Eisenach.

J Perioperative Science 2014, 1:4

http://www.perioperative-science.com/content/01/04
Journal of Perioperative Science
OPEN ACCESS REVIEW

A Practical Approach to the Perioperative Management of Heart Failure

John H. Eisenach*

Abstract
Demographic aging and its implications for healthcare delivery is a global concern. Heart failure is the
leading cause of hospital admission in patients older than age 65. It is a major risk factor for
postoperative morbidity and mortality, representing one of the most challenging and expensive
problems in medicine and surgery. Every anesthesia provider must be familiar with the definition,
classification, pathogenesis, and perioperative management associated with heart failure. This review
will focus on five key questions that anesthesiologists can incorporate into a strategic approach to
managing the surgical patient with heart failure.
Keywords: systolic heart failure; diastolic heart failure; cardiomyopathy; anesthesia; preoperative
evaluation; blood volume management
( J Perioper Sci 2014, 1:4 )

Introduction postoperative mortality than patients with coronary

The terms “coronary artery disease” and
“congestive heart failure” are common listings on
the pre-anesthesia medical record. Coronary artery
disease is a structural and readily conceptual
diagnosis. In contrast, the term “CHF” is often
vaguely listed on the pre-anesthesia record and
poorly characterized in patients for non-cardiac
surgery. Furthermore, many aspects of heart failure
(HF) are poorly understood. Every anesthesia
provider must be familiar with the definition,
classification, pathogenesis, and treatment strategies
associated with HF. Comprehensive guidelines for
the diagnosis and treatment of HF were first
published in 1995, were revised in 2001, 2009, and
recently in 2013 [1,2].
As survival in patients with coronary disease has
increased, so has the prevalence of heart failure [3].
Patients with HF have a significantly higher risk of
From the *Departments of Anesthesiology, Physiology and
Biomedical Engineering, Mayo Clinic, Rochester, MN 55905
Accepted for publication July 13, 2014.
Reprints will not be available from the authors.
Address correspondence to John H. Eisenach
Departments of Anesthesiology, Physiology and Biomedical
Engineering, Mayo Clinic. Address e-mail to
Eisenach.John@mayo.edu
disease, even in minor procedures [4]. From the
year 2010 to 2030 the prevalence of all
cardiovascular disease is projected to increase by
10%, but the prevalence of HF is projected to
increase by 25%, such that 1 in 33 Americans will
have heart failure [5]. In the same time frame, total
costs for HF are estimated to increase from $31
billion to $70 billion [3]. Heart failure is the most
common reason for hospital admission in patients
older than age 65 [6]. Taken together, HF is
emerging as one of the most challenging and
expensive problems in medicine and surgery. In a
recent surgical outcomes study of HF patients,
adverse events within one month of non-cardiac
surgery occurred in 30%; of these were death (8%),
myocardial infarction (15%), and HF exacerbation
(25%). Patient factors that increased risks of these
complications included age>80, diabetes, and
ejection fraction (EF) less that 30% [7]. Due to the
broad nature of this topic, this review will focus on
five key questions that anesthesiologists can
incorporate into a strategic approach to managing
the surgical patient with heart failure.
What is the type and cause of heart failure?
The common definitions used to classify the type of
HF are summarized in Table 1. Heart failure is the

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syndrome that results from a reduced filling of blood,
or reduced ejection of blood from the ventricle. The
unifying theme in HF is the clinical presentation of
dyspnea and fatigue which may limit exercise
tolerance. Fluid retention may lead to pulmonary
venous congestion and peripheral edema. Together,
the ultimate consequence is a reduction in quality of
life and life expectancy [8]. While there is no single
test that confirms the diagnosis of HF, the
categorical feature of systolic HF is an EF less than
40%, compared to an EF greater than 50% in
diastolic HF, while individuals with an EF between
41 and 49% are considered intermediate.

Table 1. Definitions of common terms and some key features of HF

Term Definition Comments/features

Heart Failure Structural or functional impairment of Lifetime risk is 20% for Americans
ventricular filling or ejection over age 40. Mortality is 50% within 5
years of diagnosis.
HFrEF HF with reduced EF, formerly systolic EF typically < 40% Prevalence less than
HF: Inability of heart to move blood half of HF cases. Major causes are
forward at a sufficient rate to meet the ischemic heart disease and idiopathic.
metabolic demands of the body
HFpEF HF with preserved EF, formerly EF typically > 50% Prevalence more
diastolic HF: Ability of heart to move than half of HF cases and more
blood forward only if the cardiac filling common in women. Major cause is
pressures are abnormally high hypertension.
HF intermediate HF with intermediate EF EF between 41-49%. Treated similarly
EF to HFpEF
Cardiomyopathy, Structural and functional disorders of Includes a wide range of abnormalities
LV dysfunction the myocardium that cause HF
Dilated Myocardial dysfunction characterized Most commonly idiopathic in origin
Cardiomyopathy by ventricular dilatation and and associated with better survival
decreased contractility than other causes of cardiomyopathy;
25% of cases improve in a short time
Peripartum LV dysfunction in the last trimester of After 6 months: improved LV function
cardiomyopathy pregnancy, unknown cause but risk in 50% of patients; much worse
factors include multiparity, advanced prognosis if LV function does not
maternal age, African descent, long- improve (6 year mortality 50%)
term tocolysis.
Compensated HF Moving up the Frank-Starling curve Improving NYHA class
(Na+ and water retention), LV
hypertrophy, neurohumoral activation
Decompensated Increased cardiac workload due to Worsening NYHA class
HF increases in metabolic demand,
increased circulating volume,
decreased contractility

The heart consumes more energy than any other
organ, pumping about ten tons of blood throughout
the body per day. When cells in the myocardium
become deprived of energy, this abnormality of
“myocardial energetics” plays a major role in
progression of HF. There are three components of
cellular energy metabolism: 1) substrate utilization:
the uptake and conversion of free fatty acids and
glucose into the Kreb’s cycle; 2) oxidative
phosphorylation: producing ATP from the
mitochondrial respiratory chain; and 3) transfer and
utilization of high-energy phosphates (ATP) to the
myofibrils [9]. Dysfunction in all three components
of myocardial energetics is early and integral to HF

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pathogenesis. Future therapeutic approaches will Causes of HF can be classified as cardiogenic or

target these molecular and metabolic pathways.
In contrast to the common clinical presentation of
HF, the causes of HF are widely variable. Growing
evidence suggests that there are unique
characteristics in risk factors, pathophysiology,
treatment, and outcomes in systolic vs. diastolic
heart failure [10]. Figure 1 displays common and
contrasting features of systolic and diastolic HF.
non-cardiogenic. Cardiogenic causes of HF are
inherently related to pathophysiology of the
myocardium, the valves, and the pericardium, and
can be classified as structural and functional. Non-
cardiogenic causes of HF are non-cardiac
pathologies that are injurious to myocardium or
evoke a physiological state that resembles heart
failure.

Figure 1. Common and contrasting features of heart failure with reduced HF (HFrEF) and heart failure
with preserved HF (HFpEF). HFrEF or systolic HF is generally associated with an acute injury to myocardium, or
a genetic abnormality injurious to myocardium. The pathophysiology of HFpEF, or diastolic HF, is insidious in
onset primarily from poorly controlled hypertension, but also confounded by aging and poorly controlled co-
morbidities. While initial physiologic adaptations are common between syndromes, the maladaptive processes
distinguish the two. The arrows represent the cycle of heart failure that continues when inadequate therapies
exacerbate the syndrome.

For structural changes in systolic HF, ischemic heart
disease is the leading cardiogenic cause. Myocardial
infarction changes the ventricular geometry within
hours to days. The area of myocardium expands and
becomes thinner. Global remodeling results in
ventricular dilatation (eccentric hypertrophy),
decreased systolic function, mitral valve dysfunction,
and aneurysm formation [11]. For diastolic HF,
hypertensive heart disease is the leading cardiogenic
cause associated with remodeling, as the ventricular
walls become thickened (concentric hypertrophy)
and ejection fraction is preserved.
Chemotherapy induced cardiomyopathy can be
attributed to a variety of agents, with the most
established class being anthracyclines. Doxorubicin
(Adriamycin) toxicity is thought to be due to
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oxidative stress, decreased antioxidant enzymes, and
possibly iron accumulation in cardiomyocytes
[12,13]. The incidence of heart failure after
doxorubicin is dependent on age and dose, with an
accelerated risk of myocardial toxicity when doses
exceed 550 mg/m2 [14]. Trastuzumab (Herceptin) is
a monoclonal antibody against HER2 protein for the
treatment of positive HER2 breast cancer [15].
Trastuzumab myocardial toxicity is not related to
dose, but potential cardiotoxicity increases when
combined with anthracycline therapy, and the
effects are greater if the cumulative doxorubicin
dose is > 300 mg/m² [16]. Other common
chemotherapy agents that are associated with
myocardial depression are mitoxantrone
(Novantrone), cyclophosphamide (Cytoxan),
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ifosfamide (Ifex), all-trans retinoic acid (Tretinoin),
and imatinib (Gleevec) [17].
Detailed examples of additional structural causes
of HF are beyond the scope of this review but
include: gene mutations, inborn errors of
metabolism, toxins (i.e., alcohol, smoking, illicit
drugs, lead poisoning), infections such as viral (i.e,
HIV), bacterial, Lyme disease, fungal, parasitic (i.e.,
Chagas disease), and idiopathic. Indeed, the leading
cause of non-ischemic dilated cardiomyopathy is
idiopathic, present in up to 50% of patients where no
definitive cause is found [18].
Functional causes of HF are illustrated in Figure 2.
Functional causes may overlap with structural
causes that reduce contractile function, such as
myocardial infarction. However, a major cause of
non-ischemic contractile dysfunction is chronic
volume overload due to either severe mitral
regurgitation or severe aortic regurgitation. This
leads to chamber dilation and eccentric hypertrophy.
Pressure overload is a functional cause of diastolic
HF, where chronic hypertension or chronic aortic
stenosis lead to ventricular remodeling which
increases wall thickness in attempt to reduce the
wall stress through LaPlace’s relation for a hollow
sphere:

σ = P x r / 2h, where σ = wall tension, P = pressure, r = radius, and h = wall thickness.

Figure 2. Functional causes of left sided heart failure. Impaired contractility results from a combination of
structural damage to myocardium, most commonly by myocardial infarction and ischemic heart disease, with
functional causes that perpetuate the syndrome of heart failure, such as increased sympathetic nervous system
activity and neurohormonal activation. Pressure overload can induce left ventricular (LV) systolic or diastolic
dysfunction. Diastolic dysfunction is the abnormal relaxation or myocardial stiffness associated with chronic
hypertension, pressure overload, and myocardial thickening. Without proper management diastolic dysfunction
can progress to LV systolic dysfunction or HF with preserved EF.

Diastolic dysfunction is the abnormal relaxation
associated with chronic hypertension, pressure
overload, and myocardial thickening. Without
proper management it can progress to HF with
preserved EF. Other causes of diastolic dysfunction
that aren’t directly caused from pressure overload
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include hypertrophic cardiomyopathy and restrictive
cardiomyopathy.
Another common functional cause of HF relevant
to the anesthesiologist is tachyarrhythmia-induced
cardiomyopathy. A typical surgical presentation of
tachyarrhythmia-induced cardiomyopathy is atrial
fibrillation with rapid ventricular response and
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associated arterial thrombosis (i.e., ischemic stroke,
mesenteric ischemia, or cold leg). Emergency
echocardiography may reveal severe global
hypokinesis with a severely depressed ejection
fraction. When caught early, these tachyarrhythmia-
induced cardiomyopathies are at least partially
reversible with rate control and medical
management [19].
The pathophysiology of systolic HF.is a complex
interaction between injury of the myocytes and
extracellular matrix, ventricular remodeling,
sympathetic nervous system activation, and
activation of the renin-angiotensin-aldosterone
system [20]. Sympathetic nerve activity is normally
increased in aging, but substantially increased
during HF [21]. Circulating catecholamine levels
(norepinephrine, epinephrine) are increased, which
leads to salt and fluid retention, peripheral
vasoconstriction, and down-regulation of beta-1
adrenergic receptors in the heart [22]. Vagal
function in the heart is also reduced in proportion to
the severity of heart failure [23,24].
Concomitant with overdriving sympathetic nerve
traffic, HF is associated with an over-active renal
angiotensin-aldosterone system (RAAS) [25]. This
further increases salt and fluid retention, and the
RAAS hormones mediate some of the maladaptive
effects on the myocardium[26,27]. Natriuretic
peptides are released, and circulating cytokines such
as interferons and tumor necrosis factor further
mediate dysfunctional myocardial remodeling [28].
Interestingly, co-morbid conditions tend to
segregate between systolic and diastolic HF.
Previous myocardial infarction is the major risk
factor for systolic HF, followed by sleep apnea,
hypertension, and diabetes. Diastolic HF is
associated with a greater variety of diseases, with
the major risks being obesity, hypertension, and
diabetes, followed by chronic lung disease, dialysis,
and sleep apnea [11].
What is the stage and class of heart failure?
The patient’s functional status remains a key feature
in preoperative cardiac evaluation. In previous
ACC/AHA guidelines for preoperative clinical
predictors of anesthesia risk, decompensated HF
was classified as a major clinical risk factor, and
compensated or prior HF, an intermediate risk factor
[29]. The most recent ACC/AHA guidelines for
preoperative cardiovascular evaluation list
decompensated HF as an “active cardiac condition,”
for which the HF patient should undergo evaluation
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and optimization of HF before elective surgery [30].
Compensated HF or prior HF is now considered a
clinical risk factor warranting further assessment of
functional capacity, other clinical risk factors, and
surgical risk. Adapted from the original Goldman
criteria, the Revised Cardiac Risk Index (RCRI) lists
“History of HF” as one of six independent predictors
of cardiac risk in the determination of an
individual’s RCRI [31]. More recently, Sabate and
colleagues identified HF as an independent risk
factor for major adverse cardiac and cerebrovascular
events following non-cardiac surgery [32].
Class: The New York Heart Association (NYHA)
functional classification correlates with quality of
life and survival. Because the paramount symptom
of HF is dyspnea on exertion, the NYHA class
stratifies patients based on the symptom severity as
described in Table 2. Class IV HF has a worse
prognosis than most cancers in the U.S., with a one-
year mortality approaching 45% [11].
Stage: Historically, there have not been wide-
spread screening efforts for HF. Risk factors for HF
were either poorly defined or poorly publicized. In
an attempt to prevent or reverse HF progression, the
ACCF/AHA guidelines developed clinical staging
criteria to identify patients at risk for—or in early
stages of—HF [1]. The staging criteria allow for
patients to be stratified into clinical trials. Results of
these trials form the guidelines for medical
management. In contrast to NYHA class where
patients can move up or down a continuum of
functional status, patients move through the stages
of HF in one direction, not reverse.
What are the current medications?
By understanding the treatment strategy,
summarized in Table 2, one can determine a
patient’s current HF stage. The medications in HF
serve to reduce cardiac sympathetic stimulation,
lessen sodium and water retention, and decrease
afterload, collectively breaking the cycle of
physiological adaptations and pathologic
maladaptations depicted in Figure 1.
On the electrocardiogram, a prolonged QRS
complex is present in approximately 1/3 of HF
patients, which is associated with worse outcome
[33]. The associated bundle branch block produces a
loss of ventricular coordination called dyssynchrony
or mechanoenergetic uncoupling which hastens
maladaptive remodeling [34]. Cardiac
resynchronization therapy (CRT) is an attempt to
coordinate ventricular depolarization. With pacer
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leads in both ventricles, CRT brings synchronized regurgitation if present, improve ejection fraction,
contraction to the ventricles, which reverses and can improve symptoms and NYHA class [35].
pathologic remodeling, may improve mitral

Table 2. Stage, class, and treatment algorithm of HF

NYHA Functional ACCF/AHA Stages of HF Treatment Algorithm

Classifications
A At high risk for HF but Risk-factor reduction, education; treat
without structural heart hypertension, diabetes, dyslipidemia.
disease or symptoms of HF Smoking cessation and avoidance of
cardiotoxic agents
I No limitations of B Structural heart disease but ACE inhibitor or ARB in all patients; beta-
physical activity. without signs or symptoms blocker in select patients; statins;
Ordinary physical of HF ICD in patients with ischemic
activity does not cause cardiomyopathy and at least 40 days post-
symptoms of HF. MI and EF < 30%

I No limitation of C Structural heart disease ACE inhibitors and beta-blockers in all

physical activity. with prior or current patients;
Ordinary physical symptoms of HF Dietary sodium restriction, diuretics, and
activity does not cause digoxin;
symptoms of HF. Hydralazine and isosorbide dinitrate in
II Slight limitation of African Americans;
physical activity, Aldosterone antagonist;
Comfortable at rest,
but ordinary physical Cardiac resynchronization if bundle-
activity results in branch block present
symptoms of HF. Revascularization, mitral-valve surgery
III Marked limitation of
physical activity.
Comfortable at rest,
but less than ordinary
activity causes
symptoms of HF.
IV Unable to carry on any
physical activity
D Refractory HF requiring Inotropes, ventricular assist device,
without symptoms of
specialized interventions transplantation
HF, or symptoms of HF
Hospice
at rest.
ACCF, American College of Cardiology Foundation; AHA, American Heart Association; HF, heart failure; NYHA,
New York Heart Association; MI, myocardial infarction; ARB, angiotension receptor blocker. Table adapted
from reference [1].

There is strong evidence to suggest that CRT is ECG, sinus rhythm, and NYHA class II or III
indicated in patients with left ventricular EF less symptoms [1]. Weaker evidence suggests a benefit
than or equal to 35%, a QRS complex greater than of CRT in patients with atrial fibrillation with EF
120 milliseconds, a left bundle branch pattern on less than 35%, optimal medical therapy, and fully

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dependent on ventricular pacing [1]. Importantly,
approximately 80% of biventricular pacers will
include an automated internal cardiac defibrillator
(ICD).
There are two strong indications for ICD’s in HF.
This first is to prevent sudden cardiac death in
patients with non-ischemic cardiomyopathy,
ischemic cardiomyopathy > 40 days post myocardial
infarction, an EF less than or equal to 35%, and have
a NYHA class II or III with a reasonably predicted
survival beyond one year [1]. The second indication
is to prevent sudden cardiac death in patients with
an EF less than or equal to 30%, with NYHA class I
symptoms while receiving optimal medical
management, who are also expected to live beyond
one year [1] . CRT is not indicated for patient with
comorbidities and an poor expected survival. One
must weigh the benefits against the potential for
worsening quality of life because of the discomfort
from shock delivery.
What workup does this patient need before
surgery?
The patient with HF presents in one of three ways: 1)
A noticeable onset of exertional dyspnea or decrease
in exercise tolerance; 2) Fluid retention; 3) With no
symptoms or with symptoms of another cardiac
disorder or noncardiac disorder. The complete
history and physical exam will delineate cardiac
versus noncardiac causes of presentation. The
routine ECG and chest X-ray have low sensitivity
and specificity for diagnosing a cardiac cause of HF,
but are useful in the general assessment of cardiac
and pulmonary pathology.
The most useful diagnostic test is
echocardiography to address three main questions: 1)
ejection fraction; 2) left ventricular structure,
dimension, wall motion; and 3) non-left ventricular
abnormalities (i.e., valve, pericardium, right
ventricle). Additional echocardiography indices will
include atrial size and pressure, characteristics of
LV filling, and pulmonary arterial pressure. The
comprehensive echocardiogram will also provide a
baseline for future comparison and therapeutic
management. Laboratory testing will include
natriuretic peptides (BNP and/or NT-proBNP)Figure
3, complete blood count, urinalysis, electrolyte
panel, hemoglobin A-1c, lipid panel, renal, liver,
and thyroid function, as well as viral screening.

Figure 3. Brain-type natriuretic peptide. BNP is also called brain type natriuretic peptide because it was first
discovered in brain tissue. In cardiac myocytes, dilation and pressure overload on the cell causes expression of the
gene that translates the pro-hormone. The pro-hormone gets cleaved into an N-terminal pro-BNP that is inactive
but measurable, and C-terminal BNP which is the active hormone that inhibits the renin angiotensin aldosterone
system (RAAS), promotes diuresis and vasodilation, and thereby decreases preload and afterload. NT-proBNP has
a half-life of 1-2 hours and BNP has a half-life of 20 minutes.

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The pre-operative holding area: Is this patient in
heart failure? Certainly patients in acute HF should
not undergo elective procedures, and anesthesia
providers must be prepared to diagnose and triage
HF patients in the holding area. A meta-analysis of
HF diagnostic criteria in patients presenting to the
emergency room with dyspnea can be extrapolated
to our pre-operative evaluations [36]. If a patient is
dyspneic, the positive predictors that suggest HF are
listed in Table 3. The strongest predictor of HF in a
dyspneic patient is medication non-adherence. Atrial
fibrillation is an important predictor of HF because
the prevalence of a-fib in patients with acute HF is
greater than 30% [37]. Of note, the reason serum
BNP or NT-proBNP is not listed as a positive
predictor is because it can also be elevated in
advanced age and critical illness. This would include
renal failure, acute coronary syndrome, lung disease
with cor pulmonale, acute pulmonary embolus, and
high output cardiac states such as sepsis. However,
if BNP is low, this suggests that a patient does not
have HF. The most negative predictors that would
dissuade the diagnosis of HF are also listed in Table
3.

Table 3. Is this patient in heart failure…do I cancel this case?

Suggested of systolic HF (HFrEF): Suggestive of HFpEF:

Comorbidities Hypertension, Obesity, chronic lung Poorly controlled hypertension,

disease, chronic kidney disease, diabetes, previous MI, sleep apnea, diabetes,
sleep apnea, hyper/hypothyroidism, obesity
acromegaly, alcohol, cocaine, cancer
agents, tachydysrhythmias, myocarditis,
AIDS, Chaga’s disease, peripartum
cardiomyopathy, amyoid, sarcoid,
Takotsubo

Predictors of acute decompensated HF

Positive predictors: Negative predictors:
History History of HF, past or present atrial No history of HF
fibrillation or other tachyarrhythmias, No dyspnea on exertion
peripheral edema, sleep disordered
breathing
Physical exam Presence of an S3 gallop No rales/crackles on lung
Jugular venous distention auscultation
Irregular pulse rhythm
Presence of right ventricular heave Cold
extremities
Chest X-Ray Congestion (cardiomegaly with a heart to No cardiomegaly
thorax ratio of less than 1:2, cephalization No congestion
of flow or batwing or butterfly appearance,
Kerley B lines, prominent horizontal
fissure, pleural effusions)
Electrocardiography Abnormal rhythm, ventricular morphology No abnormalities

Monitors/Laboratory BNP or N-terminal pro-BNP elevated* A normal BNP

Cardiac troponins elevated
*indicates that while BNP and/or NT-proBNP is elevated in acute HF, there are many other conditions
associated with an elevation of these markers.

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Preoperative medications: For preoperative
continuation of anti-hypertensive agents, concerns
have arisen with respect to profound and refractory
intraoperative hypotension in patients who take an
angiotensin converting enzyme inhibitor (ACEI) or
an angiotensin receptor blocker (ARB). A study at
our institution found that discontinuation of
ACEI/ARB therapy at least 10 hour before
anesthesia was associated with a reduced risk of
immediate postinduction hypotension [38].
Therefore, our pre-operative evaluation clinic
recommends that patients hold their ACEI and ARB
on the day of surgery, provided that their blood
pressure is well-controlled. If their hypertension is
poorly controlled at the time of their preoperative
visit, these medications are continued on the day of
surgery. The lipid-lowering agent is generally taken
at night, and while postoperative outcomes data are
less clear on HF patients, the use of preoperative
statins has shown a reduction in postoperative atrial
fibrillation and hospital length-of-stay in cardiac
surgery patients [39]and therefore can be continued
up to surgery.
Specific beta-blockers in HF management are
bisoprolol, carvedilol, or sustained-release
metoprolol [1]. These medications should be
continued on the day of surgery [40,41]. Diuretics
should be held on the morning of surgery, primarily
because patients are fasting and therefore may be at
risk of volume depletion with the use of their
diuretic. Aldosterone antagonists (i.e.,
spironolactone, eplerenone), digoxin, and long-
acting nitrates can be continued on the day of
surgery.
Pacemaker interrogation: Pacemaker settings vary
by patient and device manufacturer. Interrogation of
these devices is essential to determine whether a
patient’s heart rhythm is pacemaker dependent and
if so, the device should be re-programmed to
asynchronous demand pacing (e.g., VOO). The
device settings and magnet responses should be
reviewed with the manufacturer and/or the hospital
pacemaker service. If neither is available and the
device is a single chamber (right atrium) or dual-
chamber (right atrium + right ventricle) pacemaker,
a magnet placed on the chest should convert a
pacemaker to VOO. Importantly, these responses are
not universal, particularly for older devices. This
stresses the importance of reviewing all pacemakers
prior to surgery.
Stage B patients with asymptomatic ischemic
cardiomyopathy, who are at least 40 days after
myocardial infarction, and have an LVEF ≤30%,
may have an internal cardiac defibrillator (ICD) to
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prevent sudden cardiac death. Defibrillators are
accompanied by either single chamber, dual
chamber, or biventricular pacemakers. If a
biventricular pacemaker device has an ICD, a
magnet should inactivate the defibrillator but may
not change the pacemaker settings. To prevent
unnecessary shocks the ICD should be inactivated in
the holding area. Continuous ECG monitoring is
indicated until reactivation.
Stage C patients may have a biventricular
pacemaker with or without an implantable
defibrillator. Again, magnet placement should
deactivate the defibrillator, but will not change the
pacemaker settings. For electrical interference,
these devices are programmed with a ventricular
noise reversion back-up mode, referred to as the
“VNR.” This is the automatic default setting when
the pacemaker senses electrical noise such as
electrocautery. When electrical interference is
sensed, the device typically converts to VOO at a
rate between 60-90 bpm. These devices should be
interrogated postoperatively to confirm the desired
settings and reactivation of the ICD.
How should I care for this patient during and
after surgery?
Induction and maintenance of anesthesia: An
awake arterial catheter prior to induction is helpful
for any patient in acute or decompensated HF
presenting for emergency surgery, for any HF
patient in a higher functional class or stage of HF,
and for any HF patient with severe systolic or
diastolic dysfunction, pulmonary hypertension, or
significant valvular disease. Rapid atrial fibrillation
in a HF patient would also indicate arterial line
placement, with aggressive attempts to adequately
stabilize ventricular rate control prior to surgery.
The choice of medications for induction is less
critical when real-time monitoring of heart rate and
arterial pressure allow for careful titration of these
agents. For example, propofol or thiopental have the
potential to cause profound hypotension in the HF
patient because of the chronically elevated
sympathetic nervous system activity [42,43]. These
agents can be given simultaneously with pressor
administration. Etomidate and ketamine have less
effect on sympathetic-mediated maintenance of
blood pressure [42,44]. The sympathomimetic effect
of ketamine may increase myocardial oxygen
demand, but this can be offset by short-acting beta-
blockade. Maintenance of anesthesia in HF patients
is generally dependent on the surgical procedure, the
expected duration of procedure, blood loss, fluid
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shifts, and the need for additional monitoring develop hypotension secondary to low cardiac
techniques. output. If the patient has adequate intravascular
Hemodynamic supportive infusions for volume, then inotropes (dopamine, dobutamine)
perioperative management: The agents useful for should be initiated. If blood pressure is stable, then
maintaining cardiac performance and blood pressure these patients may benefit from the vasodilatory and
support are listed in Table 4. Patients with severe inotropic effect of milrinone. Milrinone may be
systolic dysfunction or dilated cardiomyopathy may bolused over 10 minutes prior to infusion.

Table 4. Intraoperative supportive medications and considerations

Indication / Drug Mech. Action Goal / Effect Starting Dose

Systolic dysfunction
(↓ CO + congestion)
Dopamine DA1, β1, α1, α2 ag. Inotropy, pressor 5 mcg/kg/min

Dobutamine β1 agonist Inotropy 2 mcg/kg/min

Milrinone PDE III inhibitor Inotropy, Bolus: 50 mcg/kg over 10 min

vasodilation Infusion:
0.5 mcg/kg/min
Diastolic dysfunction
(↑ BP + congestion)
Nitroprusside NO donor, veno- & Preload < afterload 0.5 mcg/kg/min
arteriodilator reduction
Nitroglycerin NO donor, veno- & Preload > afterload 0.5 mcg/kg/min
arteriodilator reduction
Volume Overload

Furosemide Loop diuretic Plasma volume Initial I.V. bolus one-half

reduction patient’s daily oral dose

For patients with diastolic HF, an imbalance in
myocardial oxygen supply and demand, particularly
in the setting of volume overload and severe
hypertension, may lead to deterioration of cardiac
function and flash pulmonary edema. Nitroglycerin
generally decreases preload by venodilation in order
to reduce myocardial oxygen demand, while the
arteriodilator effect reduces afterload. Nitroprusside
provides potent afterload reduction. Both agents
must be titrated with caution as patients with
diastolic HF are particularly volume sensitive. With
either decompensated systolic or diastolic HF,
furosemide is the agent of choice for diuresis.
Based on the oral bioavailability (60%), the initial
I.V. bolus dose is approximately one-half the daily
oral dose, with additional doses titrated to effect.
Nesiritide is a recombinant natriuretic peptide that
has been shown to improve dyspnea and
hemodynamic parameters in patients with
decompensated heart failure [45]but no
improvement in renal function or mortality [46].
Because the half-life and duration of action of
nesiritide is longer than the nitric oxide mediated
vasodilators, it’s use is limited in the perioperative
period.
Monitors: Regardless of surgery, the ACCF/AHA
guidelines recommend invasive hemodynamic
monitoring in HF patients whose fluid status,
perfusion, or systemic or pulmonary vascular
resistance is uncertain; whose systolic pressure

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Eisenach. J Perioperative Science 2014, 1:4
http://www.perioperative-science.com/content/01/04
remains low, or is associated with symptoms,
despite initial therapy; whose renal function is
worsening with therapy; or those who require
parenteral vasoactive agents[1]. Because of
pathophysiologic relevance of intravascular volume
for both systolic and diastolic HF, the most critical
aspect of intraoperative and postoperative
monitoring for HF patients involves careful fluid
management. “Static” variables are those that
estimate cardiac filling pressure or cardiac filling
volume (as an estimate of end-diastolic volume, or
preload) [47]. Central venous catheters are placed
for tracking changes in filling pressure but in
isolation will not discriminate between changes in
ventricular dysfunction and volume overload. The
pulmonary arterial catheter estimates changes in left
ventricular filling pressure (pulmonary diastolic and
wedge pressure) and provides thermodilution-based
measures of cardiac output.
Even with minimal user training, transesophageal
echocardiography (TEE) provides real-time image
estimates of end-diastolic ventricular volume, and
global and regional ventricular contractile function
[48]. TEE is often considered the monitor of choice
to differentiate between cardiogenic, hypovolemic,
and vasodilatory causes of shock. The intrathoracic
thermodilution method utilizes a central venous line
for injection of iced saline, and a thermodilution
catheter in a proximal artery (i.e., femoral or axillary)
to sense the temperature change from the cold saline
injection [49]. The accompanying commercial
monitor module estimates stroke volume and
intrathoracic blood volume and global end-diastolic
volume without dependence on the respiratory cycle.
“Dynamic” variables estimate changes in
intravascular volume based on characteristics of the
arterial waveform that vary with the respiratory
cycle [47]. A regular rhythm is also necessary.
During positive pressure ventilation, systolic blood
pressure variation is the difference between the
maximum and minimum systolic pressure values
over the respiratory cycle. Hypovolemia is
suggested when systolic pressure variation is greater
than 10 mmHg. Similarly, pulse pressure (PP) will
vary over the respiratory cycle in accord with
hypovolemia.
Pulse pressure variability can also be derived
from one respiratory cycle and is calculated as the
maximal PP minus the minimal PP, divided by the
average of these two pressures, expressed as a
percentage. Similarly, stroke volume (SV) varies
over the respiratory cycle in accord with
hypovolemia. The calculation of SV variability
requires a commercial module on the arterial line
Journal of Perioperative Science
that analyzes the pulse contour to estimate SV. SV
variability is derived from one respiratory cycle and
is calculated as the maximal SV minus the minimal
SV divided by the average of these two pressures. It
is also expressed as a percentage.
Finally, commercial modules exist that determine
variability in the amplitude of the pulse oximetry
waveform. The variability in pulse oximeter
plethysmography waveform (ΔPOP) is calculated as
the maximal minus minimal plethysmographic
amplitude, divided by the maximal amplitude. This
too can be determined over one respiratory cycle.
All of the examples of static and dynamic
methods of tracking intravascular volume changes
have advantages and disadvantages, including cost
and training expertise. Moreover, ventricular
systolic and diastolic dysfunction associated with
HF may have a confounding effect on these
variables. No readily available technique has
demonstrated superiority. In this context, one must
practice the basics of fluid management, including
maintenance fluid requirements, surgery-specific
insensible losses, urine output, estimated blood loss,
and careful fluid resuscitation.
Postoperative Management: Postoperative
planning for HF patients depends on the
preoperative functional status, the complexity of the
procedure including intravascular fluid shifts, and
potential for postoperative acute decompensating
HF. Cardiac devices must be interrogated and
reactivated when available. Large intraoperative
fluid shifts increase the risk for major adverse
cardiac events and acute congestion. The entire
clinical picture must be considered for postoperative
monitoring with a low threshold for intensive care.
In summary, HF is a syndrome with multiple
classifications, etiologies, and treatment strategies.
Understanding the recently-standardized treatment
algorithm will facilitate the preoperative evaluation.
Anesthesia providers need to recognize
compensated versus decompensated HF in order to
guide decision-making. Careful anesthetic planning,
device interrogation, fluid management, and
postoperative monitoring will optimize perioperative
management.
Competing interests
The authors declare that they have no conflict of
interests.
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