Scope of the Problem

According to the American Heart Association, approximately 6 million people in the United States have congestive heart failure (CHF). Available statistics indicate that the incidence of CHF in the population approaches 15.2 per 1000 after age 65, 31.7 per 1000 after age 75, and 65.2 per 1000 after age 85, with 1,106,000 hospital discharges for heart failure (HF) in 2006 alone.¹ HF is the leading cause of hospitalization in patients older than 65,² with a reported associated cost of $24 to $50 billion annually.^1–4 On a global scale, HF reportedly affects 0.4% to 2.0% of the adult population.⁵

Despite great advances in the understanding of the pathophysiology of HF and the development of medications that can potentially attenuate the progression of that pathophysiology, morbidity and mortality from this disease remain high. The incidence rate of hospitalization for HF increased by 70% during the 1990s,² and patients with New York Heart Association (NYHA) Class IV symptoms currently have a reported 1-year mortality rate of 30% to 50%.⁶ By comparison, the corresponding rates for NYHA Class I-II patients and Class II-III patients are 5% and 10% to 15%, respectively. (Table 27-1 defines the NYHA symptomatic classes.⁷) Thus, one of the major goals in the management of HF is the prevention of progression to advanced stages.

TABLE 27-1 New York Heart Association (NYHA) Functional Capacity

From The Criteria Committee of the New York Heart Association: Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels, 9th edition. Boston: Little, Brown & Co, 1994, pp 253–256.

Although many patients successfully achieve temporary relief of HF symptoms with medical management, the underlying pathophysiology inevitably progresses, and pharmacologic interventions alone eventually will become inadequate in most patients. A variety of surgical procedures can be performed to improve cardiac function and potentially arrest (or even reverse) the progression to severe dysfunction; but until very recently, surgical intervention (short of transplantation or placement of a ventricular assist device [VAD]) was considered contraindicated in patients with advanced HF. Surprisingly, good outcomes with “corrective” interventions, however, now have resulted in patients presenting for surgical treatment of their HF on a regular basis. This chapter describes the procedures typically performed in this population and the anesthetic considerations for patients with advanced HF.

Brief Review of the Pathophysiology

The current understanding of the pathophysiology of chronic HF maintains that initial increases in end-diastolic ventricular volume and pressure trigger the release of endogenous natriuretic peptides that promote diuresis.^8–10 Concurrent activation of the sympathetic nervous system causes peripheral vasoconstriction and increases the inotropic state of the myocardium. Initially, these mechanisms act to decrease excessive preload (which restores wall tension to normal) and maintain cardiac output (CO) and arterial blood pressure (BP) in the face of mildly depressed ventricular function. Eventually, however, the carotid, ventricular, and aortic arch baroreceptors are activated by the relative hypovolemia, which leads to further activation of the sympathetic nervous system (via the medullary vasomotor regulatory center), as well as the renin-angiotensin-aldosterone axis, and the release of vasopressin. The resultant peripheral vasoconstriction, mild fluid retention, and further increases in heart rate and inotropy will again compensate for the failing heart. Ultimately, however, chronic sympathetic stimulation causes myocardial β₁-adrenergic receptors to downregulate, and as ventricular function deteriorates, left ventricular (LV) end-diastolic volumes and pressures again increase, resulting in increased ventricular wall tension. During this time, increased levels of angiotensin II result in adverse myocardial remodeling. Remodeling is a key event in the progression of HF and refers to changes in not only ventricular geometry (e.g., dilation) but also myocardial composition (e.g., myocyte hypertrophy, lengthening, hyperplasia, fibrosis). In addition, increased circulating levels of angiotensin II may enhance myocyte apoptosis (programmed cell death) via a protein kinase C–mediated increase in cytosolic calcium levels.¹¹

Alterations in chamber geometry (dilation) and myocardial remodeling lead to progressively decreased forward CO, perpetuating the vicious cycle of adverse neurohumoral activation and transient, tenuous compensation. Myocardial oxygen demand increases, whereas oxygen supply potentially decreases because of shortened diastolic periods and increased diastolic wall tension. This developing diastolic dysfunction (ventricular “stiffness”) leads to increased left atrial and pulmonary pressures, pulmonary congestion, and increased right ventricular (RV) afterload. This eventually may progress to signs and symptoms of right-sided HF.

Modern medical management of chronic CHF, therefore, uses agents that have been shown to decelerate the progression to severe failure, reduce adverse myocardial remodeling, and enhance survival (e.g., angiotensin-converting enzyme inhibitors,^12–14 β-blockers,^15–18 and aldosterone antagonists^19,20), in combination with other agents that improve the symptoms but have not been shown to improve long-term survival alone (e.g., diuretics, digoxin). (See Chapter 10.)

Limitations of Current Medical Management

Given that there are currently between 300,000 and 800,000 patients in the United States who have progressed to NYHA Class III and IV status despite modern medical management,²¹ it appears that current treatment strategies have significant limitations. Part of the failure of medical management alone to control the progression of the disease may be that treatment has traditionally focused on systolic dysfunction. Four classic stages of HF have been described: (1) an initial cardiac injury or insult, (2) activation of specific neurohormonal axes with resultant cardiac remodeling, (3) compensatory fluid retention and peripheral vasoconstriction, and (4) ultimate contractile failure.²² In contrast with this traditional conception, it is now known that diastolic dysfunction (decreased lusitropic function) is the primary problem in an estimated 30% to 50% of patients with HF. Pharmacologic interventions aimed at improving diastolic dysfunction and attenuating (if not reversing) remodeling currently are the subject of randomized trials worldwide.

Revascularization

Coronary artery disease has become the most common cause of HF.²⁹ Of those patients currently listed for heart transplantation, 36% carry a primary diagnosis of ischemic heart disease, and 31% of those transplanted in 2007 had ischemia as their primary indication. Commonly used terms describing the extent of myocardial injury are defined in Table 27-2.

TABLE 27-2 Commonly Used Terms Describing the Extent of Myocardial Injury and the Potential for Recovery

Where viable myocardium and feasible targets exist, revascularization of chronically ischemic, hibernating myocardium can improve ventricular function, downgrade NYHA functional class, and improve prognosis.^30,31 Although the primary benefit of revascularization appears to be functional improvement of the left ventricle, reducing ischemic substrate for arrhythmias and retarding adverse myocardial remodeling are important secondary benefits.²⁴

Despite an increased perioperative risk for morbidity and mortality in this population, the world’s literature reports current survival rates between 57% and 75% at 5 years, with in-hospital mortality rates between 1.7% and 11%.³¹ A review reported an 83.5% survival rate at 2 years after revascularization compared with only 57.2% survival in patients with CHF who were not revascularized.³⁰ In general, morbidity and mortality tend to correlate inversely with EF and directly with NYHA functional class. Additional factors predisposing patients to greater morbidity and mortality include advanced age, female sex, hypertension, diabetes, and emergent operations³² (see Chapter 18). The decreases in morbidity and mortality after revascularization in this high-risk population in recent years are at least partially attributable to improvements in surgical technique and myocardial protection, but the concurrent performance of mitral valve repair and ventricular reshaping address the adverse ventricular loading conditions present and also may contribute to improved outcomes. The results of ongoing clinical trials evaluating combinations of surgical procedures (e.g., revascularization plus ventricular reshaping vs. revascularization alone) are discussed in detail later.

The importance of determining the viability of myocardium in the area to be revascularized cannot be overstated because the potential for recovery of function depends on residual contractile reserve, integrity of the sarcolemma, and metabolically preserved cellular function.³¹ Methods to detect viable myocardium include dobutamine stress echocardiography, single-photon emission computed tomography, positron emission tomography, and cardiac magnetic resonance imaging (see Chapters 1 and 2). Although dobutamine stress echocardio-graphy often has been shown to have the greatest predictive accuracy,³³ important limitations need to be taken into account. Dobutamine stress echocardiography does not demonstrate viability directly, but improvement in mechanical contraction under pharmacologic stimulation. An example for a false-negative result can be seen if there is loss of contractile proteins in the presence of preserved function of the muscle fiber membrane.³¹ Some centers report using only the intraoperative assessment of myocardial wall thickness and contractility to determine potential viability with revascularization of the target region.³⁴ Regardless of the specific method used, the important point is that there needs to be viable tissue to revascularize, and the best results will be obtained in properly selected individuals. Overwhelmingly, encouraging results worldwide suggest that, when feasible, revascularization is of benefit and provides survival advantage to patients with significant ventricular dysfunction.

Correction of Mitral Regurgitation

The mitral valve is a complex apparatus consisting of the anterior and posterior leaflets, the mitral annulus, the chordae tendineae, the papillary muscles, and the wall of the left ventricle. The posterior portion of the annulus is only rudimentarily developed and flexible. This explains why this portion of the annulus is prone to dilation during pathologic volume-overloaded states and mandates some form of mechanical stabilization when surgical valve repair is undertaken. The normal annulus has a three-dimensional (3D) saddle shape that is exacerbated during systole because of apical displacement of the commissures.³⁵ In addition, the aortic root bulges posteriorly during systole. These dynamic phenomena lead to the ability of the annulus to change its shape during the cardiac cycle. During systole, an elliptical shape is assumed that facilitates coaptation of the leaflets. During diastole, a more circular form increases orifice dimensions, decreasing resistance to LV inflow.³⁶ Consequently, the LV free wall, papillary muscles, and chordae play an important role in the competence of the valve, as well as in LV function during systole.

The mechanism responsible for mitral regurgitation can best be understood by utilizing the Carpentier classification (Table 27-3). This classification describes the motion of the mitral leaflets and position of the coaptation zone relative to the annular plane. The mitral regurgitation seen in patients with CHF is most often functional, primarily because of apical displacement of the papillary muscles resulting in tethering of the leaflets leading to systolic restriction of leaflet motion (type IIIb).

TABLE 27-3 Carpentier Classification of Mitral Regurgitation

From Carpentier A, Chauvaud S, Fabiani JN, et al: Reconstructive surgery of mitral valve incompetence: Ten-year appraisal. J Thorac Cardiovasc Surg 79:338, 1980.

Historically, many physicians considered mitral regurgitation advantageous for the failing left ventricle. It was believed that a low-pressure atrial “pop off” allowed the failing ventricle to protect itself from the high afterload of the systemic circulation and gave the illusion that the heart had a better overall contractile state than really existed. This misconception was “supported” by the fact that surgical replacement of the mitral valve was associated with a very high mortality rate in patients with depressed LV function.³⁷

Romano and Bolling’s³⁸ work disproved this misconception, showing that despite increased operative risk, mitral valve repair or replacement was beneficial to patients with severely depressed LV function, CHF, and mitral regurgitation. Operative mortality rates of 5% were reported, with 1- and 2-year survival rates of 80% and 70%, respectively.³⁸ Not only was long-term mortality reduced, but the increase in LV systolic function (on average by 10%) enabled a downgrading of NYHA class and resulted in an improved quality of life (see Chapter 19).

Although the majority of patients with end-stage HF will exhibit functional mitral regurgitation (as discussed earlier), there may be additional concurrent valvular pathology present in a given patient. An intraoperative transesophageal echocardiography (TEE) evaluation of the valvular anatomy, the mechanism of the mitral regurgitation, and direct surgical inspection will determine the feasibility of repair. Data obtained from patients suffering from organic mitral valve regurgitation have been extrapolated to the functional mitral regurgitation group in the belief that valve repair is preferable to valve replacement, because there are demonstrated hemodynamic advantages associated with preservation of the subvalvular apparatus,³⁹ and long-term anticoagulation is not required. However, review of the literature cannot unequivocally support this assumption. Magne et al⁴⁰ were unable to show a survival advantage between MV repair and replacement in patients with ischemic mitral regurgitation. Gillinov et al⁴¹ showed that a survival benefit could be obtained by repairing the mitral valve as opposed to replacing it, especially in lower-risk patients. However, in high-risk patients, defined as patients with extremely low EF and dilated ventricles, this survival benefit was lost, prompting them to recommend MV replacement.⁴¹ Braun et al⁴² showed that end-diastolic diameter larger than 65 mm was associated with poorer survival in 108 patients undergoing restrictive mitral annuloplasty and CABG. Reverse remodeling was seen in all patients with end-diastolic diameter smaller than 65 mm; however, it was seen in only 25% with end-diastolic diameter larger than 65 mm, making them question whether MV repair/CABG is justified in grossly dilated ventricles. Most likely a ventricular solution will need to be considered in this subset of patients.

A common dilemma that is encountered by the perioperative team is what to do with a patient with ischemic cardiomyopathy and moderate mitral regurgitation. In the setting of severe mitral regurgitation, most would agree to perform concurrent mitral regurgitation repair, and in the setting of mild mitral regurgitation, to leave the mitral valve dysfunction unaddressed. Penicka et al’s⁴³ study potentially could help shed light on this topic. They found improvement in moderate ischemic mitral regurgitation only in patients in whom viable myocardium in the region of the papillary muscles could be identified by preoperative single-photon emission computed tomographic testing. Patients with nonviable myocardium and dyssynchrony between the papillary muscles showed postoperative worsening of ischemic mitral regurgitation. Consequently, the authors argued to perform annuloplasty in all patients with nonviable myocardium and perform isolated CABG in patients with viable myocardium.⁴³

The primary repair technique in the setting of type IIIb dysfunction consists of downsized annuloplasty. Although much debate exists regarding whether the annuloplasty should be performed with the aid of a complete semirigid ring or band, most experts agree that the annulus needs to be remodeled and stabilized. Although this technique results in excellent short-term results, most surgeons realize that addressing a ventricular problem at the annular level cannot represent the ideal solution. Magne et al⁴⁴ showed that the use of annuloplasty rings eliminated severe mitral regurgitation; however, this was at the cost of leaving patients with functional mitral stenosis. One valvular disorder could be exchanged for another by undersizing the annulus (see Chapter 19).

After the procedure, TEE is used to assess the adequacy of the repair and potential improvement of overall cardiac function. Often, hemodynamic improvement is not immediately apparent, and TEE is used to optimize preload and guide pharmacologic interventions (see Chapters 12 to 14, 32, and 34).

Left Ventricular Restoration

In 1985, building on work by Cooley, Jatene, and others,^45–47 Dor et al introduced a ventricular reshaping procedure intended to improve systolic performance by excluding akinetic/dyskinetic and aneurysmal portions of the left ventricle with a circular stitch at the transitional zone between contractile and noncontractile myocardium. A small patch was used within the ventricular cavity as needed to reestablish ventricular wall continuity at the level of the purse-string suture.⁴⁸

This procedure generally was performed in conjunction with revascularization (and included mitral repair/replacement as needed) and thus helped establish important principles for a surgical ventricular restoration: revascularization of ischemic myocardium, decreasing of ventricular volume, and the restoration of ventricular shape. A subsequent publication by the same group described the results of this procedure in 130 patients (35% of whom had “heart failure” as the indication for the operation) and reported a 6% in-hospital mortality rate and a 3% late mortality rate because of recurrence of cardiac failure.⁴⁹

In 1996, Batista et al⁵⁰ introduced a procedure for the reshaping of the nonischemic, dilated, and failing left ventricle of NYHA Class IV patients through resection of a wedge of normal myocardium from the LV apex to the base (laterally, between the papillary muscles). This “partial left ventriculectomy” restored more normal ventricular geometry and decreased wall tension. Functional mitral regurgitation also was addressed during the Batista procedure by a mitral valve replacement or repair. Although many patients did benefit initially from this procedure (reduction of NYHA functional class to NYHA Class I in 57% and NYHA Class II in 33.3%),⁵¹ perioperative mortality was high (20% in both Batista’s own series and in the large Cleveland Clinic experience).^51,52 In addition, the experience of several centers was that many patients required rescue mechanical circulatory assistance after the procedure, and many patients experienced a redilatation of their left ventricle resulting in a return to NYHA Class IV status.^53–55 Thus, despite the short-lived period of initial enthusiasm in the mid- to late-1990s, the Batista procedure essentially has been abandoned. The concept of ventricular reshaping, however, remains of interest.

The modified Dor procedure (endoventricular circular patch plasty) has been used successfully to reshape large, dilated, spherical left ventricles of patients who have had an anterior wall myocardial infarction (MI) with resulting aneurysm and akinesis/dyskinesis. Essentially, a Dacron patch is placed within the LV cavity to exclude the large akinetic/dyskinetic area of the anterior wall. This restores LV geometry to a more normal elliptical shape and improves systolic function. When performed concurrently with CABG, significant early and late improvements in both NYHA functional class and EF have been demonstrated, with an in-hospital mortality rate of 12%.^56,57 A trial of 439 patients undergoing this procedure found an improved in-hospital mortality rate of 6.6% and an 18-month survival rate of 89.2%. In this series, CABG was performed concurrently in 89%, mitral valve repair in 22%, and mitral valve replacement in 4%.⁵⁸

Surgical ventricular restoration is the modern name for a modified Dor procedure, in which, in addition to exclusion of the akinetic aneurysmal segment of the anterior and/or septal wall and revascularization, a sizing balloon (or other sizer) is used to create an elliptical left ventricle of 30% to 40% smaller volume than baseline. Despite a worldwide surgical ventricular restoration database already in place including more than 5000 surgical ventricular restoration patients, a randomized, controlled trial was designed named “The Surgical Treatment for Heart failure (STICH),” with the intention to scientifically prove the efficacy of this procedure as an adjunct to revascularization. The results of this important trial have been eagerly awaited for years. Unfortunately, STICH did not demonstrate that the addition of surgical ventricular restoration to revascularization was associated with a greater improvement in symptoms or exercise tolerance, or with a reduction in the rate of death or hospitalization for cardiac causes when compared with revascularization alone.⁵⁹ The negative results from this trial have caused much controversy and the validity questioned.⁶⁰ Noted areas of concern revolve around participant eligibility for anatomic reasons, lack of standardized volumetric assessments in large numbers of participants, and alteration of the primary objective after trial commencement. In essence, the expert opinion is that the STICH trial was “well conceived, but poorly executed.” At the time of this writing, surgical ventricular restoration continues to be performed for true LV aneurysms but has fallen out of favor as a routine adjunct for the dilated end-stage left ventricle.

Cirillo’s⁶¹ recent publication described a further modification of the Dor concept wherein the shape and orientation of the patch, as well as the manner of suturing, ostensibly maintained more physiologic orientation of the myocardial fibers. Named the “KISS” procedure (Keep fIbers orientation with Strip patch reShaping), this methodology reportedly allowed for a return of normal apical rotation and ventricular torsion to optimize systolic performance. Long-term results of this new approach await further study.

Cardiac Resynchronization Therapy and Implantable Cardioverter-Defibrillators

The progression of disease resulting in advanced cardiac failure is typically accompanied by conduction defects and arrhythmias, and pacemakers and implantable cardioverter-defibrillators (ICDs) are common in this population. In addition to the well-known defects in sinus or atrioventricular node function, intraventricular conduction defects delay the onset of RV or LV systole in 30% to 50% of patients with advanced HF.^62,63 This lack of coordination of LV and RV contractions further impairs CO^64–67 and has been reported to increase the risk for death in this population^68,69 (see Chapters 4 and 25).

Cardiac resynchronization therapy (CRT) entails biventricular pacing (not to be confused with dual-chamber atrioventricular sequential pacing) to optimize the timing of RV and LV contractions. The right atrium is paced by a lead in the right atrium, the right ventricle by a lead in the right ventricle, and the left ventricle by a lead in a coronary vein (accessed via the coronary sinus). Although CRT is more an interventional cardiology procedure than a surgical procedure per se, anesthesiologists frequently are asked to provide sedation (if not general anesthesia) for these sometimes lengthy implantation procedures.

Studies have shown that atrial-synchronized biventricular pacing (pacing the left and right ventricles in a carefully timed manner) can resynchronize RV and LV contraction, improving CO and overall hemodynamics. This enhances these patients’ ability to exercise, which improves their NYHA functional class, and decreases the length and frequency of their hospitalizations, which improves their quality of life.^70–74

Sudden death from ventricular fibrillation accounts for approximately 350,000 deaths annually in the United States.¹ Patients with advanced HF experience ventricular fibrillation with a frequency six to nine times that of the general population,¹ and ventricular fibrillation causes 40% of all deaths in this population even in the absence of apparent disease progression based on symptoms.⁷⁵ Thus, ICDs commonly are indicated for patients with advanced cardiac failure. An ICD is a device capable of arrhythmia detection and automatic defibrillation. ICDs successfully terminate ventricular fibrillation in greater than 98% of episodes, and studies have demonstrated that an ICD increases survival and decreases the risk for sudden death in patients with ischemic cardiomyopathy and decreased LV function.^76–78

The COMPANION trial (Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure) studied 1500 patients with NYHA Class III/IV HF, a QRS interval of greater than 120 milliseconds, PR interval greater than 150 milliseconds, and an LVEF less than or equal to 35%. Compared with optimal pharmacologic therapy alone, CRT decreased the risk of the combined end point of death from or hospitalization for HF by 34%. The combination of CRT and ICD implantation reduced these risks by 40%.⁷⁹

The CARE-HF (Cardiac Resynchronization in Heart Failure) trial enrolled 800 patients with NYHA Class III/IV HF, a QRS interval of more than 150 milliseconds, a QRS interval of more than 120 milliseconds with echocardiographic evidence of dyssynchrony, and an LVEF of 35% or less. Compared with optimal medical therapy alone, CRT (without ICD functionality) reduced all-cause mortality by 36%. In addition, CRT showed significant improvement of cardiac dyssynchrony, ventricular function, and mitral regurgitation based on echocardiographic criteria.⁶⁸

Most recent guidelines give a Class I recommendation for placement of a CRT device with or without ICD in patients with LVEF ≤ 35%, QRS ≥ 120 milliseconds, presence of sinus rhythm, and NYHA Class III/IV symptoms on optimal medical therapy.⁸⁰ However, two recent trials have investigated the effects of CRT on patients with NYHA Class I/II HF. The REVERSE trial (Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction) randomized 610 NYHA Class I/II patients with QRS ≥ 120 milliseconds and LVEF ≤ 40% to receive a CRT device (±ICD) that was either active (CRT-ON) or disabled (CRT-OFF). This study showed a significant delay in time to first hospitalization and improvement in measures of LV remodeling in the CRT-ON group.⁸¹ The MADIT-CRT trial (Multicenter Automatic Defibrillator Implantation Trial–Cardiac Resynchronization Therapy) randomized 1820 NYHA Class I/II patients with QRS ≥ 130 milliseconds and LVEF ≤ 30% to receive CRT and ICD or ICD alone. The CRT-ICD group had a significant 41% decrease in risk for first HF event, significant reduction in LV volumes, and increase in LVEF as compared with the ICD only group.⁸² Thus, although CRT previously has been about reduction in symptoms, it is anticipated that results such as those reported from MADIT-CRT will lead to an increased utilization of CRT in relatively asymptomatic patients with developing HF to prevent the progression of the disease.

Ventricular Assist Devices: Implementation of Support

VADs can be used to take over the pumping function of the failing ventricle and provide effective CO to the arterial circulation downstream from the failing ventricle. In the case of the failing right ventricle, a right ventricular assist device (RVAD) can divert the deoxygenated venous return to the heart and pump it directly to the pulmonary arterial circulation. In the case of the failing left ventricle, a left ventricular assist device (LVAD) can divert the oxygenated blood returning to the left side of the heart and pump it directly into the aorta. Figure 27-1 demonstrates common cannulation strategies in the heart and great vessels by which MCS is implemented. Although there are a few notable exceptions (discussed later), these basic cannulation strategies are common to all manufacturers’ devices currently in use, regardless of the type of output they produce.

Figure 27-1 The Thoratec ventricular assist device (VAD) and three cannulation approaches for univentricular left-heart support (A) and biventricular support (B, C). Potential cannulation strategies for VADs are shown. B, The most commonly used cannulation approaches for most currently available VADs. Cannulas are placed in the heart and great vessels to divert blood returning to the failing side of the heart to the pump. The blood collected in the VAD blood chamber is then ejected into the arterial circulation immediately downstream of the failing ventricle. AO, aorta; Apex, left ventricular apex; IAG, cannula inserted via the interatrial groove and directed toward the LA roof; LA, left atrial appendage; PA, pulmonary artery; RA, right atrium.

(Reproduced from Thoratec Corporation, Pleasanton, CA.)

In addition to maintaining the circulation, decompression (or emptying) of the failing ventricle provides additional benefit because decompression will decrease the wall tension (and, therefore, myocardial oxygen demand) in the volume- and pressure-overloaded failing ventricle, potentially allowing for recovery of ventricular function. This is particularly relevant to short-term support of the acutely failing ventricle, but recovery of function (to varying degrees) also can be seen with chronically failing ventricles.

Mechanical Circulatory Support: Modern Practice

In prior years, VADs were regarded as either a last-ditch hope for recovery after an acute cardiac event that resulted in refractory cardiogenic shock (“bridge-to-recovery”), or as a “bridge-to-transplantation” for patients with chronic HF who were doing poorly. This has all changed now. More widespread acceptance of MCS, the recognition that outcomes are better when the support is instituted earlier rather than later, the development and use of risk scores to appropriately select patients and support strategies,^83–94 the demonstration that there is often significant improvement in multiorgan function during the time spent on VAD support,^95–97 the advent of new and improved devices, and a substantially decreased rate of VAD-associated complications^98–101 have allowed for an increased and an improved clinical utilization of this life-saving technology in the management of both acute and chronic HF.

Short-Term Ventricular Assist Device Use

The main indication for the short-term use of VADs always has revolved around the concept that the acutely failed myocardium could potentially recover after a short period of support. Depending on the cause of the acute failure (e.g., ischemic stunning, viral myocarditis), early experience revealed that myocardial recovery typically took a week or two in the majority of well-managed patients, who were then theoretically able to be weaned from support. Most short-term VAD use in prior decades was with extracorporeal, pulsatile devices, although standard centrifugal pumps producing continuous flow were also occasionally used, especially for the pediatric population and for extracorporeal membrane oxygenation (ECMO). In reality, however, regardless of the device used as a bridge-to-recovery, support often was initiated too late, complications (e.g., bleeding, thromboembolism, infection, multisystem organ failure) were frequent, and the percentage of patients who were able to be weaned from support (much less discharged from the hospital) was often disappointing.

Early experience also demonstrated that specific patient conditions or comorbidities (Table 27-4) potentially increased the risk for complications during VAD support or made support difficult to implement. It also was proposed that patients who were not potential transplant candidates should probably not be considered for VAD support. Finally, it commonly was believed for many years that patients unlikely to survive regardless of the reestablishment of effective systemic perfusion should probably not even be considered for temporary VAD support. However, society currently demands that everyone (no matter how critically ill) be given an opportunity to recover, and the new and improved MCS technology is often now used with the understanding that improvement in clinical status will allow for a continuation of support, whereas a worsening of the clinical picture will prompt a discontinuation of support. Nevertheless, it is the advancements of the technology and an increased patient management experience that have brought a new flexibility to the arena of short-term MCS.

TABLE 27-4 Conditions or Comorbidities That Make Ventricular Assist Device Placement or Use Difficult, Make the Patient More Likely to Have Major Complications, or Make Meaningful Recovery Unlikely

BSA, body surface area; ESLD, end stage liver disease; ESRD, end stage renal disease.

The traditional concept of the temporary or short-term use of a VAD as a “bridge-to-recovery” has thus been expanded to include concepts such as “bridge-to-immediate survival,” “bridge-to-next decision,” and “bridge-to-a-bridge.”

Figure 27-2 The Tandem Heart percutaneous Ventricular Assist Device (pVAD).

This recently introduced device provides circulatory support with a centrifugal pump head and the potential advantages of percutaneous cannula insertion. Partial left-heart bypass is accomplished via an interatrial septal cannulation into the left atrium across the area of the fossa ovalis, and oxygenated blood is returned to the femoral artery.

(Courtesy of CardiacAssist Inc., Pittsburgh, PA.)

Figure 27-3 The Impella.

The Impella 2.5 is a minimally invasive, catheter-based cardiac assist device designed to unload the left ventricle (thereby reducing myocardial oxygen consumption), while increasing overall cardiac output to maintain systemic perfusion. The Impella 2.5 can be percutaneously inserted into the left ventricle from the femoral artery. The tip of the catheter rests in the left ventricle during support, generating flows up to 2.5 L/min in the ascending aorta.

(Reproduced from Abiomed, Inc., Danvers, MA.)

Figure 27-4 A, The Abiomed BVS5000. B, Biventricular support with the Abiomed BVS5000. Cannulas are placed in the heart and great vessels to divert blood to the extracorporeal BVS5000 pumps. Blood collected in the pumps is ejected into the ascending aorta (left ventricular assist device [LVAD]) and main pulmonary artery (right ventricular assist device [RVAD]). Note that the pumps fill by gravity drainage and are, therefore, generally mounted below the level of the heart. Adjustments can be made to pump height to optimize filling and pump ejection. For example, lowering a pump can augment device filling but will increase the afterload against which the device must eject. Conversely, raising a pump can facilitate pump emptying but will decrease filling of the device.

(Reproduced from Abiomed Corporation, Danvers, MA.)

Figure 27-5 The Thoratec pVAD (percutaneous ventricular assist device).

(Reproduced from Thoratec Corporation, Pleasanton, CA.)

Figure 27-6 The Abiomed AB5000 ventricle.

Hookups for the inflow and outflow cannulas are at the right. Although arrows indicate the direction of flow, they also serendipitously point at the artificial unidirectional valves that mandate anticoagulation during support with this device. The driveline, which alternately provides vacuum to assist filling and compressed air to accomplish ejection, is at the left.

(Reproduced from Abiomed Corporation, Danvers, MA.)

Figure 27-7 The Thoratec CentriMag.

(From Thoratec Corporation, Pleasanton, CA.)

Though useful conceptually, the apparent distinctions between these indications can sometimes appear somewhat artificial in the clinical arena, and the current practice of short-term MCS is really more of a continuous spectrum beginning with the immediate survival of the patient.

Bridge-to-Immediate Survival

Since the late 1960s, the IABP has been the most commonly used “bridge-to-immediate survival” because it simultaneously increases myocardial O₂ supply and decreases O₂ demand, interrupting the otherwise inexorable cycle leading to ventricular failure. It is estimated that 5% to 10% of patients will experience development of cardiogenic shock after an acute MI, and early survival rates for these patients are on the order of 5% to 21%.¹⁰² However, 75% of such patients who are unresponsive to pharmacologic interventions will exhibit hemodynamic improvement with IABP therapy alone,¹⁰³ and early survival rates in these patients are reported to approach 93% when treated with IABP counterpulsation.¹⁰⁴

Although a balloon pump can improve the output from an acutely stunned ventricle, it only can augment forward CO by about 25% to 30% at maximum depending on the afterload,^105,106 and it is clear that there will be no augmentation of forward CO if there is a complete absence of LV function; thus, by itself, an IABP cannot be expected to rescue a patient from catastrophic myocardial failure (see Chapter 32).

ECMO has heretofore been the mainstay of emergent temporary MCS when there is intractable cardiorespiratory failure, and ECMO is making a comeback as an integral part of resuscitative protocols in many institutions, but the development of effective devices that can be deployed rapidly, at the first recognition of refractory ventricular insufficiency, has made “bridge-to-immediate survival” more of a reality than ever.

A key determinant of the overall survivability of acute cardiac failure is the rapidity with which the failing ventricle can be decompressed and resumption of adequate systemic perfusion assured. Although immediate implementation of support with conventional short-term VADs could potentially achieve these goals, sternotomy and CPB typically are utilized for the implantation of the requisite cannulae in the heart and great vessels. Furthermore, delays may be experienced while awaiting the availability of the operating room and necessary perioperative staff, prolonging the period of time during which the failing ventricle is pressure and volume overloaded, and the splanchnic beds and peripheral tissues are underperfused. It was considerations such as these that drove the development of several new and innovative short-term assist devices. Once immediate survival is assured, such a device conceivably can be changed later to another capable of providing longer term support.