Although there is a lack of large clinical trials of RAAS modulation in the perioperative period, such is not the case for β-adrenergic blockers. Randomized clinical trials show that these drugs should be given to prevent ischemic events and arrhythmias in high-risk cardiac patients with ischemia, arrhythmias, or hypertension or a history of these conditions and to patients with ischemia in perioperative testing submitted for noncardiac surgery (particularly vascular surgery) (108). Also, β-adrenergic blockers are indicated for the treatment of perioperative hypertension, ischemia, and arrhythmias identified preoperatively and previously untreated (108). Perioperative β-adrenergic blocker therapy in high-risk patients is underused (109). Nevertheless, whether β-adrenergic blockers should be newly initiated before surgery solely for management of HF remains highly speculative. Withdrawal of β-adrenergic blocker therapy from patients who have received it chronically may be particularly dangerous (108). Recent data also suggest that while initiating β-adrenergic blocker therapy may be highly advantageous for some surgical patient populations, it may be considerably less advantageous (perhaps even deleterious) for other patient populations (110).
In addition to ACE inhibitors and β-adrenergic blockers, diuretics and digoxin are often prescribed for patients with left ventricular systolic dysfunction and symptomatic HF. Diuretics provide rapid symptomatic relief of HF in the acute setting, and they maximize the benefits from ACE-I and β-adrenergic blockers, which are dependent on minimization of excessive intravascular volume (16). Moreover, older hypertensive patients who use diuretics in combination with β-adrenergic blockers have lower mean pulse pressures as compared with those patients receiving β-adrenergic blockers alone (111). Widened pulse pressure is an independent predictor of adverse CV outcomes in older persons (112). Diuretics continue to have a role in the outpatient management of HF in conjunction with ACE-I, β-adrenergic blockers, and (in some cases) aldosterone antagonists even though no randomized controlled trials have demonstrated a survival benefit from diuretics in HF. Importantly, hospitalization or death from worsening HF were significantly more frequent in HF patients receiving non-potassium-sparing diuretics than those not receiving diuretics (relative risk = 1.31, 95% confidence interval, 1.09–1.57) in a large post hoc review of data from SOLVD (Studies of Left Ventricular Dysfunction) patients (113).
Digoxin continues to be useful for patients with HF and left ventricular systolic dysfunction who remain symptomatic despite receiving ACE inhibitor, β-adrenergic blocker, and diuretic. Digoxin is the only positive inotropic drug that does not increase mortality in chronic HF (Fig. 4). The Digitalis Investigators Group (DIG) trial (114), enrolling more than 6500 patients with an average follow-up of 37 mo, showed that digoxin reduced the incidence of HF exacerbations but had no effect on survival. Patients with mildly symptomatic chronic HF, who were randomized to digoxin withdrawal (PROVED and RADIANCE trials), had an increased likelihood of an acute exacerbation compared with those who continued to receive digoxin (115,116). On the other hand, doubling the dose of digoxin from 0.125 to 0.25 mg daily provided no significant benefit in terms of exercise tolerance or ventricular function, suggesting that doses of digoxin should be kept small (117).
Chronic treatment with diuretics can lead to hypovolemia and an imbalance of electrolytes, particularly hypokalemia. These side effects are most common in the elderly (118). Chronic diuretic therapy can lead to hypotension and arrhythmias (119) during anesthesia. However, chronic use of diuretics for the management of HF has not been associated with perioperative CV death (within 30 days of surgery) in emergency and urgent surgical patients (120). In contrast, complications of digoxin therapy can be life-threatening and often difficult to diagnose and treat, given digoxin's narrow therapeutic index. Aggravating conditions that predispose to digoxin toxicity include hypomagnesemia, hypercalcemia, and hypokalemia, all of which may occur during the perioperative period. Treatment of digoxin toxicity, which often manifests as nausea, arrhythmias, and visual symptoms consists of correcting any underlying electrolyte imbalances, administering antiarrhythmic drugs (most commonly phenytoin), and in refractory cases, commercially prepared antibodies to digoxin (e.g., digoxin-specific Fab (Digibind; Glaxo-SmithKline, Research Triangle Park, NC), a mixture of antidigoxin Fab fragments prepared from sheep sera). Despite continuing concerns about digoxin toxicity, perioperative discontinuation of digoxin therapy remains controversial. After adjustment for the confounding effect of HF, Sear et al. (120) report that digoxin therapy was associated with an increased cardiac risk in urgent and emergent surgical patients. Given that rate and rhythm control and positive inotropy can be achieved with other drugs with shorter half-lives and less toxicity, we tend to discontinue digoxin in elderly surgical patients where age-related alterations in drug distribution and excretion may make toxicity increasingly likely (121).
Abnormal diastolic ventricular function is present in nearly all patients with symptomatic HF (122). As many as one in three patients presenting with clinical signs of chronic HF have a normal or near-normal EF (≥40%). Although the prognosis of patients with isolated diastolic HF is better than for those with systolic HF (5%–8% versus 10%–15% annual mortality), the complication rate is the same (123). The 1-yr readmission rate for patients with isolated diastolic HF approaches 50% (124).
Large randomized trials have led to the treatment guidelines for systolic HF; however, there are few completed randomized, double-blind, placebo-controlled, multicenter trials performed in patients with diastolic HF. The CHARM-Preserved Trial (58) data of 3023 patients indicate that treatment with the ARB candesartan reduces hospitalization rates but does not alter mortality in patients with diastolic HF. Findings from the I-PRESERVE (Irbesartan in HF with preserved systolic function) (125) trial of more than 4000 subjects will likely provide conclusive data regarding the primary end-point of death and the role of ARB blockade in the management of diastolic HF. Data from the Seniors trial (126) of nebivolol in 2128 HF patients, of whom 752 had diastolic HF (EF defined as >35%), suggest that β-adrenergic blockade is equally beneficial in patients with diastolic as with systolic HF. Preliminary findings from continuing studies suggest that aldosterone antagonists may also improve exercise tolerance and quality of life in patients with diastolic HF (127,128). However, until validation from adequately powered, randomized controlled trials becomes available, the contemporary treatment of chronic diastolic HF remains empiric (Table 4).
Patients with chronic HF may experience episodes of acutely decompensated HF, heralded by the classic symptoms of dyspnea or fatigue. These patients will require all the standard medications as outlined in previous sections (except for perhaps holding ACE-I when systolic BP <80 mm Hg), and may also require infusions of vasodilators or positive inotropic drugs (129) (Table 5).
IV vasodilators have long been used to treat the symptoms of low cardiac output in patients with decompensated chronic HF. In general, vasodilators reduce ventricular filling pressures and systemic vascular resistance while increasing stroke volume and cardiac output. Nitroglycerin is commonly used for this purpose and has been studied in numerous clinical trials (129). In addition, recombinant brain natriuretic peptide (BNP) has received regulatory approval as a drug (nesiritide), indicated for patients with acute HF and dyspnea. Nesiritide binds to A- and B-type natriuretic peptide receptors on endothelial and vascular smooth muscle cells. It produces venous and arterial dilation, with subsequent reductions in preload and afterload, through increasing cGMP. Nesiritide does not increase heart rate, and has no effect on cardiac inotropy. Nesiritide exerts diuretic and natriuretic effects and causes coronary vasodilation. It has a rapid onset of action with a distribution half-life of 2 min and a terminal elimination half-life of 18 min. Onset of the drug's effects is later than would be predicted based on its pharmacokinetic parameters. For example, with an initial loading dose and maintenance infusion, only 60% of the reduction in pulmonary wedge pressure that will be measured at 3 h is achieved 15 min after the bolus dose (130). Clinical effects have also been observed to persist longer than would be anticipated (based on drug levels) after the drug is discontinued.
Nesiritide is metabolized by three mechanisms: endocytotic internalization by its surface receptor, hydrolysis by neutral endopeptidase, and renal excretion (minor role) (131). When initiated in the perioperative setting (e.g., post-CPB), a starting infusion dose of 0.005 μg · kg−1 · min−1, without a bolus, is recommended to avoid hypotension in patients with increased filling pressures and low systemic vascular resistance (<800 dyne · s · cm−5) who might also be receiving ACE-I and β-adrenergic blockers. Studies have shown that nesiritide reduces symptoms of acute decompensated HF similarly to nitroglycerin, including a reduction of pulmonary artery pressure, without development of acute tolerance (132). In early studies, patients receiving nesiritide experienced fewer adverse events than those receiving nitroglycerin (133). Compared with dobutamine, nesiritide was associated with fewer instances of ventricular tachycardia or cardiac arrest (134). In the ADHERE registry (135) of more than 65,000 episodes of acute decompensated HF, treatment with either nesiritide or a vasodilator was associated with a 0.59 odds ratio for mortality compared with either milrinone or dobutamine. Recent data, however, suggest that not only may nesiritide not offer a compelling safety advantage, it may also be associated with an increased incidence of adverse side effects, including renal failure and mortality, when administered to patients with acutely decompensated chronic HF (136,137). These publications prompted the Food and Drug Administration to convene an expert panel, which made several recommendations, including that nesiritide be used only for hospitalized patients with acute decompensated HF and that the drug not be used to enhance diuresis or to “protect” the kidneys (138).
Clinical trials showed that chronic treatment with positive inotropes such as inamrinone and milrinone led to increased mortality (139–141). Nevertheless, positive inotropic drugs, principally dobutamine or milrinone, have long been used to treat decompensated HF (Fig. 4). There is a lack of data supporting their discretionary administration (142), e.g., on a monthly schedule to patients awaiting cardiac transplantation to avoid the need for ventricular assist devices. Levosimendan, a new cAMP-independent positive inotrope, may prove to have no negative outcome effects when used to treat acute decompensation of chronic HF (143). Levosimendan acts by increasing myocyte sensitivity to calcium via stabilizing the calcium-bound conformation of troponin C (Fig. 5). Levosimendan also opens KATP channels in vascular smooth muscle inducing vasodilation and in cardiac muscle, where these channels may protect against ischemia (144). When compared with dobutamine, levosimendan reduced 1-mo mortality (and reduced mortality compared with placebo at 14 days (145). Calcium sensitivity is increased during systole without causing calcium overload during diastole. This results in enhanced inotropic performance and preserved diastolic performance.
When drug treatment proves unsuccessful, HF patients may require invasive therapy, including ventricular assist devices, resynchronization with biventricular pacing, coronary bypass with or without surgical remodeling, or even cardiac orthotopic transplantation (146). These important modalities are beyond the scope of this review.
For most patients, the diagnosis of HF will have been made long before they arrive for surgery or intensive care. Current guidelines provide a helpful framework by which primary care physicians and cardiologists can make the appropriate diagnoses and follow the disease process over time (6). On the other hand, how does a perioperative physician determine quickly, conveniently, and inexpensively whether a dyspneic patient's symptoms are the result of new or worsening HF, lung disease, or a combination of the two? Clearly the issue can be settled using the medical history and physical examination, electrocardiogram, echocardiogram, chest radiograph, and consultation with either a pulmonary medicine specialist or cardiologist. On the other hand, measurements of BNP in blood are widely used to help triage patients presenting with acute dyspnea (147). Taken together with physical examination and history, if the BNP is <100 pg/mL, then HF is highly unlikely; negative predictive value, 90%, and if the BNP level is >500 pg/mL, then HF is highly likely, positive predictive value is 90%. For BNP levels of 100–500 pg/mL, one must consider whether the baseline is increased as a result of advanced age, underlying stable left ventricular dysfunction, right ventricular failure secondary to pulmonary hypertension or acute pulmonary embolism (148,149).
Current guidelines begin pharmacotherapy of HF with primary prevention of left ventricular dysfunction (6,7) (Fig. 1). Because hypertension and coronary artery disease are leading primary causes of left ventricular dysfunction, adequate control of both hypertension (according to the Joint National Committee-7 guidelines) (150) and hypercholesterolemia has been endorsed after encouraging results in prevention trials (151). ACE inhibitors, and possibly β-adrenergic blockers, should be initiated in diabetic, hypertensive, and hypercholesterolemia patients (AHA/ACC, Stage A HF) who are at increased risk for CV events, despite normal contractile function, to reduce the onset of new HF (HOPE trial) (30). In patients with asymptomatic left ventricular dysfunction (EF ≤ 40%) (Stage B), treatment with ACE inhibitors and β-adrenergic blockers can blunt the disease progression. In the symptomatic HF patient (Stage C), diuretics are titrated to relieve symptoms of pulmonary congestion and peripheral edema and to restore a normal state of intravascular volume (152). ACE inhibitors and β-adrenergic blockers are recommended to blunt disease progression. Although digoxin has no effect on patient survival, it may be considered in Stage C if the patient remains symptomatic despite adequate doses of ACE inhibitors and diuretics. An alternative for patients (particularly African-American patients) with systolic dysfunction and contraindications, intolerance, or unresponsiveness to ACE inhibitors or ARBs is isosorbide dinitrate three times a day in combination with hydralazine three times a day (153) or BiDil (fixed dose combination of isosorbide dinitrate and hydralazine hydrochloride (A-HeFT trial) (31). The use of an NO donor (isosorbide) in HF heralds the new suggestion that “NO balance” may be important in the pathophysiology of HF (154).
In general, the primary treatment objectives for Stages A–C HF are: 1) improved quality of life, 2) reduced morbidity, and 3) reduced mortality. At this time, the most important way to improve long-term outcome is through inhibiting disease progression by counteracting neurohormonal effects. Pharmacologic therapy in patients with severe, decompensated HF (Stage D) is based on hemodynamic status. Symptomatic treatment with diuretics, vasodilators, and, in palliative circumstances, IV inotropic infusions is added to “standard” treatment. Finally, some of these patients may require device therapies or surgical procedures, such as cardiac transplants.
What is an anesthesiologist to do when faced with a patient with Stage D or decompensated Stage C HF who requires emergency surgery? If tracheal intubation and positive pressure ventilation are needed to manage pulmonary edema, then there is little reason to select a regional anesthesia technique. When feasible (this will be rare because these patients often cannot lie flat on the operating table), regional nerve block techniques, rather than general anesthesia or neuroaxial block techniques, may avoid intraoperative crystalloid infusions. There is no evidence basis by which to select either an induction or a maintenance anesthetic drug in these patients. We have successfully used most IV induction drugs in these patients (including thiopental, propofol, ketamine, etomidate, midazolam, and diazepam) and have seen no obvious reason to recommend any one of them over the others. Similarly, while many authors advocate maintaining anesthesia in these very sick patients using benzodiazepines and opioids, our usual practice is to maintain anesthesia with inhaled anesthetics. We find intraoperative fluid and medical management considerably more challenging than anesthetic choice in these patients. Accordingly, when HF patients must undergo major surgery, we suggest invasive arterial BP monitoring and transesophageal echocardiography (TEE) to help guide intraoperative decision-making. TEE is especially useful in diagnosing whether hypotensive episodes are the result of inadequate circulating blood volume, worsening ventricular function, or arterial vasodilation (155–157). Pulmonary artery catheters have long been used in these patients for this purpose; if TEE is not available, pulmonary artery catheters may be a useful, if controversial, alternative (158).
Large volumes of blood, colloid, or crystalloid should be used to treat hypotension in HF patients only when there is a reasonable suspicion that true hypovolemia is present. This advice may be even more important for patients receiving spinal or epidural anesthesia (in the latter case there seems to be an even greater tendency to use IV fluid/colloid/blood rather than vasoactive drugs to treat hypotension). Patients receiving loop diuretics on an outpatient basis may prove refractory to the usual IV doses of furosemide and continuous infusions of furosemide (20 mg/h) or nesiritide (0.005–0.01 μg · kg−1 · min−1) may be needed. Finally, transfusion for perioperative anemia in a hemodynamically stable patient with a history of HF (e.g., stage C) must be approached with greater caution than usual. It is easy to produce intravascular volume overload in these patients (159).
When we consider our aging patient population in which prolonged survival with hypertension and/or coronary artery disease is expected and the better HF treatment strategies now available to them, we conclude that anesthesiologists will encounter an increasing number of patients with either a predisposition to HF (stages A and B) or a history of HF (stages C and D). Thus, knowledge of the evolving pharmacologic strategies for the management of chronic HF is essential both for patient care and for our continued credibility as perioperative physicians.
Abbreviations for Trials and Registries: ADHERE: Acute Decompensated Heart Failure National Registry, A-HeFT: African-American Heart Failure Trial, ATLAS: Assessment of treatment with lisinopril and survival, BEST: β-Blocker evaluation of survival study, CHARM: Candesartan in heart failure assessment in reduction of mortality, CIBIS: Cardiac insufficiency bisoprolol study, COMET: Carvedilol or metoprolol European trial, CONSENSUS: Cooperative North Scandinavian Enalapril Survival Study, COPERNICUS: Carvedilol prospective randomized cumulative survival, DIG: Digitalis Investigation Group, ELITE: Evaluation of losartan in the elderly, EPHESUS: Eplerenone post-MI heart failure efficacy and survival study, GISSI: Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico Investigators, HOPE: Heart outcomes prevention evaluation, I-PRESERVE: Irbesartan in heart failure with preserved systolic function, ISIS: International study of infarct survival, MERIT-HF: Metoprolol CR/XL randomized intervention trial in congestive heart failure, PROVED: Prospective randomized study of ventricular function and efficacy of digoxin, RALES: Randomized aldactone evaluation study, RADIANCE: Randomized assessment of digoxin or inhibitors of the angiotensin-converting enzyme, SAVE: Survival and ventricular enlargement, SOLVD: Study of left ventricular dysfunction, US CARVEDILOL: United States carvedilol, V-Heft: Veteran's Administration Heart Failure Trial, Val-HeFT: Valsartan in heart failure trial.
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