Temporary Mechanical Circulatory Support Devices

46  Temporary Mechanical Circulatory Support Devices Mark Gdowski, Jonathan D. Wolfe, David L. Brown

OUTLINE Intraaortic Balloon Pump, 478 Physiologic Principles, 478 Monitoring of IABP Counterpulsation, 480 Contraindications to IABP Counterpulsation, 481 Insertion, Removal, and Complications, 482 Clinical Efficacy and Indications, 483 Unstable Angina, 483 Acute Myocardial Infarction, 483 Cardiogenic Shock, 484 High-Risk Percutaneous Coronary Intervention, 484 Cardiac Surgery, 484 Other, 485 Conclusion, 485 Left Ventricle to Aorta Support Devices, 485 Physiology and Monitoring, 486 Contraindications and Complications, 486 Clinical Efficacy and Indications, 487 Cardiogenic Shock, 487 High-Risk PCI, 487 Conclusion, 487

Left Atrium to Aorta Support Devices, 487 Physiology and Monitoring, 488 Contraindications and Complications, 488 Clinical Efficacy and Indications, 488 Cardiogenic Shock, 489 High-Risk Percutaneous Coronary Intervention, 489 Conclusion, 489 Extracorporeal Membrane Oxygenation, 489 Physiologic Principles of ECMO, 489 Monitoring of ECMO, 490 Contraindications to the Use of ECMO, 491 Insertion, Removal, and Complications, 491 Insertion, 491 Removal, 491 Complications, 491 Clinical Efficacy and Indications, 491 Cardiogenic Shock, 492 Cardiac Arrest, 492 Conclusions, 492 Summary, 492

Clinicians practicing in the cardiac intensive care unit (CICU) are challenged with increasingly complex patients who often require hemodynamic support to improve end-organ perfusion and reduce mortality. The high mortality associated with cardiogenic shock has been the stimulus for technological advances that provide life-sustaining hemodynamic support when maximum pharmacologic therapy is ineffective. Numerous devices to augment cardiac output (CO) have been developed that can be placed surgically or percutaneously (Fig. 46.1). Each approach has device-specific characteristics (Table 46.1), advantages and disadvantages, different effects on hemodynamics (Table 46.2), and different complication profiles (Table 46.3). This chapter will explore four categories of devices, provide practical guidance on device management, and examine the evidence behind indications for the use of each.

used in managing cardiogenic shock, intractable angina, myocardial ischemia, during high-risk percutaneous coronary intervention (PCI), in cardiac surgery, and for patients with refractory heart failure or arrhythmias awaiting definitive therapy.1 It relies on the concept of diastolic augmentation and afterload reduction to improve the function of ischemic and/or failing myocardium. The concept was originally proposed by Moulopoulos et al. in 1962 and validated by demonstration of an improvement in hemodynamic parameters in experimental animal models.2 The first report of human use by Kantrowitz appeared 6 years later.3 Although most commonly placed in the patient in the catheterization laboratory, the IABP can be placed at the bedside by experienced operators. Practitioners in the CICU need to be familiar with the fundamental principles of IABP counterpulsation therapy to effectively manage patients. Characteristics of the IABP are summarized in Table 46.1.

INTRAAORTIC BALLOON PUMP

Physiologic Principles

The intraaortic balloon pump (IABP) is one of the most frequently placed mechanical circulatory support devices. The device is

The primary goal of IABP counterpulsation is to increase myocardial oxygen supply while decreasing oxygen demand.

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CHAPTER 46  Temporary Mechanical Circulatory Support Devices

Keywords Mechanical circulatory support device intraaortic balloon pump (IABP) Impella TandemHeart Extracorporeal membrane oxygenation (ECMO) cardiogenic shock

478.e1

479

CHAPTER 46  Temporary Mechanical Circulatory Support Devices

IABP

Impella

A

B

TandemHeart

C

ECMO

D

Fig. 46.1  Comparison of the most commonly used temporary mechanical circulatory support devices. (From Scheidt S, Wilner G, Mueller H, et al. Intraaortic balloon counterpulsation in cardiogenic shock. N Engl J. Med. 1973;288:979).

TABLE 46.1  Characteristics of Temporary Mechanical Circulatory Support Devices Device Characteristics

IABP

Impella

TandemHeart

VA ECMO

Pump mechanism Cannula size Insertion Maximum implant duration Delivered flow

Pneumatic 8 Fr Percutaneous 7–10 days 0.5–1 L/min

Axial flow 13–23 Fr Percutaneous or surgical cutdown 7–21 days (model dependent) 1.5–5 L/min (model dependent)

Centrifugal 21 Fr inflow, 15–17 Fr outflow Percutaneous 14–21 days 4 L/min

Centrifugal 18–21 Fr inflow, 15–17 Fr outflow Percutaneous and surgical 21–28 days 3–6 L/min

IABP, Intraaortic balloon pump; VA ECMO, venoarterial extracorporeal membrane oxygenation. From Combes A, Brodie D, Chen Y, et al. The ICM research agenda on extracorporeal life support. Intensive Care Med. 2017;43:1306–1318.

TABLE 46.2  Effect of Temporary Mechanical Circulatory Support Devices on Hemodynamics Hemodynamic Parameter

IABP

Impella

TandemHeart

VA ECMO

MAP Afterload Coronary perfusion LV stroke volume LV preload LVEDP Peripheral tissue perfusion

Increase Reduced Slightly Increased Slightly Increased Slightly Reduced Slightly Reduced Neutral

Increase Neutral Unknown Reduced Slightly Reduced Reduced Improved

Increase Increased Unknown Reduced Reduced Reduced Improved

Increase Increased Unknown Reduced Reduced Increased Improved

IABP, Intraaortic balloon pump; LV, left ventricular; LVEDP, left ventricular end-diastolic pressure; MAP, mean arterial pressure; VA ECMO, venoarterial extracorporeal membrane oxygenation. Modified from Werdan K, Gielen S, Ebelet H, et al. Mechanical circulatory support in cardiogenic shock. Eur Heart J. 2014;35:156–167; and Combes A, Brodie D, Chen Y, et al. The ICM research agenda on extracorporeal life support. Intensive Care Med. 2017;43:1306–1318.

During diastole, the balloon inflates, resulting in a volume of blood being displaced toward the proximal aorta. During systole, the balloon rapidly deflates, creating a vacuum effect resulting in a decrease in left ventricular (LV) afterload. To optimize these two hemodynamic effects, the IABP must inflate and deflate in synchrony with the cardiac cycle. The single most important determinant of effective counterpulsation is the timing of the IABP relative to the cardiac cycle.4 Once proper timing has been

established, IABP counterpulsation improves myocardial oxygen delivery via an increase in coronary perfusion pressure, reduces cardiac work by decreasing systolic blood pressure and afterload, and improves forward blood flow in patients with impaired cardiac contractile function.5 Modern IABPs now use a closed-loop control system to automatically optimize pump timing.6–10 Several factors influence the hemodynamic effect of an IABP: the volume of the balloon, its position in the aorta, the underlying

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TABLE 46.3  Complications of Temporary

Mechanical Circulatory Support Devices Complication Limb ischemia Hemolysis Hemorrhage

USP

IABP

Impella

TandemHeart

VA ECMO

+ + +

++ ++ ++

+++ ++ +++

+++ ++ +++

IABP, Intraaortic balloon pump; VA ECMO, venoarterial extracorporeal membrane oxygenation. From Combes A, Brodie D, Chen Y, et al. The ICM research agenda on extracorporeal life support. Intensive Care Med. 2017;43:1306–1318.

INF

T

P

Monitoring of IABP Counterpulsation The appropriate timing of balloon counterpulsation to the mechanical events of the cardiac cycle must be monitored to ensure that the patient is deriving maximal hemodynamic benefit (Fig. 46.2). To maximize diastolic augmentation, the balloon should inflate at end systole, immediately after closure of the aortic valve. Balloon inflation augments coronary perfusion pressure, thereby providing greater myocardial oxygen delivery. Mean diastolic pressure (MDP) correlates well with coronary perfusion and, hence, oxygen delivery.5 Smith and colleagues confirmed that maximal coronary perfusion occurs when balloon inflation coincides with end systole.8,15 The timing of balloon deflation, which decreases LV oxygen consumption, should occur at end diastole. Deflation before the LV ejection of blood creates a vacuum effect in the proximal aorta that, in turn, reduces afterload and peak systolic pressure. The triggering of balloon counterpulsation requires a predictable, reproducible, and reliable trigger event. The most commonly used trigger is the electrocardiographic (ECG) waveform. Inflation of the balloon begins at end systole, which correlates with the

UEDP

AEDP R

R

QS

heart rate and rhythm, the compliance of the aorta, and systemic vascular resistance.11 An increase in arterial elastance (a property that is affected by compliance) is associated with a greater degree of hemodynamic improvement from an IABP.12 Despite the presence of multiple factors that can cause variability in the effects of an IABP, a majority of patients exhibit a specific hemodynamic response (see Table 46.2), including a decrease in systolic pressure, an increase in diastolic pressure (which may subsequently enhance coronary blood flow to a territory perfused by an artery with a critical stenosis), a reduction in heart rate, a decrease in the mean pulmonary capillary wedge pressure (PCWP), and an increase in CO.13 The reduction in aortic pressure caused by the rapid deflation of the balloon decreases LV afterload and diminishes myocardial workload.5 Two indices that are measured during IABP counterpulsation are the tension-time index (TTI), which is the time integral of LV pressures during systole, and the diastolic pressure-time index (DPTI), which is the time integral of the proximal aortic pressures during diastole. Proper balloon inflation augments diastolic pressure (i.e., increases DPTI), whereas rapid balloon deflation decreases LV afterload (i.e., decreases TTI). The endocardial viability ratio (DPTI:TTI), which reflects the relationship between myocardial oxygen supply and demand, will increase with optimal IABP counterpulsation.5,14

ASP

R T

P QS

R T

P QS

T

P

P

QS

Fig. 46.2  Optimal timing of an intraaortic balloon pump (IABP). Arterial pressure tracing from a patient with an IABP. The balloon was set at 2 : 1 to evaluate timing. Inflation (INF) was timed to the dicrotic notch to follow aortic valve closure. There is augmentation of diastolic pressure (ADP) and reduction of the end-diastolic pressure with augmented beats (AEDP) compared with the unaugmented end-diastolic pressure (UEDP). The augmented systolic pressure (ASP) is often lower than the unaugmented systolic pressure (USP) as well. (Modified from Hollenberg S, Saltzberg M, Soble J, Parrillo J. Heart failure and cardiomyopathy. In: Crawford MH, Dimarco JP, Paulus WJ, eds. Cardiology. London: Mosby; 2001.)

middle of the T wave, while deflation of the balloon begins at end diastole and correlates with the R wave. IABP systems recognize other potential triggers, such as arterial pressure waveforms (most often used during cardiopulmonary resuscitation [CPR]) and ventricular or atrioventricular pacer spikes. A suboptimal hemodynamic effect results when IABP counterpulsation is not appropriately timed to the mechanical events of the cardiac cycle.16 Loss of the optimal hemodynamic effect occurs when balloon IABP counterpulsation is not appropriately timed to the mechanical events of the cardiac cycle. Mahaffey and colleagues have described four different scenarios involving faulty coupling of balloon IABP counterpulsation with the cardiac cycle16 (Fig. 46.3). During early inflation, the balloon inflates before closure of the aortic valve. Pressure augmentation is thus superimposed upon the systolic aortic pressure tracing, leading to a decrease in LV emptying (a decrease in stroke volume), a decrease in cardiac output, an increase in LV afterload, and an overall increase in myocardial oxygen consumption. In this scenario, there is loss of the distinct systolic peak of the central aortic pressure waveform and loss of the dicrotic notch (see Fig. 46.3A). To correct early inflation, the timing interval should be slowly increased until the onset of inflation occurs at the dicrotic notch. During late inflation, the dicrotic notch on the aortic pressure waveform is clearly visualized. The balloon inflates well beyond closure of the aortic valve. In this scenario, diastolic augmentation of the central aortic pressure is decreased, whereas LV afterload is minimally affected. The classic morphologic finding on the central aortic pressure tracing is the presence of a distinct dicrotic notch, with the augmented diastolic pressure wave occurring well afterward (see Fig. 46.3B). To correct late inflation of the

CHAPTER 46  Temporary Mechanical Circulatory Support Devices



Diastolic Augmentation

Unassisted Systole

481

Diastolic Augmentation Assisted systole

Assisted Systole

Dicrotic Notch

A

Assisted Aortic End Diastolic Pressure Diastolic Augmentation

B Assisted Systole

Assisted Aortic End Diastolic Pressure

Unassisted Systole

Widened Appearance

C

Assisted Aortic End Diastolic Pressure

Unassisted Aortic End Diastolic Pressure

D

Prolonged Rate of Rise of Assisted Systole

Assisted Aortic End Diastolic Pressure

Fig. 46.3  Incorrect timing in intraaortic balloon counterpulsation. (A) Early inflation: loss of dicrotic notch and distinct systolic peak of the aortic pressure waveform. (B) Late inflation: dicrotic notch is clearly visualized with the augmented diastolic pressure curve occurring well afterward. (C) Early deflation: peaked augmented diastolic wave along with a U-shaped wave preceding the onset of systole. (D) Late deflation: loss of a distinct valley representing the end-diastolic pressure before the central aortic systolic waveform. (From Krishna M, Zacharowski K. Principles of intraaortic balloon pump counterpulsation. Continuing education in anaesthesia. Crit Care Pain. 2009;9(1):24–28. Reproduced with permission from Datascope.)

IABP, the timing interval should be gradually decreased until the onset of inflation coincides with the dicrotic notch on the arterial pressure waveform. During early deflation, the balloon deflates prematurely; consequently, the benefits of diastolic augmentation are lost. Analysis of the arterial pressure tracing reveals the presence of a peaked diastolic augmentation wave along with a U-shaped wave preceding the onset of systole (Fig. 46.3C). To correct early deflation, the timing interval should be increased until the augmented diastolic wave becomes appropriate. During late deflation, the balloon is deflated after the onset of systole and the opening of the aortic valve. The resultant hemodynamic profile is like the one observed with early inflation: afterload is increased, leading to increased LV work and myocardial oxygen consumption along with reduced stroke volume and CO. Analysis of the arterial pressure tracing usually reveals the loss of a distinct valley representing the end-diastolic pressure before the central aortic systolic wave (see Fig. 46.3D). To correct late deflation, the timing interval should be decreased gradually until the balloon deflates before the onset of systole.

Contraindications to IABP Counterpulsation When IABP therapy is being considered, the risks and benefits of this modality must be individually assessed for each patient.

Absolute contraindications include significant aortic regurgitation, suspected aortic dissection, clinically significant abdominal or thoracic aortic aneurysm, distal aortic occlusion or severe stenosis, and chronic end-stage heart disease with no anticipation of recovery. Relative contraindications include severe peripheral arterial disease (PAD), contraindications to anticoagulation, uncontrolled sepsis, and sustained tachyarrhythmias (heart rate >160 beats/min).17 IABP counterpulsation in a patient with aortic regurgitation can potentially lead to further cardiac decompensation. During balloon inflation, an increased regurgitant volume may be generated across the incompetent aortic valve, resulting in increased LV volumes. Data from animal studies have demonstrated increased regurgitant flow but also enhanced LV stroke volumes, despite the increased diastolic volumes.18 Therefore, although patients with severe aortic valvular insufficiency should be excluded from IABP therapy, patients with lesser degrees of aortic regurgitation can be considered but with close monitoring during the initial phase of therapy. Patients with vascular abnormalities—such as distal aortic stenosis, aortic dissection, or aortic aneurysm—have a significantly increased risk of catastrophic vascular complications. The presence of PAD or iliofemoral grafts increases the risk of complications associated with balloon insertion and removal. Sustained tachyarrhythmias with heart rates exceeding 160 beats/

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BOX 46.1  Insertion and Removal of the

BOX 46.2  Insertion and Removal of the

The following steps are involved during insertion of an intraaortic balloon pump: 1. An initial physical examination focusing on peripheral vasculature should be conducted, including palpation and demarcation of the femoral, popliteal, dorsalis pedis, and posterior tibial pulses and auscultation for femoral and abdominal bruits. 2. The side with the better arterial pulsations should be selected for insertion. 3. The inguinal region should be inspected for landmarks and the femoral artery should be identified. 4. The inguinal region should be prepared and draped in a sterile fashion. 5. Following administration of a local anesthetic agent, a skin incision is made 2 to 3 cm below the inguinal ligament. 6. Using a modified Seldinger technique, the femoral artery is cannulated with a needle and a J-tipped guidewire is then advanced through the needle after brisk flow of arterial blood is confirmed. 7. The guidewire should be advanced to the level of the descending aorta under fluoroscopic guidance. 8. A dilator is inserted and removed until an arterial sheath can be safely placed. 9. The intraaortic balloon is passed over the guidewire to a position just distal to the origin of the left subclavian artery. 10. The guidewire is subsequently removed and the catheter lumen is aspirated to remove any residual air or thrombus. 11. The intraaortic balloon is connected to the drive system console and counterpulsation can subsequently begin. 12. The hemodynamic tracing should be inspected for proper timing. 13. A chest radiograph should be obtained to document correct positioning. 14. The intraaortic balloon catheter and femoral sheath should be secured with sutures.

1. Anticoagulation should be stopped; confirm that the activated clotting time is less than 180 seconds or the activated partial thromboplastin time is less than 40 seconds. 2. Conscious patients should receive a low-dose narcotic and/or analgesic agent. 3. The securing sutures are cut. 4. The drive system console is turned off. 5. The intraaortic balloon is completely deflated by aspiration with a 20-mL syringe attached to the balloon inflation port. 6. The sheath and intraaortic balloon catheter are pulled as one unit. 7. Blood is allowed to flow from the arterial access site for a few seconds to remove any thrombi. 8. Manual pressure is applied above the puncture site for 30 minutes or longer if hemostasis is not obtained. A mechanical compression device can also be used to help apply pressure to promote hemostasis. 9. Distal arterial pulsations are palpated. 10. The patient should remain recumbent for a minimum of 6 hours to prevent any subsequent hemorrhage or vascular complications at the arterial access site.

Intraaortic Balloon Pump

min hamper the ability of the balloon to accurately track the mechanical events of the cardiac cycle and provide hemodynamic support.

Insertion, Removal, and Complications The most commonly used approach for percutaneous placement is cannulation of the femoral artery. Once it is concluded that the patient no longer requires circulatory support, the removal of the IABP is also a straightforward process. Mahaffey and colleagues have devised a simple stepwise approach to device insertion and removal (Boxes 46.1 and 46.2).16 A thorough vascular examination should precede the insertion of the IABP. This examination should include palpation of all lower extremity pulses along with auscultation of the lower half of the abdomen and of the femoral arteries. The femoral artery with the best palpable pulsation should be selected to minimize vascular complications.1 The balloon (7.5 Fr) is inserted percutaneously over a guidewire using a sheath (8–9 Fr) although a sheathless approach has been used. The downsizing of IABP catheters (from early single-lumen balloons) has significantly reduced the incidence of ischemic peripheral vascular complications, especially in patients with small or atherosclerotic arteries. In patients with severe peripheral atherosclerosis or distal

Intraaortic Balloon Pump

abdominal aortic aneurysms, the IABP can be inserted through the axillary, subclavian, or brachial arteries. Following insertion of the device (see Box 46.1), fluoroscopy can be used to confirm that the device has been placed in the descending thoracic aorta distal to the origin of the left subclavian artery. IABP counterpulsation can begin thereafter, with augmentation using one inflation for each cardiac cycle (1 : 1 ratio) being ideal for optimal hemodynamic support. However, adjusting counterpulsation timing is best done with the console set at 1 : 2 pumping so that the pressure tracings with and without counterpulsation can be compared. Daily chest radiographs and continuous monitoring of hemodynamic parameters ensures stable placement and appropriate timing of the device. No conclusive data support the requirement for intravenous anticoagulation in the setting of IABP use. A trial of 153 patients found no difference in vascular complications in patients undergoing IABP therapy with and without continuous heparin anticoagulation.19 Industry guidelines do not require continuous anticoagulation therapy, especially when the device is set at a 1 : 1 assist ratio. Currently, it is reasonable to use intravenous heparin with the goal of maintaining an activated partial thromboplastin time (aPTT) of 60 to 75 seconds in a patient without contraindications to anticoagulation and when IABP counterpulsation therapy is planned for longer than 24 hours or at lower assist ratios.1 Although no conclusive data exist in the literature, some authorities recommend gradual weaning of the balloon pump before it is finally removed. In patients in whom the IABP was placed to treat hemodynamic instability, a gradual reduction in the assist ratio from 1 : 1 to 1 : 2 and then to 1 : 3 over several hours is frequently employed. If hemodynamic stability is demonstrated at lesser assist ratios, the device can be safely removed (see Box 46.2). Complications arising from IABP counterpulsation therapy can be categorized into vascular and nonvascular events. In two



CHAPTER 46  Temporary Mechanical Circulatory Support Devices

studies of nearly 40,000 patients, death due directly to an IABP or IABP placement was less than 0.05%. Major complications— including major limb ischemia, severe bleeding, balloon leak, and death related directly to device insertion or to device failure—occurred in 2.6% of patients (see Table 46.3).20 The true incidence of complications associated with placement of an IABP is difficult to ascertain. Studies citing complication rates differ in the indications for IABP counterpulsation therapy, insertion technique (surgical or percutaneous), duration of use, and the specific definitions of complications.20–24 The most commonly reported complications are bleeding and arterial trauma.1 Vascular complications remain the most common serious complications to occur in patients with an IABP. The most common types of vascular complications include limb ischemia, vascular laceration necessitating surgical repair, and major hemorrhage.25–27 Arterial obstruction and limb ischemia can occur when the IABP is inadvertently placed into either the superficial or profunda femoral artery instead of the common femoral artery, as these arteries are usually too small to accommodate the IABP without compromising blood flow to the leg. Prompt removal of the device and contralateral insertion (with avoidance of an excessively low needle puncture) is recommended. Arterial dissection can occur with improper advancement of a guidewire with subsequent insertion of the IABP into a false lumen. Less common vascular complications include spinal cord or visceral organ ischemia, cholesterol embolization, cerebrovascular accidents, sepsis, and balloon rupture. Balloon rupture is uncommon and usually owing to the balloon inflating against calcified plaque in the aorta. Because the helium gas used to inflate the balloon is insoluble in blood, helium embolization can cause prolonged ischemia or stroke. These patients can be treated with hyperbaric oxygen to maintain tissue viability. Numerous analyses have been attempted to identify clinical variables that predispose to a higher rate of complications. The presence of PAD (including a history of limb claudication, femoral arterial bruit, or absent pulsations) has been the most consistent clinical predictor of complications.28–30 These complications are more common in women (related to the size of the vessels) and patients with a history of diabetes mellitus and hypertension who are more likely to have PAD.

Clinical Efficacy and Indications IABP counterpulsation therapy improves the hemodynamic and metabolic derangements that result from circulatory collapse.17 Historically, this modality has been mainly used in the setting of acute ischemic syndromes associated with hemodynamic decompensation. In the decades since its introduction, more data have accumulated supporting the use of IABP therapy in a variety of clinical scenarios.

Unstable Angina.  Data are sparse regarding the use of IABP counterpulsation in patients with unstable angina. These data date back several decades; the use of IABP counterpulsation in this patient population is based on observational studies and clinical experience. Gold and colleagues studied 11 patients experiencing persistent angina despite aggressive medical therapy

483

after an acute myocardial infarction (MI); nine of these patients exhibited symptomatic improvement following placement of an IABP.31 Fuchs and colleagues examined seven patients who had proximal left anterior descending coronary arterial stenoses exceeding 90% along with unstable angina.32 The use of IABP counterpulsation before intervention improved symptoms and enhanced coronary blood flow as assessed with a Doppler flow wire.32 The 2014 American College of Cardiology/American Heart Association (ACC/AHA) practice guidelines for the management of patients with non-ST elevation acute coronary syndromes state that it may be reasonable to consider IABP counterpulsation therapy in patients with unstable angina that is continuing or recurring despite intensive medical therapy.33

Acute Myocardial Infarction.  Routine use of IABP counterpulsation in patients with acute MI, including ST segment elevation myocardial infarction (STEMI), is not indicated, though there may be patients who benefit from its use. Primary PCI in patients with STEMI has reduced mortality but it is widely recognized that some patients develop reperfusion injury or fail to achieve reperfusion at the cellular level owing to microvascular embolization that limits myocardial salvage even if the occluded coronary artery has been successfully recanalized by PCI.34–36 In the pre-PCI era, Ohman and colleagues conducted a trial of 182 patients with acute MI who were randomized to prophylactic IABP counterpulsation therapy for 48 hours or standard medical therapy.37 Patients randomized to IABP experienced less recurrent ischemia and a significantly lower rate of reocclusion of the infarct-related artery (8% vs. 21%; P < .03) at follow-up angiography 5 days later. The composite endpoint of death, stroke, reinfarction, need for emergent revascularization, or recurrent ischemia was significantly lower in patients randomized to IABP (24% vs. 13%; P < .04). The Primary Angioplasty in Myocardial Infarction-II (PAMI-2) trial randomized 437 patients who underwent primary percutaneous transluminal coronary angioplasty (PTCA) to 36 to 48 hours of IABP following primary or standard care. Prophylactic IABP counterpulsation after primary PTCA showed no benefit over standard therapy in decreasing all-cause mortality or adverse cardiovascular events, including infarct-related artery reocclusion.38 A registry of 1490 acute MI patients treated by primary PTCA was analyzed by Brodie and colleagues.39 In this observational study, 105 patients had an IABP placed before PCI, whereas 108 patients had an IABP inserted following the completion of PCI. Although the patients with an IABP placed before PCI exhibited a higher prevalence of cardiogenic shock and multivessel coronary artery disease, they experienced substantially higher procedural success rates and fewer adverse events (e.g., dysrhythmias and shock) during the PCI. In this observational study, the initiation of IABP counterpulsation therapy before PCI was an independent predictor of lower periprocedural complications. The Counterpulsation to Reduce Infarct Size Pre-PCI Acute Myocardial Infarction (CRISP AMI) trial randomized 337 patients with anterior STEMI without cardiogenic shock to routine IABP counterpulsation before primary PCI or primary PCI alone to determine if its use reduced infarct size, assessed by cardiac

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magnetic resonance imaging.40 Patients randomized to IABP showed no reduction in infarct size at 3 to 5 days compared to those who received no IABP. All-cause mortality at 6 months (2% vs. 5%; P = .12) and the composite endpoint of death, new or worsening heart failure and shock favored IABP use (5% vs. 12%; P = .03). More important, a substudy of patients with large MIs (defined by summed ST deviation ≥15 mm) and persistent ischemia (ST resolution after PCI >50%) showed a significant mortality reduction with IABP placement (0 vs. 5 deaths; P = .046).41 A meta-analysis of IABP use in acute MI patients in the absence of cardiogenic shock showed no mortality benefit.42 Thus the routine use of IABP counterpulsation in patients with acute MI, including STEMI, is not indicated.

Cardiogenic Shock.  Cardiogenic shock occurs in 5% to 10% of patients with acute MI and is associated with high mortality rates even in patients who undergo early revascularization with PCI or coronary artery bypass graft surgery (CABG).43 The 30-day mortality rate for the 0.8% of Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO I) trial patients with cardiogenic shock treated with thrombolytic therapy was 58%.44 In the interventional era, the mortality rate of cardiogenic shock remains as high as 50%.45,46 Early use of IABP in acute MI complicated by cardiogenic shock was based predominantly on small retrospective studies performed in the thrombolytic era that suggested improved outcomes.47,48 A meta-analysis of IABP use in patients with acute MI suggested a reduction in in-hospital mortality in patients with cardiogenic shock.49 The Intraaortic Balloon Pump in Cardiogenic Shock (IABP-SHOCK) trial randomized 45 patients with cardiogenic shock complicating acute MI treated with PCI to IABP or standard therapy. Mechanical support was associated only with modest reductions of the Acute Physiology and Chronic Health Evaluation (APACHE) II score as a marker of severity of disease, improvement in cardiac index, reduction of inflammatory state, or reduction of brain natriuretic peptide (BNP) biomarker status compared with medical therapy alone.50 The Intraaortic Balloon Pump in Cardiogenic Shock II (IABPSHOCK II) trial was one of the first large, multicenter randomized trials to compare IABP counterpulsation and standard medical therapy alone in patients with acute MI complicated by cardiogenic shock and treated with early revascularization.51 A total of 600 patients were randomized to IABP or no standard care. All patients underwent early revascularization (by PCI or CABG) and received optimal medical therapy. At 30 days, 119 patients in the IABP group and 123 patients in the control group died (39.7% vs. 41.3%; P = .69). There were no significant differences in secondary endpoints, including length of stay in the intensive care unit, duration of catecholamine therapy, and renal function. There was no difference in 1-year mortality (52% vs. 51%; P = .91) between the groups.52 Despite being the largest randomized trial performed in patients with cardiogenic shock, there were many limitations. The trial anticipated a 30-day mortality of 56% in the control group, but it was significantly lower than anticipated and thus was underpowered to address the primary

hypothesis. Despite evidence suggesting that IABP placement before primary PCI results in reduced mortality compared with insertion after primary PCI, 86% of patients in the IABP-SHOCK II trial had the IABP inserted following PCI.53 Also, there was a large crossover from the control group to the IABP group and use of LV assist devices in the control group. Based on clinical trials, routine use of IABP in acute MI patients with cardiogenic shock is not indicated. The 2013 ACC/AHA practice guidelines for the management of STEMI currently give the use of IABP counterpulsation a class IIa indication for acute MI patients in cardiogenic shock who do not stabilize with pharmacologic therapy.

High-Risk Percutaneous Coronary Intervention.  An IABP is often used for mechanical circulatory support in patients undergoing high-risk PCI. These patients often have a higher risk of procedural morbidity and mortality due to severe LV dysfunction, multivessel coronary artery disease, or uncontrolled angina. In this subset of patients, placement of an IABP before the intervention may be beneficial from the enhancement of coronary perfusion pressure and stabilization of hemodynamic parameters. The IABP may also allow them to better tolerate procedural complications, such as coronary artery dissection or the development of no-reflow. Small retrospective studies of elective IABP counterpulsation support before high-risk PCI have found favorable outcomes with no major adverse events within 72 hours of the intervention.54,55 Briguori and colleagues described 133 consecutive patients who underwent high-risk PCI.56 The patients were divided into those with an elective preprocedural placement of an IABP and those with provisional (i.e., standby) usage of an IABP. Among patients with a low LV ejection fraction (LVEF), the rate of major adverse cardiac events (acute MI, shock, stroke, emergent CABG, or death) was 17% in the standby IABP group versus 0% in the group that received a preprocedural IABP (P = .001). The Balloon Pump-Assisted Coronary Intervention Study (BCIS-1) was one of the first randomized controlled trials to examine the use of elective IABP in high-risk PCI patients.57 A total of 301 patients scheduled to undergo high-risk single-vessel or multivessel PCI were randomized to PCI with or without an IABP. There was no significant difference in major adverse cardiovascular events, including MI or stroke, in the elective IABP group compared with the control group (15.2% vs. 16.0%; P = .85). There were no differences in major secondary endpoints between the two groups except for major procedural complications, including ventricular tachycardia/fibrillation, cardiopulmonary arrest, and prolonged hypotension, all of which were less common in the IABP group. All-cause mortality at 51 months was significantly lower in the elective IABP group compared to the control group (42 patients vs. 58 patients; P = .039).58 The 2011 ACC/AHA/Society of Cardiovascular Angiography and Intervention (SCAI) practice guidelines currently assign the use of elective IABP as an adjunct to PCI in a carefully selected subgroup of patients with a class IIb indication. Cardiac Surgery.  The literature regarding the use of IABP counterpulsation in cardiac surgery is conflicting. Low cardiac



CHAPTER 46  Temporary Mechanical Circulatory Support Devices

output syndrome occurs in approximately 5% to 10% of patients following open-heart surgery and is associated with increased mortality. Some studies suggest that placement of prophylactic IABP before CABG in patients with certain high-risk features— including critical coronary arterial anatomy (including left main disease), severe LV dysfunction, or unstable angina—may be beneficial.59–61 In a small prospective study, Christenson and colleagues randomized 60 consecutive high-risk patients who were to undergo CABG to either conservative management or to preoperative IABP commencing 2, 12, or 24 hours before surgery.60 Most of these patients had LV dysfunction, unstable angina, and/or left main stenosis. Although no mortality benefit was observed, patients who were randomized to preoperative IABP of any duration had significantly higher cardiac output, a shorter duration of mechanical ventilation, and a reduced length of hospitalization. In 141 hemodynamically stable, high-risk patients who underwent CABG, 38 (27%) of whom underwent prophylactic IABP before surgery, after risk-adjustment, prophylactic IABP was associated with a reduction in postoperative low cardiac output syndrome (adjusted odds ratio [OR] 0.07; P = .006) and postoperative MI (adjusted OR, 0.04; P = .04) as well as a shorter length of hospital stay (10.4 days vs. 12.2 days; P < .0001).62 A meta-analysis performed by Field and colleagues of five randomized clinical trials of prophylactic IABP before CABG or standard care concluded that preoperative IABP counterpulsation may be beneficial in specific high-risk patient groups.63 Future clinical trials are needed to assess its true effectiveness.

Other.  IABP counterpulsation can also be used in a variety of other clinical situations. In patients with severe end-stage cardiomyopathy with refractory heart failure who are awaiting cardiac transplantation or LV assist device (LVAD) placement, IABP counterpulsation can be used as a bridging modality. There have been several case series and studies that have reported successful bridging with IABP counterpulsation in patients with cardiogenic shock who require cardiac transplantation or an LVAD.64,65 IABP counterpulsation in this setting decreases aortic systolic pressure and impedance; thus, it can promote systolic unloading of the LV, leading to an increased stroke volume. The use of IABP counterpulsation has also been shown to improve right ventricular (RV) failure, as unloading the LV can increase performance of the RV and improve outcomes in carefully selected patients.66 Incessant ventricular tachyarrhythmias are occasionally treated with IABP counterpulsation to unload the LV or to improve perfusion to ischemic myocardium. Several anecdotal reports have described cessation of ventricular tachycardia and fibrillation following the initiation of IABP counterpulsation therapy.17

Conclusion IABP counterpulsation is one of the most frequently used mechanical circulatory support devices in the CICU setting owing to its ease of use, safety, and availability. Based on the dual physiologic concept of diastolic augmentation and systolic afterload reduction, it can be an important strategy to improve the function of an ischemic and failing heart in selected patients.

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Blood inlet area

Catheter diameter: 9 Fr Flow rate: up to 4.0 L/min

Blood outlet area 14 Fr pump motor

Fig. 46.4  Components of the Impella CP device. (Courtesy of Abiomed, Inc.)

Although routine use is clearly not indicated in a variety of clinical settings based on randomized clinical trials, IABP counterpulsation may still be beneficial in selected subgroups of patients. Future randomized clinical trials are required to help understand which patients may benefit from IABP counterpulsation.

LEFT VENTRICLE TO AORTA SUPPORT DEVICES Catheter-mounted, temporary ventricular pumps were described as early as 1975 and were first used in humans in the 1990s.67 The concept evolved into the Impella (Abiomed, Inc.) LV to aorta support devices. The Impella is a miniature axial flow pump attached to a catheter (Fig. 46.4). Most commonly, devices are inserted percutaneously or surgically to position the pump across the aortic valve with the inflow in the LV and the outflow into the aorta (Fig. 46.5). The first device was approved by the US Food and Drug Administration (FDA) in 2008 for partial circulatory support during cardiac procedures not requiring cardiopulmonary bypass.68 Subsequent FDA-approved indications have expanded as alterations have been made to the device, resulting in a family of devices that are used for cardiac support during high-risk percutaneous procedures, LV support in cardiogenic shock and, most recently, for circulatory assistance in the setting of RV failure. Current device models include the Impella 2.5, Impella CP, Impella 5.0, and Impella RP (Video 46.1). All devices except the Impella RP provide LV circulatory support. The recently approved Impella RP provides RV circulatory support.69–71 This section will focus on the LV Impella devices.

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Fig. 46.5  Illustration of an Impella device positioned across the aortic valve. (From Thiele H, Smalling RW, Schuler GC. Percutaneous left ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2007;28:2057–2063.)

Physiology and Monitoring The Impella devices contain a miniature pump with a rotating impeller based on the principle of the Archimedes Screw.72 The pump is mounted on a flexible catheter and inserted percutaneously or surgically through the arterial system and advanced to position the distal end of the pump in the LV apex with the proximal end in the ascending aorta. Blood is aspirated out of the LV and ejected into the aorta. The devices are most commonly inserted through the femoral artery but alternative access sites, such as the subclavian and axillary arteries, have been described (see Table 46.1).73–75 Unlike the IABP, the Impella systems do not require timing or a trigger based on the ECG or arterial pressure. By unloading the LV, the pump reduces myocardial oxygen consumption, improves mean arterial pressure, and reduces PCWP (see Table 46.2).76 Adequate RV function is necessary to maintain LV preload in cases of biventricular failure or unstable ventricular arrhythmias.77 The 12 Fr Impella 2.5, 14 Fr Impella CP, and 21 Fr Impella 5.0 provide a maximum flow rate of 2.5, 3 to 4, and 5 L/min, respectively.68,78 The Impella 2.5 and Impella CP are inserted percutaneously (see Video 46.1). The Impella 5.0 requires surgical cutdown due to the large cannula size. The pumps consist of inflow and outflow areas, a motor, and a pump pressure monitor. Heparin and glucose are continuously infused into the motor housing to prevent backflow of blood. The pump is attached to a flexible 9 Fr catheter that houses the motor power leads and lumens for pressure measurement and heparin infusions. The catheter’s most proximal end contains a hub for attachment of

a console cable and side arms for attachment of pressure measurement tubing. Impella devices are used with an automatic controller that can be run off a built-in rechargeable battery or from an electric power cord. The controller features a display that users interact with to determine pump positioning and the quality of pumping function. The degree of support for patients can be set by changing the revolutions per minute (RPM) in set levels designated as P1 to P9 on the controller.79 The flow of heparin and saline into the motor is regulated by the “purge cassette” and can be monitored on the controller display.80 In addition to the use of radiography and echocardiography, appropriate Impella placement may be verified by the pressure waveform generated from the pressure sensor at the distal end of the pump. The placement signal is used to verify whether the Impella pump is correctly positioned in the LV or the aorta by evaluating the pressure differential on a pulsatile waveform. Appropriate placement can also be assessed on the display using the motor current waveform, which is a measure of the energy intake of the Impella pump. The energy used by the Impella varies with motor speed and the pressure difference between the inflow and outflow areas of the pump. When the Impella is positioned correctly with the inlet area in the LV and the output in the ascending aorta, the motor current should be pulsatile because of the pressure difference between the two areas. When the intake and output are on the same side of the aortic valve, the motor current will be dampened owing to the lack of a pressure differential.80 The Impella 2.5 and CP devices have been approved for up to 4 days and the Impella 5.0 is approved for up to 6 days. Although much longer use has been reported, the requirement for hemodynamic support beyond these timelines should result in consideration of a more durable form of cardiac support.81 Once weaning is desired, the pump power can be slowly reduced over time to reduce the level of cardiac support. If the patient’s hemodynamics remain stable, the device can be pulled proximally into the aorta. If continued hemodynamic stability is observed, the device can then be removed entirely.

Contraindications and Complications Appropriate evaluation prior to insertion of an Impella device is crucial in determining potential contraindications or patient-specific risk factors for complications. Careful physical examination and imaging technology are necessary to assess the patient’s vasculature and select an appropriate arterial access site. Traditional angiography, magnetic resonance angiography, or computed tomography angiography are often used for this purpose. Echocardiography is important to assess for LV thrombus, mechanical aortic valves, severe aortic stenosis, or aortic regurgitation. Insertion of a pulmonary artery catheter should also be considered to provide continuous hemodynamic monitoring of cardiac output, central venous pressures, and mixed venous oxygen saturation (SvO2). Contraindications to the use of Impella devices include mechanical aortic valves or LV thrombus. The device should not be placed in patients with severe PAD owing to the risk of embolism during insertion. A minimum vessel diameter of 7 mm



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is required for the Impella 5.0 owing to the cannula size. Preexisting septal defects are considered a relative contraindication as, theoretically, the device could worsen right-to-left shunting. Severe aortic stenosis and regurgitation are considered relative indications, although Impella use in critical aortic stenosis has been reported.82 Anticoagulation is necessary to prevent thrombus formation on the pump housing and catheter. Therefore the device should not be inserted in patients who cannot tolerate anticoagulation. Obesity, scar tissue related to previous vascular procedures, and tortuous vasculature may increase the risk of complications. The most common complications include limb ischemia, vascular injury, and bleeding (see Table 46.3).83 Vascular complications include hematoma or pseudoaneurysm formation, arteriovenous fistula creation, and retroperitoneal hemorrhage. Hemolysis is reported in up to 10% of patients with Impella devices due to the sheer stress of the rotating impeller on red blood cells. Repositioning the device may reduce the degree of hemolysis. Patients with persistent hemolysis associated with acute kidney injury should have the device removed.84

Clinical Efficacy and Indications Numerous case reports, case series, and observational studies of various Impella devices have been reported for a wide range of indications. Many demonstrate improved hemodynamics and outcomes. Unfortunately, few randomized controlled trials are available. Most available data address Impella use in patients with cardiogenic shock and prophylactic use in patients undergoing PCI.

Cardiogenic Shock.  Several observational studies have evaluated the role of Impella in the setting of cardiogenic shock. Three studies evaluated the use of the Impella 2.5 in the setting of acute MI complicated by cardiogenic shock and demonstrated improved hemodynamics.83,85,86 Two studies evaluated the Impella 5.0 in refractory cardiogenic shock and also demonstrated improved hemodynamics.87,88 Most studies report mortality but, as these are observational studies, none report mortality compared to a control population. One retrospective cohort study compared the Impella 2.5 to IABP counterpulsation in patients with cardiogenic shock following cardiac arrest or in patients with risk factors for cardiogenic shock after angiography. Mortality between the two groups was similar, with equal rates of vascular complications. There was a trend toward a higher rate of bleeding with the Impella device.89 Only one randomized controlled trial evaluated the utility of an Impella device in cardiogenic shock. In the Efficacy Study of LV Assist Device to Treat Patients With Cardiogenic Shock (ISAR-SHOCK), 26 patients with cardiogenic shock after acute MI were randomized to Impella 2.5 versus IABP. The primary outcome was the change of cardiac index from baseline to 30 minutes after implantation. Mortality at 30 days was considered a secondary outcome. The trial demonstrated that the cardiac index was significantly higher in the Impella arm versus the IABP arm (Impella ΔCI: 0.49 ± 0.46 L/min/m2; IABP ΔCI: 0.11 ± 0.31 L/min/m2; P = .02). There was no difference in mortality between the two groups.90

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High-Risk PCI.  Numerous observational studies in over 1000 patients have demonstrated the safety and efficacy of the Impella device in the setting of high-risk PCI.91–96 Some of the studies were funded by the manufacturers of Impella devices, introducing a risk of bias. Studies are limited to the Impella 2.5; data regarding the use of the Impella CP or Impella 5.0 in this setting are lacking. A retrospective cohort study comparing outcomes of patients undergoing high-risk PCI with periprocedural support from Impella 2.5 (n = 13) versus IABP (n = 62) showed similar efficacy and a similar incidence of bleeding complications between the two groups.97 Only one randomized controlled trial exists that evaluates the utility of Impella in patients undergoing high-risk PCI. In the Prospective, Multicenter, Randomized Controlled Trial of Impella 2.5 Versus Intra-aortic Balloon Pump in Patients Undergoing High-Risk Percutaneous Coronary Intervention (PROTECT II), patients with symptomatic, complex three-vessel coronary artery disease or unprotected left main coronary artery disease and severely depressed LV function undergoing nonemergent high-risk PCI were randomized to Impella 2.5 (n = 225) versus IABP (n = 223). The primary endpoint was adverse events during and after the PCI procedure at discharge or at 30-day follow-up, whichever was longer. Components of the primary outcome included all-cause mortality, MI, stroke or transient ischemic attack, repeat revascularization procedure, need for cardiac or vascular operation, acute renal insufficiency, severe intraprocedural hypotension requiring therapy, CPR, ventricular tachycardia requiring cardioversion, aortic insufficiency, or angiographic failure of PCI. The study demonstrated that, relative to IABP, Impella provided superior cardiac power output. However, there was no difference in the primary outcome between the two groups at 30 days. At 90 days, there was a statistically nonsignificant trend toward improved outcomes with Impella. PROTECT II was terminated early owing to futility.98

Conclusion Impella use is increasing in frequency and is an intriguing option for patients with cardiogenic shock or as prophylaxis during high-risk PCI. Compared to the IABP, Impella devices consistently demonstrate improved hemodynamics (see Table 46.2). However, Impella use has not translated into improved outcomes and is associated with a high rate of complications. Current evidence is largely limited to the Impella 2.5 and Impella 5.0 devices; whether the percutaneous design and enhanced cardiac support provided by the Impella CP will translate into improved outcomes is unknown. Further randomized clinical trials evaluating the use of Impella are necessary.

LEFT ATRIUM TO AORTA SUPPORT DEVICES The TandemHeart percutaneous ventricular assist device (Cardiac Assist, Inc.) is the only commercially available left atrium to aorta assist device. This percutaneous device pumps blood extracorporeally from the left atrial via a transseptally inserted cannula to the ileofemoral arterial system, thereby bypassing the LV (see Table 46.1). This device entered the market in 2005 and

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is FDA approved to provide extracorporeal circulatory support for up to 6 hours.68,79

Physiology and Monitoring The TandemHeart has four components: a transseptal cannula, a centrifugal pump, a femoral arterial cannula, and a control console. A 21 Fr cannula is inserted into the right femoral vein, advanced to the right atrium, and finally into the left atrium via a transseptal puncture (Fig. 46.6A).72,99 The fenestrated cannula aspirates blood from the left atrium via a large end hole and 14 smaller side holes (Fig. 46.6B).79 Blood flows to a 15 to 19 Fr arterial perfusion cannula inserted into the common femoral artery. The flow of blood is propelled by an extracorporeal centrifugal pump containing a spinning impeller. The pump has both a motor chamber and a blood chamber that are separated by a polymer membrane. An electromagnetic motor rotates the impeller between 3000 and 7500 RPM. The size of the arterial cannula determines the maximum flow rate. The 15 Fr arterial cannula can support flow rate up to 3.5 L/min, whereas the 19 Fr arterial cannula can achieve flow up to 5 L/min.79 Heparinized saline flows continuously into the lower chamber of the pump, providing lubrication, cooling, and preventing thrombus formation. An external controller controls the pump and contains a 60-minute backup battery in case of power failure.

An FDA-approved oxygenator can be added to the circuit to provide oxygenation in addition to circulatory support. The hemodynamic effects of the TandemHeart are superior to the IABP (see Table 46.2). Similar to the Impella device and unlike the IABP, the TandemHeart does not require a trigger or timing based on the cardiac cycle. As the TandemHeart device works in parallel with the LV, any intrinsic CO from the LV is additive to the support of the device. By virtue of unloading the LV, the TandemHeart results in increased CO, increased mean atrial pressure, decreased PCWP, and decreased central venous pressure.100 Both the LV and RV have decreased filling pressures, resulting in reduced ventricular workload and oxygen demand, and an increase in cardiac power index.101,102 However, due to an increase in afterload and a decrease in preload, ventricular contraction may decrease. As a result, the LV often provides only a minimal contribution to CO, resulting in relatively nonpulsatile arterial pressure tracing. The amount of cardiac support provided by TandemHeart can be increased or decreased by changing the RPM on the centrifugal pump. Although only FDA approved for 6 hours, in practice, devices are often used for a week or more.103 Weaning is facilitated by monitoring hemodynamic stability while slowly reducing the RPM on the centrifugal pump. If hemodynamic stability is confirmed, the pump can be turned off and removed.

Contraindications and Complications

Fig. 46.6  Illustration of the TandemHeart device. (A) Placement of the TandemHeart demonstrating an arterial catheter and a transseptal venous catheter connected to the centrifugal pump. (B) Close-up of the transseptally inserted fenestrated venous catheter. (From Thiele H, Smalling RW, Schuler GC. Percutaneous left ventricular assist devices in acute myocardial infarction complicated by cardiogenic shock. Eur Heart J. 2007;28:2057–2063.)

Initial evaluation is similar to other percutaneous support devices. Imaging modalities and physical examination are necessary to evaluate the patient’s vasculature. Expertise with transseptal puncture technique is required and is often a barrier to the use of TandemHeart given that proficiency with this technique is not universal among interventional cardiologists. Upon insertion of the transseptal cannula, appropriate placement must be verified using a combination of echocardiography, pressure transduction, and blood gas analysis from the distal port. Contraindications for the use of TandemHeart include severe PAD, which may preclude the placement of the arterial cannula, contraindications to anticoagulation, and left atrial thrombus. Adequate RV function or support is necessary to maintain appropriate left atrial pressure for optimal device function.77 There is limited experience using the TandemHeart in the setting of ventricular septal defects or severe aortic regurgitation.104,105 Obesity, scar tissue related to previous vascular access procedures, and tortuous vasculature may increase the risk of complications. Complications include arterial dissection, groin hematoma, limb ischemia, hemolysis, and thromboembolism (see Table 46.3).106 Complications unique to the transseptal puncture technique, such as cardiac tamponade, may be increased in anticoagulated patients. Additionally, dislodgement of the left atrial cannula back into the right atrium will cause severe rightto-left shunting and associated hypoxemia. The cannula may also migrate into a pulmonary vein, which may cause device malfunction.

Clinical Efficacy and Indications There are currently no randomized control trials evaluating the TandemHeart device. The TandemHeart to Reduce Infarct Size



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(TRIS) trial that intended to randomize patients with STEMI to either TandemHeart or usual care prior to PCI was withdrawn before enrollment. Current evidence is limited to case series or observational comparisons with other types of percutaneously inserted cardiac support devices.

Cardiogenic Shock.  In one of the earliest trials describing its use, 18 patients with acute MI complicated by cardiogenic shock were treated with TandemHeart. Patients were noted to have improved hemodynamics, including increased cardiac index and mean arterial pressure with decreased PCWP and central venous pressure. Mortality was 44%.99 In a much larger study of 117 patients with cardiogenic shock despite vasopressors and/or IABP, support with TandemHeart was used for a mean of 5.7 days. TandemHeart resulted in improved cardiac index and decreased lactate. Mortality at 30 days was 40.2%. Complications were numerous and included bleeding around the arterial cannula in 29% of patients, vascular complications in 5% of patients, and limb ischemia in 3.4% of patients.106 Two studies compared outcomes between TandemHeart and the IABP in patients with cardiogenic shock. A 2005 study of patients with cardiogenic shock after MI compared outcomes between patients treated with an IABP (n = 20) and TandemHeart (n = 21). Compared with the IABP, TandemHeart demonstrated improved hemodynamics, including improved cardiac power index. However, mortality at 30 days was similar between the two groups (45% vs. 43%). Furthermore, TandemHeart was associated with more complications, including severe bleeding (IABP, n = 8 vs. TandemHeart, n = 19) and limb ischemia (IABP, n = 0 vs. TandemHeart, n = 7).101 A 2006 randomized control trial of 42 patients across 12 centers compared patients with cardiogenic shock randomized to IABP (n = 14) or TandemHeart (n = 19). Patients treated with TandemHeart had improved hemodynamics compared to those treated with an IABP. However, survival was not different between the two groups at 30 days; TandemHeart use was associated with more adverse events than the IABP.102 High-Risk Percutaneous Coronary Intervention. A 2016 single-center observational study of 74 patients treated with TandemHeart for elective, urgent, emergent, and emergent salvage cases suggested that TandemHeart is a viable option for high-risk PCI. Up to 13% of patients had ischemic limb injury associated with the arterial catheter and 31% of patients had major bleeding.107 Two trials compare TandemHeart with Impella devices for high-risk PCI. In a 2013 single-center observational study, 68 patients underwent high-risk PCI with TandemHeart support (n = 32) or Impella 2.5 (n = 36). There was no difference in mortality or major vascular complications at 30 days between the two groups.108 A 2016 meta-analysis reviewed 8 studies of 205 combined patients that utilized TandemHeart and 12 studies of 1345 patients that utilized Impella 2.5 for support during high-risk PCI. Mortality at 30 days was 8% for the TandemHeart group and 3.5% for the Impella group. Bleeding rates were 3.6% with the TandemHeart group and 7.1% with the Impella group.109

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Conclusion The TandemHeart device provides impressive hemodynamic support and remains an option for patients with cardiogenic shock or high-risk PCI. However, its insertion requires experience with transseptal puncture, which is a major barrier, and the device is used infrequently at many centers as a result. Additionally, rates of complications, including bleeding and limb ischemia, warrant careful considering of the use of this device if other options are available, particularly in emergency settings.

EXTRACORPOREAL MEMBRANE OXYGENATION Cardiopulmonary bypass was used as early as the 1950s during cardiac surgery.110,111 Modifications of cardiopulmonary bypass led to the development of extracorporeal membrane oxygenation (ECMO) that was first used successfully in humans for treatment of respiratory failure in 1972.112 Early devices were fraught with complications, limiting their utility. ECMO technology has advanced dramatically in the past several decades. Subsequent improvements have reduced complications and allowed for expanded use of these devices for a variety of indications.79 The two basic configurations of ECMO are venovenous (VV) ECMO and venoarterial (VA) ECMO. VV ECMO can be used to oxygenate blood and remove carbon dioxide in patients with respiratory failure. VA ECMO provides both hemodynamic and respiratory support. This section will focus on VA ECMO used to provide temporary cardiac support.

PHYSIOLOGIC PRINCIPLES OF ECMO The ECMO circuit consists of a blood pump, membrane oxygenator, conduit tubing, and a heat exchanger (see Table 46.1).113 In VA ECMO, a drainage catheter is inserted into the venous circulation, which drains blood through an oxygenator and returns it to the arterial system using a pump (Fig. 46.7). VA ECMO is a supportive therapy with the goals of improving oxygen delivery and carbon dioxide removal while resting the heart and lungs to facilitate recovery. When recovery is not possible, VA ECMO may be used as a bridge to definitive therapy with a permanent ventricular assist device or cardiac transplant. Minimizing complications in this setting is crucial.114 The VA ECMO circuit can be set up in different ways. Although other vessels may be used, most commonly the femoral artery and vein are cannulated. Regardless of the setup, the drainage cannula is positioned in the vena cava or right atrium and the return cannula is positioned to deliver blood retrograde to the aorta. Blood flowing anterograde from the LV will meet resistance from blood flowing retrograde from the ECMO circuit. This nonphysiologic configuration has differing effects on the RV and LV. For the RV, drainage of blood from the venous system results in decreased preload, reduced RV output, and reduced pulmonary blood flow. For the LV, blood delivered retrograde into the arterial system results in increased mean arterial pressure and, consequently, increased afterload (see Table 46.2).114 The

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Fig. 46.7  Illustration of a patient with femoral venoarterial (VA) extracorporeal membrane oxygenation (ECMO). Deoxygenated venous blood from the femoral vein is infused through the ECMO circuit, and oxygenated blood is returned retrograde to the femoral artery (red arrow). Poorly oxygenated blood flowing anterograde from the left ventricle (purple arrow) will meet with resistance from the blood returned retrograde from the ECMO circuit. (From Abrams D, Combes A, Brodie D. Extracorporeal membrane oxygenation in cardiopulmonary disease in adults. J Am Coll Cardiol. 2014;63(25):2769–2778.)

resultant increase in afterload often leads to reductions in LV stroke volume. The degree of reduction depends on residual LV function and the integrity of the aortic and mitral valves. Increasing hemodynamic support by increasing flow through the VA ECMO circuit further increases afterload. Concomitant increases in LV end-diastolic pressure may cause LV dilation, decreased coronary blood flow, and reduced subendocardial perfusion. The amount of support can be titrated by changing the flow rate on the blood pump. Rates as high as 10 L/min can be accommodated with large-bore cannula.79 However, ECMO generally provides between 3 and 6 L/min of support.115 High flow also increases left atrial pressure and may precipitate pulmonary edema. Increases in afterload may be further exacerbated by the vasoconstrictive effects of vasopressor medications. Systemic hypertension is common; weaning of vasopressors and the addition of antihypertensive medications may be necessary to prevent complications. Oxygenation and removal of carbon dioxide is facilitated by an oxygenator that uses a semipermeable membrane as an artificial lung to separate gas from blood. In VA ECMO, deoxygenated blood is pulled from the venous system and oxygenated blood is returned to the arterial system. Oxygenation is determined by the amount of blood flow through the ECMO circuit, gas flow through the oxygenator, and the contribution from the patient’s own pulmonary function. The rate of carbon dioxide removal is regulated by the flow of blood through the ECMO circuit and gas flow through the oxygenator, known as the sweep gas flow rate. Adjustments may be made guided by arterial blood gas analysis.116,117

Monitoring of ECMO Once cannulation has occurred and patients are connected to the ECMO circuit, flow through the circuit is slowly uptitrated

to achieve appropriate respiratory and hemodynamic targets. Frequent adjustments may be necessary to achieve adequate arterial oxyhemoglobin saturation, mean arterial pressure, and venous oxygen saturation. Light sedation may be necessary to maintain patient comfort. Anticoagulation is essential during ECMO and is typically achieved with intravenous unfractionated heparin. Anticoagulation with the direct thrombin inhibitors argatroban and bivalirudin has been reported and is used in the case of heparin-induced thrombocytopenia.118 Anticoagulation is usually titrated based on activated clotting time (ACT). There is no universally agreed upon anticoagulation protocol; target ACT varies between institutions.117 Alternatives to the ACT have been proposed and include titration based on aPTT, anti-factor Xa levels, and thromboelastography.119 The artificial material in the ECMO circuit results in activation of the coagulation, fibrinolytic, and complement pathways, which can result in both bleeding and thrombotic complications. As a result, platelets are continuously consumed.120 Current practice is to maintain platelet levels over 50,000/mL; some centers maintain levels over 100,000/mL. Hemolysis, hemorrhage, and decreased bone marrow production due to critical illness may result in a decreased hemoglobin concentration. Hemoglobin levels have historically been kept at or near normal levels because adequate oxygen delivery depends not only on adequate blood flow but also on hemoglobin concentration. Accordingly, hemoglobin is often maintained between 12 and 14 mg/dL.121 Recent reports using newly improved ECMO circuits suggest that ECMO may be safely performed with a hemoglobin below 8 mg/dL. However, these data have not yet been incorporated into widespread practice.115,122 Owing to the requirement for aggressive transfusion parameters, patients frequently receive dozens of blood product tranfusions.123 For ventilated patients, ventilator settings should be minimized once adequate oxygenation and carbon dioxide removal is facilitated with the ECMO circuit. This allows avoidance of ventilator-associated lung injury and oxygen toxicity. An ultraprotective lung strategy with target plateau pressures less than 20 cm H2O and FiO2 less than 0.5 is often used to improve outcomes.124 Reduction in ventilator settings decreases intrathoracic pressure, which may facilitate venous return and CO. Early tracheostomy may be beneficial. While near maximum flow rates are typically used for patients on VV ECMO, the flow rates used with patients on VA ECMO must be high enough to facilitate hemodynamic and oxygenation goals but low enough to allow for sufficient preload to maintain intrinsic CO. LV output must be monitored frequently owing to the risk of LV distention. Aggressive diuresis may be necessary. Ultrafiltration can also be added to the ECMO circuit to facilitate volume removal. LV output is assessed using the pulsatility on an arterial line waveform in combination with echocardiography. If LV output cannot be maintained, ionotropes, an IABP, or Impella devices may be inserted to improve forward flow.125–127 If cardiac output remains low despite these interventions, LV decompression may be necessary. Techniques include transatrial balloon septostomy or surgical insertion of an LV or right upper pulmonary vein drainage catheter.120



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Contraindications to the Use of ECMO General criteria for initiating VA ECMO include severe cardiac failure that is potentially reversible and unresponsive to standard therapy. ECMO should not be considered for patients who have preexisting conditions that are incompatible with recovery, such as severe neurologic injury and advanced malignancy.

Insertion, Removal, and Complications Insertion.  ECMO requires a multidisciplinary team, including a surgeon, anesthesiologist, perfusionist, cardiologist, pulmonologist, and intensivist. Once it has been decided that ECMO will be initiated, the patient is anticoagulated and the cannula are inserted. If ECMO is initiated after cardiac surgery, the cannulas may be connected centrally to the same outlets used for cardiopulmonary bypass. If peripheral cannulation is desired, the cannulas are inserted percutaneously using the Seldinger technique. The size of the cannulas chosen is determined based on the expected amount of circulatory support required for the patient based on residual LV function. Often, the largest possible cannula is used. For adults, inflow cannulas are available between 18 and 21 Fr and outflow cannulas are between 15 and 22 Fr.115 In VA ECMO, a venous cannula is typically placed in the femoral vein and advanced to the venocaval junction. The arterial cannula is typically placed in the common femoral artery. Given the large cannula sizes used in ECMO, ischemia to the limb ipsilateral to the arterial cannula is common. To compensate, a distal arterial cannula may be inserted into the posterior tibial artery to provide flow to perfuse the lower limb.128 If the femoral vessels are unsuitable for cannulation owing to severe PAD or prior arterial bypass, other arteries may be utilized. The right carotid, right subclavian, and axillary arteries have been used.129 Cannulation of the right carotid carries the risk of cerebral infarction and should be used cautiously. The subclavian artery has the advantage of potentially allowing patient ambulation. Removal.  The duration of ECMO support is typically 5 to 10 days, with a maximum implant time of 3 to 4 weeks.115 Once patients have recovered sufficiently to warrant consideration of weaning, weaning may be initiated as a series of trials. To facilitate a trial, the support provided by the ECMO circuit is decreased incrementally while monitoring hemodynamic and respiratory stability. There is no universally accepted protocol for weaning. As VA ECMO also provides for gas exchange, the pump flow cannot be decreased without ensuring that respiratory support is adequate. Also, completely turning off the pump increases the risk of thrombus formation in the ECMO circuit, but short periods of reducing flow to 1 L/min can be performed. Since assessment of LV function may be compromised when the VA ECMO circuit is providing full support, cardiac monitoring during the weaning process with transthoracic or transesophageal echocardiography has been proposed.130 If weaning is successful and the decision is made to discontinue ECMO entirely, the cannulas are removed and the venous and arterial access sites are compressed manually for at least 30 minutes to achieve hemostasis.

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Complications.  Advances in ECMO technology aimed at reducing complications include low-resistance gas exchange membranes, highly durable centrifugal pumps, heparin-coated tubing, and improved cannulas.120 Major complications include bleeding, thromboembolism, neurologic injury, and cannulation-related injury (see Table 46.3). Bleeding is the most common complication, occurring in 27% to 50% of patients, and may be severe enough to require intervention.119,123,131 Both anticoagulation and platelet dysfunction contribute to bleeding. Cannulation-related injury includes hemorrhage, dissection, distal ischemia, and compartment syndrome. Major bleeding from surgical wounds should prompt exploration. Modern heparin-coated ECMO circuits allow for anticoagulation to be held. Discontinuation of anticoagulation for up to 20 days has been reported without complication.132 Thrombus may develop within the ECMO circuit or the patient’s vasculature with an incidence of 8% to 16%.119,123 Routine inspection of all tubing and connectors for signs of clot formation is necessary. Changes in the pressure gradient across the oxygenator may reflect thrombus formation. Large clots necessitate immediate circuit exchange. If anticoagulation must be held or if there is heightened concern for thrombus development, circuits primed with anticoagulant may be kept at the bedside for urgent exchange. Intracardiac thrombosis may also develop if there is stasis owing to poor LV function. Neurologic injury occurs in up to 50% of patients with cardiac failure or those for whom ECMO is administered during cardiopulmonary resuscitation.133 Coma, encephalopathy, anoxic brain injury, stroke, brain death, and myoclonus have all been observed. Cerebral hypoxia is of particular concern for patients with femoral artery cannulation. Oxygenated blood returning from the circuit to the aorta will preferentially perfuse the abdominal viscera instead of the brain, heart, and upper extremities. To detect this complication, arterial oxyhemoglobin saturation should be monitored in the upper extremities. Other complications include pulmonary edema and pulmonary hemorrhage due to elevated LV end-diastolic and left atrial pressures that may warrant LV or left atrial venting. Infection related to cannulation may result in prolonging the duration of ECMO or increased length of hospital stays.134 Heparin-induced thrombocytopenia may also develop and should prompt changing the anticoagulant to a direct thrombin inhibitor. Hemolysis, thrombocytopenia, acquired von Willebrand’s syndrome, disseminated intravascular coagulation, acute kidney injury, and air emboli have all been reported.120,135

Clinical Efficacy and Indications ECMO has numerous indications in adult populations. While randomized controlled trials exist demonstrating the utility of ECMO in respiratory failure and acute respiratory distress syndrome, there are no such trials for cardiac support or following cardiopulmonary arrest.136 In practice, ECMO is often used as a salvage therapy or a temporary bridge to definitive therapy with ventricular assist devices or cardiac transplant.115 As a result, conducting a controlled trial for cardiac failure is challenging owing to the lack of an ethically defensible control group. The

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available evidence supporting the use of VA ECMO in cardiogenic shock and cardiopulmonary arrest is presented next.

indication for VA ECMO. Among 9025 adult patients with cardiogenic shock, survival to discharge was 41%.145

Cardiogenic Shock.  Studies have demonstrated the utility of ECMO for patients with cardiogenic shock from acute MI, acute decompensated heart failure, myocarditis, stress-induced cardiomyopathy, and postcardiotomy shock.115,137–139 Miniaturized VA ECMO devices have even been shown to facilitate interhospital transfer for patients with cardiogenic shock.140 A 2008 observational study of 81 patients with refractory cardiogenic shock due to medical causes (n = 55), postcardiotomy (n = 16), or following cardiac transplantation (n = 10) and treated with VA ECMO found a 42% patient survival to discharge. More than half of patients had at least one major ECMO-related complication. Long-term quality of life for ECMO survivors was worse than age-matched controls but better than patients on dialysis, after acute respiratory distress syndrome, or with advanced heart failure.141 A 2010 study compared 30-day outcomes between STEMI patients with cardiogenic shock refractory to IABP and ionotropic agents in two different time periods. One group (n = 115) received usual care, but ECMO therapy was available to the other group (n = 219) and used in 46 patients. Mortality at 30 days was lower in the group with ECMO availability (41% vs. 30%; P < .04).142 A 2017 meta-analysis of 24 studies and 1926 patients placed on ECMO for refractory cardiogenic shock after cardiac surgery showed a survival to discharge rate of 31%.143 A 2016 study of 4227 Taiwanese patients placed on ECMO for cardiogenic, postcardiotomy, traumatic or septic shock showed an average 30-day mortality of 60% and 1-year mortality of 77%. In patients with cardiogenic shock, mortality at 30 days was 66% and 77% at 1 year.144 The Extracorporeal Life Support Organization has maintained an international registry of patients receiving ECMO support since 1989. Their most recent report of 78,397 adults and children showed that survival for patients on ECMO was higher when it was used for respiratory support than for cardiac failure or following CPR. However, cardiogenic shock was the most common

Cardiac Arrest.  VA ECMO support has emerged as an intriguing option for patients with refractory cardiopulmonary arrest and has been the subject of numerous trials.146–153 In one of the largest trials comparing patients with refractory cardiac arrest treated with conventional CPR (n = 321) to those treated with VA ECMO support (n = 85), the primary outcome was survival to discharge with minimal neurologic impairment. Among propensity-matched patients, patients treated with ECMO showed improved 6-month survival (OR, 0.48; P = .003).154 In a meta-analysis of 20 studies, including 833 patients for whom VA ECMO was initiated for refractory out-of-hospital cardiac arrest, overall survival to discharge was 22%. Thirteen percent of patients were considered to have a good neurologic outcome.155 In a 2016 meta-analysis of nine studies of ECMO used in patients with refractory cardiopulmonary arrest, ECMO was associated with an absolute increase of 30 days survival of 13% compared with patients in whom ECMO was not used (95% CI, 6% to 20%; P < .001; number needed to treat [NNT], 7.7) and a higher rate of favorable neurologic outcome at 30 days (absolute risk difference, 14%; 95% CI, 7% to 20%; P < .0001; NNT, 7.1).121 According to the Extracorporeal Life Support Organization registry, VA ECMO has been used for 2885 adult patients with refractory cardiopulmonary arrest since 1989. Overall survival to discharge was 29%.145

Conclusions VA ECMO is becoming a commonly used method of temporary cardiac support. It has advantages of providing full cardiac and respiratory support as well as utility in biventricular failure. Considerable expertise is required for proper maintenance of ECMO circuits and complications are common and may be severe. However, ECMO remains an exciting and unique option for otherwise viable patients as salvage therapy for cardiogenic shock and cardiopulmonary arrest refractory to conventional resuscitation methods.

SUMMARY Numerous devices are available to provide temporary mechanical cardiac support for a variety of indications. Selection of a device should be based on individual patient characteristics in addition to a thorough understanding of device concepts, advantages, and disadvantages. While each device can augment CO and provide hemodynamic support, evidence suggests that improving

The full reference list for this chapter is available at ExpertConsult.com.

hemodynamics alone may not translate into improved survival. Therefore, while mechanical support devices may be life saving for an individual patient, continued improvement in technology and high-quality evidence are necessary before routine use should be considered.

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REFERENCES 1. Santa-Cruz RA, Cohen MG, Ohman EM. Aortic counterpulsation: a review of the hemodynamic effects and indications for use. Catheter Cardiovasc Interv. 2006;67: 68–77. 2. Moulopoulos SD, Topaz S, Kolff WJ. Diastolic balloon pumping (with carbon dioxide) in the aorta - a mechanical assistance to the failing circulation. Am Heart J. 1962;63:669. 3. Kantrowitz A, Tjonneland S, Freed PS, et al. Initial clinical experience with intraaortic balloon pumping in cardiogenic shock. JAMA. 1968;203:113–118. 4. Jaron D, Tomeck J, Freed PS, et al. Measurement of ventricular load phase angle as an operating criterion for in series assist devices: hemodynamic studies using intraaortic balloon pumping. Trans Am Soc Artif Intern Organs. 1970;16:466–471. 5. Lucas WJ. Anstandt MP: Triggering and timing of the intraaortic balloon pump. In: Maccioli GA, ed. Intraaortic Balloon Pump Therapy. Baltimore: Williams and Wilkins; 1997:57–67. 6. Jaron D, Moore TW, He P. Control of intraaortic balloon pumping: theory and guidelines for clinical applications. Ann Biomed Eng. 1985;13(2):155–175. 7. Zelano JA, Li JK, Welkowitz W. A closed-loop control scheme for intraaortic balloon pumping. IEEE Trans Biomed Eng. 1990;37(2):182–192. 8. Smith B, Barnea O, Moore TW, et al. Optimal control system for the intraaortic balloon pump. Med Biol Eng Comput. 1991;29(2):180–184. 9. Barnea O, Smith BT, Dubin S, et al. Optimal controller for intraaortic balloon pumping. IEEE Trans Biomed Eng. 1992;39(6):629–634. 10. Kantrowitz A, Freed PS, Cardona RR, et al. Initial clinical trial of a closed loop, fully automatic intraaortic balloon pump. ASAIO J. 1992;38(3):M617–M621. 11. Weber KT, Janicki JS. Intraaortic balloon counterpulsation. A review of physiological principles, clinical results, and device safety. Ann Thorac Surg. 1974;17:602. 12. Marchionni N, Fumagalli S, Baldereschi G, et al. Effective arterial elastance and the hemodynamic effects of intraaortic balloon counterpulsation in patients with coronary heart disease. Am Heart J. 1998;135:855–861. 13. Scheidt S, Wilner G, Mueller H, et al. Intraaortic balloon counterpulsation in cardiogenic shock. N Engl J Med. 1973;288:979. 14. Maccioli GA, Lucas WJ, Norfleet EA. The intraaortic balloon pump: a review. J Cardiothorac Anesth. 1988;2(3):365–373. 15. Barnea O, Moore TW, Dubin SE, et al. Cardiac energy considerations during intraaortic balloon pumping. IEEE Trans Biomed Eng. 1990;37(2):170–181. 16. Mahaffey KW, Kruse KR, Ohman EM. Intraaortic balloon pump counterpulsation: physiology, patient management, and clinical efficacy. In: Brown DL, ed. Cardiac Intensive Care. Philadelphia: WB Saunders; 1998:647–656. 17. Mahaffey KW, Kruse KR, Ohman EM. Perspectives on the use of intraaortic balloon counterpulsation in the 1990s. In: Topol EJ, ed. Textbook of Interventional Cardiology, Update Series, No. 21. Philadelphia: WB Saunders; 1996:303–320. 18. Yellin E, Levy L, Bregman D, et al. Hemodynamic effects of intraaortic balloon pumping in dogs with aortic incompetence. Trans Am Soc Artif Intern Organs. 1973;19:389–394.

492.e1

19. Jiang CY, Zhao LL, Wang JA, et al. Anticoagulation therapy in intraaortic balloon counterpulsation: does IABP really need anticoagulation? J Zhejiang Univ Sci. 2003;4:607–611. 20. Ferguson JJ, Cohen M, Freedman RJ, et al. The current practice of intraaortic balloon counterpulsation: results from the Benchmark Registry. J Am Coll Cardiol. 2001;38:1456–1462. 21. Urban PM, Freedman RJ, Ohman EM, et al. In-hospital mortality associated with the use of intraaortic balloon counterpulsation. Am J Cardiol. 2004;94:181–185. 22. Cohen M, Urban P, Christenson JT. Intraaortic balloon counterpulsation in US and non-US centers: results of the Benchmark Registry. Eur Heart J. 2003;24:1763–1770. 23. Arceo A, Urban P, Dorsaz PA, et al. In-hospital complications of percutaneous intraaortic balloon counterpulsation. Angiology. 2003;54:577–585. 24. Cohen M, Ferguson JJ 3rd, Freedman RJ Jr, et al. Comparison of outcomes after 8 vs 9.5 French size intraaortic balloon counterpulsation catheters based on 9332 patients in the prospective Benchmark Registry. Catheter Cardiovasc Interv. 2002;56:200–206. 25. Barnett MG, Swartz MT, Peterson GJ, et al. Vascular complications from intraaortic balloons: risk analysis. J Vasc Surg. 1994;19:81–87, discussion 87–89. 26. Funk M, Ford CF, Foell DW, et al. Frequency of long-term lower limb ischemia associated with intraaortic balloon pump use. Am J Cardiol. 1992;70:1195–1199. 27. Patel JJ, Kopisyansky C, Boston B, et al. Prospective evaluation of complications with percutaneous intraaortic balloon counterpulsation. Am J Cardiol. 1995;76:1205–1207. 28. Cohen M, Dawson MS, Kopistansky C, et al. Sex and other predictors of intraaortic balloon counterpulsation-related complications: a prospective study of 1119 consecutive patients. Am Heart J. 2000;139(2 Pt 1):282–287. 29. Alderman JD, Gabliani GI, McCabe CH, et al. Incidence and management of limb ischemia with percutaneous wire-guided intraaortic balloon catheters. J Am Coll Cardiol. 1987;9:524–530. 30. Rapoport S, Sniderman KW, Morse SS, et al. Pseudoaneurysm: a complication of faulty technique in femoral arterial puncture. Radiology. 1985;154:529–530. 31. Murphy DA, Craver JM, Jones EL, et al. Surgical management of acute myocardial ischemia following percutaneous transluminal coronary angioplasty. Role of the intraaortic balloon pump. J Thorac Cardiovasc Surg. 1984;87:332–339. 32. Fuchs RM, Brin KP, Brinker JA, et al. Augmentation of regional coronary blood flow by intraaortic balloon counterpulsation in patients with unstable angina. Circulation. 1983;68:117–123. 33. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-STelevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130:2354–2394. 34. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intra-venous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13–20. 35. Rezkalla SH, Kloner RA. No-reflow phenomenon. Circulation. 2002;105:656–662. 36. van Nunen LX, Marko N, Kapur NK. Usefulness of intra-aortic balloon counterpulsation. Am J Cardiol. 2016;117:469–476.

492.e2

PART VI  Advanced Diagnostic and Therapeutic Techniques

37. Ohman EM, George BS, White CJ, et al. Use of aortic counterpulsation to improve sustained coronary artery patency during acute myocardial infarction. Results of a randomized trial. Circulation. 1994;90:792–799. 38. Stone GW, Marsalese D, Brodie BR, et al. A prospective, randomized evaluation of prophylactic intraoartic balloon counterpulsation in high risk patients with acute myocardial infarction treated with primary angioplasty. Second primary angioplasty in myocardial infarction (PAMI-II) trial investigators. J Am Coll Cardiol. 1997;29:1459–1467. 39. Brodie BR, Stuckey TD, Hanson C, et al. Intraaortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces catheterization laboratory events in high-risk patients with acute myocardial infarction. Am J Cardiol. 1999;84:18–23. 40. Patel MR, Smalling RW, Thiele H, et al. Intra-aortic balloon counterpulsation and infarct size in patients with acute anterior myocardial infarction without shock: the CRISP AMI randomized trial. JAMA. 2011;306: 1329–1337. 41. van Nunen LX, van’t Veer M, Schampaert S, et al. Intra-aortic balloon counterpulsation reduces mortality in large anterior myocardial infarction complicated by persistent ischemia: a CRISP-AMI substudy. EuroIntervention. 2015;11: 286–292. 42. Sjauw KD, Engstrom AE, Vis MM, et al. A systematic review of and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? Eur Heart J. 2009;30:459–468. 43. Goldberg RJ, Spencer FA, Gore JM, et al. Thirty-year trends (1975 to 2005) in the magnitude of, management of, and hospital death rates associated with cardiogenic shock in patients with acute myocardial infarction: a population-based perspective. Circulation. 2009;119:1211–1219. 44. Holmes DR, Bates ER, Kleiman NS, et al. Contemporary reperfusion therapy for cardiogenic shock: the GUSTO I trial experience. J Am Coll Cardiol. 1995;26:668–674. 45. Hochman JS, Boland J, Sleeper LA, et al. Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an international registry. SHOCK Registry investigators. Circulation. 1995;91:873–881. 46. Hollenberg SM, Kavinsky CJ, Parillo JE. Cardiogenic shock. Ann Intern Med. 1999;131:47–59. 47. Sanborn TA, Sleeper LA, Bates ER, et al. Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK trial registry. J Am Coll Cardiol. 2000;36:1123–1129. 48. Ohman EM, Nanas J, Stomel RJ, et al. Thrombolysis and counterpulsation to improve survival in myocardial infarction complicated by hypotension and suspected cardiogenic shock or heart failure: results of the TACTICS trial. J Thromb Thrombolysis. 2005;19:33–39. 49. Bahekar A, Singh M, Singh S, et al. Cardiovascular outcomes using intra-aortic balloon pump in high-risk acute myocardial with or without cardiogenic shock: a meta-analysis. J Cardiovasc Pharmacol Ther. 2012;17:44–56. 50. Prondzinsky R, Lemm H, Swyter M, et al. Intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP SHOCK trial for attenuation of multiorgan dysfunction syndrome. Crit Care Med. 2010;38:152–160.

51. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367:1287–1296. 52. Thiele H, Zeymer U, Neumann FJ, et al. Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomized, open-labal trial. Lancet. 2013;382:1638–1645. 53. Abdel-Wahab M, Saad M, Kynast J, et al. Comparison of hospital mortality with intra-aortic balloon counterpulsation insertion before versus after primary percutaneous coronary intervention for cardiogenic shock complicating acute myocardial infarction. Am J Cardiol. 2010;105:967–971. 54. Kahn JK, Rutherford BD, McConahay DR, et al. Supported “high risk” coronary angioplasty using intraaortic balloon pump counterpulsation. J Am Coll Cardiol. 1990;15: 1151–1155. 55. Kreidich I, Davies DW, Lim R, et al. High-risk coronary angioplasty with elective intraaortic balloon pump support. Int J Cardiol. 1992;35:147–152. 56. Briguori C, Sarais C, Pagnotta P, et al. Elective versus provisional intraaortic balloon pumping in high-risk percutaneous transluminal coronary angioplasty. Am Heart J. 2003;145:700–707. 57. Perera D, Stables R, Thoams M, et al. Elective intra-aortic balloon counterpulsation during high-risk percutaneous coronary intervention: a randomized controlled trial. JAMA. 2010;304:867–874. 58. Perera D, Stables R, Clayton T, et al. Long-term mortality data from the balloon pump-assisted coronary intervention study (BCIS-1): a randomized, controlled trial of elective balloon counterpulsation during high-risk percutaneous coronary intervention. Circulation. 2013;127:207–212. 59. Baskett RJ, Ghali WA, Maitland A, et al. The intraaortic balloon pump in cardiac surgery. Ann Thorac Surg. 2002;74:1276–1287. 60. Christenson JT, Simonet F, Badel P, et al. Optimal timing of preoperative intraaortic balloon pump support in high-risk coronary patients. Ann Thorac Surg. 1999;68:934–939. 61. Kang N, Edwards M, Larbalestier R. Preoperative intraaortic balloon pumps in high-risk patients undergoing open heart surgery. Ann Thorac Surg. 2001;72:54–57. 62. Miceli A, Fiorani B, Danesi TH, et al. Prophylactic intra-aortic balloon pump in high-risk patients undergoing coronary artery bypass grafting: A propensity score analysis. Interact Cardiovasc Thorac Surg. 2009;9:291–294. 63. Field M, Rengarajan A, Khan O, Spyt T, Richens D. Preoperative intraaortic balloon pumps in patients undergoing coronary artery bypass grafting. Cochrane Database Syst Rev. 2007;(1):CD004472. 64. Cochran RP, Starkey TD, Panos AL, et al. Ambulatory intraaortic balloon pump use as bridge to heart transplant. Ann Thorac Surg. 2002;74:746–751, discussion 751–752. 65. Sintek MA, Gdowski M, Lindman B, et al. Intra-aortic balloon counterpulation in patients with chronic heart failure and cardiogenic shock: Clinical response and predictors of stabilization. J Card Fail. 2015;21:868–876. 66. Arafa OE, Geiran OR, Anderson K, et al. Intraaortic balloon pumping for predominantly right ventricular failure after heart transplantation. Ann Thorac Surg. 2000;70:1587–1593. 67. Sweeney MS. The Hemopump in 1997: A clinical, political, and marketing evaluation. Ann Thorac Surg. 1999;68:761–763. 68. Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/ STS Clinical expert consensus statement on the use of



CHAPTER 46  Temporary Mechanical Circulatory Support Devices percutaneous mechanical circulatory support devices in cardiovascular care. J Am Coll Cardiol. 2015;65:e7–e26. 69. Cheung AW, White CW, Davis MK, et al. Short-term Mechanical Circulatory Support for Recovery from Acute Right Ventricular Failure: Clinical Outcomes. J Heart Lung Transplant. 2014;33(8):794–799. 70. Anderson MB, Goldstein J, Milano C, et al. Benefits of a novel percutaneous ventricular assist device for right heart failure: The prospective RECOVER RIGHT study of the Impella RP device. J Heart Lung Transplant. 2015;34(12):1549–1560. 71. Yan I, Grahn H, Blankenberg S. Right ventricular temporal assist device for cardiac recompensation. ESC Heart Fail. 2017;4(3):376–378. 72. Basra SS, Loyalka P, Kar B. Current status of percutaneous ventricular assist devices for cardiogenic shock. Curr Opin Cardiol. 2011;26(6):548–554. 73. Jurmann MJ, Siniawski H, Erb M, et al. Initial experience with miniature axial flow ventricular assist devices for postcardiotomy heart failure. Ann Thorac Surg. 2004;77:1642–1647. 74. Siegenthaler MP, Brhem K, Strecker T, et al. The Impella Recover microaxial left ventricular assist device reduces mortality for postcardiotomy failure: a three-center experience. J Thorac Cardiovasc Surg. 2004;127:812–822. 75. Sassard T, Scalabre A, Bonnefoy E, et al. The right axillary artery approach for the Impella Recover LP 5.0 microaxial pump. Ann Thorac Surg. 2008;85(4):1468–1470. 76. Ouweneel DM, Henriques JP. Percutaneous cardiac support devices for cardiogenic shock: current indications and recommendations. Heart. 2012;98(16):1246–1254. 77. Ostadal P, Mlcek M, Holy F, et al. Direct comparison of percutaneous circulatory support systems in specific hemodynamic conditions in a porcine model. Circ Arrhythm Electrophysiol. 2012;5(6):1202–1206. 78. Werdan K, Gielen S, Ebelet H, et al. Mechanical circulatory support in cardiogenic shock. Eur Heart J. 2014;35:156–167. 79. Nagpal AD, Singal RK, Arora RC, et al. Temporary mechanical circulatory support in cardiac critical care: a state of the art review and algorithm for device selection. Can J Cardiol. 2017;33:110–118. 80. Abiomed Inc. (2017). Impella ventricular support systems for use during cardiogenic shock and high-risk PCI. Instructions for use and clinical reference manual. Danvers, MA. 81. Lemaire A, Anderson MB, Lee LY, et al. The Impella device for acute mechanical circulatory support in patients in cardiogenic shock. Ann Thorac Surg. 2014;97:133–138. 82. Martinez CA, Singh V, Londoño JC, et al. Percutaneous retrograde left ventricular assist support for interventions in patients with aortic stenosis and left ventricular dysfunction. Catheter Cardiovasc Interv. 2012;80:1201–1209. 83. Lauten A, Engström AE, Jung C, et al. Percutaneous leftventricular support with the impella-2.5–assist device in acute cardiogenic shock results of the Impella–EUROSHOCK Registry. Circ Heart Fail. 2013;6:23–30. 84. Badiye AP, Hernandez GA, Novoa I, et al. Incidence of hemolysis in patients with cardiogenic shock treated with Impella percutaneous left ventricular assist device. ASAIO J. 2016;62:11–14. 85. O’Neill WW, Schreiber T, Wohns DHW, et al. The current use of Impella 2.5 in acute myocardial infarction complicated by cardiogenic shock: results from the USpella Registry. J Interv Cardiol. 2014;27:1–11.

492.e3

86. Casassus F, Corre J, Leroux L, et al. The Use of Impella 2.5 in severe refractory cardiogenic shock complicating an acute myocardial infarction. J Interv Cardiol. 2015;28:41–50. 87. Engström AE, Granfeldt H, Seybold-Epting W, et al. Mechanical circulatory support with the Impella 5.0 device for postcardiotomy cardiogenic shock: a three-center experience. Minerva Cardioangiol. 2013;61:539–546. 88. Griffith BP, Anderson MB, Samuels LE, et al. The RECOVER I: a multicenter prospective study of Impella 5.0/LD for postcardiotomy circulatory support. J Thorac Cardiovasc Surg. 2013;145:548–554. 89. Manzo-Silberman S, Fichet J, Mathonnet A, et al. Percutaneous left ventricular assistance in post cardiac arrest shock: comparison of intra aortic blood pump and IMPELLA Recover LP2.5. Resuscitation. 2013;84:609–615. 90. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol. 2008;52:1584–1585. 91. Alasnag MA, Gardi DO, Elder M, et al. Use of the Impella 2.5 for prophylactic circulatory support during elective high-risk percutaneous coronary intervention. Cardiovasc Revasc Med. 2011;12:299–303. 92. Cohen MG, Matthews R, Maini B, et al. Percutaneous left ventricular assist device for high-risk percutaneous coronary interventions: real-world versus clinical trial experience. Am Heart J. 2015;170:872–879. 93. Iliodromitis KE, Kahlert P, Plicht B, et al. High-risk PCI in acute coronary syndromes with impella lp 2.5 device support. Int J Cardiol. 2011;153:59–63. 94. Maini B, Naidu SS, Mulukutla S, et al. Real-world use of the Impella 2.5 circulatory support system in complex high-risk percutaneous coronary intervention: The USpella Registry. Catheter Cardiovasc Interv. 2012;80:717–725. 95. Sjauw KD, Konorza T, Erbel R, et al. Supported high-risk percutaneous coronary intervention with the Impella 2.5 device the Europella registry. J Am Coll Cardiol. 2009;54:2430–2434. 96. Dixon SR, Henriques JPS, Mauri L, et al. A Prospective Feasibility Trial Investigating the Use of the Impella 2.5 system in patients undergoing high-risk percutaneous coronary intervention (the PROTECT I trial). JACC Cardiovasc Interv. 2009;2:91–96. 97. Boudoulas KD, Pederzolli A, Saini U, et al. Comparison of Impella and intra-aortic balloon pump in high-risk percutaneous coronary intervention: Vascular complications and incidence of bleeding. Acute Card Care. 2012;14:120–124. 98. O’Neill WW, Kleiman NS, Moses J, et al. A prospective, randomized clinical trial of hemodynamic support with Impella 2.5 versus intra-aortic balloon pump in patients undergoing high-risk percutaneous coronary intervention: the PROTECT II Study. Circulation. 2012;126:1717–1727. 99. Thiele H, Lauer B, Hambrecht R, et al. Reversal of cardiogenic shock by percutaneous left atrial-to-femoral arterial bypass assistance. Circulation. 2001;104(24):2917–2922. 100. Kapur NK, Paruchuri V, Urbano-Morales JA, et al. Mechanically unloading the left ventricle before coronary reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation. 2013;128(4):328–336. 101. Thiele H, Sick P, Doudriot E, et al. Randomized comparison of intra-aortic balloon support with percutaneous left ventricular assist device in patient with revascularized acute myocardial

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infarction complicated by cardiogenic shock. Eur Heart J. 2005;26(13):1276–1283. 102. Burkhoff D, Cohen H, Brunckhorst C, et al. A randomized multicenter clinical study to evaluate the safety and efficacy of the TandemHeart percutaneous ventricular assist device versus conventional medical therapy with intraaortic balloon pumping for treatment of cardiogenic shock. Am Heart J. 2006;152(2):469.e1–469.e8. 103. Berg DD, Sukul D, O’Brien M, et al. Outcomes in patients undergoing percutaneous ventricular assist device implantation for cardiogenic shock. Eur Heart J Acute Cardiovasc Care. 2016;5(2):108–116. 104. Gregoric ID, Bieniarz MC, Arora H, et al. Percutaneous ventricular assist device support in a patient with a postinfarction ventricular septal defect. Tex Heart Inst J. 2008;35(1):46–49. 105. Pham DT, Al-Quthami A, Kapur NK, et al. Percutaneous left ventricular support in cardiogenic shock and severe aortic regurgitation. Catheter Cardiovasc Interv. 2013;81(2):399–401. 106. Kar B, Gregoric ID, Basra SS, et al. The percutaneous ventricular assist device in severe refractory cardiogenic shock. J Am Coll Cardiol. 2011;57(6):688–696. 107. Nascimbene A, Loyalka P, Gregoric ID, et al. Percutaneous coronary intervention with the TandemHeartTM percutaneous left ventricular assist device support: six years of experience and outcomes. Catheter Cardiovasc Interv. 2016;87:1101–1110. 108. The Impella Recover 2.5 and TandemHeart ventricular assist devices are safe and associated with equivalent clinical outcomes in patients undergoing high-risk percutaneous coronary interventions. Catheter Cardiovasc Interv. 2013;82:E28–E37. 109. Meta-Analysis of usefulness of percutaneous left ventricular assist devices for high-risk percutaneous coronary interventions. Am J Cardiol. 2016;118:369–375. 110. Miller B, Gibbon JH, Gibbon MH, et al. recent advances in the development of the mechanical heart and lung apparatus. Ann Surg. 1951;134(4):694–708. 111. Gibbon JH. The development of the heart-lung apparatus. Am J Surg. 1978;135:608–619. 112. Hill JD, O’Brien TG, Murray JJ, et al. Prolonged extracorporeal oxygenation for acute post-traumatic respiratory failure (shock-lung syndrome). Use of the Bramson membrane lung. N Engl J Med. 1972;286(12):629–634. 113. Squiers JJ, Lima B, DiMaio JM. Contemporary extracorporeal membrane oxygenation therapy in adults: fundamental principles and systematic review of the evidence. J Thorac Cardiovasc Surg. 2016;152:20–32. 114. Lim HS, Howell N, Ranasinghe A. extracorporeal life support: physiological concepts and clinical outcomes. J Card Fail. 2017;23(2):181–196. 115. Combes A, Brodie D, Chen Y, et al. The ICM research agenda on extracorporeal life support. Intensive Care Med. 2017;43:1306–1318. 116. Brodie D, Bacchetta M. Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011;365(20):1905–1914. 117. Abrams D, Combes A, Brodie D. Extracorporeal membrane oxygenation in cardiopulmonary disease in adults. J Am Coll Cardiol. 2014;63(25):2769–2778. 118. Pieri M, Agracheva N, Bonaveglio E, et al. Bivalirudin versus heparin as an anticoagulant during extracorporeal membrane oxygenation: a case-control study. J Cardiothorac Vasc Anesth. 2013;27(1):30–34.

119. Sklar MC, Sy E, Lequier L, et al. Anticoagulation practices during venovenous extracorporeal membrane oxygenation for respiratory failure. a systematic review. Ann Am Thorac Soc. 2016;13(12):2242–2250. 120. Raleigh L, Ha R, Hill C. Extracorporeal membrane oxygenation applications in cardiac critical care. Semin Cardiothorac Vasc Anesth. 2015;19(4):342–352. 121. Ouweneel DM, Schotborgh JV, Limpens J, et al. extracorporeal life support during cardiac arrest and cardiogenic shock: a systematic review and meta-analysis. Intensive Care Med. 2016;42:1922–1934. 122. Agerstrand CL, Burkart KM, Abrams DC, et al. Blood conservation in extracorporeal membrane oxygenation for acute respiratory distress syndrome. Ann Thorac Surg. 2015;99(2):590–595. 123. Sy E, Sklar MC, Lequier L, et al. Anticoagulation practices and the prevalence of major bleeding, thromboembolic events, and mortality in venoarterial extracorporeal membrane oxygenation: a systematic review and meta-analysis. J Crit Care. 2017;39:87–96. 124. Kolla S, Awad SS, Rich PB, et al. Extracorporeal life support for 100 adult patients with severe respiratory distress syndrome. Ann Surg. 1997;226(4):544–564. 125. Koeckert MS, Jorde UP, Naka Y, et al. Impella LP 2.5 for left ventricular unloading during venoarterial extracorporeal membrane oxygenation support. J Card Surg. 2011;26(6):666–668. 126. Kawashima D, Gojo S, Nishimura T, et al. Left ventricular mechanical support with impella provides more ventricular unloading in heart failure than extracorporeal membrane oxygenation. ASAIO J. 2011;57:169–176. 127. Meani P, Gelsomino S, Natour E, et al. Modalities and effects of left ventricle unloading on extracorporeal life support: a review of the current literature. Eur J Heart Fail. 2017;19(suppl 2):84–91. 128. Madershahian N, Nagib R, Wipperman J, et al. A simple technique of distal perfusion during prolonged femoro-femoral cannulation. J Card Surg. 2006;21:168–169. 129. Navia JL, Atik FA, Beyer EA, et al. Extracorporeal membrane oxygenation with right axillary artery perfusion. Ann Thorac Surg. 2005;29:2163–2165. 130. Aissaoui N, Brehn C, El-Banayosy A, Intech, et al (2016) Weaning strategy from veno-arterial extracorporeal membrane oxygenation. Chapter 15, pp 305-318. 131. Mazzeffi M, Greenwood J, Tanaka K, et al. Bleeding, transfusion, and mortality on extracorporeal life support: ECLS Working Group on Thrombosis and Hemostasis. Ann Thorac Surg. 2016;101:682–690. 132. Prolonged venovenous extracorporeal membrane oxygenation without anticoagulation: a case of Goodpasture syndromerelated pulmonary haemorrhage. Crit Care Resusc. 2014;16(1):69–72. 133. Mateen FJ, Muralidharan R, Shinohara RT, et al. Neurological injury in adults treated with extracorporeal membrane oxygenation. Arch Neurol. 2011;68(12):1543–1549. 134. Schmidt M, Bréchot N, Hariri S, et al. Nosocomial infections in adult cardiogenic shock patients supported by venoarterial extracorporeal membrane oxygenation. Clin Infect Dis. 2012;55(12):1633–1641. 135. Heilmann C, Geisen U, Beyersdorf F, et al. Acquired von Willebrand syndrome in patients with extracorporeal life support (ECLS). Intensive Care Med. 2012;38(1):62–68.



CHAPTER 46  Temporary Mechanical Circulatory Support Devices

136. Tramm R, Ilic D, Davies AR, et al. Extracorporeal membrane oxygenation for critically ill adults. Cochrane Database Syst Rev. 2015;(1):CD010381. 137. Asaumi Y, Yasuda S, Morii I, et al. Favourable clinical outcome in patients with cardiogenic shock due to fulminant myocarditis supported by percutaneous extracorporeal membrane oxygenation. Eur Heart J. 2005;26:2185–2192. 138. Smedira NG, Blackstone EH. Postcardiotomy mechanical support: risk factors and outcomes. Ann Thorac Surg. 2001;71:S60–S66. 139. Doll N, Kiaii B, Borger M, et al. Five-year results of 219 consecutive patients treated with extracorporeal membrane oxygenation for refractory postoperative cardiogenic shock. Ann Thorac Surg. 2004;77:151–157. 140. Arlt M, Philipp A, Voelkel S, et al. Hand-held minimised extracorporeal membrane oxygenation: a new bridge to recovery in patients with out-of-centre cardiogenic shock. Eur J Cardiothorac Surg. 2011;40:689–694. 141. Combes A, Leprince P, Luyt C, et al. Outcomes and long-term quality-of-life of patients supported by extracorporeal membrane oxygenation for refractory cardiogenic shock. Crit Care Med. 2008;36:1404–1411. 142. Sheu J, Tsai T, Lee F, et al. Early extracorporeal membrane oxygenator-assisted primary percutaneous coronary intervention improved 30-day clinical outcomes in patients with ST-segment elevation myocardial infarction complicated with profound cardiogenic shock. Crit Care Med. 2010;38:1810–1817. 143. Khorsandi M, Doughtery S, Bouamra O, et al. Extra-corporeal membrane oxygenation for refractory cardiogenic shock after adult cardiac surgery: a systematic review and meta-analysis. J Cardiothorac Surg. 2017;12(1):55. 144. Chang C, Chen H, Caffrey JL, et al. Survival analysis after extracorporeal membrane oxygenation in critically ill adults a nationwide cohort study. Circulation. 2016;133:2423–2433. 145. Thiagarajan RR, Barbaro RP, Rycus PT, et al. Extracorporeal life support organization registry international report 2016. ASAIO J. 2017;63:60–67.

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146. Kagawa E, Dote K, Kato M, et al. Should we emergently revascularize occluded coronaries for cardiac arrest? Rapidresponse extracorporeal membrane oxygenation and intraarrest percutaneous coronary intervention. Circulation. 2012;126:1605–1613. 147. Arlt M, Philipp A, Voelkel S, et al. Early experiences with miniaturized extracorporeal life-support in the catheterization laboratory. Eur J Cardiothorac Surg. 2012;42:858–863. 148. Chen Y, Lin J, Yu H, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet. 2008;372:554–561. 149. Younger JG, Schreiner RJ, Swaniker F, et al. Extracorporeal resuscitation of cardiac arrest. Acad Emerg Med. 1999;6:700–707. 150. Pagani FD, Aaronson KD, Swaniker F, et al. The use of extracorporeal life support in adult patients with primary cardiac failure as a bridge to implantable left ventricular assist device. Ann Thorac Surg. 2001;71(3 suppl):S77–S81. 151. Massetti M, Tasle M, Page OL, et al. Back from irreversibility: extracorporeal life support for prolonged cardiac arrest. Ann Thorac Surg. 2005;79:179–184. 152. Bednarczyk JM, White CW, Ducas RA, et al. Resuscitative extracorporeal membrane oxygenation for in hospital cardiac arrest: a Canadian observational experience. Resuscitation. 2014;85:1713–1719. 153. Stub D, Bernard S, Pellegrino V, et al. refractory cardiac arrest treated with mechanical cpr, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88–94. 154. Shin TG, Choi J, Jo IJ, et al. Extracorporeal cardiopulmonary resuscitation in patients with inhospital cardiac arrest: a comparison with conventional cardiopulmonary resuscitation. Crit Care Med. 2011;39:1–7. 155. Ortega-Deballon I, Hornby L, Shemie SD, et al. Extracorporeal resuscitation for refractory out-of-hospital cardiac arrest in adults: a systematic review of international practices and outcomes. Resuscitation. 2016;101:12–20.