updates on perioperative management of heart failure

Updates on Perioperative Management of Heart Failure Patients Presenting

for Non-Cardiac Surgery

LESSON 7Volume 4210/21/2021*

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79Curr Rev Clin Anesth 42(7): 77-92 2021

Updates on Perioperative Management of Heart Failure Patients Presenting

for Non-Cardiac Surgery

Sandeep Khanna, MDAssistant Professor

Department of Cardiothoracic Anesthesiology Department of General Anesthesiology

Department of Outcomes Research Cleveland Clinic Foundation

Cleveland, Ohio

LESSON OBJECTIVES

Current Reviews in Clinical Anesthesia® designates this lesson for 1½ CME contact hours in Pharmacology/Therapeutics.

Upon completion of this lesson, the reader will be able to: 1. Define, classify and stage Heart Failure. 2. Describe the advantages and disadvantages of the NYHA classification. 3. Explain the process of diagnosing Heart Failure. 4. Identify treatment modalities for Heart Failure. 5. Illustrate the mechanism of action of Sacubitril/valsartan. 6. List indications and contraindications for Sacubitril/valsartan. 7. Describe the mechanism of action of Ivabradine. 8. Identify the perioperative implications of Sacubitril/valsartan and Ivabradine. 9. Manage the perioperative medication in a Heart Failure patient.10. Construct a perioperative plan for Heart Failure patients.

Introduction Heart failure (HF) presently afflicts more than 6 million adults in the United States, and projections suggest that by 2030 9 million patients will seek care for heart failure. The increasing prevalence of HF has been attributed to an ageing population. Additionally, introduction of innovative technolo-gies for treatment (such as specialized mechanical circulatory support devices) and prolonged survival in patients with cardiovascular disorders (includ-ing coronary artery disease and cardiomyopathy) is creating circumstances wherein anesthesiology teams are likely to encounter HF patients seek-ing surgical care. Despite advancements in clini-cal care, the 5 year mortality rate after a hospital-

ization related to HF remains high at 40-50%. In 2013, the American College of Cardiology/American Heart Association (ACC/AHA) introduced guide-lines for management of HF; a focused update was released in 2017.

Definition, Classification and Staging of Heart Failure

HF is a progressive clinical syndrome that is char-acterized by compromised cardiac performance. Diminished cardiac function can be related to im-paired ejection of blood and/or ventricular filling. The ensuing systolic and diastolic dysfunction pre-


cipitate symptoms such as dyspnea, decreased ex-ercise tolerance and fatigue.

Currently, ejection fraction (EF) is used to de-fi ne various types of heart failure (Table 1). The adoption of EF as a defi ning characteristic of HF recognizes that most HF eventually affects left ventricular function. This defi nition also acknowl-edges that EF can change over time and endeavors to account for EF variability. Let us take the exam-ple of a 70 year old woman who suffers an acute an-terior myocardial infarction related to left anterior descending artery thrombosis. Her baseline EF decreases from 60% to 30%. Loss of myocardium leads to a decline in pumping capacity, systolic dys-function and reduced EF. Over time, pathophysi-ologic remodeling, fi brosis, and scarring lead to a stiff left ventricle and diastolic dysfunction. Con-sequently, adequate fi lling of her left ventricle ne-cessitates higher fi lling pressures. When assessed 3 years after the episode of myocardial infarction, her EF has recovered to 48% with guideline di-rected medical therapy, but her exercise tolerance remains decreased due to her diastolic impairment.

Systolic and diastolic abnormalities often co-exist in Heart Failure patients, regardless of their Ejection Fraction.

While terms such as systolic/diastolic or con-gestive heart failure have been commonly used to describe the type of HF, we now recognize that patients labeled with systolic HF invariably have measurable diastolic dysfunction and vice a versa, especially if newer echocardiography modalities such as strain and tissue Doppler imaging are em-

ployed for evaluation. In addition to the EF based defi nition, HF can

be classifi ed on the basis of functional status. The New York Heart Association (NYHA) defi nes four functional classes of HF independent of EF. These functional classes are based on the presence of symptoms such as shortness of breath, fatigue, an-ginal pain and palpitations, and are categorized in relation to level of activity. Additionally, other clas-sifi cation schema exist such as the Specifi c Activity Scale (Table 2).

NYHA functional classifi cation, fi rst published in 1928 and last updated in 1994, remains very popular for classifying HF. Despite its simplicity, it is able to assess effi cacy of treatment, prognosis for survival, and predict peak oxygen consumption. However, it is subjective and non-specifi c as non-cardiac conditions like emphysema, obesity, ane-mia, and neuromuscular diseases (such as myas-thenia) can compromise functional status and lead to fatigue and dyspnea with exercise. Additionally, ongoing treatment, disease progression, and altera-tions in loading circumstances invariably change the NYHA functional class, sometimes dramatical-ly. Lastly, what constitutes ordinary activity is un-clear and the subjective nature of the classifi cation may pose interpretation diffi culties. Going back to our prior example, let us assume that the 70 year old woman referred to above presented in cardio-genic shock during her massive anterior wall myo-cardial infarction. At presentation, her functional class would be NYHA IV. Yet, when assessed 3 years later at an offi ce visit, she reports she is able to swim leisurely with some shortness of breath.

In 2013, ACC/AHA introduced staging of HF. The staging highlights the progressive, yet irre-

Defi nition % EF Comments

HF with reduced EF (HFrEF) ≤ 40 Effi cacious therapies are currently present and well delineated.

HF with preserved EF (HFpEF) ≥ 50 To date, effi cacious therapies have not been identifi ed.

HF with preserved EF, improved > 40 Patients who had reduced EF in the past but now have a recovered EF

HF with preserved EF, borderline 41–49 Patients fall into an intermediate or borderline group

EF: Ejection fraction; HF: Heart failure; HFrEF: Heart failure reduced ejection fraction HFpEF: Heart failure preserved ejection fraction.

Table 1: Defi nition of Heart Failure


Functional Class

NYHA classifi cation Specifi c Activity Scale

I No limitation; ordinary physical activity does not precipitate HF symptoms

Can participate in activities that require ≥ 7 METs

II Slight limitation; ordinary physical activities cause HF symptoms. However, patient is asymptomatic and comfortable at rest

Can participate in activities that require ≥ 5 but < 7 METs

III Marked limitation; less-than-ordinary physical activities cause HF symptoms but the patient is comfortable at rest

Can participate in activities that require ≥ 2 but < 5 METs

IV Symptoms of HF are present at rest and are accentuated by activity

Unable to participate in activities that require > 2 METs

Table 2: Functional Classifi cation of Heart Failure

NYHA: New York Heart Association; METs: Metabolic equivalents

Stage of HF

Defi nition Examples Recommended Therapeutic Strategies

A At high risk for HF in the absence of structural heart disease or symptoms of HF.

Patients with hypertension, diabetes mellitus or meta-bolic syndrome.

Lifestyle modifi cation, statins, ACEI or ARB for patients with DM

B Structural heart disease is present. However, signs or symptoms of HF are absent.

Patients with previous myo-cardial infarction, asymptom-atic valvular disease such as bicuspid aortic valve with mild aortic stenosis and insuffi ciency

ACEI or ARB, beta- blockers as appropriate.

Interventions such as ICD placement, revascularization, or valvular surgery in select patients as appropriate.

C Structural heart disease with prior or current symptoms of HF.

Symptomatic valvular dis-ease such as presence of bicuspid aortic valve with dyspnea related to aortic stenosis and insuffi ciency

ACEI or ARB, beta-blockers, aldosterone antagonists and diuretics. In selected patients hydralazine/isosorbide dinitrate and/or digoxin.

Interventional therapies such as CRT, ICD placement, revas-cularization, or valvular surgery as appropriate.

D Refractory HF requiring specialized interventions.

NYHA Class IV patient with recurrent hospitalizations for HF

Chronic inotropes, heart trans-plant, temporary or permanent mechanical circulatory support, hospice or palliative care.

Table 3: Stages of Heart Failure


versible nature of HF, while recognizing that pa-tients can be in different functional classes; it also outlines treatment recommendations (Table 3).

NYHA functional classifi cation, although sim-ple to use, suffers from subjectivity.

In stark contrast to the NYHA classifi cation, HF patients cannot revert back to a previous stage but can progress to a higher stage. For example, a patient could be categorized as Stage C HF after suffering a myocardial infarction. Although the

NYHA class may vary from class I to class IV (de-pending upon her circumstances and symptoms), a patient is at risk of progressing to Stage D and cannot revert back to either Stage A or B. Stag-ing allows visualization of HF as a continuous, pro-gressive and irreversible process that commences as asymptomatic systolic or diastolic dysfunction (Stage A and B), progresses to a symptomatic state (Stage C) and culminates as advanced or end stage heart failure (Stage D).

The clinical diagnosis of HF usually applies to patients with Stage C and Stage D HF. Although imaging modalities like echocardiography and car-

Parameters evaluated Comments

History and Physical Examination Symptoms: Dyspnea on exertion, orthopnea or PND, abdominal swelling, fatigue and recent weight gain

Signs: Audible S3, lung rales, presence of pedal edema and/or ascites, raised JVP, +ve hepato-jugular refl ex

Acute HF patients may display pallor, peripheral cyanosis, cool extremities and labored breathing in addition to the signs and symp-toms associated with chronic HF

Modifi ed Framingham clinical criteria

Major Criteria: PND, orthopnea, elevated JVP, presence of S3, Cardiomegaly on CXR, Pulmonary edema on CXR, weight loss ≥ 4.5 kg in 5 days in re-sponse to presumed HF treatment

Minor Criteria: Bilateral leg edema, dyspnea on ordinary exertion, nocturnal cough, hepatomegaly, pleural effusion, tachycardia (HR > 120 beats/min)

Diagnosis requires 2 major or 1 major + 2 minor criteria

Laboratory evaluation BNP, liver and renal function tests, serum electrolytes, TSH, CBC, Urinalysis, HbA1C, lipid profi le

BNP < 100 pg/mL suggests that HF is UNLIKELY to be the cause of dyspnea

Other modalities Echocardiography

CXR

Stress testing

Left and Right heart catheterization

BNP: Brain natriuretic peptide; CBC: Complete blood count; CXR: Chest X-ray; HF: Heart Failure HR: Heart rate; JVP: Jugular venous pressure; PND: Paroxysmal Nocturnal Dyspnea, S3: Third heart sound; TSH: Thyroid stimulating hormone

Table 4: Diagnosis of Heart Failure


diac biomarkers (including brain natriuretic pep-tide) play an important role in evaluation, current-ly there is no single test that can reliably make the diagnosis of HF. The modifi ed Framingham clinical criteria are often used for diagnosing HF (Table 4).

Temporal defi nitions of HF are surprisingly ar-bitrary. While ‘chronic HF’ patients have had HF for some time (months), patients with symptoms and signs that have remained unchanged on cur-rent treatment, for at least 1 month are labeled as having ‘stable chronic HF’. Acute HF syndrome or decompensated HF, defi ned as a change in signs and symptoms of HF that necessitates urgent therapy and/or hospital admission, generally occurs when chronic stable HF worsens. Patients often present with increasing dyspnea secondary to severe pul-monary congestion, with or without a low cardiac

Diagnosis of Heart Failure relies mostly on conducting a thorough and careful clinical assessment.

output and diminished systemic perfusion. New onset or ‘de novo’ HF patients previously did not have signs and symptoms suggestive of HF. Pa-tients can present with sudden onset of symptoms (acute myocardial infarction) or subacutely (as in a patient with hypertrophic cardiomyopathy) and gradually develop exercise induced dyspnea. Ad-vanced or refractory HF is present when patients exhibit NYHA III-IV functional status, despite

optimal guideline directed management therapy, and suffer from recurrent episodes of pulmonary or systemic congestion, low cardiac output and/or ma-lignant arrhythmias causing 2 or more unplanned visits or hospitalizations in the last year.

Guideline Directed Management Therapy for Chronic Heart Failure

Guideline directed management therapy (GDMT) emphasizes the importance of lifestyle modifi ca-tions, pharmacotherapy, electrophysiologic strat-egies and surgical intervention for achieving op-timal outcomes in patients with chronic HF. A dysregulated neurohormonal response, activa-tion of the renin angiotensin aldosterone system (RAAS) and sympathetic nervous system in HFrEF lead to sodium and fl uid retention, ventricular re-modeling and vasoconstriction. Pharmacotherapy targets these dysregulated mechanisms to achieve clinical benefi t (Table 5, Figure 1). Drugs that have shown to have a morbidity and mortality benefi t in HFrEF patients include angiotensin converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs), beta-blockers, aldosterone an-tagonists and vasodilators (Table 5). As noted in Table 5, only specifi c beta-blockers have been shown to be effi cacious in HF. In heart failure with preserved ejection fraction (HFpEF), the mor-tality benefi t from a particular drug class is yet to be established. In such patients, clinical care is fo-

Figure 1: Role of Pharmacotherapy in Chronic Heart Failure with Reduced Ejection Fraction


cused on appropriately managing underlying con-ditions such as hypertension, coronary artery dis-ease (CAD), atrial fi brillation, sleep apnea, obesity

Reduction in mortality in HFrEF patients is greater with Sacubitril-valsartan when com-pared to ACEIs.

and kidney disease. Additionally, optimization of volume status with diuretics is encouraged. In 2017, the ACC/AHA incorporated two new class-es of medications as part of GDMT for patients in Stage C HFrEF: an angiotensin receptor-neprilysin inhibitor (ARNI), valsartan/sacubitril, and a sino-atrial node modulator, ivabradine.

Sacubitril/valsartan was approved in July 2015. This novel drug combination has a unique mecha-nism of action (Figure 2). It incorporates a nepri-lysin inhibitor, sacubitril, and the ARB, valsartan. Neprilysin, a neutral endopeptidase, metabolizes natriuretic peptides, bradykinin, and angiotensin II. Inhibition of neprilysin increases the levels of these vasoactive peptides, thereby providing ben-efi t by reducing vasoconstriction, sodium retention and remodeling. Addition of an ARB is necessary to prevent activation of the RAAS as levels of angio-tensin II also increase with neprilysin inhibition. Adverse reactions of ARNIs mimic those of ACEI and ARBs. Common side effects may include hypo-tension, hyperkalemia, increased serum creatinine, angioedema, cough, and renal failure. Additionally, ARNIs can cause profound vasodilatation and cau-

tious use in patients with aortic/mitral stenosis, re-nal artery stenosis, or renal/hepatic impairment is warranted.

ARNI use is recommended in patients with chronic symptomatic HFrEF NYHA class II or III in conjunction with beta-blocker therapy (Table 6). Patients who are already on ACEI or ARBs may benefi t from replacing those medications with an ARNI. However, ARNIs should not be administered with ACEIs or within 36 hours of the last dose of an ACEI due to the increased risk of angioedema.

Ivabradine, like sacubitril/valsartan, was ap-proved in 2015. It decreases the heart rate without compromising inotropy of the heart by selectively inhibiting the “funny current” or the I(f) ion chan-nel. This channel is predominantly expressed in the sinoatrial node, the atrioventricular node and the Purkinje fi bers and conducts the “funny cur-rent” (a mixed Na/K inward current that activates on hyperpolarization). Consequently, the funny current plays an important role in determining the rate of spontaneous activity of the sinoatrial node and, thereby, the heart rate.

Ivabradine is indicated in patients with stable, symptomatic, chronic HF with an EF of 35% or less and sinus rhythm with a resting heart rate ≥ 70 bpm (Table 6).

Patients with heart rates > 70 bpm suffer from increased rates of cardiovascular death and hospi-talization for heart failure. Addition of ivabradine in these select patients who demonstrate elevated heart rates, despite being on maximally tolerated beta-blocker therapy, is benefi cial. As it can precipi-

Figure 2: Mechanism of Action of the Angiotensin Receptor-Neprilysin Inhibitor Sacubitril/Valsartan


tate profound bradycardia, ivabradine is avoided in patients with resting heart rates < 60 bpm. Addition-ally, patients with baseline hypotension, decompen-sated HFrEF, and conduction abnormalities (such as sick sinus syndrome or third-degree heart block) are not suitable candidates for ivabradine therapy. Cautious use in patients with a prolonged QT in-terval is warranted as it can precipitate torsades de pointes, a life threatening polymorphic ventricular

Ivabradine can precipitate profound bradyar-rhythmias as well as polymorphic ventricular tachyarrhythmia in susceptible patients.

arrhythmia. Phosphenes, described as transient enhanced brightness in a limited area of the visual fi eld, and image decomposition can occur with iv-abradine use and is most likely related to its effects on the hyperpolarization current in the retina.

HF patients often suffer from additional comor-bidities including hypertension, diabetes, anemia,

atrial fi brillation and chronic kidney disease. In addition to pharmacotherapy, certain conditions, such as atrial fi brillation, may be amenable to cath-eter ablation or a pulmonary vein isolation proce-dure. In other instances, electrophysiologic thera-pies may help optimize HF (Table 7).

Perioperative Management of Heart Failure Patients Presenting

for Non-Cardiac SurgeryWe are likely to take care of HF patients in a vari-ety of settings: preoperatively in the clinic, intraop-eratively in the operating room and postoperatively in the recovery room or critical care unit. Although preoperative optimization is generally possible in patients presenting for elective procedures, the need for urgent or emergent surgery in HF patients may make optimization diffi cult, if not impossible. Answers to certain pivotal questions help the team formulate a safe anesthetic plan.

Therapy Target and Mechanism for benefi t Contraindications

ACEI: captopril, enalapril

RAAS; decreased conversion of angiotensin I to II leads to vasodi-latation and inhibition of ventricular remodeling

Hypersensitivity, previous angio-edema due to any ACEI, concomi-tant use with aliskiren in diabetic patients as can lead to profound hyperkalemia and hypotension.

ARB: (candesartan, losartan, valsartan)

RAAS; inhibits binding of angioten-sin II to its AT1 receptor

Hypersensitivity, concomitant use with aliskiren in diabetic patients

Beta Blockers:bisoprolol, carvedilol, metoprolol succinate

Sympathetic system; block beta 1 receptors in the heart inhibiting ventricular remodeling

Severe bradycardia, Bradyarrhyth-mias like second or third degree heart block, sick sinus syndrome, cardiogenic shock, decompensated HFrEF

Loop diuretics: furosemide, torsemide

Congestion; inhibit sodium and chloride absorption at the level of thick ascending limb of loop of Henle

Hypersensitivity, anuria

Thiazide diuretics: metolazone, hydrochlorothiazide

Congestion; inhibit sodium chloride cotransporter at the level of distal convoluted tube

Hypersensitivity, anuria, If creati-nine clearance < 10 ml/min, hydro-chlorothiazide should not be used.

Aldosterone antagonists: spironolactone, eplerenone

RAAS; aldosterone antagonism inhibits ventricular remodeling

Anuria, hyperkalemia, signifi cant renal dysfunction.

Vasodilators:hydralazine, isosorbide dinitrate

Vascular smooth muscle; balanced vasodilatation and stress modula-tion.

For nitrates: hypersensitivity, con-comitant use of phosphodiesterase 5 inhibitors or riociguat

Table 5: Guideline Directed Therapy for Heart Failure Reduced Ejection Fraction


Q1. What kind of HF syndrome is the patient presenting with?

It is important to clarify the type of HF (HFrEF or HFpEF), determine current functional status (NYHA class), inquire about recent changes in symptoms and ascertain the stage of HF. Addition-ally, it is important to establish if the patient is in stable chronic HF or in an acute decompensated state. Patients with advanced or end stage HF and new onset ‘de novo’ HF are at high risk for decom-pensation and hemodynamic instability during the perioperative period.

In addition to a thorough history and physi-cal examination, it is imperative that the team reviews or reassesses cardiac biomarkers (brain natriuretic peptide, troponins), electrocardiogram, chest x-ray, echocardiography and right or left heart catheterization results. If the hospital has a dedicated Heart Failure team, it is prudent to seek consultation, especially if the patients are expected to decompensate perioperatively, require mechani-cal circulatory support (MCS) for cardiogenic shock prior to surgery or if the anesthesia team needs guidance regarding perioperative management of an in situ MCS device such as an Impella or left ventricular assist device (LVAD). For example, a patient with HFrEF with an EF of 10% present-ing for debulking of ovarian cancer for palliative purposes may benefi t from pre-surgical intra-aortic

balloon pump counter pulsation support or place-ment of an Impella device.

Q2. What Guideline Directed Management therapy is the patient currently on and what are its perioperative implications?

In stable chronic HF patients who are already on beta-blocker therapy, it is important to continue the medication perioperatively. In unstable patients it is reasonable to individualize management.

For patients who are currently on ARNIs and are coming for surgery, the decision pathway re-mains unclear. As for ACEI and ARBs, it may be reasonable to stop therapy 24 hours prior to sur-gery and reinstitute therapy within 48 hours of the operation. If large fl uid shifts, bleeding or va-soplegic shock is anticipated, an approach can be tailored.

Although anesthetic experience with ivabradine has been limited, concomitant use of QT prolonging and bradycardia inducing drugs such as verapamil should be avidly avoided. Ivabradine bradycardia may be resistant to atropine. Consequently, it is important to ensure immediate availability of transcutaneous pacing and direct beta ag-onists such as epinephrine to increase heart rate if hemodynamically signifi cant brady-cardia is present. A variety of conditions, includ-ing anesthetic drugs and electrolyte abnormalities,

Therapy Target and mechanism for benefi t

Indication Contraindications

ARNI: valsartan/sacubitril

RAAS; inhibition of neprilysin by sacubitril and inhibition of RAAS activation by valsartan

a. HFrEF (EF ≤ 40%)b. NYHA class II or III HF

Previous angioedema due to any ACEI, concomitant use of ACEI or use within 36 hours, concomitant use with aliskiren in diabetic patients, severe hepatic impairment

Sinoatrial node modulator: ivabradine

Inhibits "funny current" I(f) in the sinus node, decreases depolariza-tion and heart rate

a. HFrEF (EF ≤ 35%)b. On maximum tolerated doses of beta blockerc. Sinus rhythm with a resting heart rate >70 bpmd. NYHA class II or III HF

Hypersensitivity, HFpEF, Acute decompensated HFrEF, Severe bradycardia (resting Heart Rate < 60 beats per minute), Brady-arrhythmias like second or third degree heart block, sick sinus syndrome, atrial pacemaker dependence

Table 6: Recently Added Medications for Heart Failure Reduced Ejection Fraction

ACEI: Angiotensin converting enzyme inhibitor, ARNI: Angiotensin receptor-neprilysin inhibitor RAAS: Renin angiotensin aldosterone system, HFrEF: Heart failure reduced ejection fraction; HFpEF, Heart failure with pre-served ejection fraction


can prolong the QT interval in conjunction with ivabradine and precipitate torsades de pointes. It is prudent to place defi brillation pads prior to po-sitioning the patient for surgery in such patients. If available, continuous QT interval monitoring on the anesthesia workstation monitor should be en-abled. Lastly, concomitant use of potent inhibitors of CYP3A4, such as diltiazem, itraconazole, keto-conazole, ritonavir, and verapamil, can precipitate ivabradine toxicity.

HF patients are often on anticoagulant drugs. Patients on warfarin may need bridging antico-agulation for elective surgery under certain cir-cumstances: CHADS2 score of 5 or 6 with atrial fi brillation, mechanical mitral or aortic valve with risk factors for stroke, a left ventricular assist de-vice or recent pulmonary or systemic embolism or deep vein thrombosis within 3 months. Emergent reversal of the anticoagulation effect of warfarin may necessitate use of prothrombin complex con-centrates or plasma products. Patients who do not need bridging with heparin, are advised to stop their warfarin 5 days prior to elective surgery.

Patients on direct oral anticoagulants such as dabigatran and apixaban need an individualized approach depending on dosing, creatinine clear-ance and the bleeding risk of surgery. Discontinu-ation of these drugs varies from 2 to 5 days. For emergent reversal of the anticoagulation effect, andexanet alfa can be employed in patients tak-ing apixaban or rivaroxaban while idarucizumab is recommended for patients on dabigatran.

If a cardiac implantable electronic device such as a pacemaker, ICD or CRT device is present, it is important to elicit the following information: last date of interrogation, indication for placement, bat-

tery longevity, any leads placed within the last 3 months, current programming, pacemaker depen-dence, device response to magnet placement and the need for altering device therapy due to the sur-gery site. Ideally, pacemakers should be checked or interrogated every 12 months and ICD checks should occur every 6 months.

Patients on chronic inotropic drugs and pulmo-nary vasodilators should continue to receive their vasoactive medications in an uninterrupted fash-ion as withholding these medications could precipi-tate decompensated HF.

Lastly, anemia in HF patients is multifactorial. Iron defi ciency, volume overload leading to dilution, chronic infl ammation and decreased kidney func-tion often lead to anemia. However, there is no role for using erythropoietin stimulating medications in this patient population. Correction of iron defi -ciency prior to surgery is encouraged.

Q3. Decision making in HF patients: Should we proceed with surgery?

Broadly three possible decision pathways exist for such patients: A. Proceed with surgery without any additional testing or new medical interventions B. Postpone surgery and proceed only after HF has been stabilized C. Reconsider need for surgery or explore alter- native procedures and therapies.

In 2014, ACC/AHA proposed guidelines for cardio-vascular evaluation and management of patients undergoing non-cardiac surgery and suggested a 7 step algorithm. While the guidelines predominant-

Table 7: Electrophysiologic and Other Therapy for Heart Failure Reduced Ejection Fraction

Therapy Target and Mechanism Comments

CRT and ICD Ventricular dyssynchrony due to conduction abnormalities

Sudden death due to ventricular arrhythmias

Avoid in blood stream infections, lack of vascular access for lead placement. Individualize ap-proach in presence of ventricular assist device, prosthetic tricus-pid valve or chronic inotropic therapy.

Chronic inotropic therapy, MCS and Heart Transplantation

Failing Myocardium and cardio-genic shock; maintenance of systemic and coronary perfusion

Patients with LVADs need anti-coagulation with warfarin

CRT: Cardiac resynchronization therapy; ICD: Implantable cardio-defi brillatorLVAD: Left Ventricular Assist Device; MCS: Mechanical circulatory support


ly focus on detecting and managing coronary artery disease (CAD) prior to elective surgery, the authors acknowledge that patients with active HF have a signifi cantly higher risk of postoperative mortality than do patients with CAD. Decision making for HF patients may vary in different institutions and a suggested algorithm is provided in Figure 3.

Although patients with chronic stable HF can undergo guideline directed evaluation as recom-mended, those with new onset or acute HF benefi t from specialized consultation. These patients ben-efi t from optimization prior to undergoing elective surgery, including titration of pharmacotherapy, which may require 1 to 3 months. Patients with re-fractory or advanced HF should proceed to elective surgery when benefi t outweighs risk. In these pa-tients, consultation with a HF team and bioethicist may be required for appropriate decision making (Figure 3).

Q4. Does choice of anesthesia affect periop-erative outcomes?

The evidence to support preferential use of neurax-ial or general anesthesia is limited in HF patients. Regardless of the anesthetic technique employed, optimal pain control with or without the use of re-gional techniques is important as pain and its as-sociated hypertension and tachycardia can lead to decompensation of stable HF. Drug choices during the conduct of general or regional anesthesia are important in HF patients with prolonged QT inter-

vals to avoid iatrogenic precipitation of malignant ventricular arrhythmias.

Q5. What anesthetic goals and considerations are important?

Goals include identifying and treating factors that may lead to decompensation in stable HF patients or worsen any existing hemodynamic instability. Perioperative factors including hypertension, pain, anemia, excessive fl uid administration, tachy or bradyarrhythmias, ischemia, infection, hypother-mia, hypoxia, hypo or hypercarbia, sepsis and inap-propriate medication management can precipitate cardiogenic shock.

Monitoring and vascular access needs are deter-mined by the surgery and the pre-surgical status of HF. Standard ASA monitors may suffi ce for stable HF patients undergoing minor or intermediate risk procedures. Invasive arterial monitoring, pulmo-nary artery catheterization and echocardiography may be needed for decompensated and advanced HF patients, even if they are undergoing minor surgical procedures. Additionally, intraoperative decompensation in patients with stable HF may necessitate institution of such monitoring.

Optimal fl uid resuscitation is challenging as static indices like central venous pressure and dy-namic indices of fl uid status (such as pulse pres-sure variation) are not accurate in patients with re-duced EF or right HF. It is feasible to follow ASA’s practice guidelines for perioperative blood manage-

Figure 3: Suggested Algorithm for Heart Failure Patients Presenting for Elective Non-Cardiac Surgery


ment. Consequently, patient’s whose hemoglobin levels are < 6 g/dL merit transfusion, while there is minimal benefit in transfusing HF patients whose hemoglobin levels exceed 10 g/dL. On the contrary, overzealous blood transfusion can precipitate de-compensated HF.

SummaryBy 2030, the US will have 80 million seniors. Pro-jections suggest that 6 million seniors will seek care for HF. HFpEF will become the leading type of HF in the future and our cost of taking care of these patients will approximate 70 billion dollars. The recent addition of sacubitril/valsartan and ivabradine has expanded the armamentarium of drugs that help reduce mortality in patients with HFrEF. Our quest for developing effective drug therapy to reduce mortality in patients with HF-pEF is ongoing. Importantly, anesthesiology teams are very likely to provide care to patients with HF on a more frequent basis in the near future.

References Heidenreich PA, Albert NM, Allen LA et al. Fore-casting the impact of heart failure in the United States: a policy statement from the American Heart Association. Circ Heart Fail. 2013; 6:606–619.

Yancy CW, Jessup M, Bozkurt B et al. 2013 ACCF/AHA guideline for the management of heart fail-ure: a report of the American College of Cardiol-ogy Foundation/American Heart Association task force on practice guidelines. Circulation. 2013; 128:e240–327.

Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the Management of Heart Failure: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines and the Heart Failure Society of America. Circulation. 2017; 136(6):e137–61.

Raphael C, Briscoe C, Davies J, et al. Limitations of the New York Heart Association functional classifi-cation system and self-reported walking distances in chronic heart failure. Heart. 2007;93(4):476-482.

Ponikowski P, Voors AA., Anker SD et al.: 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiol-ogy (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.Eur J Heart Fail 2016; 18: pp. 891-975.

Fleisher LA, Fleischmann KE, Auerbach AD et al. 2014 ACC/AHA guideline on perioperative cardio-vascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Cir-culation. 2014; 130:e278–e333

Douketis JD, Spyropoulos AC, Spencer FA, Mayr M, Jaffer AK, Eckman MH, Dunn AS, Kunz R. Peri-operative management of antithrombotic therapy: Antithrombotic Therapy and Prevention of Throm-bosis, 9th ed: American College of Chest Physi-cians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e326S-e350S

Smit-Fun, Valérie; Buhre, Wolfgang F. The patient with chronic heart failure undergoing surgery, Cur-rent Opinion in Anaesthesiology. 2016; 29(3):391-396

Sessler DI, Bloomstone JA, Aronson S, Berry C, Gan TJ, Kellum JA, Plumb J, Mythen MG, Grocott MPW, Edwards MR, Miller TE; Perioperative Qual-ity Initiative-3 workgroup; POQI chairs, Miller TE, Mythen MG, Grocott MP, Edwards MR; Physiology group; Preoperative blood pressure group; Intraop-erative blood pressure group; Postoperative blood pressure group. Perioperative Quality Initiative consensus statement on intraoperative blood pres-sure, risk and outcomes for elective surgery. Br J Anaesth. 2019 May;122(5):563-574

American Society of Anesthesiologists Task Force on Perioperative Blood Management. Practice guidelines for perioperative blood management: an updated report by the American Society of Anesthe-siologists Task Force on Perioperative Blood Man-agement. Anesthesiology. 2015 Feb;122(2):241-75


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ERRATUMVolume 42, Lesson 2

The third point listed in “Tips for Your Clinical Practice” on page 27 should state:

Several of the chemicals found in cigarette smoke are powerful inducers of cytochrome P450 enzymes. This can increase the dose requirements for many anesthetic drugs (e.g., propofol, opioids,muscle relaxants).


• Heart Failure (HF) now affects more than 6 million adults in the United States; by 2030, projections suggest that 9 million patients will seek care for HF.

• Regardless of the anesthetic technique employed, optimal pain control is essential since its associated tachycardia and hypertension can lead to cardiac decompensation.

• The anesthesiologist needs to identify and manage those factors that can worsen the stable HF patient’s hemodynamic stability. These factors include hypertension, tachycardia, anemia, volume overload, ischemia, arrhythmias, infection, and temperature and CO2 alterations.

• Although standard monitoring may suffice for stable HF patients undergoing minor procedures, invasive monitors may be needed for certain patients and procedures. Consultation with the patient’s cardiologist can be invaluable.

• Some HF patients (e.g., those who may decompensate perioperatively) may require mechanical circulatory support (MCS). Guidance may be required regarding the management of appropriate devices.

• Ivabradine is indicated in stable, symptomatic HF with an EF less than 35% and a sinus rhythm with a rate equal to or greater than 70. It’s important to recognize that bradycardia in patients on ivabradine does not respond well to atropine.

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Tips for Your Clinical Practice: Key Points

Monte Lichtiger, MD Editor, Current Reviews®

MARK ONLY THE ONE BEST ANSWER PER QUESTION ON YOURANSWER CARD OR ONLINE EXAM FORM AT WWW.CURRENTREVIEWS.COM

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POST-STUDY QUESTIONS

LESSON

MARK ALL ANSWERS ON BOTH THIS PAGE AND YOUR ANSWER CARD 7

CORRECT ANSWERS TO LESSON 6 VOLUME 42 (MCGOLDRICK)

1. B 2. D 3. A 4. C 5. C 6. B 7. C 8. B

1. A 50 year old woman with symptomatic moderate mitral stenosis presents for colonoscopy. Her Ejection Frac- tion (EF) is 45% and currently she develops dyspnea after climbing one flight of stairs. She has been regu- larly following up with her cardiologists for the last 2 years. She MOST likely has: □ A. Heart Failure with reduced EF □ B. Stage C Heart Failure □ C. NYHA IV symptoms □ D. De Novo’ Heart Failure

2. An 80 year old man presents for emergent coronary artery bypass grafting. He was doing well at home when he suddenly developed crushing chest pain. He now has left anterior descending artery disease. His current EF is 20%, he has Grade II diastolic dysfunction and he is dyspneic at rest. Physical examination reveals cool, clammy extremities and bilateral lung rales. He MOST likely has: □ A. Stage A Heart Failure □ B. NYHA III symptoms □ C. Heart Failure with preserved EF □ D. Acute decompensated heart failure 3. Which of the following drug classes is MOST likely to help alleviate heart failure symptoms related to fluid overload? □ A. Angiotensin receptor blockers □ B. Diuretics □ C. Beta-blockers □ D. Sinoatrial node modulators

4. Which of the following drugs acts by inhibiting the sodium-chloride-cotransporter in the distal convoluted tubule? □ A. Spironolactone □ B. Eplerenone □ C. Metolazone □ D. Torsemide

5. Which of the following beta-blockers MOST likely decreases mortality in Heart Failure with reduced ejection fraction patients? □ A. Bisoprolol □ B. Propranolol □ C. Labetalol □ D. Atenolol

6. A Heart failure patient with reduced ejection fraction has symptomatic sinus node dysfunction (sick sinus syndrome). Which therapy is MOST likely to benefit this patient? □ A. Pulmonary Venous Isolation procedure □ B. Pacemaker implantation □ C. Ivabradine □ D. Metoprolol succinate

7. A 75 year old man with Heart Failure with reduced ejection fraction and atrial fibrillation presents with acute renal insufficiency. His oral medications include warfarin, carvedilol, spironolactone and as needed acetaminophen for knee pain. Which of the following drugs should MOST likely be discontinued due to risk of hyperkalemia? □ A. Spironolactone □ B. Acetaminophen □ C. Carvedilol □ D. Warfarin

8. Sacubitril inhibits which endogenous peptidase? □ A. Tryptase □ B. Aldolase □ C. Neprilysin □ D. Transaminase

updates on perioperative management of heart failure

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