory pressure (PEEP). Depending on the etiology,inadequate lung function may be addressed by performingrecruitment maneuvers to decrease atelectasis, diuresing todecrease pulmonary edema, instituting antibiotic therapyfor pneumonia, or utilizing thoracentesis or bronchoscopyfor significant pleural effusions or secretions and mucousplugging. Upper body hypoxemia may also be remediedby manipulating aspects of VA ECMO support. VA ECMOflows can be increased in an attempt to better perfuse theaortic root with retrograde arterialized blood. In addition,the arterial outflow cannulation site can be switched from thefemoral artery to the axillary or carotid artery. As they arein closer proximity to the aortic arch, these cannulation sitesmay be more effective in washing the root with oxygenatedblood. However, cannulation of these smaller vessels willrequire a smaller cannula, which will decrease the maximumachievable flows. A VA-V ECMO circuit can also be createdwhere a portion of arterialized blood from the arterial outflowcannula is diverted via the right internal jugular artery to

the right heart. This enriches the blood traveling throughthe pulmonary circulation and to the left ventricle to providebetter oxygen delivery to the coronary and cerebral circula-tions. Finally, if cardiac function has recovered sufficiently,VA ECMO can be converted to VV ECMO to provide onlygas exchange support until the lungs fully recover function.

6.3. SvO2and Lactate. SvO

2, a measure of total body oxy-

genation and the balance between oxygen consumption anddelivery, should be routinely assessed in the patient on VAECMO. The body responds to a decrease in oxygen delivery(DO2) by increasing the extraction ratio (ER) of oxygen from

the blood. Recall that

ER = VO2

DO2

, (2)

where VO2is oxygen consumption. Simplification of this

equation results in the following:

ER =(SaO2− SvO

2)

SaO2

. (3)

Given a constant arterial oxygen saturation (SaO2), this

equation reflects the inverse relationship of ER with SvO2.

Assuming a SaO2of 100%, a normal extraction of 25–35%

results in a normal SvO2of 65–75%. A state of high extraction

will result in a low SvO2of <65–75%; once oxygen extraction

reaches a maximum of 50–60% and the SvO2decreases to

40–50%, the body will begin to produce lactate due to theinitiation of anaerobic metabolism.

A high ER or low SvO2due to inadequate oxygen delivery

may be secondary to inadequate ECMO support. Recall that

DO2= CO × CaO

2, (4)

where CaO2is oxygen content. Given that the main compo-

nents of CaO2are hemoglobin (Hb) and SaO

2the equation

may be simplified to

DO2= CO ×Hb × SaO

2. (5)

Thus, increasing VA ECMO flows (via increases in volumeor RPM) to increase total CO will increase DO

2and may

improve a suboptimal SvO2. Oxygen delivery can also be

increased by red cell transfusion as well as by ensuringadequate arterial saturation. Because the anemic patientrequires higher ECMO flows to achieve the same oxygendelivery, optimization of Hb prior to manipulation of flowsmay be desirable. A high ER or low SvO

2may also be caused

by an increase in oxygen consumption; thus, interventionsto decrease VO

2(antipyretics, cooling, antishivering agents,

increasing sedation, etc.) can also be made concomitantly. Amore complete description of oxygen delivery on VA ECMOmay be delineated with this equation:

DO2= (native cardiac output × CaO

2of native lung)

+ (ECMO Flow × CaO2of membrane lung) .

(6)

A true SvO2cannot be measured because venous return

is split between the native and ECMO circulations. However,


Table 4: Different sites of VA ECMO arterial cannulation and arterial catheter placement.

Arterial Cannula Location of mixing Arterial catheter site Comments

Right commoncarotid artery Aortic arch Avoid right radial

Right radial blood gasesinaccurate due to sampling ofimmediate downstreamarterialized blood

Right axillary artery Aortic arch Avoid right radialRight radial blood gases notreflective of blood to which restof body is exposed

Left axillary artery Aortic arch Avoid left radialLeft radial blood gases notreflective of blood to which restof body is exposed

Femoral artery

Between aortic root anddescending aorta—exact locationdepends on native cardiac outputand magnitude of retrograde flow

Preferred site right radialAvoid dorsalis pedis ofcannulated limb

Right radial cannulation detectsupper body hypoxemia (see text)

Aorta Aortic root Any

because the majority of blood flows through the VA ECMOcircuit, it can be reasonably estimated by interrogating thevenous cannula leading towards the membrane oxygenatoreither by blood gas analysis or a saturation probe to obtaina premembrane saturation. The minority of blood flowsthrough the native pulmonary circulation. Hence, measure-ment of SvO

2from a pulmonary artery catheter may not be

accurate.Rearrangement of the equation for VO

2renders another

equation for the variables that affect SvO2:

SvO2= SaO

2−

VO2

CO ×Hb. (7)

6.4. Pulsatility. VA ECMO provides rest to the myocardiumby decreasing venous return and subsequently the volumework and wall tension of the heart. In addition, the decreasein preload decreases left ventricular end-diastolic volume(LVEDV) and pressure (LVEDP), thus promoting bettercoronary perfusion pressure due to a greater pressure gradi-ent (coronary perfusion pressure = diastolic pressure – leftventricular end diastolic pressure). However, the return ofblood into the arterial system increases afterload and thepressure work of the myocardium. The overall effect of thedecrease in volume work and the increase in pressure workdepends on the level of ECMO support as well as myocardialfunction and its response to these phenomena.

The ejection of blood flow out of the left ventriclegenerates a stroke volume and its arterial correlate, a pulsepressure. The absence of pulsatility in the arterial waveformin the setting of an appropriate level of support (60–80% ofthe predicted cardiac output allowing for the remaining 20–40% to pass through the lungs and heart) may be a signof poor contractility and the heart’s inability to overcomethe increase in afterload despite the decrease in preloadand volume work. Without pulsatility, blood within theleft ventricle and at the aortic root may stagnate. In thissituation, the risk of thrombus formation and subsequentembolic complications is increased. In addition, without the

adequate ejection of blood, persistent venous return fromthebesian and bronchial veins into the left atrium (LA) andventricle will result in overdistension of the LV. This increasein LVEDV will cause an increase in LVEDP, which can com-promise coronary perfusion pressure and cause additionalischemic damage to the myocardium. Finally, an increase inafterload in the setting of severe mitral regurgitation mayresult in left atrial hypertension and the transmission ofpressures to the pulmonary system resulting in pulmonaryedema and hemorrhage. Such a complication may occureven without preexisting valvular pathology, as the stasis ofblood may cause left ventricular dilation and a functionalmitral insufficiency due to dilation of the annulus. In thisscenario, a pulmonary artery catheter may demonstrate anincrease in the pulmonary capillary occlusion pressure.Whileassessment of the heart in a partially bypassed state can bechallenging, transesophageal echocardiography may aid inconfirming aortic valve opening as well as by providing anassessment of the left ventricular end-diastolic dimension.

VA ECMO flows can be reduced in an attempt to reduceafterload. However, this maneuver may not be possible ifit compromises oxygen delivery and end-organ perfusiondue to the inability of the heart to produce a compen-satory increase in native cardiac output. Inotropic supportcan be instituted or escalated to increase contractility ofthe myocardium. In addition, afterload reduction with avasodilator or intra-aortic balloon pump (IABP) may beimplemented. An IABPbrings the added benefit of improvingcoronary perfusion with balloon inflation during diastole.If these maneuvers fail to promote left ventricular ejection,decompression of the left ventriclemay be necessary. Decom-pression may be accomplished by a percutaneous left atrialseptostomy, which allows blood from the LA to drain downits pressure gradient into the right atrium (RA) to then bedrained via the venous cannula. A catheter may also beplaced into the LA through a transseptal puncture to facilitatedrainage [14]. In addition, the left atrium or left ventriclecan be directly cannulated allowing blood to be vented intothe venous arm of the ECMO circuit. Finally, use of a left


Table 5: Summary of monitoring in VA ECMO.

Monitor for Treatment

Rhythm Dysrhythmias such as ventricular fibrillation thatmay prevent ventricular ejection

AntiarrhythmicsCardioversionPacingAblation

MAPHypotension (MAP = CO × SVR)

(i) Inadequate VA ECMO flow(ii) Inadequate SVR

(i) See “Flow” below(ii) Start vasoconstrictor

Pulsatility

Lack of pulsatility on arterial waveform caused by(i) poor myocardial function(ii) excessive VA ECMO support(iii) Inadequate preload(iv) RV failure

May result in(i) thrombus(ii) myocardial ischemia(iii) pulmonary edema (assess CXR, wedge)

If poor myocardial function, consider:decreasing VA ECMO flowstarting or increasing inotropestarting or increasing vasodilatorIABPmyocardial decompression

Flow(liters/min)

Low flows (assuming centrifugal pump)(i) Inadequate preload

(a) Hypovolemia (may see hemolysis,chattering)

(b) Mechanical obstructive(ii) Excessive afterload (thrombus, kink, SVR)(iii) Inadequate RPM

(i) Volume: crystalloid/colloid/transfusionRelease of mechanical obstruction

(ii) Exchange oxygenator, relieve cannula kink,vasodilator to decrease SVR

(iii) Increase RPM

Gas exchange

Inadequate PaO2 inadequate or excessive CO2elimination

(i) VA ECMO settings(a) FDO2(b) VA ECMO flow(c) Sweep gas flow rate

(i) If hypoxemia, increase FDO2 or flow.If hypercarbia, increase sweep. Ifhypocarbia, decrease sweep or add CO2.

(ii) Oxygenator function(a) Pre- and postmembrane pressures(b) Pre- and postoxygenator gases

(ii) Increased Δ𝑃 and inadequate arterializationof postoxygenator gases suggest oxygenatormalfunction

(iii) Upper body hypoxemia (femoral-femoralcannulation)

(iii) Increase pulmonary venous O2 contentAdjust ventilator settingsTreat etiology of pulmonary dysfunctionIncrease VA ECMO flowChange to axillary/carotid cannulationVA-V ECMOVV ECMO

Oxygendelivery: SvO2and lactate

Decreased SvO2 and increasing lactate suggestinadequate oxygen delivery (DO2 = CO × CaO2)

(i) VA ECMO flow(ii) Hemoglobin(iii) SaO2

Excessive oxygen consumption (ER = VO2/DO2)(i) Febrile(ii) Shivering

(i) Increase VA ECMO flow(ii) Transfuse(iii) Ensure adequate gas exchange

(i) Antipyretics(ii) Consider agents such as meperidine ordexmedetomidine

Distal limbischemia

Loss of pulsesCyanosis and coolness of limb

Femoral-femoral cannulation:DP or PT anterograde perfusion catheter

Anticoagulation Adequate heparinization by PTTTemperature Normothermia unless therapeutic hypothermia


ventricular assist device such as the Impella 2.5 (Abiomed,Danvers, MA) to provide left ventricular decompression aswell as forward flow has been described [15, 16].

Pulsatility is a dynamic property. Loss of pulsatility maysignal worsening myocardial function, while the appearanceof pulsatility or an improvement in pulse pressure may signalrecovery. The differential diagnosis for loss of pulsatility alsoincludes:

VA ECMO Flows That Are Too High. The greater the ECMOflows, the more blood that drains into the circuit causinga greater decrease in LV preload, stroke volume, and pulsepressure. Total bypass, where the ECMO circuit takes over100% of the cardiac output, creates a flat, nonpulsatile arterialtracing and signifies the lack of ejection of blood from the leftventricle.

Hypovolemia/Mechanical Obstruction.Adecrease in intravas-cular volume or a mechanical cause of decreased venousreturn may result in a decrease in LV preload that leads toa decreased stroke volume and pulse pressure.

RV Failure. VA ECMO decreases RV preload and the volumework of the ventricle. However, pulmonary edema, lungcollapse, or other parenchymal disease may cause hypoxicpulmonary vasoconstriction and may result in clinicallysignificant pulmonary hypertension and an increase in RVpressure work. If this occurs to a significant extent, the rightventricle may be unable to deliver volume to the left side ofthe heart, resulting in a decrease in stroke volume and inpulsatility. In this scenario, pulmonary afterload reductionwith nitric oxide or with inodilators such as milrinone anddobutamine (which will also provide inotropic assistance)may be beneficial. If systemic pressures allow, nitroglycerinor nitroprusside may also be utilized.

6.5. Rhythm. While it may be possible to maintain adequatehemodynamic and gas exchange support with VA ECMOduring dysrhythmias that would otherwise be fatal, nonsinusrhythms such as ventricular fibrillation should be rectifieddue to the ineffective ejection of blood flow from the LV.Such arrhythmias should be addressed with direct currentcardioversion, antiarrhythmics, pacing, or ablation.

6.6. Other Considerations

Pre- and Postmembrane Oxygenator Pressures. Exposure ofblood to nonbiologic surfaces results in contact activation ofthe coagulation system resulting in a propensity to developclot in the VA ECMO circuit. Premembrane pressures shouldbe followed to assess for increases greater than 300–400mmHg. The postmembrane pressure can give useful contextto the pre-membrane pressure. An elevated premembranepressure in the setting of a normal post-membrane pressuresuggests that the source of the increased resistance lies withinthe oxygenator. This scenario produces an increase in thedifference between pre- and post-membrane pressures (i.e.,an increase in ΔP, significant if >40mmHg) and may beindicative of thrombus on the membrane lung. If thrombus

is suspected and is accompanied by a deterioration in gasexchange, the oxygenator may need to be replaced. Anelevated pre-membrane pressure in the setting of an elevatedpost-membrane pressure suggests that the source of increasedresistance is located downstream to the oxygenator, perhapsas a clot or kink in the cannula.

Partial Thromboplastin Time/Activated Clotting Time. Hep-arinization is used to decrease the risk of developing clot.Adequate anticoagulation is monitored by partial throm-boplastin time (PTT) and/or the activated clotting time(ACT). Heparin levels and antithrombin III levels may alsobe followed.

Distal Ischemia. Ipsilateral distal pulses as well as limb colorand warmth should be assessed routinely with peripheralcannulations such as the axillary artery (arm ischemia) andthe femoral artery (leg ischemia). In the case of femoralcannulations, a dorsalis pedis (DP) or posterior tibial (PT)distal perfusion cannula can be placed to promote perfusionto the lower extremity. Ischemic brain injury may occur as aconsequence of carotid cannulation.

Central Venous Pressure. The CVP is altered by venousdrainage during VA ECMO support; however, a rise inCVP in the setting of stable settings may be indicative of amechanical obstructive process.

7. Recovery

Myocardial recovery onVAECMOsupport is suggested by anincrease in pulse pressure and by improved contractility onechocardiography. The ultimate test of myocardial recovery,however, is accomplished by assessing hemodynamic stabilityon minimal or no support. The RPMs can be decreased toachieve ∼1 liter/min of flow or the VA ECMO cannulas can bebriefly clamped. The native ventricle must be able to handlethe full load of native cardiac output. If the myocardium hasrecovered, a decrease in or the temporary withdrawal of VAECMO support should result in acceptable contractility onechocardiography and a stable MAP and CVP. Hypotension,a rising CVP, and a poorly contractile myocardium onechocardiography suggest inadequate recovery.

8. Conclusion

VA ECMO, a form of mechanical circulatory support, had itsorigins in the operating roomas cardiopulmonary bypass andhas evolved for use in the intensive care unit and beyond.Its purpose is simple—to replace some of the function ofa failed cardiopulmonary system and to provide some restto the myocardium. The successful achievement of such anaim, however, requires a thorough understanding of basicphysiologic principles so that the weaknesses inherent to thistherapy can be identified and rectified. As this technologycontinues to improve and becomes more accessible, knowl-edge of the principles underlying VA ECMO will only growin importance to those involved in the care of the critically ill.


Conflict of Interests

The authors declare that there is no conflict of interestsregarding the publication of this paper.

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