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Management Strategies for High-Risk Cardiac Surgery: Improving Outcomes in Patients with Heart Failure
(#2000-0734 ... September 11, 2000)
Steven F. Bolling, MD,1 Marc L. Dickstein, MD,2 Jerrold H. Levy, MD,3 Patrick M. McCarthy, MD,4 Mehmet C. Oz, MD,2 Robert M. Savage, MD, FACC4
1University of Michigan, Ann Arbor, Michigan
2Columbia Presbyterian Medical Center, New York, New York
3Emory University Hospital, Atlanta, Georgia
4The Cleveland Clinic Foundation, Cleveland, Ohio
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The Heart Surgery Forum #2000-0734
3(4):337-349, 2000
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ABSTRACT
Background: Surgical heart failure management is the fastest growing aspect of cardio-vascular surgery. Advances in cardiac surgical techniques have changed the number and types of operations permitted physicians and thus broadened the complexity of patients recommended for operation.
Methods: Surgeons, anesthesiologists and cardiologists face hemodynamic and patho-physiological challenges that can be optimally overcome only by modifying treatment strategies. Because many treatment standards are still evolving in this rapidly advancing field, a team of cardiovascular surgeons and anesthesiologists convened to share clinical experience and impres-sions and discuss practical issues related to high-risk patients undergoing heart surgery.
Results: Heart failure pathophysiology, surgical heart failure management, including mitral reconstruction and left ventricular remodeling, cardiopulmonary bypass weaning, inotropic support, transesophageal echocardiography and acute cardiovascular collapse after cardiac surgery are discussed.
Conclusion: This article is intended to guide clinicians to improve patient care and outcomes in this special population by providing specific guidance on the appropriate use of inotropic and mechanical support in patients undergoing high-risk procedures using innovative techniques.
INTRODUCTION
Advances in cardiac surgical techniques have changed the number and types of operations permitted physicians and thus broadened the complexity of patients recommended for operation. Not only has the overall number of individuals undergoing elective cardiac surgery since the early 1980s increased, but today?s patients are also proportionately older and at higher risk [Warner 1997]. Among patients undergoing major vascular surgery, cardiovascular complications are the most important causes of perioperative morbidity and mortality [Poldermans 1999], and patients with advanced heart failure have the highest risk for perioperative events and decreased survival [Ferraris 1998]. Continued improvements in combined medical and surgical approaches [Christenson 1997, McCarthy 1997, Smedira 1997, Bolling 1998, Goldstein 1998, McCarthy 1998, Beck 1999, Kˆrfer 1999, Kuhn 2000] together with novel postoperative monitoring techniques [Ninomiya 1997, Savage 1997, Savage 1999, Shanewise 1999] are enabling patients with ad-vanced heart failure to receive surgical therapy in an attempt to improve cardiac function and survival [Warner 1997, Dalrymple-Hay 1999, McCarthy 1999, Nashef 1999].
Finally, surgical heart failure management is the fastest growing aspect of cardiovascular surgery. Surgeons, anesthesiologists and cardiologists face hemodynamic and physiological challenges that can be optimally overcome only by modifying treatment strategies. Because many treatment standards are still evolving in this rapidly advancing field, an expert panel was convened to review contemporary treatment strategies in the high-risk cardiac surgical patient. This article reviews cutting edge approaches to the management of patients with compromised ventricular function using pharmacological and mechanical means.
DISCUSSION
Heart Failure
Despite significant advances in the management of cardiovascular diseases, heart failure prevalence has been increasing [Gheorghiade 1998, American Heart Association 1999], mainly because the age of the population is also increasing [Ho 1993]. Heart failure afflicts approximately four to five million individuals in the United States at an annual cost in excess of $12 billion [Levit 1991, O?Connell 1994]. Clinical estimates suggest that approximately 5% of patients with heart failure are New York Heart Association (NYHA) Class IV patients [Adams 1998].
Definition and Classification
Heart failure is the term used to characterize the pathophysiological condition in which the heart cannot pump blood at a rate sufficient to meet the metabolic requirements of the tissues or can do so only from elevated filling pressures [Lenfant 1994, Colucci 1997]. Heart failure is usually the result of "primary" myocardial failure. However, an indistinguishable syndrome may occur with normal myocardial function and excessively deranged loading conditions.
The pathophysiological definition of heart failure implies that it can be caused by abnormalities in systolic or diastolic function. Systolic heart failure is the inability of the active contractile phase of the cardiac cycle to meet the body?s metabolic demands, whereas diastolic heart failure is the condition where the heart cannot sustain an adequate preload volume for the maintenance of normal systolic function. This may be associated with normal or inadequate cardiac output [Gaasch 1994]. Clinical manifestations of heart failure are due to inadequate cardiac output and/or damming up of blood behind one or both ventricles (i.e., the forward or backward pressure theories of heart failure). Implicit in the backward failure theory is the idea that intravascular volume redistributes behind the specific cardiac chamber that is initially affected. Patients with left ventricular (LV) myocardial infarction (MI), hypertension and aortic and mitral valve disease initially manifest symptoms of pulmonary congestion (i.e., left heart failure). Over time, patients experience generalized fluid accumulation including ankle edema, congestive hepatomegaly, ascites and pleural effusion (i.e., right heart failure) [Little 1997].
Myocardial Cell Structure and Function
The contractile cells of the heart (cardiomyocytes), composed of myofibrils (actin and myosin), mitochondria, the sarcoplasmic reticulum (SR) and a centrally located nucleus, constitute 75% of the heart [Opie 1997]. Figure 1 shows myocardial cell structure [Opie 1997]; Figure 2 shows myocardial function with action-potential activation [Opie 1997].
A cell membrane (sarcolemma) surrounds the cell and invaginates into its interior as the t-tubule network. The mitochondria are responsible for energy generation (i.e., ATP) for contractile function and maintenance of transmembrane ion gradients. The SR is a fine network throughout the cell (parts of which lie in close proximity to the t-tubules) and is responsible for calcium (Ca++) release into the cell during contraction and ATP-dependent uptake during relaxation. The myofibrils are composed of thin actin and thick myosin filaments. Myosin filaments are attached to the z-line by the protein titin, whereas actin filaments are attached directly. At regular intervals on the actin filaments are troponin complexes. These complexes are composed of troponin C, which binds Ca++ and then is able to bind the inhibitory protein troponin I. This repositions troponin M on the actin filament, which removes the inhibition exerted by tropomyosin on the actin-myosin interaction. ATP binds to the bridging myosin and weakens the binding state. With the inhibitory influence of troponin I once again dominating the actin-myosin interaction, the cross-bridging is inhibited. In the presence of calcium (Ca++), the process occurs repetitively, and the actin moves more centrally along the myosin filament.
With action-potential activation of the sarcolemma, small amounts of Ca++ enter the cell, which results in a greater Ca++-induced Ca++ release from the SR, leading to a 10-fold Ca++ concentration increase and troponin C binds Ca++ forming a complex that inhibits troponin I. Beta receptors on the sarcolemma (t-tubules near SR Ca++ release channels) serve to open the Ca++ in addition to increasing the uptake of Ca++ into the SR. Ca++ is taken into the SR by a Ca++ pump that is ATP-dependent. Phospholamban is the protein receptor that, when phosphorylated, triggers the Ca++ uptake into the SR and storage with calsequestrin. Protein kinases, which provide the phosphyloration for phospholamban, are stimulated by cyclic adenosine monophosphate (cAMP (increased by beta stimulation)) and enhanced intracellular Ca++. The sarcolemma Ca++ channels are voltage-gated and with beta stimulation there is a larger opening and more channels are open for increased Ca++ flux into the cell. Beta receptors on the sarcolemma convert an extracellular hormone or drug into an intracellular physiologic change via intermediary messengers (G-protein, cAMP and kinase A). With end-stage heart failure, the SR Ca++ release receptor, the Ca++ uptake pump and phospholambans are decreased. In addition, there is major down-regulation of the beta-1 receptor, beta-2 uncoupling from adenyl cyclase, diminished adenyl cyclase activity, and increased levels of the Gi protein, which inhibits the Gs protein that activates adenyl cyclase.
Contractile Performance
The cardiac cycle is composed of seven distinct phases: atrial contraction, isovolumetric contraction, rapid ejection, slowed ejection (protodiastole), isovolumetric relaxation, rapid ventricular filling and slowed ventricular filling (diastasis). The three major determinants of cardiac contractile performance are the Frank-Starling mechanism (preload and afterload), heart rate and the con-tractile state of the heart [Opie 1997]. Myocardial performance and its determinants may be easily visualized using pressure volume loops, which demonstrate the relation between preload, afterload, contractility and stroke volume [see Figure 3 :1737:] [Little 1997]. Increased afterload can decrease LV systolic emptying in the absence of myocardial contractility depression. Increased preload, if it occurs without a change in end-systolic pressure, results in a larger stroke volume. A primary increase in myocardial contractility effects a steeper ESPVR. If preload and afterload remain constant, an increase in stroke volume occurs.
Adaptive Mechanisms in Heart Failure
When the myocardium does not meet systemic metabolic demands, several adaptive mechanisms activate to maintain normal pumping function [see Table 1 :1746:] [Katz 1990]. Most important among theses are the Frank-Starling mechanism, myocardial hypertrophy and activation of neu-rohumoral mechanisms [Katz 1990, Katz 1994]. With the onset of primary myocardial failure, the contractility curve of the Frank-Starling performance relation is shifted downward and to the right. To maintain adequate myocardial performance, the LV end-diastolic volume (EDV) in-creases (through diminished stroke volumes and central volume redistribution) with a resulting compensation in pump function maintaining output. As further deterioration in myocardial con-tractility occurs, a point is reached where cardiac pump function is only maintained in the presence of increased preload, which results in pulmonary congestion. With persistence of elevated loads, myocardial cells are stimulated. The resulting increase in mitochondria synthesis serves to meet the elevated energy demands in the failing heart. Eventually, persistence of this hemodynamic load results in cardiac hypertrophy with increased myocardial myofibrils and mitochon-dria. Unless the loading conditions are normalized, the ventricle eventually undergoes a remodeling process with myocardial cell necrosis, fibrosis and LV dilation.
In response to reduced cardiac output and elevated atrial pressures, a series of neurohumoral changes occurs, including increased sympathetic activation (with parasympathetic withdrawal), activation of the renin-angiotensin-aldosterone system and the elicitation of an inflammatory cytokine response [Francis 1984, Dzau 1987]. The activation of the sympathetic system occurs as a result of increased excitatory inflow from the arterial and cardiopulmonary baroreceptors. The overall response to sympathetic activation and withdrawal of parasympathetic tone is eleva-tion of circulating catecholamine concentrations, primarily norepinephrine, with increased heart rate and excessive vasoconstriction, increased circulating renin concentrations and subsequent increased sodium reabsorption by the renal tubules [see Figure 4a :1738:, and Figure 4b :1739:] [Colucci 1997, Schrier 1999]. The elevation of circulating norepinephrine may result from a com-bination of increased release from nerve endings and consequent excess in plasma, and reduced uptake by adrenergic nerve endings. Patients with heart failure demonstrate increased adrenergic nerve outflow, and the level of nerve activity correlates with the concentration of plasma norepi-nephrine. The extent of elevation of plasma norepinephrine concentration correlates directly with the severity of the LV dysfunction [Colucci 1997]. In patients studied in the Studies on Left Ventricular Dysfunction (SOLVD) trial, plasma norepinephrine, renin activity, atrial natriuretic factor, and arginine vasopressin were elevated in patients with symptomatic heart failure [Francis 1990]. In addition, plasma angiotensin II concentration was significantly elevated, even in asymptomatic heart failure patients studied in SOLVD [Francis 1990]. Angiotensin II is a potent peripheral vasoconstrictor and contributes, along with increased adrenergic activity, to the excessive elevation of systemic vascular resistance in heart failure patients. Angiotensin II also enhances the adrenergic nervous system?s release of norepinephrine. Several important mediators, including arginine vasopressin, natriuretic peptides, and endothelin, have important effects on the myocardium and vasculature and are involved in heart failure pathophysiology [Colucci 1997]. Inflammatory responses to heart failure also occur, including production of tumor necrosis factor (a direct myocardial depressant), interleukin 1B and other peptide growth factors, which induce further myocardial hypertrophy. The role of inflammatory cytokines in the pathophysiology of heart failure remains to be elucidated.
The primary goals of heart failure management are to improve quality of life, reduce the frequency of heart failure exacerbations and extend survival [Rich 1999]. To achieve these goals, optimal management requires surgical correction of the underlying cause whenever possible, prudent pharmacological support, and nonpharmacological and rehabilitative regimens of care.
Surgical Heart Failure Management: Selected Approaches
Heart transplantation is standard treatment for patients with severe congestive heart failure. The International Society for Heart and Lung Transplantation maintains a registry of heart transplantation. The number of transplantations reported to the registry per year [see Figure 5 :1740:] has plateaued since 1990 at approximately 3500 per year [Hunt 1998]. Because the procedure is limited both by the availability of donor hearts and its unsuitability in older patients or those with comorbid medical conditions [Hunt 1998], new surgical strategies to manage severe end-stage heart disease have evolved such as coronary artery revascularization, cardiomyoplasty, LV myoreduction surgery and mitral valve repair [McCarthy 1999].
Mitral Valve Annuloplasty
Functional mitral regurgitation (MR) is a significant complication of the ventricular dilation associated with advanced heart failure [Kono 1992] and a predictor of poor survival. Reported one-year mortality for such patients is between 46% and 70% [Stevenson 1987, Anguita 1993]. His-torically, mitral valve replacement was the surgical approach to patients with MR. Little was understood about the adverse consequences that interrupted annulus-papillary muscle continuity had on LV systolic function [Pitarys 1990], and this procedure was associated with very high mortality rates [Phillips 1981, Pinson 1984]. The concept of an MR "pop-off" effect originated in this patient population. It was incorrectly thought that reversal of blood flow was beneficial to the heart failure patient. Subsequently, preservation of annulus-papillary muscle continuity has been demonstrated to be of paramount importance to LV function preservation [David 1983, Sarris 1988]. Preservation of the mitral valve apparatus and the LV in mitral valve repair en-hances and maintains LV function and geometry with an associated decrease in wall stress [Goldman 1987, Tischler 1994]. This procedure has been shown to be safe, with a significant decrease in operative morbidity and mortality and good long-term outcomes [Gallino 1987, Rankin 1988, Akins 1994, Alvarez 1996]. Patient mortality from mitral valve replacement is ascribed to disruption of the subvalvar apparatus and loss of LV function. Maintenance of the chordal, annular, subvalvar continuity and mitral geometric relationships are essential to preserv-ing overall ventricular function and may be even more crucial in patients with compromised LV function. MR in this patient cohort arises from a ventricular pathology; therefore, a solution directed at the mitral valve that encompasses the entire left ventricle would be ideal.
With this goal in mind, 92 patients with end-stage cardiomyopathy and refractory MR underwent mitral valve repair with an undersized flexible annuloplasty ring [see Figure 6 :1741:] [Bolling 1998] at the University of Michigan from 1993 to 1999. Detailed methodology has been previously described [Bolling 1998]. All patients had severe LV systolic dysfunction (defined as an LV ejection fraction (LVEF) <25%) and NYHA Class III or IV heart failure despite receiving maximal medical therapy. Overall operative mortality was 5%. Five mortalities, including intraoperative death due to right ventricular failure (1), cardiac failure (1), stroke (1) and multisystem organ failure (2), were reported at 30 days. Five patients required intra-aortic balloon pump (IABP) support, and no patients required the use of an LV assist device (LVAD). The duration of follow-up has been 1-68 months (mean 38 months), with a one- and two-year actuarial survival of 80% and 70%, respectively. A total of 26 late deaths have occurred. At 24-month follow-up, all remaining patients are in NYHA Class I or II, with a mean LVEF of 26%. Interim results are presented in Table 2 Table 2; however final results will soon be available. The NYHA class improved for each patient, and all patients reported subjective improvement in functional status. Improvement in LVEF, cardiac output and EDV was demonstrated for all patients with a reduction in sphericity index and regurgitant fraction. Although significant undersizing of the mitral annulus was employed to overcorrect for the zone of coaptation, no mitral stenosis was induced, nor was any systolic anterior motion (SAM) noted in this study. SAM was avoided because of the widening of the aorto-mitral angle and increased LV size seen in cardiomyopathic patients. Acute remodeling of the base of the heart from the undersizing of the mitral annular ring may contribute to the improvement seen in these myopathic hearts. This may reestablish the ellipsoid shape and somewhat normal geometry to the base of the LV [Bach 1995, Bolling 1995, Bach 1996, Bolling 1998]. Importantly, all patients remain on maximal medical therapy; most have been able to tolerate a better regime with increased beta blockers and angiotensin-converting enzyme inhibitors. Mitral reconstruction by means of aggressive annuloplasty effectively corrects MR in patients with severe cardiomyopathy.
Further evidence exists to support the success of mitral valve repair in patients with cardiomyopathy. Akasaka et al. assessed coronary flow characteristics before and after mitral valve reconstruction in patients with MR and no coronary artery disease [Akasaka 1998]. Prior to reconstruction, coronary flow reserve was limited because of increased baseline coronary flow and flow velocity related to LV volume overload, hypertrophy and LV wall stress. The restriction improved following mitral valve reconstruction; reduction in baseline coronary flow and flow velocity occurred after LV preload, work and mass reduction [Akasaka 1998]. A restriction in the coronary flow reserve would seem probable in patients with MR and cardiomyopathy, and improved flow reserve and velocity would be expected following mitral valve repair. Ultimately, the mitral valve repair in this setting should lead to improvement in LV geometry.
Left Ventricular Remodeling
Patients with severe ventricular dilation from either ischemic or idiopathic cardiomyopathy have a very poor prognosis. Aside from transplantation, surgical interventions in patients with refractory heart failure have been generally contraindicated. Improved surgical therapies involving ventricular reconstruction to reduce wall stress and ventricular chamber dimensions are rapidly expanding and evolving.
Batista and coworkers developed an operation for patients with end-stage dilated cardiomyopathy of various etiologies [Batista 1996, Batista 1997]. The objective of the operation is to return the enlarged heart to a normal diameter, thereby reducing LV wall tension (via a mechanism related to the law of Laplace). To reduce heart diameter, large segments of LV wall are resected. The heart is then reconstructed to decrease LV diameter. Reported perioperative mortality is approximately 22%, and two-year mortality is approximately 45%. Most survivors have improved clinical condition [Batista 1997].
Of the 62 patients who underwent partial left ventriculectomy at the Cleveland Clinic Foundation between May 1996 and December 1998, 59 also had concomitant mitral valve repair. A complete description of study population, methodology and a report of early results has previ-ously been presented [McCarthy 1997]. Although 30% of patients continue to do well, this surgery is associated with a high risk of both early and late failure, which remains largely unpredictable. It is thought that detrimental effects on diastolic compliance offset the presumed benefits of improved systolic function [Dickstein 1997]. McCarthy and colleagues at the Cleveland Clinic Foundation have abandoned this procedure as an alternative to cardiac transplantation.
A more promising operation is LV reconstruction for ischemic cardiomyopathy. Revascularization following an anterior MI may improve survival [Bertelsen 1997, Senior 1999], but the infarcted anterior wall and septum segment remain akinetic unless repaired surgically. Remote (nonin-farcted) myocardia must compensate to ensure adequate cardiac output. Ultimately, heart failure ensues as LV geometry becomes spherical [Dor 1997a].
For many years, cardiac specialists have felt that patients with ventricular aneurysms show improvement in heart failure symptoms following ventricular aneurysmectomy [Cooley 1959]. The operative mortality and concerns over the ideal means of ventricular remodeling have prompted continuous interest in improving surgical approaches. Ventricular reconstruction, benefiting both dyskinetic ventricles and akinetic ventricles, has evolved from linear aneurysm repairs to more complicated repairs that exclude the infarcted septum and free wall [McCarthy 1999].
Infarct exclusion, the technique adopted at the Cleveland Clinic Foundation that evolved from the combined experience of Jatene, Dor, Cooley and David [Jatene 1985, Dor 1997b, Moreira 1998], excludes the akinetic areas of the LV apex and septum, resulting in a more elliptical shape and thus improved cardiac function [see Figure 7 :1742:]. More than 100 Cleveland Clinic patients have undergone this infarct exclusion, which is frequently associated with coronary artery bypass (86%) and mitral valve surgery (44%). Low perioperative mortality (2%) and late failure rates (90%) have been demonstrated. As documented by three-dimensional echocardiography, decreased LV volumes and improved LVEFs have been observed.
Surgical therapies for heart failure are rapidly expanding and evolving. The concept of high mortality and morbidity of surgical interventions in patients with end-stage heart disease no longer applies because of improvements in preoperative selection, intraoperative techniques and post-operative care. Results are acceptable when operative techniques are combined with optimal medical management of heart failure, and many patients can avoid or postpone transplantation. This strategy will allow preservation of the limited number of donor organs for patients who have no other alternative.
Cardiopulmonary Bypass Weaning
The selection of an appropriate therapeutic regimen, especially in patients with preexisting car-diac dysfunction prior to surgery, is a crucial element for successful separation from cardiopulmonary bypass (CPB). No definitive studies exist to determine which treatment modality, or combination of treatments, is optimal in this patient population. This is further evidenced by the observation that the use of certain proven treatments such as milrinone administration varies from less than 10% to 80%. However, several trends and guidelines are evident. Prophylactic inotrope administration, used to assist separation from CPB, does not result in damage to the myocardium. When tachycardia is avoided and coronary perfusion pressure maintained, prophylactic inotropes might benefit patients with preexisting myocardial dysfunction by facilitating a smooth and accelerated separation from CPB [Hardy 1993].
Down-regulation of beta-receptors during cardiac surgery has led to the development of agents that act independently of this system [Boldt 1993]. Phosphodiesterase inhibitors (PDEIs) have demonstrated remarkable effectiveness in facilitating weaning from CPB [Hamada 1999]; in fact, Columbia University and others such as the Cleveland Clinic Foundation [Boldt 1992, Butterworth 1993, Hardy 1993, Badner 1994, De Hert 1995, Orime 1998a, Orime 1998b] have come to refer to these agents as "balloon pumps in a bottle" [Orime 1999]. Prophylactic support of the circulation during separation from CPB, especially with PDEIs, may be indicated in this specific patient population as part of the strategy to ensure maximal preservation of myocardial function.
In addition to inotropic support regimens, appropriate early use of mechanical support can pre-serve end-organ function while allowing the heart precious time for recovery. Especially after an acute MI, repletion of ATP stores can take three days and will occur more quickly in a well-supported patient with a decompressed LV. Although a benefit of IABPs is their ease of insertion, the net additional power supplied to the left-sided circulation is only about 10%. At Columbia University, the criteria for institution of more aggressive support includes hemodynamic requirements: low cardiac output, elevated pulmonary arterial pressures (PAPs), elevated central venous pressures (CVPs) and tachycardia with arrhythmias. In addition, continual monitoring of physiologic criteria (e.g., mixed venous oxygen saturation, urine output) is employed. Use of LV support systems in this setting might be warranted and should be instituted early enough to prevent irreversible end-organ injury.
Transesophageal Echocardiography and High-Risk Cardiac Surgery
Patient Case. The patient was transferred to the operating room for a cardiac transplant after three weeks of biventricular assist with the Thoratec device (see Movie). During the device insertion period, the patient had experienced repeated episodes of bleeding with intermittent drops in the ventricular assist device (VAD) flow. Although the patient was hemodynamically stable at the time of transplantation, echocardiography demonstrated several well-defined, loculated collections of fluid around the heart that were confirmed at explantation to be pericardial effusions.
Transesophageal echocardiography (TEE) has become an indispensable monitoring tool in high-risk cardiac surgical procedures [Shanewise 1999]. Early recognition of the utility of intraoperative TEE focused on the assessment of the adequacy of mitral valve repair [Freeman 1992]. Today, its role has expanded to include the diagnosis of hemodynamic disorders and assessment of both anatomical and functional abnormalities as well as monitoring the rapid changes in cardiac function that occur during cardiac surgical procedures [Swenson 1996, Poelaert 1998, Garduno 1999, Lambert 1999, Swenson 1999, Willens 1999, Willens 2000].
Clinical studies have examined the role of TEE and its indications in intraoperative decision-making. In patients with acute or chronic hemodynamic disturbances or patients at risk for myocardial ischemia who were monitored with two-lead electrocardiography, radial and pulmonary artery catheters and biplane or multiplane TEE, the most important guiding factor in 25% of surgical interventions was TEE. Further, TEE was the most important monitor in guiding anti-ischemic therapy, fluid administration, vasopressor or inotrope administration, vasodilator therapy and depth of anesthesia [Kolev 1998]. In addition, Bergquist et al. have reported that TEE is often influential in guiding decision-making during elective myocardial revascularization proce-dures [Bergquist 1996]. To guide clinical decisions, the American Society of Echocardiography (ASE) and Society of Cardiovascular Anesthesiologists (SCA) have established guidelines for performing comprehensive intraoperative TEE examinations [Shanewise 1999].
The numerous pitfalls that can accompany the sophisticated TEE technology are associated with the physics of ultrasound, presence of artifacts and the ability to alter images with changes in console settings. Practical limitations include operator dependence and the imperfect relationship between echocardiography findings and physiological reality. For example, the amount of mitral insufficiency observed in an anesthetized patient may not reflect the competence of the valve during activities of normal living. In the following review of the limits of intraoperative echocardiography, EF will serve as an illustrative example.
The most common systolic function index determined from echocardiography is EF. Typically, EF is derived from the change in the area of the short-axis slice of the LV at the midpapillary level. Since TEE provides two-dimensional images, it is assumed that area is linearly related to volume and an area change would be identical to a volume change. This assumption may be invalid, however, secondary to the heterogeneity of the chamber. For example, a dilated, akinetic apex would not impact the above-described EF calculation. More broadly stated, the estimation of EF is less robust in the presence of regional wall motion abnormalities. Another practical limitation stems from the fact that the change in chamber area is not typically measured, which requires laborious planimetry or problematic automated edge detection, but rather is derived from a visual gestált that is obviously prone to observer error.
EF was established as a parameter to track systolic function deterioration in patients with heart disease. However, in the perioperative period, profound changes occur in the conditions under which the heart ejects. These conditions may result in EF changes that are unrelated to systolic function. One obvious example is the seemingly poor contractile function of the LV while on partial CPB. Two important alterations in loading conditions include reduced preload due to the diversion of venous return to the bypass pump and increased afterload due to maintenance of aortic pressure with the bypass pump. Clearly, assessment of systolic function is impossible under these extremely altered loading conditions. One less obvious example of the limitations associated with EF was noted during partial left ventriculectomy (Batista procedure): increased EF was accomplished by a reduction in EDV; the perceived benefits to heart function were not realized.
Acute Cardiovascular Collapse After Cardiac Surgery
A high index of suspicion is important when evaluating a patient with unexplained acute cardiovascular dysfunction following cardiac surgery. A variety of clinical problems can produce car-diovascular collapse, and multiple mechanisms may be responsible. Diagnosis and treatment are important when acute decompensation occurs. A differential diagnosis of acute-onset hypotension includes evaluation of the cardiac, inflammatory, neoplastic, degenerative, toxic, congenital, autoimmune, traumatic and endocrine pathophysiological processes [Hravnak 1997]. Because blood pressure (BP) is the product of cardiac output and total peripheral resistance, hypotension results from an abnormality in one or both of these parameters. Artifactual BP changes should be evaluated before instituting immediate therapy.
Administration of Sedative, Hypnotic or Anesthetic Drugs
Precipitous hypotension often follows administration of intravenous sedative, hypnotic or anesthetic drugs in critically ill patients [Levy 1992, Wahr 1996]. The effect typically occurs in patients who are hypovolemic or require a high sympathetic tone to maintain perfusion pressure [Shafer 1998]. Sedating these patients with one agent or a combination (e.g., benzodiazepines or opioids) causes their basal catecholamine levels to fall and BP to decrease.
Anaphylaxis/Bronchospasm
Any medication or blood product administered in the perioperative setting can be associated with unintended consequences or side effects. Patients are exposed to occult antigens, including latex, drug additives and drug preservatives, and serious adverse drug reactions may occur. As a result, clinicians must be prepared to treat anaphylaxis, the most life-threatening form of adverse reaction [Levy 1992]. When acute hypotension ensues following blood administration, anaphylaxis should always be considered as a cause [Levy 1992]. Bronchospasm and wheezing can also exacerbate right ventricular dysfunction. Furthermore, transfusion-related acute lung injury, an immunological reaction, presents similarly to anaphylaxis.
Disconnection or Overdosage of Vasoactive Infusions
Inadvertent discontinuation of vasoconstrictor infusions in critically ill patients must be considered a cause of precipitous hypotension. Catecholamines should be infused into central venous catheters whenever possible to avoid this problem. In addition, inadvertent overdosage when sodium nitroprusside or nitroglycerin is administered intravenously can occur after accidental flushing. Infusion rates, administration sites and patency of intravenous cannulas should be reevaluated after precipitous hypotension in patients receiving vasoactive medications.
Dysrhythmias
Bradycardia, rapid ventricular rates or sudden loss of sinus rhythm in patients with valvular heart disease (e.g., mitral or aortic stenosis) may seriously compromise LV filling and decrease cardiac output to produce shock. Heart rate and rhythm should be evaluated in all patients who develop acute cardiovascular dysfunction. Amiodarone administration has produced life-saving results in patients with recurrent ventricular tachycardia or ventricular fibrillation [Levy 1992, Kowey 1995].
Myocardial Ischemia
Following protamine reversal of anticoagulation, patients are acutely hypercoagulable, and graft closure, especially when target vessels were problematic, is always important to consider. Incomplete revascularization of a patient or even coronary or internal mammary artery spasm may compromise myocardial blood flow. In addition, open chamber procedures carry the risk of coronary air emboli, which can manifest as acute myocardial ischemia after resumption of LV output. TEE is extremely useful in assessing the adequacy of de-airing maneuvers.
Tamponade
Cardiac tamponade may occur and is often associated with excessive chest tube drainage that suddenly decreases following chest closure [Chuttani 1994]. If the heart is edematous and the chest cavity is small, chest closure can also cause acute hemodynamic compromise in a critically ill patient.
Pneumothorax/Hemothorax
An unrecognized pneumothorax or hemothorax may appear as precipitous hypotension with or without wheezing during mechanical ventilation in the operating room or intensive care unit; it may be confused with anaphylaxis. Chest auscultation and clinical suspicion are important for diagnosing this reversible problem. Signs of tension pneumothorax include acute hypotension, hypoxemia and hyperresonance to percussion, decreased breath sounds on the affected side and increased peak inspiratory pressure [Barton 1999]. Time should not be wasted obtaining a portable chest radiograph if life-threatening hypotension is present. Air should be immediately aspirated with a 14-gauge intravenous catheter placed in the second intercostal space over the midclavicular line on the affected side or with chest tube insertion.
Progressive Biventricular Dysfunction
Patients with preexisting heart failure or patients without adequate myocardial preservation may develop reperfusion injury and, thus, progressive ventricular dysfunction. In addition to beta-adrenergic down regulation, stress responses from surgery and extracorporeal circulation may further exacerbate ventricular dysfunction [Levy 1993].
Complications of Inotropic Support
Despite major advances in inotropic medications and the understanding of their proper use, ap-proximately 6% of patients require more aggressive therapy. Failure of inotropic therapy can be heralded by end-organ dysfunction, including oliguria and coagulopathy, and can be predicted by poor mixed venous oxygen saturation. Solutions include earlier use of appropriate inotropic sup-port, combined with adjunctive techniques to provide stability during the critical first 12 hours following CPB. For example, aggressive administration of a PDEI such as milrinone results in improved biventricular contractility and reduced right-sided circulatory failure in patients other-wise dying after cardiac surgery [Feneck 1991, George 1992, Sherry 1993, Kikura 1997]. However, despite improved hemodynamics, systemic hypotension, which can be disconcerting, periodically occurs with PDEIs. In patients with vasodilatory shock, use of arginine vasopressin (AVP) at physiologic rather than pharmacologic doses (0.1 units/min.) has demonstrated reliable increases in systemic BP without causing end-organ ischemia [Argenziano 1997]. Patients with neurohormonal heart failure changes are often resistant to alpha-agonist medications as monotherapy and require restoration of depleted AVP to regain appropriate response to sympathetic agents. In the reparative surgery population at Columbia University, a 10% incidence of vasodilatory shock, defined as a mean arterial pressure below 65 mm Hg despite a cardiac index above 2.4 L/min./m2 has been identified [Argenziano 1998]. Unlike patients with cardiogenic shock who have appropriately elevated AVP levels, vasodilatory shock patients have subphysi-ological circulating hormone concentrations.
Similarly, the inability to substantively improve the ventricular contractility and hemodynamics of critically ill cardiac patients mandates mechanical support in suitable candidates. Traditionally at Columbia University, IABP support is initiated if patients remain tachycardic with elevated right-sided pressures despite combined use of milrinone and norepinephrine with additional vasopressin as indicated. However, in the absence of ongoing myocardial ischemia, IABP support only increases net left-sided power output by 10%. In profound ventricular failure, early institution of a VAD [see Figure 8 :1743:] will support end-organ perfusion while allowing the ischemic myocardium the required two-to-three days to regenerate depleted energy stores. If, after this short period, attempts to reduce VAD flows after reinstitution of inotropic medications prove unsuccessful, insertion of longer-term implantable VADs is considered [see Figure 9 :1745:] [Goldstein 1998]. This approach has resulted in hospital discharge rates in excess of 70% rather than the historical standard of 25%.
Patient Case. A 69-year-old woman with a history of coronary artery disease presented with MR (4+), EF 20% and an apical aneurysm. Preoperatively, patient hemodynamic measurements included BP 110/60 mm Hg, pulmonary artery pressure (PAP) 50/24 mm Hg and central venous pressure (CVP) 9 mm Hg without inotropic support. The patient underwent Dor aneurysmectomy, bow-tie mitral valve repair, and coronary artery bypass grafting. Postoperatively, the patient was administered intravenous dobutamine; hemodynamics on dobutamine were BP 75/40 mm Hg; PAP 40/20 mm Hg and CVP 16 mm Hg. The patient experienced increasing tachycardia on dobutamine, and CPB weaning was difficult. Intravenous milrinone was started. The patient?s LV function and hemodynamics improved (BP 120/60 mm Hg; PAP 28/12 mm Hg; CVP 11 mm Hg), and the patient was successfully separated from CPB.
CONCLUSION
Management of the high-risk cardiac surgical patient requires the best of modern medicine, namely, sophisticated technology and a team of concerned medical and nursing specialists. Several options are now available for physicians to treat the ever-increasing number of heart failure patients. Surgical techniques, including mitral valve repair with an undersized flexible annuloplasty ring, and infarct exclusion, have shown promising results. Similarly, advances in moni-toring techniques, including TEE, and medical therapy with aggressive inotropic support, provide the practitioner with options to improve patient outcome.
AUTHOR/ARTICLE INFORMATION
Submitted August 29, 2000; accepted September 11, 2000.
Address correspondence and reprint requests to: Mehmet C. Oz, MD, Irving Assistant Professor of Surgery, Division of Cardiothoracic Surgery, College of Physicians & Surgeons, Columbia University, Milstein 7-435, 177 Ft. Washington Ave., New York, NY 10032, Phone: 212-305-4434, Fax: 212-305-2439, Email: mco2@columbia.edu
Key words: Cardiomyopathy, cardiopulmonary bypass, heart failure, infarct exclusion, inotropic support, mitral valve, transesophageal echocardiography, ventricular assist device
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