Interventions for Advanced Heart Failure

Dr. Kapur has received preclinical research support from Heartware Inc. and Cardiac­Assist Inc. and has worked as a speaker and consultant for Maquet and Thoratec Inc.


Heart disease remains the number one cause of mortality in the United States. Over the past 50 years, pharmacologic advancements for cardiovascular risk factors and device innovation for the management of coronary disease including acute myocardial infarction (AMI) have radically changed the landscape of heart disease. No longer is AMI considered a terminal event as in-hospital mortality rates have been reduced to less than 10% and more individuals are now surviving their incident and subsequent heart attacks. However, with each myocardial insult, nearly 25% of individuals develop chronic heart failure after an AMI leading to a growing number of patients with heart failure entering the catheterization laboratory (cath lab).

An estimated 2.6% of the total American population and nearly 11% of the elderly population over age 80 suffer from heart failure, which is defined as “a syndrome caused by cardiac dysfunction, generally resulting from myocardial muscle dysfunction or loss and characterized by either LV (left ventricle) dilation or hypertrophy or both.” Of the 10.5 million emergency department visits for acute heart failure each year, nearly 50% occur in patients with preserved systolic function. By 2030, more than 8 million people in the United States (1 in every 33) will be diagnosed with heart failure. Direct and indirect costs for heart failure are projected to increase from $31 billion in 2012 to $70 billion in 2030. The increasing population of individuals with heart failure has also increased the number of coronary and non-coronary procedures being performed in patients with high-risk features including advanced age, low ejection fraction, renal insufficiency, and decompensated hemodynamics. The approach to this high-risk interventional population now requires a better understanding of their heart failure status. There exists a growing demand for operators trained in invasive hemodynamics who can interface with a heart failure/mechanical support/cardiac transplant program and who have experience with emerging cutting-edge techniques for the management of advanced heart failure.

Defining Advanced Heart Failure

Symptoms of heart failure may occur secondary to disease of the myocardium, endocardium, pericardium, cardiac valves, systemic vasculature, and metabolic or neurohormonal stress. Several classification systems for heart failure exist. First, heart failure can be broadly categorized as being associated with reduced (HFrEF) or preserved (HFpEF) left ventricular ejection. HFrEF is defined as symptoms of heart failure in patients with a left ventricular ejection fraction (LVEF) ≤40%. HFpEF may be further categorized as diastolic heart failure (LVEF >50%), borderline HFpEF (LVEF 41% to 49%), or improved HFpEF (prior HFrEF). Second, the New York Heart Association (NYHA) functional classification categorizes patients based on symptom severity ( Table 33-1 ). Third, the American College of Cardiology and the American Heart Association have defined progressive stages of heart failure with specific goals and strategies to facilitate management at each level of heart failure ( Table 33-1 ). Fourth, the term “advanced heart failure” is often reserved for Stage D patients who exhibit symptoms refractory to guideline-based management strategies. The European Society of Cardiology has defined advanced heart failure using several criteria ( Table 33-2 ). For Stage D patients being considered for surgical ventricular assist devices the Interagency for Mechanically Assisted Circulatory Support (INTERMACS) has further defined distinct patient profiles for risk stratification ( Table 33-3 ).

TABLE 33-1

Heart Failure Definition, Stages, and New York Heart Association Classification

Heart failure definition based on ejection fraction (HF r EF)HF p EF
HFpEF, borderline
Referred to as “systolic heart failure”
Referred to as “diastolic heart failure”
HFpEF, improved >40 Outcomes appear similar to HF p EF patients
Subset of HF p EF with previous HF r EF
ACC/AHA heart failure stages

  • Stage A: At risk for HF but without evidence of structural heart disease or HF symptoms

  • Stage B: Structural heart disease but without signs or symptoms of HF

  • Stage C: Structural heart disease with prior or current symptoms of HF

  • Stage D: Refractory HF requiring specialized interventions

New York Heart Association classification

  • Class I: No limitations to physical activity. No symptoms of HF with ordinary activity

  • Class II: Slight limitation to physical activity. Symptoms of HF with ordinary activity

  • Class III: Marked limitation to physical activity. Symptoms of HF with less than ordinary exertion

  • Class IV: Inability to carry on any physical activity. Symptoms of HF at rest

ESC definition of heart failure Diagnosis of HFrEF requires the following three conditions to be satisfied

  • Symptoms typical of HF

  • Signs typical of HF

  • Reduced LVEF

Diagnosis of HFpEF requires the following four conditions to be satisfied

  • Symptoms typical of HF

  • Signs typical of HF

  • Normal or only mildly reduced LVEF, non-dilated LV

  • Relevant structural heart disease: LV hypertrophy, LA enlargement, and/or diastolic dysfunction

HF, Heart failure; HFrEF, heart failure with reduced ejection fraction; HFpEF, heart failure with preserved ejection fraction; LA, left atrium; LV, left ventricular; LVEF, left ventricular ejection fraction.

TABLE 33-2

Definition of Advanced Heart Failure

Markers of advanced heart failure (ACC/AHA)

  • ≥2 Hospitalizations or emergency department visits for HF in past 12 months

  • Persistent NYHA class IV symptoms

  • Progressive weight loss

  • Hypotension

  • Inability to tolerate ACE inhibitors or beta-blockers, increasing diuretic dose

  • Progressive decline in renal function

  • Progressive hyponatremia

  • Frequent ICD shocks

ESC definition of advanced heart failure

  • Persistent NYHA class III-IV symptoms

  • ≥1 HF hospitalization in past 6 months

  • Episodes of fluid retention and/or systemic hypoperfusion at rest

  • Evidence of severe cardiac dysfunction

    • LVEF <30%

    • Pseudonormal or restrictive mitral inflow pattern

    • Mean PCWP >16 mm Hg and/or CVP >12 mm Hg

    • High BNP or NT-proBNP plasma levels

  • Impaired functional capacity

    • Inability to exercise

    • Peak VO 2 <12-14 mL/kg/min

    • 6-Minute walk distance <300 m

ACE, Angiotensin converting enzyme; BNP, brain natriuretic peptide; CVP, central venous pressure; HF, heart failure; ICD, implantable cardioverter defibrillators; LVEF, left ventricular ejection fraction; NT-proBNP, N-terminal-pro-brain natriuretic peptide; NYHA, New York Heart Association; PCWP, pulmonary capillary wedge pressure.

TABLE 33-3

INTERMACS Profiles—Updated Version

Profile 1 Critical cardiogenic shock despite escalating support
Profile 2 Progressive decline despite inotropes
Profile 3 Clinically stable but inotrope dependent
Profile 4 Recurrent, not refractory, advanced heart failure
Profile 5 Exertion intolerant, comfortable at rest
Profile 6 Exertion limited, can perform mild activity
Profile 7 Advanced NYHA class III

NYHA, New York Heart Association.

Hemodynamics of Heart Failure

Nearly all approaches to treat heart failure reduce ventricular wall stress, which is defined by the law of Laplace as the product of ventricular pressure and volume (i.e., LV diameter) and is inversely related to wall thickness ( Figure 33-1 ). Across all phases of heart failure progression, from an inciting event (i.e., myocardial infarction) to chronic dilated cardiomyopathy, increased left ventricular pressure and volume promotes LV wall stress. Increased wall stress, in turn, activates multiple signaling cascades that stimulate myocardial hypertrophy, fibrosis, and inflammation. Both pharmacologic and mechanical therapies for heart failure limit LV wall stress by reducing LV volume and pressure.


Hemodynamics of heart failure.

Cardiac remodeling is a term that broadly refers to changes in myocardial structure and function in response to injury. Irrespective of the injurious mechanism (i.e., myocardial infarction, hypertensive heart disease, valvulopathy, myocarditis, or primary myocyte failure), a decline in ventricular function activates the sympathetic nervous system and the renin-angiotensin-aldosterone system, which increase left ventricular end-systolic (ESP) and end-diastolic pressure. Sustained neurohormonal activation promotes systolic failure and can lead to a dilated cardiomyopathy, where left ventricle end-diastolic volume (EDV) is increased. Ventricular afterload is defined as wall stress generated during systolic ejection. The law of Laplace quantifies ventricular wall stress, which can be represented as the product of ESP and EDV.

EDP, End-diastolic pressure; EDV, end-diastolic volume; ESP, end-systolic pressure; LV, left ventricle.

The hemodynamics of heart failure and the effect of therapeutic interventions can be represented in the pressure-volume (PV) domain using data derived from a conductance catheter. Each pressure-volume loop represents one cardiac cycle ( Figure 33-2 ). Various pharmacologic interventions such as increasing preload with volume resuscitation, increasing afterload with vasopressors, or increasing inotropy will modulate ventricular PV relationships differently. In most cases, these interventions are adequate to stabilize hemodynamics, augment native stroke volume, and increase vital organ perfusion. However, the net effect of each of these therapies is increased LV wall stress ( Figure 33-3 ), which increases myocardial oxygen demand, promotes myocardial ischemia, and can trigger ventricular arrhythmias.


Cardiac hemodynamics in the pressure-volume domain.

Each pressure-volume loop represents one cardiac cycle. Beginning at the end of isovolumic relaxation (Point 1), left ventricular (LV) volume increases during diastole (Phase 1 to 2). At end-diastole (Point 2), LV volume is maximal and isovolumic contraction (Phase 2 to 3) begins. At the peak of isovolumic contraction, LV pressure exceeds aortic pressure and blood begins to eject from the LV into the aorta (Point 3). During this systolic ejection phase, LV volume decreases until aortic pressure exceeds LV pressure and the aortic valve closes, which is known as the end-systolic pressure-volume point (ESPV) (Point 4). Stroke volume is represented by the width of the PV loop as the difference between end-systolic and end-diastolic volumes (Point 1—Point 2). Load-independent contractility, also known as elastance at end-systole (Ees), is defined as the maximal slope of the ESPV point under various loading conditions, known as the ESPV relationship (ESPVR). Effective arterial elastance (Ea) is defined as the ratio of end-systolic pressure and stroke volume. Under steady state conditions, optimal LV pump efficiency occurs when the ratio of Ea :  Emax approaches 1 (Ref). Arterial elastance is a component of afterload, which is defined as the resistance to LV ejection throughout systole and can be represented as the product of end-systolic pressure (ESP) and end-diastolic volume (EDV).

EDV, End-diastolic volume; ESP, end-systolic pressure; LV, left ventricle; PV, pressure-volume; SV, stroke volume.


Impact of modulating preload, afterload, and inotropy on pressure-volume relationships in the left ventricle.

A, Increasing preload augments left ventricular (LV) stroke volume (SV; horizontal arrows ) and increases both end-systolic pressure (ESP) and end-diastolic volume (EDV) without changing elastance at end-systole (Ees) or arterial elastance (Ea). The net effect is increased LV wall stress (i.e. afterload) due to increased ESP and EDV. B, Vasopressors increase ESP and reduce SV without affecting EDV or Ees. Both Ea and LV wall stress are increased due to elevated ESP. C, Inotropes increase myocardial contractility (Ees), ESP, and SV without affecting EDV. Ea is decreased due to increased SV, but LV wall stress is increased due to increased ESP. Inotropes also increase heart rate and promote myocardial oxygen demand. Solid lines represent baseline conditions (1). Dashed lines represent modulated conditions (2).

In 1914, Ernest Starling extended findings from Otto Frank and defined the Frank-Starling mechanism, which describes the intrinsic ability of the heart to increase stroke volume in response to increases in LV pressure or volume. Numerous studies have confirmed these early observations and further shown that in heart failure the slope of the operating curve defined by LV pressure and volume is reduced and small changes in LV pressure or volume can lead to hypotension or pulmonary congestion ( Figure 33-4 ). At each of these stages (acute heart failure, stable chronic heart failure, and decompensated heart failure/cardiogenic shock), the objectives of therapy are to improve stroke volume and reduce intracardiac volume and pressure overload, while maintaining an adequate mean arterial pressure to support end-organ tissue perfusion. For these reasons, careful timing and selection of pharmacologic therapy can impact patient outcomes. Invasive diagnostic evaluation and monitoring can guide therapy in advanced heart failure management ( Table 33-4 ).


Hemodynamic conditions associated with stages of cardiac injury and treatment profiles.

A, Frank-Starling curves represent the relationship (slope) between stroke volume (or cardiac output) and left ventricular end-diastolic pressure or end-diastolic volume (LVEDP or LVEDV). B-D, Pressure-volume (PV) loops represent the relationship between LV pressure and LV volume. A-D) Resting conditions are represented by Slope 1 and solid-lined PV loops. Increased LVEDP or LVEDV is associated with increased stroke volume. B, Acute cardiac injury reduces the Frank-Starling curve (Slope 2) and elastance at end-systole (Ees; dashed line ) and increases end-diastolic volume and pressure. C, Chronic systolic heart failure is associated with a reduced Frank-Starling curve (Slope 3) and Ees. Patients with compensated systolic heart failure may demonstrate preserved stroke volume (width of the PV loop), increased LVEDV, and normal or mildly increased LVEDP. Increased LVEDP or LVEDV is associated with small increases in stroke volume. D, Decompensated systolic heart failure or cardiogenic shock is associated with reduced Ees and a flat Frank-Starling curve (Slope 4). In this condition, increased LVEDP or LVEDV is not associated with increased stroke volume.

TABLE 33-4

Guidelines for the Use of Pulmonary Artery Catheters in Advanced Heart Failure

COR , Class of recommendation; HF, heart failure; LOE, level of evidence.

Reproduced with permission from Yancy CW, Jessup M, Bozkurt B, et al: 2013 ACCF/AHA Guideline for the Management of Heart Failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 62:e147–e239, 2013.

Percutaneous Mechanical Circulatory Support

The use of surgically implanted left ventricular assist devices (LVADs) as an approach to “bridge” patients to recovery or cardiac transplantation or as “destination therapy” has opened new opportunities for patients with advanced heart failure whose condition might otherwise have been rendered medically futile. Guidelines for the management of Stage D advanced heart failure recommend considering inotropic therapy, mechanical support, or cardiac transplantation ( Table 33-5 ). 7 Nearly 2000 LVADs are implanted annually in the United States alone. LVADs have evolved from large, bulky, pulsatile systems to smaller, compact, fully implantable continuous flow (CF) pumps that generate minimally pulsatile blood flow when functioning optimally. These CF-LVADs use rotodynamic pumps to transfer kinetic energy from a circulating impeller to the bloodstream, thereby generating forward flow. CF-LVADs can be divided into two categories: axial-flow and centrifugal-flow pumps. In both cases, blood is pulled into the impeller of the pump via an inlet cannula connected to the left ventricular apex and delivered to the systemic circulation via an outflow cannula connected to either the ascending or descending aorta ( Figure 33-5 ; ).

TABLE 33-5

Guidelines for the Management of Stage D, Advanced Heart Failure

BTT, bridge to transplantation; GDMT, guideline-directed medical therapy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; MCS, mechanical circulatory support.

*Although optimal patient selection for MCS remains an active area of investigation, general indications for referral for MCS therapy include patients with LVEF <25% and NYHA class III-I functional status despite GDMT, including, when indicated, CRT, with either high predicted 1- to 2-year mortality (eg, as suggested by markedly reduced peak oxygen consumption and clinical prognostic scores) or dependence on continuous parenteral inotropic support. Patient selection requires a multidisciplinary team of experienced advanced HF and transplantation cardiologists, cardiothoracic surgeons, nurses and ideally, social workers and palliative care clinicians.

Reproduced with permission from Yancy CW, Jessup M, Bozkurt B, et al: 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 62:e147–e239, 2013.


Hemodynamic profile of continuous flow left ventricular assist devices (CF-LVAD).

A, Fluoroscopic image of a HeartMate-II CF-LVAD (Thoratec Corp., Pleasanton, Calif.). B, Activation of a continuous flow LVAD reduces left ventricular end-systolic pressure, end-diastolic pressure, and end-diastolic volume with no significant change in arterial elastance, but a significant reduction in wall stress.

Ea, Arterial elastance; EDV, end-diastolic volume; ESP, end-systolic pressure; LVAD, left ventricular assist devices.

In parallel to the evolution of surgical LVADs, percutaneously delivered mechanical circulatory support (pMCS) systems have also grown from counterpulsation balloon systems to centrifugally driven circuits, or catheter-mounted axial-flow pumps. Both surgical LVADs and pMCS systems are subject to changes in preload and afterload. Inadequate LV preload due to volume depletion, poor right ventricular function, hypotension, pulmonary obstruction, or valvular disease will reduce flow generation. Similarly, increased afterload due to hypertension, elevated systemic vascular resistance, or valvular disease will reduce device flow. For these reasons, careful hemodynamic interrogation before, during, and after initiation of pMCS is essential for optimal device function.

The overall goals of pMCS systems are to: (1) increase vital organ perfusion, (2) augment coronary perfusion, and (3) reduce ventricular volume and filling pressures, thereby reducing wall stress, stroke work, and myocardial oxygen consumption. Clinical scenarios where these devices are commonly used include: cardiogenic shock, mechanical complications after AMI, high-risk coronary and non-coronary intervention, and for high-risk electrophysiologic ablations. Percutaneous circulatory support devices can be categorized by the type of pump used as either pulsatile or continuous blood flow devices. Each device impacts native ventricular function in a unique way and requires adequate preload for optimal use.

Intra-aortic Balloon Pump Counterpulsation

The intra-aortic balloon counterpulsation pump (IABP) is the most widely used MCS device with over 4 decades of clinical experience and registry data supporting its use. The IABP is a catheter-mounted balloon that augments pulsatile blood flow by inflating during diastole, which displaces blood volume in the descending aorta and increases mean aortic pressure, thereby potentially augmenting coronary perfusion. Upon deflation, during systole, the IABP generates a pressure sink, which is filled by ejecting blood from the heart. Optimal IABP function should increase diastolic aortic pressure, reduce aortic and LV systolic pressure, increase systemic mean arterial pressure, reduce LV diastolic volume and pressure, and increase coronary perfusion pressure. The hemodynamic effect of an IABP can be directly measured using tracings obtained from the IABP console to determine the magnitude of systolic unloading and diastolic augmentation ( Figure 33-6 ).


Hemodynamic profile of intra-aortic balloon counterpulsation pumps (IABPs).

A, IABP tracings acquired at a balloon to heart beat synchronization ratio of 1 : 2 can identify nonaugmented diastolic (A) and systolic (B) pressures, dicrotic-notch pressure (C), augmented diastolic (D) pressure, reduced aortic end-diastolic pressure (E), and augmented or reduced systolic pressure (F). Systolic unloading can be calculated as the difference between nonaugmented and augmented systolic pressures (B-F). Diastolic augmentation is the difference between non-augmented and augmented diastolic pressures (D-A). Diastolic unloading can be calculated as the difference between nonaugmented diastolic pressure and reduced aortic end-diastolic pressure (A-E). The change in aortic pressure at balloon deflation (deflation pressure) is measured as the difference between augmented diastolic pressure and reduced aortic end-diastolic pressure (D-E). The slope of deflation pressure is measured as the deflation pressure divided by time. B, Optimal IABP function reduces left ventricular end-systolic pressure (ESP) and end-diastolic volume (EDV), while increasing stroke volume. Arterial elastance is reduced due to increased stroke volume and reduced ESP. Wall stress is reduced due to decreased ESP and EDV.

The pioneering work of Kantrowitz, Weber, Janicki, Sarnoff, Schreuder, Kern, and many others have established that the hemodynamic impact of balloon counterpulsation is primarily determined by four factors: (1) the magnitude of diastolic pressure augmentation, (2) the magnitude of reduced systolic pressure, (3) the magnitude of volume displacement, and (4) the timing of balloon inflation and deflation. IABP balloon capacity ranges from 34 cc to 50 cc. Larger capacity IABPs potentially offer better hemodynamic support than standard 40 cc IABPs. In addition to balloon capacity, the hemodynamic effects of IABP are determined by frequency and timing of IABP inflation and deflation, its position in the descending aorta, shape and occlusivity, as well as biologic factors including heart rate, blood pressure, and aortic compliance.

IABP advantages include its relative cost compared with other assist devices, ease of insertion, and widespread familiarity with its insertion technique. However, its use in the setting of cardiogenic shock is best when deployed early in the management of cardiogenic shock and decompensated heart failure. Major complications, including acute limb ischemia, severe bleeding, IABP failure or leak, or death directly related to IABP insertion, occurred at a frequency of 2.6% in 16,909 patient case records in the Benchmark Registry. Clinician expertise, sheathless insertion, and smaller IABPs are associated with decreased incidence of vascular complications.

Percutaneous Rotodynamic Pumps

Both the Impella (Abiomed Inc., Danvers, Massachusetts) and TandemHeart (CardiacAssist Inc., Pittsburgh, Pennsylvania) devices are rotodynamic pumps that generate continuous, minimally pulsatile blood flow when functioning optimally. The Impella devices are catheter-mounted axial-flow pumps that are placed into the left ventricle in retrograde fashion across the aortic valve. The pump transfers kinetic energy from a circulating impeller to the bloodstream, which results in continuous blood flow from the left ventricle to ascending aorta. The Impella 2.5 LP and CP devices can be deployed without the need for surgery, while the Impella 5.0 device requires surgical vascular access ( Figure 33-7 ; ; ). At present, there is growing experience with the CP device in the United States. In contrast, the TandemHeart device is an extracorporeal centrifugal flow pump that reduces left ventricular preload by transferring oxygenated blood from the left atrium to the descending aorta via two cannulas: a transseptal inflow cannula in the left atrium and an arterial outflow cannula in the femoral artery. The net effect of these devices is to reduce native left ventricular volume and pressure, while increasing mean arterial pressure without greatly influencing ventricular afterload ( Figure 33-8 ; ; ). An advantage of the Impella 2.5 and CP devices is ease of insertion via a single arterial access, while an advantage of the TandemHeart device is the magnitude of support provided without the need for surgical vascular access ( Table 33-6 ). No studies comparing these continuous flow devices head-to-head exist.


Hemodynamic profile of the Impella pump.

A-B, The Impella pump is an intracorporeal axial-flow catheter deployed into the arterial circulation via either percutaneous or surgical access. The pump rests across the aortic valve and withdraws blood from the LV into the ascending aorta. C, Optimal Impella pump function reduces left ventricular ESP and EDV, while decreasing native left ventricular stroke volume by directly displacing blood from the LV. Ea is slightly increased due to reduced stroke volume; however, LV afterload or wall stress is reduced due to decreased ESP and EDV.

Ea, Arterial elastance; EDV, end-diastolic volume; ESP, end-systolic pressure; LV, left ventricular; RA, right atrium; RV, right ventricular.


Hemodynamic profile of the TandemHeart pump.

A and B, The TandemHeart pump is an extracorporeal, centrifugal-flow pump that delivers oxygenated blood from the LA via a transseptal inflow cannula into the systemic circulation via a femoral arterial outflow cannula. C, Optimal TandemHeart pump function reduces LV ESP and EDV, while decreasing native left ventricular stroke volume by reducing LV preload. Ea is slightly increased due to reduced stroke volume; however, LV afterload or wall stress is reduced due to decreased ESP and EDV.

Ea, Arterial elastance; EDV, end-diastolic volume; ESP, end-systolic pressure; LA, left atrium; LV, left ventricular; RA, right atrium; RV, right ventricular.

TABLE 33-6

Advantages and Disadvantages of Percutaneous Mechanical Circulatory Support Devices


  • Ease of insertion

  • Widespread familiarity with insertion technique

  • Relative cost compared with other devices

  • Bedside placement is feasible

  • Improves coronary perfusion

  • Anticoagulation is recommended but not required

  • Moderate hemodynamic support in moderate to severe cardiogenic shock

  • Contraindicated in severe aortic insufficiency

Impella devices

  • Provides up to 3.5 L/minute of flow (surgical 5.0 implant provides 5.0 L/minute)

  • Ease of insertion

  • Improves coronary perfusion

  • Requires fluoroscopy for placement

  • Impella 5.0 requires surgical cutdown for placement

  • Requires systemic anticoagulation

  • Contraindicated in mechanical aortic valves or severe aortic stenosis

  • Contraindicated in patients with LV thrombus


  • Provides up to 5.0 L/minute of flow

  • Can be used to support left and/or right ventricles

  • Can be used in severe aortic insufficiency

  • No surgical cutdown necessary for placement

  • Improves coronary perfusion

  • Requires fluoroscopy for placement

  • Transseptal puncture for LV support

  • Requires systemic anticoagulation


  • Ease of insertion

  • Does not require fluoroscopy for placement

  • Offers complete cardiopulmonary support

  • Requires systemic anticoagulation

  • Acute increase in LV afterload necessitating venting of the LV

  • Requires a perfusionist at bedside

  • Does not improve coronary perfusion

IABP, Intraaortic balloon pump; LV, left ventricular; VA-ECMO, venoarterial extracorporeal membrane oxygenation.

Other centrifugal pumps include the Centrimag (Thoratec Inc., Pleasanton, California), Rotaflow (Maquet Getinge Group, Wayne, New Jersey), and Biomedicus (Medtronic, Minneapolis, Minnesota) pumps, which are more commonly implanted surgically or used to provide flow for venoarterial extracorporeal membrane oxygenation (VA-ECMO). VA-ECMO is more commonly used to enhance systemic oxygenation during cardiorespiratory collapse or biventricular failure. The major effect of VA-ECMO is to displace blood volume from the venous to the arterial circulation. As a result, a reduction in both right and left ventricular volumes can be observed with a concomitant increase in mean arterial pressure and both LV systolic and diastolic pressures. This increase in LV afterload or wall stress occurs in contrast to the Impella or TandemHeart devices since there is no direct venting of the left ventricle with VA-ECMO ( Figure 33-9 ; ). For this reason, operators have combined VA-ECMO with either an IABP, Impella device, or a transseptal left atrial cannula to negate the effect of increased left ventricular afterload during VA-ECMO support ( Figure 33-10 ). Advantages of VA-ECMO include the relative ease of insertion, the ability to support systemic oxygenation or biventricular failure, and the ability to provide cardiopulmonary support during ventricular tachycardia or fibrillation ( Table 33-7 ).


Hemodynamic profile of venoarterial extracorporeal membrane oxygenation.

A and B, Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is an extracorporeal, centrifugal-flow pump that delivers deoxygenated blood from the venous system via an inflow cannula through an oxygenator and into the systemic circulation via a femoral arterial outflow cannula. C, Optimal VA-ECMO pump function reduces LV stroke volume and increases ESP and EDP. Ea and LV afterload or wall stress are significantly increased due to increased ESP.

Ea, Arterial elastance; ESP, end-systolic pressure; LA, left atrium; LV, left ventricular; RA, right atrium; RV, right ventricular.

FIGURE 33-10

Hemodynamic profile of venoarterial extracorporeal membrane oxygenation with and without left ventricular venting.

A, A double-lumen pigtail catheter during activation of venoarterial extracorporeal membrane oxygenation (VA-ECMO) shows increased LV systolic pressure and reduced aortic pulse pressure. B, Initiation of an IABP with VA-ECMO shows reduced LV systolic pressure (venting) and elevated aortic diastolic pressure. C, Venting of the LV with either an IABP, Impella device, or transseptal left atrial cannula during VA-ECMO support reduces LV end-systolic pressure and end-diastolic volume.

Ea, Arterial elastance; LV, left ventricular.

TABLE 33-7

Hemodynamic Effects of Percutaneous Mechanical Circulatory Support Devices

Impella 5.0 ↓↓ ↓↓ ↓↓ ↑↑
TandemHeart ↓↓ ↓↓ ↓↓ ↑↑ ↓↓
VA-ECMO ↑↑ ↑↑

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Mar 21, 2019 | Posted by in CARDIAC SURGERY | Comments Off on Interventions for Advanced Heart Failure
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