Mechanical Support of Cardiopulmonary Function: Extracorporeal Membrane Oxygenation, Ventricular Assist Devices, and the Intraaortic Balloon Pump

7 Mechanical Support of Cardiopulmonary Function


Extracorporeal Membrane Oxygenation, Ventricular Assist Devices, and the Intraaortic Balloon Pump



Nancy A. Pike, Laura A. Klee, Beth A. Zemetra




image Be sure to check out the supplementary content available at http://evolve.elsevier.com/Hazinski.



Pearls




• Signs of critically low cardiac output requiring mechanical circulatory support include: mixed venous oxygen saturation less than 40%, increased ventricular end-diastolic filling pressure, cardiac index less than 2 L/min per m2 body surface area (BSA), persistent metabolic acidosis, oliguria, poor peripheral perfusion, increased inspired oxygen requirements, and poor ventricular function by echocardiogram.


• Mechanical circulatory support (MCS) is indicated when low cardiac output persists despite maximal medical treatment, including afterload reduction combined with inotropes/catecholamines, diuretics, a phosphodiesterase-III inhibitor, fluid and transfusion management, and mechanical ventilation.


• In the pediatric population, ventricular assist devices (VADs) are used to support the failing heart as a “bridge to recovery” or “bridge to transplant.”


• MCS should be anticipated and every attempt should be made to initiate support before the development of end-organ dysfunction or circulatory collapse.


• Persistent low filling of a left ventricular assist device (LVAD) pump with rising right atrial pressure is an indication of right-sided heart failure. An echocardiogram is indicated to evaluate ventricular function and check for a pericardial effusion.


• The oxygen index (OI) is often used to identify possible indication for extracorporeal membrane oxygenation (ECMO) for children with respiratory failure.



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OI greater than 35 on three or more postductal arterial blood gases 30 to 60 minutes apart is an indication for ECMO support.



• Alveolar-arterial (A-a) gradient of 600 to 624 mm Hg is a clinical indication for ECMO. This is computed as follows (NOTE: 47 mm Hg = partial pressure of water vapor):



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• Signs to change venovenous (VV) ECMO to venoarterial (VA) ECMO include: persistent hypoxia in the presence of hypotension and poor cardiac output on maximal ventilator and inotropic support, nonperfusing arrhythmias, or cardiac arrest.



Introduction


The child with life-threatening cardiac or respiratory failure that is refractory to maximal medical support may require MCS. Over the last few years, substantial advances in pediatric MCS have occurred, with expanding indications for use, greater availability of devices suitable for pediatrics, and improved outcomes.16,20


ECMO and centrifugal ventricular assist devices remain the mainstay of MCS for children.23 MCS is not a treatment but rather a therapeutic support to provide adequate tissue oxygen delivery and maintain end-organ perfusion and function while the reversible disease responds to treatment. This support has many potential complications and should be used in appropriate patients with specific criteria for initiation.


Use of MCS in the pediatric population requires knowledge of the pathophysiology and treatment of cardiac and respiratory failure (see Chapters 6 to 9). In addition, the critical care nurse and the ECMO specialist require advanced training in MCS, because they must be familiar with the function of the support device, components of the circuit or console, potential complications, and troubleshooting for the device.


The purpose of this chapter is to provide an overview of MCS options in the pediatric population, with an emphasis on ECMO and VAD physiology, patient selection, indications and contraindications, complications, and postoperative nursing care.



Device Selection


The selection of MCS device is influenced by the indication for the device, the duration of support anticipated, and the devices available. Devices are categorized for short- or long-term support. ECMO, centrifugal VADs, and intraaortic balloon pumps (IABPs) are considered short-term modalities. Pulsatile and rotary-axial devices are typically considered long-term modalities.11


Pediatric MCS offers a potential “bridge to transplant” or a “bridge to recovery.” The term destination therapy is used to describe long-term support for patients who are not heart transplant candidates and those whose heart function is unlikely to recover. Currently, no devices are approved by the U.S. Food and Drug Administration (FDA) for destination therapy in children. Three devices approved by the FDA for destination therapy in adults are the HeartMate VE/XVE LVAS and HeartMate II (Thoratec Corporation, Pleasanton, Calif.), and the AbioCor Implantable replacement heart (Abiomed, Danvers, Mass.).11,55



Extracorporeal membrane oxygenation


ECMO remains the most common form of MCS in the pediatric population. ECMO support evolved directly from cardiopulmonary bypass devices beginning with development of the membrane oxygenator in the 1950s.13,41 In the 1970s, intraoperative cardiopulmonary bypass was successfully used for infants during surgical correction of congenital heart disease.3 In 1972, successful ECMO support of a 24-year-old trauma victim with acute respiratory distress syndrome by Hill et al.37 led to a multicenter National Institutes of Health clinical trial of ECMO versus medical management of adult acute respiratory distress syndrome that failed to show a survival advantage with ECMO support, but did lead to widespread improvement in mechanical ventilation in adults.


In 1976, Bartlett et al.6 reported the first successful use of ECMO for treatment of severe neonatal respiratory distress. Since that time, ECMO has been used successfully in the treatment of neonates with meconium aspiration, congenital diaphragmatic hernia, pneumonia, sepsis, or persistent pulmonary hypertension.57 ECMO is now used as rescue therapy for pediatric patients with severe refractory respiratory or heart failure unresponsive to maximal conventional treatment.


In 1989, the ECMO centers formed a national organization, the Extracorporeal Life Support Organization to coordinate clinical research, develop ECMO guidelines, and maintain a national registry of all ECMO centers and cases. ECMO follow-up data have documented the cost effectiveness of ECMO compared with conventional support and improved patient outcomes with the use of ECMO.49



ECMO Terminology


Bypass therapy outside of the operating suite has been called extracorporeal carbon dioxide removal, extracorporeal heart assist, extracorporeal lung assist, ECMO, and most recently, extracorporeal life support (ECLS). These terms are often used interchangeably, but the term ECMO will be used in this chapter.


ECMO therapy supports cardiopulmonary function through the use of external cardiopulmonary bypass with an oxygenator. ECMO is designed to deliver well-oxygenated blood to an artery or vein, remove carbon dioxide, and normalize acid-base balance and metabolic processes. This system provides temporary pulmonary and possibly cardiac support for infants or children with severe refractory respiratory failure, heart failure, or cardiorespiratory failure, so the failing organs have time to recover or the child is supported until transplantation.


The two types of ECMO support are VA and VV ECMO. VA ECMO provides both cardiac and respiratory support, whereas VV ECMO provides only pulmonary support. The differences between the VA and VV ECMO are summarized in Table 7-1.


Table 7-1 Differences Between VA and VV ECMO
























VA ECMO VV ECMO
Achieves higher PaO2 Achieves lower PaO2
Requires lower perfusion rates Requires higher perfusion rates
Bypasses pulmonary circulation Maintains pulmonary blood flow
Decreases pulmonary artery pressures Elevates mixed venous PO2
Provides cardiac support to assist systemic circulation Does not provide cardiac support to assist systemic circulation
Requires arterial cannulation Requires only venous cannulation

ECMO, Extracorporeal membrane oxygenation; PaO2, partial pressure of arterial oxygenation; PO2, partial pressure of oxygen; VA, venoarterial; VV, venovenous.


The appropriate ECMO circuit size is determined by the weight of the child; the larger the circuit membrane surface area, the greater the potential gas exchange. However, the larger the surface area of the membrane, the higher the platelet consumption and the larger the circuit priming volume. Because the circuit is not typically primed with blood, a high priming volume relative to the child’s circulating blood volume will result in hemodilution.



Venoarterial ECMO



Circuit


The VA ECMO circuit is composed of polyvinyl chloride tubing attached to venous and arterial cannulas (Fig. 7-1). The venous cannula is inserted into the internal jugular vein and advanced through the superior vena cava and right atrium to the tricuspid valve. The arterial cannula is placed into the right common carotid artery with the tip of the cannula advanced to the innominate artery. Postoperative cannulation immediately after cardiac surgery is often accomplished through the median sternotomy incision with direct cannulation of the right atrial appendage and the aorta. In adolescent or adult patients, the femoral artery and vein are often used for VA ECMO cannulation.


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Fig. 7-1 Venoarterial extracorporeal membrane oxygenation circuit.


(From Biddle M, Gulanick M, Berra K: Interdisciplinary team in cardiac rehabilitation. In Moser DK, Riegel B, editors: Cardiac nursing: a companion to Braunwald’s heart disease. Philadelphia, 2008, Saunders.)


The bridge connects the arterial and venous lines and is located near the cannula. The bridge is routinely clamped during ECMO support with brief periods of unclamping to prevent clot formation caused by stagnation of blood in the bridge. If the patient must be separated from ECMO for mechanical complications or for trial periods off ECMO support, the open bridge isolates the patient from the circuit while allowing blood flow to continue through the circuit to prevent stagnation and circuit thrombosis.


Blood from the venous cannula drains passively into a small reservoir called the bladder. The ECMO pump draws blood from the bladder, which works like the right atrium. The function of this bladder is to prevent negative pressure from pulling the vessel wall into the cannula, so it reduces risk of damage to the vena cava. The bladder is connected to a servo regulator mechanism that reduces or stops the pump flow if venous return decreases below a minimum threshold.


The tubing from the bladder joins to the ECMO pump, which is either a roller pump or a centrifugal pump. For the past few decades, the roller pump has been used most commonly for ECMO. However, centrifugal pumps are becoming more popular, especially in cardiac ECMO programs and for extracorporeal cardiopulmonary resuscitation. The roller pump functions on the principles of compression and displacement; blood is displaced as rollers travel the length of the raceway (the segment of tubing contained within the pump head). A strong polymer tubing, called Tygon, is used in the raceway because it is resistant to creasing and erosion.


Blood leaving the pump enters the membrane oxygenator. The membrane consists of a thin silicon rubber sheath with a plastic screen spacer inside to create a semipermeable membrane separating the gas compartment from the compartment containing the patient’s blood. As the patient’s blood flows past one side of the membrane, oxygen diffuses from the gas side across the membrane into the blood, and carbon dioxide from the blood diffuses through the membrane into the gas compartment. The carbon dioxide is then removed, or “swept out” of the system, by the ventilating gas. This ventilating gas is also referred to as the sweep gas, and it is regulated by a flow meter from an oxygen blender. The amount of oxygen in the sweep gas and the available surface area for diffusion determines the amount of oxygen delivered to the patient’s blood as it flows through the oxygenator. The rate of carbon dioxide removal is also dependent on the amount of sweep gas flow and the surface area. The movement of both oxygen and carbon dioxide are dependent on the pressure gradients for the gases across the membrane.


As the blood moves through the ECMO circuit, heat is lost, so ECMO systems use a heat exchanger to keep the blood warm. The heat exchanger is located either between the oxygenator and the patient or integrated into the oxygenator. When the heat exchanger is placed between the oxygenator and the patient, it also serves as a bubble trap.


The blood returns to the patient from the heat exchanger through an arterial cannula inserted into the right common carotid artery. The tip of the cannula is just proximal to the junction of the brachiocephalic artery and the aorta. With this type of cannulation, ECMO becomes essentially a cardiopulmonary bypass system. The greater the ECMO pump flow, the greater the oxygen delivery.



Venoarterial ECMO Flow and Function


In VA ECMO, blood is drained from the right side of the heart and is returned to the arterial side of the circulation, so that it bypasses the heart. Highly oxygenated blood is returned to the arterial circuit, where it mixes with the blood that the native heart is ejecting into the arterial circulation. Ventilator support is minimal, so blood returning from the lungs is relatively desaturated. As ECMO flow increases, the relative percentage of highly oxygenated blood in the arterial circulation is increased. Therefore, the patient’s partial pressure of arterial oxygen (PaO2) increases with increased ECMO flow. With inadequate ECMO flow, the relative percentage of desaturated blood is increased, so the PaO2 is low.


Flow from the ECMO circuit delivered into the aorta is continuous and nonpulsatile. As a result, as ECMO flow increases the patient’s native (intrinsic) cardiac output decreases and the systemic arterial blood pressure waveform is dampened by the nonpulsatile blood flow into the aorta. At 100% ECMO flow, the arterial pressure waveform is flat with only an occasional pulse that may result when slow ventricular filling triggers occasional ventricular systole. Such complete bypass is not typically provided if the patient has some cardiac function.


Typically VA ECMO is run at 80% bypass, so approximately 80% of the patient’s total cardiac output is diverted to the ECMO circuit and then returned to the arterial circulation. At this level of flow, the blood pressure waveform is dampened but preserved, with a pulse pressure of approximately 10 to 15 mmHg. At 80% bypass, the resulting admixture of saturated blood (80% of normal cardiac output) and desaturated blood (from intrinsic cardiac activity) will create sufficient arterial oxygen tension (PaO2), hemoglobin saturation and oxygen delivery. The PaO2 can be expected to be normal or even high.


One method to assess adequacy of oxygen delivery is monitoring of the oxygen saturation of blood in the venous side of the circuit; this oxygen saturation is the effective mixed venous oxygen saturation (SvO2). An SvO2 of approximately 70% to 75% indicates that the ECMO flow is providing sufficient oxygen delivery. Because the normal range of cardiac output varies widely between and within pediatric age ranges, the typical ECMO flow rate varies widely. Approximations of flow are 100 for infants, 80 for children, and 50 mL/kg per minute for adults.



Hemodynamic Changes During Venoarterial ECMO


During VA ECMO, the patient’s PaO2, SvO2, and blood pressure will be affected by changes in the ECMO flow and the patient’s intrinsic (native) cardiac output and differences between the two.



Extremely High PaO2 or Fall in Native Cardiac Output


During ECMO support, an extremely elevated PaO2 typically indicates deterioration rather than improvement in the patient’s cardiac output. Any decrease in native cardiac output is likely to increase the relative percentage of arterial flow that consists of highly oxygenated blood from the ECMO circuit. As a result, the PaO2 rises.


The patient’s cardiac output may fall as the result of hypovolemia and decreased preload, hypertension, and increased afterload or myocardial dysfunction. Hypovolemia can result from hemorrhage, frequent blood sampling that is not replaced, diuresis, and capillary leak (e.g., with septic shock). Hypertension and increased afterload can also worsen myocardial dysfunction and reduce native cardiac output, so these conditions can also cause the PaO2 to rise substantially. If hypertension develops during VA ECMO, aggressive treatment with vasodilators is indicated because hypertension increases the risk of intracranial hemorrhage.


Myocardial dysfunction can cause a fall in native cardiac output. An extreme form of myocardial dysfunction during VA ECMO is known as cardiac stun. When cardiac stun develops, the ventricles barely contract. The electrocardiogram (ECG) and heart rate may be normal, but with little contractility observed by echocardiogram. The blood pressure waveform is severely dampened and pulse pressure approaches zero because the mean arterial pressure is generated almost completely from the ECMO flow.


The etiology of cardiac stun is multifactorial, including increased ventricular wall stress, inadequate coronary perfusion, coronary hypoxia from poorly oxygenated left ventricular output during partial ECMO flow, reperfusion injury, and potential hypocalcemia from the use of older or citrated blood products to prime the ECMO circuit. Calcium is precipitated by the phosphate in the citrate-phosphate-dextrose anticoagulant in bank blood. Cardiac stun is usually reversible with time and adequate VA support. ECMO flow must be adjusted to maintain adequate mean arterial pressure while reversible causes such as acid-base and electrolyte imbalances are corrected and myocardial function recovers.


Native cardiac output can also be reduced by cardiac tamponade, hemothorax, or pneumothorax. These problems decrease venous return to the heart and reduce pulmonary blood flow and native cardiac output so the patient’s PaO2 rises because most flow in the aorta is directly from the ECMO pump. If venous return to the right atrium is severely compromised, drainage to the ECMO circuit will drop; if the condition develops suddenly, the fall in drainage to the circuit will be precipitous. The ECMO circuit contains a safety mechanism (either a mechanical bladder box or pressure modulation) that will stop the pump when venous drainage is inadequate to maintain flow through the circuit. In circuits with pressure control modules, a decrease in the venous pressure indicates a fall in venous return.


If ECMO flow is not increased to compensate for a fall in native cardiac output, oxygen delivery will be compromised and the SvO2 will fall. Systemic venous oxygen saturation can also fall if oxygen consumption is increased by conditions such as pain, anxiety, fever, and seizures.



Falling PaO2 or Increase in Native Cardiac Output


The PaO2 will fall during VA ECMO if the patient’s pulmonary blood flow and cardiac output increase, because mechanical ventilation support is minimal and the lungs do not oxygenate the blood effectively. Thus, pulmonary venous return and blood ejected by the left ventricle will be relatively hypoxemic or desaturated. Anything that increases pulmonary blood flow and native cardiac output will increase the proportion of aortic flow that is provided by this relatively hypoxemic/desaturated blood, so the PaO2 falls. Hyperdynamic heart function and hypervolemia secondary to increased volume administration or decreased urine output can increase cardiac output and pulmonary blood flow.


When the PaO2 falls, ECMO flow is usually increased to maintain systemic oxygen delivery while hypervolemia is treated with diuretic therapy or hemofiltration as appropriate. If the ECMO flow is increased appropriately, the systemic venous oxygen saturation should return to previous levels.



ECMO Support with Single Ventricle Physiology


In patients with single ventricle physiology or shunt-dependent pulmonary blood flow, controversy exists about management of the shunt during MCS. There is debate regarding whether the shunt should be completely closed, partially closed, or left open during MCS. The challenge is to maintain balance between systemic and pulmonary circulation. If the shunt is completely closed during support, there is a risk of pulmonary infarction. If the shunt is open during ECMO, increased ECMO flow may be needed to maintain adequate pulmonary and systemic blood flow and systemic oxygen delivery.53


There are limited data regarding the role of ECMO after stage 1 palliation (and its variants) for hypoplastic left heart syndrome. ECMO is a useful tool for treatment of potentially reversible conditions, such as acute shunt thrombosis and transient depressed ventricular function53; ECMO may be used electively in the immediate postoperative period. However, the use of ECMO after the Norwood procedure remains controversial because the infant’s anatomy is complicated, the therapy is expensive, and survival rate is low.18,51,53,57



Venovenous ECMO



Circuit


VV ECMO is an alternative to VA ECMO that may be preferred for treatment of respiratory failure. In VV ECMO, venous blood is drained, sent through the circuit for oxygenation and carbon dioxide removal (ventilation), and returned to the venous side of the circulation.


The VV ECMO circuit has the same major components and flow pattern as the VA ECMO circuit (described previously), but blood is infused back into the venous circulation by a second venous cannula or a double-lumen single venous cannula. In infants, a double-lumen cannula is placed in the right internal jugular vein and blood is withdrawn through this catheter and returned to the right atrium. In older patients, two or more venous cannulas are placed, often in the right internal jugular vein, the femoral vein, or both.



Venovenous ECMO Flow and Function


Because VV ECMO delivers highly oxygenated/saturated blood to the venous side of the heart, the right heart cannula must be carefully positioned and rotated, and native cardiac function must be adequate. The range of PaO2 typical during VV ECMO is 50 to 70 mmHg, lower than during VA ECMO.


Because both the venous drainage and reinfusion cannula are in the venous system, some blood will be cycled through the ECMO circuit over and over again. This phenomenon is known as recirculation. As ECMO flow increases, so does the percentage of blood that will be recirculated. The greater the volume of blood that is recirculated, the lower the amount of blood flow that is sent forward through the tricuspid valve, into the lungs, left heart, and to the body, and the lower the efficiency of gas transfer between the oxygenator and the patient. The degree of recirculation is monitored by comparing the oxygen saturation of the venous drainage (SvO2) with the arterial saturation (SaO2). If the SvO2 is higher than normal and the SaO2 is low, the volume of recirculation is excessive and either the blood flow rate or cannula placement requires adjustment.



Hemodynamic Changes during Venovenous ECMO


Venous cannula position can impede forward flow, as can right or left atrial volume, and poor contractility. If forward flow is impeded, PaO2, cardiac output and oxygen delivery fall.


If the PaO2 is low or falls during VV ECMO, the cannula position should be checked and the physician should be notified to make any adjustments. In addition, therapy to improve cardiac output may include volume administration with packed red blood cells (to maximize oxygen-carrying capacity) and initiation of inotropic support. Occasionally, conversion from VV ECMO to VA ECMO is needed if hypoxia persists, particularly in the presence of hypotension and poor cardiac output despite maximal ventilator and inotropic support. VA ECMO is also considered if the child develops nonperfusing arrhythmias or cardiac arrest.


Although there is no difference in the rate of survival, or rates of intracranial hemorrhage and infarction, seizures and brain death in pediatric respiratory patients for VV versus VA ECMO, VV ECMO is associated with significantly more cannula problems, higher incidence of CPR on ECMO, and use of inotropic support. In addition, there is also a trend toward more renal failure and use of hemofiltration on VV ECMO.62



Advantages and Disadvantages of VA and VV ECMO


The major advantage of VA ECMO is that it provides both cardiac and pulmonary support. The disadvantages of VA ECMO are: the need to ligate the right common carotid artery and internal jugular vein after decannulation, that the blood flow it provides to body organs is nonpulsatile, that it may result in lower oxygen delivery to the coronary arteries, and that there is a potential for emboli directly into the arterial circulation.


The advantages of VV ECMO are that the carotid artery is spared, pulsatile flow is maintained, and potential emboli from the circuit are trapped in the pulmonary vascular bed. The major disadvantage of VV ECMO is lack of cardiac support. However, the most common cause of myocardial dysfunction in the neonate is respiratory failure. VV ECMO delivers high concentrations of oxygen to both the lungs and the coronary arteries. The high oxygen levels can produce pulmonary vasodilation, decreasing pulmonary hypertension and reversing hypoxic myocardial dysfunction.



Indications and Contraindications of ECMO Support


The indications and contraindications differ for neonatal, pediatric, and cardiac ECMO. Although specific inclusion and exclusion criteria exist, the use of ECMO remains a center specific decision and has to be considered on a case-by-case basis. The inclusion criteria for neonatal and pediatric ECMO are summarized in Box 7-1.



Box 7-1 Inclusion Criteria for Neonatal and Pediatric Respiratory ECMO Support



Neonatal




• Gestational age >34 weeks


• Weight >2 kg


• Mechanical ventilation <14 days


• Reversible lung injury


• Oxygenation index >35


• No major congenital heart disease


• No lethal malformations or congenital anomalies


• No evidence of irreversible brain injury



Pediatric




• Potentially reversible etiology for pulmonary failure


• Oxygenation index >40 and worsening respiratory failure despite maximal ventilator support


• Hypercarbia and pH <7.1


• PaO2/FiO2 ratio <100


• Ventilator support for <14 days


• No other major contraindication to ECMO support such as severe central nervous system abnormality, ongoing hemorrhagic condition or coagulopathy, or multiple organ system failure in >3 organ systems


ECMO, Extracorporeal membrane oxygenation; FiO2, fraction inspired oxygen; PaO2, arterial partial pressure of oxygen.



Neonatal Respiratory Failure


Neonatal ECMO has generally been considered an invasive rescue therapy with an identified set of risks; it is reserved for patients with a high predicted mortality who fail to respond to optimal conventional therapies. In newborns, a predicted mortality rate of 80% or greater was historically the main indication for ECMO. Much work was done in the early years of ECMO therapy to establish criteria for 80% predicted mortality. The most commonly used variable is the OI. An OI greater than 35 on three or more postductal arterial blood gases, 30 to 60 minutes apart, is consistent with an 80% predicted mortality. In addition, a single OI of 60 is a significant predictor of mortality.


Some centers used the A-a oxygen difference (A-a DO2), also known as the A-a O2 gradient. An A-a difference or gradient of more than 600 for a period between 4 and 12 hours is an accepted indication for ECMO support. However, some centers simply report the use of ECMO in patients with severe hypoxemia (PaO2 <50 mm Hg), severe acidosis (pH <7.25), and acute deterioration resulting in a PaO2 of approximately 30 to 40 mm Hg; these are all considered indications for ECMO.


ECMO may be initiated for patients with 50% to 80% predicted mortality if ECMO offers a higher potential for survival than conventional therapy. Examples of such patients include those with meconium aspiration and congenital diaphragmatic hernia with an OI of 25 to 40. The inclusion criteria of a minimum gestational age greater than 34 weeks’ gestation and weight greater than 2 kg is somewhat arbitrary, but is based on the increased risk of intraventricular hemorrhage (IVH) and difficult intravenous access in premature neonates.


Contraindications for neonatal ECMO include the presence of irreversible and uncontrolled bleeding or coagulopathy, IVH greater than grade II, birth weight <2 kg, or gestational age <34 weeks, lethal chromosomal abnormality or congenital malformation incompatible with life, and duration of mechanical ventilation >14 days.43


With more extensive use of therapies such as high-frequency ventilation, surfactant, and nitric oxide, there has been a marked decline in the need for neonatal ECMO.38 If patients do not respond to these therapies, ECMO should be offered in a timely manner.



Pediatric Respiratory Failure


There is less consensus regarding indications for ECMO support for pediatric patients than for neonates with respiratory failure. Severe respiratory failure in children has many etiologies. A child is generally considered to be a candidate for ECMO if death is believed to be nearly certain despite maximal conventional therapy, and the lung disease is believed to be reversible and other organ systems are intact.29 In children, the OI has not been shown to be as predictive of mortality as it is in neonates. Many centers use the criteria of OI >40 and rising, hypercarbia and pH <7.1, a PaO2:FiO2 ratio less than 100 and falling, ventilator support for less than 14 days, and no contraindications such as significant neurologic or hemorrhagic conditions, or failure of more than three organ systems.43 With the use of lung protective strategies and adjunctive therapies such as high-frequency ventilation, surfactant, and nitric oxide, it has become harder to establish criteria for initiation of ECMO support. Contraindications for pediatric ECMO are similar to those in the neonatal period; these include diagnoses incompatible with life, intractable hemorrhage or coagulopathy, or severe central nervous system abnormality.



Cardiac Failure


Cardiac ECMO support has steadily increased over the past decade.24 Although isolated left ventricular failure is relatively rare in children, right ventricular failure, pulmonary hypertension, and hypoxemia are often associated with circulatory collapse in children with congenital heart disease. The most common causes of circulatory failure in infants and children are cardiovascular surgery (postcardiotomy), end-stage cardiomyopathy, and acute myocarditis. The most common indications for ECMO in cardiac patients are severe hypoxia, severe pulmonary artery hypertension, cardiogenic shock, cardiac arrest, and failure to wean from cardiopulmonary bypass after surgical repair.


With ECMO support, postcardiotomy myocardial recovery should occur in approximately 72 hours to 7 days. If there are no signs of myocardial recovery during this time, a cardiac catheterization is needed to assess for residual structural defects. If none exist, the child is listed as a candidate for cardiac transplant. If residual structural defects are identified, surgical reintervention is scheduled.


Contraindications for the use of cardiac ECMO include incurable malignancy, advanced and presumed irreversible multisystem organ failure, extreme prematurity, and severe central nervous system abnormality or hemorrhage.59 In addition, if a patient will not be a transplant candidate, the patient should be carefully evaluated before ECMO. During the past 10 years, many contraindications have been removed from the list or labeled as relative rather than absolute contraindications.



Weaning from ECMO


There are two basic approaches to weaning patients from VA ECMO. Neither method has been shown to be superior to the other.32


In the gradual approach, as lung function improves ECMO is slowly withdrawn and ventilator support is slowly increased. Weaning with this approach may take a period of several days to reach idling flow, or approximately 20 mL/kg per minute. Clinical improvements in pulmonary function and chest radiograph, and loss of edema with a return to pre-ECMO weight faciitate the weaning process.


In the second, more abrupt approach to weaning, ECMO is maintained at full flow of 100 mL/kg per minute with minimal ventilator support until moments before the ECMO circuit is clamped. At that time, the ECMO flow is decreased over a few minutes while ventilator support is simultaneously increased. The circuit is then clamped off and blood gases are obtained to assess pulmonary function. The rationale for this more abrupt termination of ECMO support is that it allows a longer period of low ventilator support to maximize the resting time for lungs to heal.


To discontinue ECMO therapy, the patient must be able to maintain adequate blood pressure, perfusion, acid-base balance, and oxygenation with acceptable ventilator settings without ECMO support. Hypoxia, acidosis, increased serum lactate, decreased cardiac function, and hypotension may be indications to resume ECMO support. During the weaning process, it is not uncommon to increase the ECMO flow or to have more than one unsuccessful attempt to remove ECMO before successful weaning.


Weaning VV ECMO is slightly different than weaning VA ECMO. When weaning VV ECMO, after the ventilator settings are increased, both of the membrane oxygenator gas ports are isolated from ambient air. Eventually, the blood entering and exiting the membrane oxygenator is in equilibrium and reflects typical venous values. This eliminates the need to clamp the venous cannula and allows a longer trial off VV ECMO.32



Complications of ECMO


ECMO has historically been reserved for those with the highest predicted mortality, so its use has a favorable benefit-to-risk ratio. There are a number of identified complications of ECMO therapy. Some of these complications are related to the use of ECMO and some are related to the complications of the initial disease process. With any cause of severe cardiorespiratory failure there is the antecedent injury associated with hypoxemia, acidosis, and shock; if ECMO is provided, there are additional potential complications related to altered flow dynamics of ECMO cannulation and bypass. In addition, there are issues of reperfusion injury and heparinization. It can become difficult to separate the complications actually related to ECMO from those related to the initial illness.


The two most common complications of ECMO are bleeding and clot formation in the circuit. Bleeding and hemorrhage are related to the use of heparin for anticoagulation of the circuit; this heparin then anticoagulates the patient too. As blood flows through the circuit, coagulation factors and platelets are activated and clot formation is triggered in the circuit. A consumptive coagulopathy can develop, causing bleeding complications. The tubing and the oxygenator trap platelets, causing thrombocytopenia. A large percentage of the circulating platelets will have reduced function.


During ECMO, patients requiring any surgical intervention (even just chest tube placement) are at increased risk for bleeding at incision sites. Gastrointestinal hemorrhage and IVH are known ECMO complications.


Because the clotting cascade is activated, clots can develop in the ECMO circuit. These clots can obstruct flow if they are sufficiently large. When clots develop in the oxygenator they can cause oxygenator failure.


Once ECMO is initiated, antithrombin III (AT III) replacement is necessary. AT III acts in concert with heparin to provide anticoagulation. Without adequate levels of AT III, the heparin infusing in the patients during ECMO cannot be truly effective as an anticoagulant. Levels of AT III have been shown to be low in most patients requiring ECMO.


The art of managing patients during ECMO involves assessing each patient’s activated clotting time (ACT) and other measures of coagulation including AT III levels, platelets, prothrombin time (PT)/activated partial thromboplastin time (aPTT) and international normalized ratio (INR) values, anti Xa heparin activity, and thromboelastrography. Heparin and blood product administration and factor replacement should be tailored to patient needs.


Other complications of ECMO include neurologic, cardiovascular, and renal complications in addition to infectious and metabolic problems. Neurologic complications include seizures, IVH, cerebral infarction, and the potential for brain death. It is important to note that even before ECMO is initiated, the patient suffers an insult to the central nervous system secondary to hypoxia and poor perfusion. Cannulation for ECMO alters perfusion and can also contribute to reperfusion injury to the brain. It is therefore difficult to identify whether a neurologic complication is related to the use of ECMO, the antecedent injury suffered before ECMO, or a combination of factors.


Cardiovascular complications of ECMO therapy include arrhythmias, hypotension, hypertension, tamponade, and cardiac stun. In addition, newborns are at risk for maintenance or persistence of a patent ductus arteriosus.


Pulmonary complications include pneumothorax or other air leaks as well as pulmonary hemorrhage and hemothoraces. Pneumothoraces are often minimized by the use of rest ventilator settings. However, when increased settings are used to try to wean ECMO support, a spontaneous pneumothorax may develop.


Infectious complications include culture-proven infections and signs of inflammation, such as neutropenia and elevated C-reactive protein that suggest infection. Attachment to an extracorporeal circuit for an extended period provides a portal for potential infection, but these patients are also intubated and have many catheters and tubes that contribute to infection risk. Meticulous attention to aseptic care of the ECMO circuit can diminish the risks of an ECMO-related infection.


Finally, there are a number of metabolic complications of ECMO therapy, including glucose, electrolyte, and acid-base abnormalities. Banked blood may contain high quantities of glucose and citrate, so glucose and calcium imbalances can be problematic. Older blood has a high potassium concentration. In addition, patients may have a high bilirubin level or high plasma-free hemoglobin, indicating significant hemolysis secondary to ECMO.



ECMO Troubleshooting



ECMO Circuit Emergencies


There are many types of ECMO circuit emergencies, so ECMO staff and the bedside nurse must be constantly vigilant to prevent a circuit problem and rapidly respond to and correct any circuit emergency. The following circuit components need to be rapidly assessed in an ECMO emergency:



• Is blood ejecting from the circuit?


• Is air being pumped in the circuit?


• Is the pump delivering forward flow?


• Does the post-oxygenator blood appear red?


• Is the sweep gas being delivered and vented from the oxygenator?


• Are the circuit and equipment functioning properly?


The circuit check can direct the ECMO specialist’s immediate response to the emergency. If there is blood ejecting from the circuit and air being pumped, then immediate removal from ECMO is required before the problem can be repaired. The ECMO specialist must identify and fix the pump problem while the patient’s nurse and additional critical care unit (PCCU) staff support the patient off ECMO. Immediately clamp the venous line, open the bridge, and clamp the arterial line to remove the patient from the ECMO circuit. Because the patient is dependent on the ventilator, provide ventilation with 100% oxygen or shift the patient back to pre-ECMO ventilator settings. In addition, increased volume and inotropic support may be required, and full cardiopulmonary resuscitation may be needed.


If there is no squirting blood or air being pumped, the patient can be maintained on ECMO while the problem is corrected. ECMO circuit emergencies and problem troubleshooting are summarized in Table 7-2.


Table 7-2 Troubleshooting the ECMO Circuit











































Problem Signs and Symptoms Response
Clots in circuit Dark zones or streaks seen; can cause bleeding due to coagulopathy (decreased platelets or fibrinogen unresponsive to transfusion) Monitor circuit, monitor for coagulopathy, change circuit
Oxygenator failure Failure to remove CO2 or add adequate levels of oxygen in spite of increasing sweep gases and FiO2; may see blood or serum leaking from gas exhaust port Remove air and debubble circuit if present; check that all gas lines are intact and not leaking to rule out gas line failure; replace oxygenator if it has failed
Air in venous side of circuit Bubbles seen Correct source of problem, remove air
Air in arterial side of circuit Bubbles seen Remove patient from ECMO by clamping arterial and venous lines to patient; place patient in Trendelenburg position; replace/repair the component identified as cause; remove all air, recirculate, and then return to ECMO
Power failure Pump stops with no AC power Plug into emergency hospital power; use battery or UPS; hand crank
Accidental decannulation With partial removal on venous side, air entrainment can be seen; with complete decannulation, cannula will be out of the body with bleeding from cannulation site and possible pumping of air or blood Cease ECMO and stop pump; put direct pressure on site; call surgeon for immediate replacement of cannula and to control bleeding; replace volume losses with available blood products and crystalloid
Water heater failure Patient exhibits hypothermia; bradycardia with reflex hypertension may be seen with pallor Obtain new water heater and connect to circuit
Raceway rupture Blood spurts out of damaged tubing in pump head Cease ECMO; turn pump off; replace raceway segment with new tubing; clean pump head; place new raceway segment into the pump head and recirculate; return to ECMO
Cracks in tubing or connectors or loose stopcocks On venous side [negative pressure side] air will entrain into the circuit. On positive pressure side of the circuit, blood will leak out Tighten connections or replace cracked tubing or connectors; cease ECMO; stop pump; cut out and replace the damaged segments

AC, Alternating current; ECMO, extracorporeal membrane oxygenation; UPS, universal power source.



Ventricular assist devices


The development and clinical application of circulatory support devices have closely paralleled the development of cardiac transplantation. Denton Cooley and colleagues achieved the first successful bridge to cardiac transplantation with an artificial heart in the late 1960s. Routine bridging to transplantation began in 1984 with the short-term use of the total artificial heart by Jack Copeland, the Pierce-Donachy (Thoratec) VAD by Donald Hill and colleagues, and the Novacor electrical VAD by Oyer and colleagues.


The options for MCS for infants and children with cardiac failure are limited. There are currently no devices approved by the FDA for specific use in infant patients. However, several devices have been used successfully to support infants and children through the following: off-label use of devices approved by the FDA for use in adults, compassionate use of investigational adult VADs, the use of devices that have received an FDA Humanitarian Device Exemption, the use of devices fabricated from FDA-approved components (such as ECMO circuits), and devices that are approved on a case-by-case basis by the FDA for emergency use.7,8,12,20–22,27,28,31,44,56 Table 7-3 lists ventricular assist devices currently being used in the pediatric population under various exemptions or adult approved devices used in older children.2,26,30,35,42,45,46,61 Additional information regarding VADs used in children is included in Evolve Table 7-1 in the Chapter 7 Supplement on the Evolve Website.



Table 7-3 Mechanical Cardiac Support Devices Currently Used in Pediatrics

image


Components and Function of VAD Support


A VAD is a heart pump that can be used to support the right ventricle (called a right ventricular assist device [RVAD]), the left ventricle (called an LVAD), or both ventricles (called a BiVAD). Most VADs have three major components: a pump (located inside or outside the body), a control system, and an energy source. The control system and energy source are found outside the body. The energy source can be a battery or compressed air (pneumatic).23


In the pediatric population, most VAD pumps are extracorporeal (outside the body) and connected to inflow and outflow cannulae (Fig. 7-2). The critical care nurse should understand the components of the VAD and VAD function.


image

Fig. 7-2 Extracorporeal pneumatic biventricular assist device (Berlin Heart EXCOR).


(Redrawn from an illustration of the Berlin EXCOR by Berlin Heart, Berlin, Germany.)


The placement of the VAD cannula differs if the device is a bridge to recovery, compared with a bridge to transplantation. If the VAD support is serving as a bridge to recovery, the inflow cannula is often connected to the patient’s atrium.19 This cannulation is technically easier and spares the ventricle further injury. However, ventricular cannulation enables higher flow rates, so this form of cannulation is used when VAD support is used as a bridge to transplant, because ventricular injury is not a concern.


When an LVAD is used, the inflow cannula (carrying blood from the patient to the pump) is inserted in either the left atrium or the left ventricle. The outflow cannula (carrying blood from the pump to the patient) is inserted in the ascending aorta. When an RVAD is used, the inflow cannula is inserted in either the right atrium or right ventricle, and the outflow cannula is inserted in the pulmonary artery.



Ventricular Assist Device Flow and Function


Most VAD pumps used in children are either displacement pumps (pulsatile or pneumatic devices) or rotary pumps (continuous flow devices). The pulsatile or pneumatic pumps mimic the natural contraction (pumping action) of the heart. Flow rates depend on preload and the size of the external pump. Average flows for an infant-sized pump (12 or 15 mL) are 0.5 to 1.3 L/min and for a child-sized pump (25 or 30 mL) are 1.3 to 3.3 L/min.4 The external pump size can be changed to accommodate the child’s growth and increased stroke volume.


The most common continuous flow devices are axial or centrifugal pumps. Both types have a central rotor containing permanent magnets. Controlled electric currents that run through coils in the pump housing apply forces to the magnets causing the rotors to turn. Axial flow rates vary depending on the size of the device implanted. The child-sized device has been reported to provide an average flow of 0.3 to 2.5 L/min.4 The pediatric centrifugal Bio-Medicus Bio-pump (Medtronic, Inc. Minneapolis, MN) has both a 50- and 80-mL pump head size to accommodate infants <10 kg and children >10 kg, respectively. The 50-mL pump can provide flow up to 1.5 L/min and the 80-mL pump can provide >2 L/min.27


The VAD console and energy source varies depending on the VAD type. Most pneumatic consoles display both left- and right-sided heart support, the pump rate in beats per minute, systolic and diastolic or fill pressures, and vacuum drive pressures. The consoles also have backup units in case of malfunction. These backup units can be automatically or manually converted, depending on the device. In addition, the consoles can be operated by external electrical power as well as internal batteries. Battery life varies by device with an average of 1 to 2 hours. External backup pumping devices should be attached to the console in case of an emergency.


The console of the centrifugal pump displays the speed and blood flow rate, which are manually adjusted by the operator. Inlet and outlet pressure monitors can be used to guide pump speed and prevent tubing collapse. External electrical power and internal batteries operate the console if transport is needed.


All VADs are preload dependent—the amount of blood returning to the heart is the amount of blood pumped to the body. The VAD is sensitive to impedance to flow, so hypertension and mechanical obstruction must be corrected. Both the LVAD and RVAD allow blood to bypass the failing ventricle. This decompresses that ventricle, decreases myocardial work, and reduces oxygen demand while maintaining adequate systemic perfusion to sustain end-organ function. VAD support has been shown to improve myocardial contractility. It also reverses beta receptor downregulation (documented to occur with heart failure), restoring myocardial response to the inotropic effects of adrenergic stimulation.48 VAD support can also normalize chamber geometry and reduce myocardial fibrosis, hypertrophy, and disruption in cytoskeletal proteins.10,34



Types of Ventricular Assist Device Pumps


Several VAD pumps made for adult patients are available for clinical use. Some are implanted internally and others are external pumps. The VAD pumps can be broadly subdivided into continuous flow (nonpulsatile) and pulsatile pumps. Both types have a central rotor containing permanent magnets; the magnets cause the rotors to turn.



Continuous Flow Pumps


The continuous flow (nonpulsatile) VADs use either centrifugal or axial flow pumps. Each has advantages and disadvantages.



Centrifugal Pump


The centrifugal pump is external, requires cannulation via a thoracotomy or sternotomy, and can be used for single or biventricular support. The most common centrifugal pump is the Bio-Medicus Bio-Pump (Medtronic, Inc. Minneapolis, Minn). The Bio-Pump uses two magnetically coupled, polycarbonate rotator cones that spin to create centrifugal force along a vertical axis.11 The rotors are shaped to accelerate the blood circumferentially and thus cause it to move toward the outer rim of the pump. The constrained vortex pump design creates subatmospheric pressure at the tip of the cone, establishing suction in the venous cannula.40 Blood enters at the apex of the cone and is ejected tangentially at the base of the cone (Fig. 7-3). The cone design retains any small air bubbles.


image

Fig. 7-3 Bio-Medicus centrifugal pump.


(From Karl TR, Horton SB, and Brizard C: Postoperative support with the centrifugal pump ventricular assist device (VAD). Seminars in Thoracic and Cardiovascular Surgery: Pediatric Cardiac Surgery Annual 9:83–91, 2006.)


The pump output is proportional to revolutions per minute and is adjusted according to the venous return. Spins averaging 10,000 to 20,000 rpm will create a blood flow of 5 to 6 L/min in larger pumpheads.36 This type of pump can support neonates and older children with postoperative cardiac failure but competent lung function.36,58


The advantages of the centrifugal pump include: no need for an oxygenator, low priming volume (pediatrics, 50 mL), low requirements for heparin and little hemolysis, adequate decompression of the left ventricle, easy transport, and low cost. However, adequate pulmonary function is required and the chest must remain open, as with ECMO.


The centrifugal VADs include Bio-Medicus Bio-pump, Levitronix CentriMag (Levotronix, Waltham, Mass.), RotaFlow (Jostra, Hirrlingen, Germany), and the Capiox Terumo (Terumo Cardiovascular Systems, Ann Arbor, Mich.). The Levitronix CentriMag is marketed in Europe, but available in the United Stated only as an investigational device.11 The advantage to this device is that it can be attached to cardiopulmonary bypass cannula already in place. However, cannula adaptors may be needed for smaller patients.

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Dec 3, 2016 | Posted by in NURSING | Comments Off on Mechanical Support of Cardiopulmonary Function: Extracorporeal Membrane Oxygenation, Ventricular Assist Devices, and the Intraaortic Balloon Pump

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