Heart Failure: Pathophysiology, Risk Assessment, Community Management PDF

Heart failure: pathophysiology, risk assessment, community management and anaesthesia Alwyn Kotzé MB ChB FRCA Simon J. Howell MA FRCA MRCP(UK) MSc MD...

Heart failure: pathophysiology, risk assessment, community management and anaesthesia Alwyn Kotzé MB ChB FRCA Simon J. Howell MA FRCA MRCP(UK) MSc MD Key points Heart Failure is a common and serious condition that increases perioperative risk Heart failure is a complex clinical syndrome The mechanisms underlying ventricular dys- significantly. caused by impaired ventricular performance. It function are death or dysfunction of cardiac Patients with heart failure is the final common pathway for a variety of myocytes and longstanding pressure or volume have a vulnerable cardiovascular disease processes, leading to overload. As myocardial contractility decreases, myocardium and a circulation potentially disabling symptoms and shortened the stroke volume drops and the end-diastolic that is dependent on life expectancy.1 Heart failure is common; cur- volume and pressure increase. This, according sympathetic nervous system rently, 1% of the population aged 50 –59 yr, to the Frank-Starling law, will restore myocar- activation. and 10% of those over 80 yr, have heart dial contractility and thus cardiac output. If sus- Perioperative risk is failure.2 Heart failure is the only major cardio- tained in the long-term, this volume increase proportional both to the vascular condition that is increasing in preva- leads to what is termed cardiac remodelling. severity of the patient’s heart lence, because of an ageing population and This involves myocardial hypertrophy, chamber failure and the surgical risk. improved survival from other cardiovascular enlargement and an increase in ventricular wall The medical management of diseases.2 Therefore, increasing numbers of stress, and increases oxygen demand. An heart failure is aimed at patients with established heart failure will increase in ventricular stiffness also occurs due preventing disease present for surgery. to increased collagen deposition in the heart, progression. The benefits of A diagnosis of heart failure has serious which impairs filling and exacerbates the long-term therapy should be implications. If the underlying cause cannot be situation.1 maintained perioperatively where possible. rectified, heart failure alone has a 50% 4 The decrease in cardiac output leads to sym- yr-mortality, and 50% of patients with severe pathetic activation and stimulation of the renin– There is no strong evidence heart failure (those who are symptomatic and angiotensin–aldosterone (RAAS) system, with that any one anaesthetic require frequent medical attention) will die salt and water retention and an increase in circu- technique is superior for patients with heart failure. within 1 yr of diagnosis.3 Decompensated heart lating volume. This will initially restore cardiac failure is a major clinical predictor of perio- output, again in accordance with the Frank– Close attention to fluid perative risk.4 If heart failure is present at the Starling law. However, it also compounds the balance and cardiovascular time of major vascular surgery, the risk of injury to the heart and leads to a vicious cycle stability is essential to prevent an acute exacerbation of cardiac death is 12 times higher than in patients of increased and inefficient cardiac energy heart failure or other major without heart failure.5 expenditure and reduced myocardial perfusion, cardiovascular morbidity. This article will describe the pathophysio- particularly in the subendocardial region.1 2 logy, diagnosis and anaesthetic implications of The combination of cardiac remodelling and Alwyn Kotzé MB ChB FRCA heart failure in the setting of non-cardiac the vicious neurohumoral cycle results in a Consultant surgery. myocardium vulnerable to ischaemia and a cir- Department of Anaesthesia culation which is dependent on sympathetic Airedale General Hospital tone (Fig. 1). Steeton BD20 6TD Pathophysiology UK Tel: þ44 (0)1535 292185 Ischaemic heart disease and hypertension are Fax: þ44 (0)1535 292162 Diagnosis and staging E-mail: [email protected] the two most important causes of heart failure (for correspondence) in the Western world. Other common causes The diagnosis of heart failure requires the pre- include diabetes mellitus, valvular heart disease sence of clinical signs and symptoms and objec- Simon J. Howell MA FRCA MRCP(UK) (especially aortic stenosis and mitral regurgita- tive evidence of ventricular dysfunction.3 The MSc MD tion) and other cardiomyopathies.1 Infective Senior Lecturer in Anaesthesia symptoms and signs may be difficult to inter- Academic Unit of Anaesthesia and nutritional causes are still common in the pret, and are not in themselves enough to make Leeds General Infirmary developing world. Advanced age and male a diagnosis of heart failure.3 Furthermore, the Leeds LS25 5EG gender are also risk factors (Table 1).1 pattern of symptoms is not always the same. UK doi:10.1093/bjaceaccp/mkn028 Advance Access publication August 25, 2008 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 8 Number 5 2008 161 & The Board of Management and Trustees of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected] Heart failure assay of serum Brain Natriuretic Peptide) may provide additional information. The American College of Cardiology and American Heart Association (ACC/AHA) guidelines for heart failure management include a four-stage classification that emphasizes interventions to slow disease progression (Table 2).6 Risk assessment Surgery-specific risk factors A commonly used classification of surgical risk is detailed in the ACC/AHA guidelines.4 Surgery is classified as low-risk and inter- mediate risk, corresponding to the potential for perioperative haemodynamic changes, fluid shifts and the likely severity of the Fig. 1 The pathophysiology of heart failure. RAAS, renin– angiotensin – stress response to surgery. In the 2007 guidelines, open aortic aldosterone system. surgery and peripheral vascular surgery are considered as high-risk (Table 3). Table 1 Causes of heart failure Mechanism Disease process Patient risk factors Detailed enquiry into the patient’s functional capacity gives an Myocyte death Ischaemic heart disease Toxins, e.g. alcohol, antineoplastic drugs indication of their cardiovascular reserve, unless exercise capacity Infective cardiomyopathy, including viral myocarditis, AIDS is compromised by disease of other systems (e.g. pulmonary, peri- Infiltrative conditions, e.g. sarcoid, cardiac neoplasms pheral vascular, musculoskeletal). Limitation of exercise tolerance Idiopathic dilated cardiomyopathy Age-related cardiomyopathy (apoptotic cardiomyopathy) to less than that required to climb one flight of stairs without rest Myocyte Pregnancy-related cardiomyopathy (exercise that equates to four metabolic equivalents or METS) is a dysfunction recognized marker for cardiovascular disease and a predictor of Nutritional deficiencies Endocrine disorders, e.g. chronic thyrotoxicosis, acromegally risk. Perioperative cardiovascular risk is inversely proportional to Circulatory Valvular heart disease: rheumatic, congenital, senile maximal functional capacity.4 Objective measurement of maximal dysfunction calcification, infective endocarditis oxygen consumption with treadmill or bicycle exercise testing may Restrictive pericardial disorders High output heart failure, e.g. protracted severe anaemia, be useful in patients with poor functional capacity, or if high-risk arteriovenous malformation surgery is planned.4 Pressure overload, e.g. severe hypertension An echocardiogram provides measurements of both systolic and diastolic function. The left ventricular ejection fraction (LVEF) is the most commonly used measure of systolic function. An LVEF.50% is regarded as good, ,40% as abnormal and ,30% as an Some patients have functional limitation but little evidence of fluid indication of severe LV dysfunction. A decreased LVEF has been retention, whereas others complain primarily of oedema and report found to be a predictor of perioperative mortality and morbidity, few symptoms of dyspnoea or fatigue.6 The patient with symptoms with the highest risk group being those with an LVEF ,35%.4 suggestive of ventricular dysfunction should be investigated as a Accurate calculation of the LVEF is operator-dependent, and matter of course. requires that the ventricle be uniform in shape. Subjective com- A normal ECG is very unusual in patients with heart failure, ments on ventricular motion may be all that is possible in some and should prompt review of the diagnosis.3 Key ECG findings are cases. Currently, the ACC and AHA do not recommend periopera- chamber hypertrophy, ventricular strain patterns and signs of tive transoesophageal echocardiography solely to predict risk. It ischaemia or previous infarction. Atrial fibrillation is also common gives no additional information over transthoracic imaging, but in heart failure patients. may offer improved image quality if the transthoracic sonographic Echocardiography is a key investigation,6 as it allows assess- windows are poor (e.g. in the obese or in ventilated patients). ment of severity of myocardial dysfunction, and may also diagnose the cause (e.g. valvular disease, hypertrophic cardiomyopathy). It is technically challenging and very operator-dependent. In particu- Medical management lar, assessment of ventricular function is often subjective. The vicious neurohumoral cycle of RAA system activation, More detailed investigations of cardiac function and structure decreasing cardiac output and cardiac remodelling is the target for (e.g. cardiac MRI, coronary catheterization, radionucleotide scans, the long-term treatment of heart failure. 162 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008  Heart failure Table 2 ACC/AHA guidelines for long-term management of heart failure in adults. AT1, angiotensin 1 receptor Reprinted with permission. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult—Summary Article A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): Developed in Collaboration With the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: Endorsed by the Heart Rhythm Society. (Circulation 2005;112:1825 –52.). &2005, American Heart Association, Inc. The only ‘cure’ for early heart failure remains definitive treat- severe hypotension in patients taking ACE inhibitors, when the ment of the cause, or heart transplantation if the disease has pro- raised sympathetic tone of heart failure is attenuated during anaes- gressed. Medical management is directed at decreasing symptoms thesia. This was reported in 22% of patients in one study, if the and preventing disease progression.3 Drugs used in the treatment ACE inhibitor was given less than 10 h before surgery.6 On the of heart failure have significant implications for perioperative care. other hand, there is evidence that recovery of the RAA system can be quick, and deleterious to both the myocardium and kidneys,2 and that hypotension associated with ACE inhibitors and general Angiotensin-converting enzyme inhibitors anaesthesia is relatively easy to rectify.7 In addition, there is cur- Angiotensin-converting enzyme (ACE) inhibitors are rec- rently no parenteral formulation of an ACE-inhibitor available. ommended as first-line treatment for the patient with left ventricu- A decrease in venous return or co-administration of negative lar dysfunction, with or without symptoms. They have been shown inotropic drugs such as amiodarone may exaggerate hypotension to decrease the risk of myocardial infarction and death in patients under anaesthesia, whether ACE inhibitors are withdrawn or not.2 with symptomatic heart failure.2 Patients may also be taking ACE Hypotensive episodes during anaesthesia are first treated with con- inhibitors for the treatment of hypertension without heart failure. ventional vasopressors or sympathomimetics and cautious expan- There is continuing controversy over how to manage periopera- sion of intravascular volume. Rarely, particularly in association tive ACE inhibition.2 On the one hand, there is concern over with high-dose ACE inhibitor treatment and neuraxial blockade, an Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008 163 Heart failure Table 3 ACC/AHA classification of surgical risk resolution of symptoms.3 Angiotensin receptor (AT) blockers are Risk stratification Procedure examples relatively long-acting competitive inhibitors of the actions of angiotensin II at the AT1 receptor.2 Vascular (High) (reported cardiac risk Aortic and other major vascular surgery During anaesthesia, blood pressure may become angiotensin- often more than 5%*) Peripheral vascular surgery dependent, particularly in hypovolaemic patients.9 As is true for Intermediate (reported cardiac risk Intraperitoneal and intrathoracic surgery patients on ACE inhibitors, those taking AT blockers are thus more generally 1% to 5%*) prone to hypotension during anaesthesia. These hypotensive spells Carotid endarterectomy Head and neck surgery may be resistant to first-line sympathomimetics where high-dose Orthopaedic surgery AT blockers have been used preoperatively and drugs such as nore- Prostate surgery pinephrine or vasopressin are sometimes required in this situation.2 Low (reported cardiac risk generally less Endoscopic procedures than 1%*) The hypotension is also sometimes associated with bradycardia, Superficial procedures which has led some authors to recommend prophylactic glycopyr- Cataract surgery rolate before anaesthesia in AT-blocked patients.2 11 The same Breast surgery Ambulatory surgery concerns as with ACE inhibitors over ARF in patients with hypo- volaemia or renal dysfunction apply.10 *Combined incidence of cardiac death and non-fatal myocardial infarction. A decision to continue AT blockers in the perioperative period Reprinted with permission. ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for may be made subject to the same cautions as with ACE inhibitors. Noncardiac Surgery: Executive Summary. If an AT-blocker is withdrawn perioperatively, the drug should be A Report of the American College of Cardiology/American Heart Association Task stopped at least 24 h before surgery, as the duration of action is Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). prolonged.2 (Circulation 2007;116:1971– 1996.). &2007, American Heart Association, Inc. Beta-adrenoreceptor antagonists infusion of phenylephrine, norepinephrine or epinephrine may be All patients with chronic, stable heart failure and without con- needed.2 traindications should be considered for treatment with beta- Another concern over the perioperative use of ACE inhibitors is adrenoreceptor antagonists (beta-blockers). The beta-blockers now ACE-inhibitor-induced acute renal failure. This occurs when glo- recommended for use in chronic heart failure are metoprolol, biso- merular afferent arteriolar blood flow is reduced (e.g. hypovolae- prolol and carvedilol.11 These drugs reduce hospital admissions, mia), and the glomerular filtration rate (GFR) therefore becomes prevent disease progression and improve long-term survival in dependent on angiotensin-II-mediated efferent arteriolar vasocon- heart failure after cardiac ischaemia.3 striction. GFR in an ACE-inhibitor treated kidney is blood There is consensus that withdrawing long-term beta-blocker pressure-dependent, and most ACE inhibitors are renally excreted. treatment in the perioperative period is harmful.2 4 Therefore, sub- This can cause a vicious cycle of accumulation and further hypo- stitution with intravenous beta-blockers should be considered if tension, resulting in renal failure.8 Regular monitoring of renal prolonged fasting is anticipated. There is much less clarity about function is recommended, particularly on initiation of treatment whether new beta-blockade in the perioperative period is indicated. and during hospital admissions.3 While there is some evidence that it is useful for the prevention of If significant fluid or blood loss is anticipated, or if the patient cardiac ischaemia and arrhythmias in certain patient groups,4 there develops renal dysfunction in the postoperative period, stopping is no equivalent evidence for heart failure. ACE inhibitors may theoretically be beneficial. In this situation, While beta-blockers are helpful in the long-term, in the short- substitution with oral nitrate and hydralazine therapy may provide term they limit the sympathetic response. This can prevent com- comparable cardiac benefits, although potentially at the cost of pensation for hypovolaemia, sepsis or the myocardial depressant exacerbating hypotension. effects of many anaesthetic agents. Therefore, hypotension is fre- The decision whether to continue or stop ACE inhibitors in the quent and relatively resistant to simple sympathomimetics. Should perioperative period must be judged on a case-by-case basis. It inotropic support be necessary, phosphodiesterase inhibitors may may be safe to continue therapy unless major blood loss is antici- prove useful as second line after beta-agonists.12 pated, the patient becomes hypovolaemic, or renal dysfunction develops. Diuretics Diuretics are very useful for symptom control, and enhance the Angiotensin receptor antagonists antihypertensive effects of ACE inhibitors and beta-blockade, but These drugs are indicated as an alternative in symptomatic heart there is no strong evidence that diuretic therapy improves survival failure patients who are intolerant to ACE inhibitors, or in combi- in heart failure.3 Chronic therapy can lead to electrolyte abnormal- nation where ACE inhibitors and beta-blockers do not give a ities, hypovolaemia and arrhythmias, particularly in the elderly.2 164 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008  Heart failure This can exacerbate heart failure. Conversely, patients who are nil Anaesthetic management by mouth and therefore omitting diuretics may retain fluid and also develop pulmonary congestion.3 Close attention to perioperative The anaesthetic management of patients with heart failure depends fluid and electrolyte balance is essential whether diuretics are con- on (i) the degree of heart failure, (ii) the cause and nature of the tinued or stopped. cardiomyopathy and (iii) the surgical procedure. Anaesthesia for patients with Stage A and B heart failure centres on avoiding drug interactions with their long-term therapy, Digoxin and maintenance of the benefits of such therapy throughout the Digoxin is most often used for symptom control in patients who are perioperative period. Drugs that worsen heart failure should be still symptomatic despite treatment with ACE inhibitors, beta- avoided if possible, and close attention should be paid to fluid blockers and diuretics. It is also used for the management of the ven- balance, analgesia, maintenance of normothermia and sinus tricular rate in AF, a common problem in heart failure.2 Digoxin is rhythm, and optimal treatment of any co-morbid conditions. the only positively inotropic drug that does not increase mortality Patients with Stage C and D heart failure present significant chal- when used as maintenance heart failure treatment. Though digoxin lenges of perioperative fluid and medical management in addition to confers no long-term survival benefit, withdrawal of digoxin therapy the challenges of anaesthesia.2 There is little evidence that any one may increase the incidence of acute heart failure exacerbations. anaesthetic technique is superior to another in this group.1 2 Digoxin has a narrow therapeutic index, and digoxin toxicity ‘Stable’ anaesthesia, with as little myocardial depression or can be difficult to diagnose and treat. Conditions that make change in afterload as possible, is a reasonable goal for patients digoxin toxicity more likely include hypomagnesaemia, hypercal- with heart failure. Traditionally, cardiovascularly ‘stable’ agents caemia, and hypokalaemia, all of which may occur during the peri- such as etomidate and benzodiazepines have been advocated, both operative period.2 Digoxin therapy has also been found to be for induction and maintenance. There is little evidence for this, associated with mortality and serious morbidity in patients under- and the use of most i.v. induction drugs and volatile agents have going urgent or emergency surgery, even after adjusting for the been described in heart failure patients.2 severity of heart failure.8 The majority of patients with disabling heart failure (Stage D, There are published recommendations both to continue1 and or symptomatic Stage C) are dependent on their preload to main- stop2 digoxin therapy before surgery. If digoxin is stopped peri- tain ventricular filling. Many patients with heart failure also rely operatively, heart rate control and positive inotropy should be on increased sympathetic tone to maintain tissue perfusion and maintained with other drugs. Should perioperative digoxin therapy cardiac output.1 Induction, emergence and fluid shifts during the be considered essential, close monitoring of serum electrolytes and perioperative period may cause the pre- or afterload to move digoxin concentrations is necessary. outside the narrow range in which the patient functions. Though there is no strong evidence published that invasive arterial and Other inotropes central venous monitoring improves outcome, information from these monitors may help the anaesthetist to anticipate or limit An increase in intracellular cyclic AMP may be achieved with these changes. In addition, a means of estimating cardiac output beta-agonists or phosphodiesterase inhibitors. As the long-term use may prove useful.2 of these drugs has been found to be associated with worse survival, Regional techniques are an alternative to general anaesthesia they are reserved for patients with severe heart failure.1 Patients for certain procedures. The sympatholysis associated with neuraxial receiving inotropic support are likely only to present to the anaes- blockade may cause severe hypotension, especially if ACE inhibi- thetist in the intensive care setting or in specialist centres, for con- tors or AT blockers have been continued preoperatively.2 However, sideration of transplant or ventricular reduction surgery. a moderate reduction in afterload may increase cardiac output without increasing oxygen demand. The superior analgesia associ- Timing of surgery ated with well-functioning regional techniques may also limit The correct timing of elective non-cardiac surgery is important to hypertensive spells, tachycardia and cardiac ischaemia postopera- decrease patient risk. The ACC/AHA guidelines identify decom- tively. Peripheral nerve block techniques have similar advantages pensated or untreated heart failure as a major clinical predictor of and disadvantages. Despite these considerations, there is no strong risk. Where possible, surgery should be postponed for the purpose evidence that either regional or general anaesthesia leads to of medical therapy, modification of risk factors and further investi- improved survival after surgery in patients with heart failure. gations (including coronary angiography, if appropriate).4 Compensated heart failure, or a history thereof, represents an inter- mediate clinical predictor. Low-risk surgical procedures can safely References continue, but formal assessment of the patient’s functional capacity 1. Magner JJ, Royston D. Heart Failure. Br J Anaesth 2004; 93: 74– 85 should be considered if intermediate risk or vascular surgery is 2. Groban L, Butterworth J. Perioperative management of chronic heart planned.4 failure. Anesth Analg 2006; 103: 557–75 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008 165 Heart failure 3. Swedberg K, Cleland J, Dargie H, et al. European Society of 8. Sear JW, Howell SJ, Sear YM, et al. Intercurrent drug therapy and perio- Cardiology Guidelines for the diagnosis and treatment of chronic heart perative cardiovascular mortality in elective and urgent/emergency surgi- failure: executive summary (update 2005). Eur Heart J 2005; 26: cal patients. Br J Anaesth 2001; 86: 506–12 1115– 40 9. Colson P, Ryckwaerdt F, Coriat P. Renin angiotensin system antagonists 4. American College of Cardiology and American heart Association. and anesthesia. Anesth Analg 1999; 89: 1143–52 ACC/AHA 2007 Guidelines on perioperative cardiovascular 10. Main J. Atherosclerotic renal artery stenosis, ACE inhibitors, and avoid- evaluation and care for noncardiac surgery. Available from http:// ing cardiovascular death. Heart 2005; 91: 548– 52 www.americanheart.org/presenter.jhtml?identifier=3004542 (accessed December 2007) 11. López-Sendó J, Swedberg K, McMurray J, et al. Expert consensus docu- ment on ß-adrenergic receptor blockers: The Task Force on 5. Sprung J, Abdelmalak B, Gottlieb A, et al. Analysis of risk factors for Beta-Blockers of the European Society of Cardiology. Eur Heart J 2004; myocardial infarction and cardiac mortality after major vascular surgery. 25: 1341–62 Anesthesiology 2000; 93: 129– 40 12. Metra M, Nodari S, D’Aloia A, et al. Beta-blocker therapy influences 6. American College of Cardiology. ACC/AHA 2005 Guideline update for the hemodynamic response to inotropic agents in patients with heart the diagnosis and management of chronic heart failure in the adult. failure: a randomized comparison of dobutamine and enoximone Available at http://content.onlinejacc.org/cgi/reprint/46/6/e1 (accessed before and after chronic treatment with metoprolol or carvedilol. J Am November 2007) Coll Cardiol 2002; 40: 1248– 58 7. Comfere T, Sprung J, Kumar MM, et al. Angiotensin system inhibitors in a general surgical population. Anesth Analg 2005; 639: 636–44 Please see multiple choice questions 10 –13 166 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 8 Number 5 2008