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CHAPTER
Heart Failure

• Heart failure (HF) is a progressive syndrome that can result from any changes in car-
diac structure or function that impair the ability of the ventricle to fill with or eject
blood. HF may be caused by an abnormality in systolic function, diastolic function, or
both. HF with reduced systolic function (ie, reduced left ventricular ejection frac-tion,
LVEF) is referred to as HF with reduced ejection fraction (HFrEF). Preserved LV
systolic function (ie, normal LVEF) with presumed diastolic dysfunction is termed HF
with preserved ejection fraction (HFpEF).

PATHOPHYSIOLOGY
• Causes of systolic dysfunction (decreased contractility) include reduced muscle mass
(eg, myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hyper-
trophy. Ventricular hypertrophy can be caused by pressure overload (eg, systemic or
pulmonary hypertension and aortic or pulmonic valve stenosis) or volume overload
(eg, valvular regurgitation, shunts, high-output states).
• Causes of diastolic dysfunction (restriction in ventricular filling) include increased
ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myo-
cardial ischemia and MI, mitral or tricuspid valve stenosis, and pericardial disease
(eg, pericarditis and pericardial tamponade).
• The leading causes of HF are coronary artery disease and hypertension.
• Regardless of the index event, decreased cardiac output (CO) results in activation of
compensatory responses to maintain circulation: (1) tachycardia and increased
contractility through sympathetic nervous system activation, (2) the Frank–Starling
mechanism, whereby increased preload (through sodium and water retention)
increases stroke volume, (3) vasoconstriction, and (4) ventricular hypertrophy and
remodeling. Although these compensatory mechanisms initially maintain cardiac
function, they are responsible for the symptoms of HF and contribute to disease
progression.
•In the neurohormonal model of HF, an initiating event (eg, acute MI) leads to decrease
CO; the HF state then becomes a systemic disease whose progression is mediated
largely by neurohormones and autocrine/paracrine factors that drive myocyte injury,
oxidative stress, inflammation, and extracellular matrix remodeling.
These substances include angiotensin II, norepinephrine, aldosterone, natriuretic
peptides, and arginine vasopressin (AVP).
• Chronic activation of the neurohormonal systems results in a cascade of events that
affect the myocardium at the molecular and cellular levels. These events lead to
changes in ventricular size (left ventricular hypertrophy), shape, structure, and func-
tion known as ventricular remodeling. The alterations in ventricular function result in
further deterioration in cardiac systolic and diastolic functions that further promotes
the remodeling process.
• Common precipitating factors that may cause a previously compensated HF patient to decompensate
include myocardial ischemia and MI, pulmonary infections, non-adherence with diet or drug therapy,
and inappropriate medication use. Drugs may precipitate or exacerbate HF through negative inotropic
effects, direct cardiotoxicity, or increased sodium and water retention.

CLINICAL PRESENTATION
• Patient presentation may range from asymptomatic to cardiogenic shock.
• Primary symptoms are dyspnea (especially on exertion) and fatigue, which lead to
exercise intolerance. Other pulmonary symptoms include orthopnea, paroxysmal
nocturnal dyspnea (PND), tachypnea, and cough.

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• Fluid overload can result in pulmonary congestion and peripheral edema.

• Nonspecific symptoms may include fatigue, nocturia, hemoptysis, abdominal pain, anorexia, nausea,
bloating, ascites, poor appetite or early satiety, and weight gain or loss.

• Physical examination may reveal pulmonary crackles, S3 gallop, cool extremities,

Cheyne–Stokes respiration, tachycardia, narrow pulse pressure, cardiomegaly, symp-
toms of pulmonary edema (extreme breathlessness and anxiety, sometimes with
coughing and pink, frothy sputum), peripheral edema, jugular venous distention (JVD),
hepatojugular reflux (HJR), hepatomegaly, and mental status changes.

DIAGNOSIS
• Consider the diagnosis of HF in patients with characteristic signs and symptoms. A
complete history and physical examination with appropriate laboratory testing are
essential in evaluating patients with suspected HF.
• Laboratory tests for identifying disorders that may cause or worsen HF include complete
blood cell count; serum electrolytes (including calcium and magnesium); renal, hepatic,
thyroid function tests, and iron studies; urinalysis; lipid profile; and A1C. Hyponatremia
(serum sodium <130 mEq/L [mmol/L]) may indicate worsening volume overload and/or
disease progression and is associated with reduced survival. Serum creatinine may be
increased due to hypoperfusion; Pre-existing renal dysfunction can contribute to volume
overload. B-type natriuretic peptide (BNP) is usually >100 pg/mL (29 pmol/L) and NT-
proBNP >300 pg/mL (35 pmol/L).

• Ventricular hypertrophy can be demonstrated on chest radiograph or electrocardio-gram

(ECG). Chest radiograph may also show pleural effusions or pulmonary edema.
• Echocardiogram can identify abnormalities of the pericardium, myocardium, or heart
valves and quantify LVEF to determine if systolic or diastolic dysfunction is present.

• The New York Heart Association Functional Classification System is intended primarily
to classify symptoms according to the physician's subjective evaluation.
Functional class (FC)-I patients have no limitation of physical activity, FC-II patients have
slight limitation, FC-III patients have marked limitation, and FC-IV patients are unable to
carry on physical activity without discomfort.
• The American College of Cardiology/American Heart Association (ACC/AHA) stag-ing
system provides a more comprehensive framework for evaluating, preventing, and
treating HF (see further discussion below).

TREATMENT OF CHRONIC HEART FAILURE

• Goals of Treatment: Improve quality of life, relieve or reduce symptoms, prevent or
minimize hospitalizations, slow disease progression, and prolong survival.
GENERAL APPROACH
• The first step is to determine the etiology or precipitating factors. Treatment of underlying
disorders (eg, hyperthyroidism) may obviate the need for treating HF.
• ACC/AHA Stage A: These are patients at high risk for developing HF. Identify and modify
risk factors to prevent development of structural heart disease and subse-quent HF.
Strategies include smoking cessation and control of hypertension, diabetes mellitus, and
dyslipidemia. Although treatment must be individualized, angiotensin-converting enzyme
(ACE) inhibitors or angiotensin receptor blockers (ARBs) are recommended for HF
prevention in patients with multiple vascular risk factors.
• ACC/AHA Stage B: These patients have structural heart disease but no HF signs or
symptoms. Treatment is targeted at minimizing additional injury and preventing or slowing
the remodeling process. In addition to treatment measures outlined for stage A, patients
with reduced LVEF (<40%) should receive an ACE inhibitor

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(or ARB) and an evidence-based ÿ-blocker to prevent development of HF, regard-less of whether
they have had an MI. Patients with a previous MI and reduced LVEF should also receive an ACE
inhibitor or ARB, evidence-based ÿ-blockers, and a statin.

• ACC/AHA Stage C: These patients have structural heart disease and previous or cur-
rent HF symptoms and include both HFrEF and HFpEF. In addition to treatments for
stages A and B, patients with HFrEF in stage C should receive guideline-directed
medical therapy (GDMT) that includes an ACE inhibitor, ARB, or angiotensin receptor–
neprilysin inhibitor (ARNI; valsartan–sacubitril) together with an evi-dence-based ÿ-
blocker, and an aldosterone antagonist in eligible patients to reduce morbidity and
mortality (Fig. 9-1). Loop diuretics, hydralazine–isosorbide dinitrate (ISDN), digoxin,
and ivabradine are also used in select patients.
• ACC/AHA Stage D HFrEF: These patients have persistent HF symptoms despite
maximally tolerated GDMT. They should be considered for specialized interventions,
including mechanical circulatory support, continuous IV positive inotropic therapy,
cardiac transplantation, or hospice care (when no additional treatments are appropriate).

NONPHARMACOLOGIC THERAPY OF CHRONIC HEART FAILURE

•Interventions include cardiac rehabilitation and restriction of fluid intake and dietary
sodium intake (<2–3 g of sodium/day) with daily weight measurements.
•In patients with hyponatremia (serum sodium <130 mEq/L [mmol/L]) or persistent volume
retention despite high diuretic doses and sodium restriction, limit daily fluid intake to 2 L/
day from all sources.
• Revascularization or anti-ischemic therapy in patients with coronary disease may reduce
HF symptoms.
• Drugs that can aggravate HF should be discontinued if possible.

PHARMACOLOGIC THERAPY FOR STAGE C HFrEF

•In general, patients with stage C HFrEF should receive an ACE inhibitor, ARB, or ARNI
along with an evidence-based ÿ-blocker, plus an aldosterone antagonist in select
patients (Fig. 9-1). Administer a diuretic if there is evidence of fluid retention.
A hydralazine–nitrate combination, ivabradine, or digoxin may be considered in select
patients. Drug dosing recommendations are provided in Table 9-1.

Diuretics
• Compensatory mechanisms in HF stimulate excessive sodium and water retention, often leading to
systemic and pulmonary congestion. In conclusion, diuretic therapy (in addition to sodium restriction)
is recommended for all patients with clinical evidence of fluid retention. However, because they do
not alter disease progression or prolong survival, diuretics are not required for patients without fluid
retention.

• Thiazide diuretics (eg, hydrochlorothiazide) are relatively weak and are infrequently
used alone in HF. However, thiazides or the thiazide-like diuretic metolazone can be
used in combination with a loop diuretic to promote very effective diuresis. Thiazides
may be preferred over loop diuretics in patients with only mild fluid retention and
elevated BP because of their more persistent antihypertensive effects.
• Loop diuretics (furosemide, bumetanide, and torsemide) are usually necessary to
restore and maintain euvolemia in HF. In addition to acting in the thick ascending limb
of the loop of Henle, they induce a prostaglandin-mediated increase in renal blood flow
that contributes to their natriuretic effect. Unlike thiazides, loop diuret-ics maintain their
effectiveness in the presence of impaired renal function, although higher doses may be
necessary.
• Adverse effects of diuretics include hypovolemia, hypotension, hyponatremia, hypo-
kalemia, hypomagnesemia, hyperuricemia, and renal dysfunction.

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GDMT for HFrEF Stage C

ACEI or ARB (Class I Evidence A)

AND
GDMT ÿ-blocker (Class I Evidence A)

Loop diuretic if needed for volume overload (Class I Evidence C)

Aldosterone antagonista (Class I Evidence A)

ARNIb (sacubitril/valsartan) (Class I Evidence BR)

Isosorbide dinitrate/hydralazine (Class I Evidence A if African-American and

persistently symptomatic on GDMT)
(Class IIa Evidence B if ACEI/ARB intolerant)

Ivabradinec (Class II Evidence BR)

Digoxind (Class IIa Evidence B if persistently symptomatic on GDMT)

a
NYHA class II-IV symptoms, estimated creatinine clearance >30 mL/min
and K+ <5.0 mEq/L
bNYHA class II-III symptoms tolerating an ACEI or ARB – switching to ARNI can
further reduce morbidity/mortality
c
NYHA class II-III symptoms in normal sinus rhythm and HR ÿ70 bpm on
maximally tolerated ÿ-blocker dose
dIndication is to reduce hospitalizations

(ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; ARNI, angiotensin
receptor–neprilysin inhibitor; bpm, beats per minute; GDMT, guideline-directed medical therapy; HFrEF,
heart failure with reduced ejection fraction; K+, serum potassium.)

FIGURE 9-1. Guideline-directed treatment algorithm for patients with ACC/

AHA stage C heart failure with reduced ejection fraction. (Adapted from Yancy
CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management-
ment of heart failure: A report of the American College of Cardiology Foundation/
American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62:e147–
e239.)

Angiotensin-Converting Enzyme Inhibitors

• ACE inhibitors decrease angiotensin II and aldosterone, attenuating many of their
deleterious effects that drive HF initiation and progression. ACE inhibitors also
inhibit the breakdown of bradykinin, which increases vasodilation and also leads
to cough. ACE inhibitors improve symptoms, slow disease progression, and
decrease mortality in patients with HFrEF. Current guidelines recommend that all
patients with HFrEF, regardless of whether or not symptoms are present, should
receive an ACE inhibitor to reduce morbidity and mortality, unless there are contraindicatio
• Clinical trials have documented favorable effects of ACE inhibitors on symptoms,
HF progression, hospitalizations, and quality of life. ACE inhibitors improve survival

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TABLE 9-1 Drug Dosing Recommendations for Stage C Heart Failure with Reduced Ejection
Fraction (HFrEF)

Usual Range with Normal

Generic (Brand) Name Initial Dose Renal Function

Loop Diuretics
Furosemide (Lasix) 20–40 mg once or twice daily 20–160 mg once or twice daily
Bumetanide (Bumex) 0.5–1 mg once or twice daily 1–2 mg once or twice daily
Torsemide (Demadex) 10–20 mg once daily 10–80 mg once daily
ACE Inhibitors

Captopril (Capoten) 6.25 mg three times daily Enalapril 50 mg three times daily
(Vasotec) 2.5 mg twice daily Lisinopril (Prinivil, 10–20 mg twice daily
Zestril) 2.5–5 mg once daily Quinapril (Accupril) 5 20–40 mg once daily
mg twice daily Ramipril (Altace) 1.25–2.5 mg 20–40 mg twice daily
once daily Fosinopril (Monopril) ) 5–10 mg once daily 10 mg once daily
Trandolapril (Mavik) 1 mg once daily Perindopril 40 mg once daily
(Aceon) 2 mg once daily Angiotensin 4 mg once daily
Receptor Blockers 8–16 mg once daily

Candesartan (Atacand) 4–8 mg once daily 32 mg daily

Valsartan (Diovan) 20–40 mg twice daily 160 mg twice daily
Losartan (Cozaar) 25–50 mg once daily 150 mg once daily
Angiotensin Receptor Blocker–Neprilysin Inhibitor
Sacubitril/Valsartan 49/51 mg sacubitril–valsartan 97/103 mg sacubitril–valsartan
(Entresto) twice daily twice daily
ÿ-Blockers
Bisoprolol (Zebeta) 1.25 mg once daily 10 mg once daily
Carvedilol (Coreg) 3.125 mg twice daily 25 mg twice daily
Carvedilol phosphate 10 mg once daily 80 mg once daily
(Coreg CR)
Metoprolol succinate 12.5–25 mg once daily 200 mg once daily
CR/XL (Toprol-XL)
Aldosterone Antagonists
Spironolactone 12.5–25 mg once daily (Aldactone) 25–50 mg once daily

Eplerenone (Inspra) 25 mg once daily 50 mg once daily

Other

Hydralazine–Isosorbide Hydralazine 37.5 mg 3 times daily Hydralazine 75 mg 3 times daily

Dinitrate (Bidil)
Isosorbide dinitrate 20 mg 3 Isosorbide dinitrate 40 mg 3 times
daily times daily
Digoxin (Lanoxin) 0.125–0.25 mg once daily 0.125–0.25 mg once daily
Ivabradine (Corlanor) 5 mg twice daily 5–7.5 mg twice daily

a Regimens proven in large clinical trials to reduce mortality.

ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker.
Data from Brater DC. Pharmacology of diuretics. Am J Med Sci. 2000;319:38-50; Yancy CW, Jessup
M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: A report of
the American College of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines. J Am Coll Cardiol. 2013;62:e147–e239.

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by 20%–30% compared with placebo. The benefits are independent of HF etiology

(ischemic vs nonischemic) and are greatest in patients with the most severe symptoms.

• Start therapy with low doses followed by gradual titration as tolerated to the target or
maximally tolerated doses (Table 9-1). Dose titration is usually accomplished by
doubling the dose every 2 weeks. Evaluate blood pressure (BP), renal function, and
serum potassium at baseline and within 1–2 weeks after the start of therapy and after
each dose increase. Although symptoms may improve within a few days of starting
therapy, it may take weeks to months before the full benefits are apparent. Even if
symptoms do not improve, continue long-term therapy to reduce mortality and
hospitalizations.
• The most common adverse effects include hypotension, renal dysfunction, and
hyperkalemia. A dry, nonproductive cough (occurring in 15%–20% of patients) is the
most common reason for discontinuation. Because cough is a bradykinin-mediated
effect, replacement with an ARB is reasonable; However, caution is required because
crossreactivity has been reported. Angioedema occurs in approximately 1% of patients
and is potentially life threatening; ACE inhibitors are contraindicated in patients with a
history of angioedema. ACE inhibitors are contraindicated in pregnancy due to various
congenital defects.

Angiotensin Receptor Blockers

• The ARBs block the angiotensin II receptor subtype AT1 , preventing the deleterious
effects of angiotensin II on ventricular remodeling. Because they do not affect the ACE
enzyme, ARBs do not affect bradykinin, which is linked to ACE inhibitor cough and
angioedema.
• ARBs are now a guideline-recommended alternative in patients who are unable to
tolerate an ACE inhibitor due to cough or angioedema. Although numerous ARBs are
available, only candesartan, valsartan, and losartan are recommended in the
guidelines because efficacy has been demonstrated in clinical trials. As with ACE
inhibitors, initiate therapy with low doses and then titrate to target doses. Evaluate BP,
renal function, and serum potassium within 1–2 weeks after starting therapy and after
dosage increases, with these parameters used to guide subsequent dose changes.

• ARBs are not suitable alternatives in patients with hypotension, hyperkalemia, or renal
insufficiency due to ACE inhibitors because they are just as likely to cause these
adverse effects. Careful monitoring is required when an ARB is used with another
inhibitor of the renin-angiotensin-aldosterone (RAAS) system (eg, ACE inhibitor or
aldosterone antagonist) because this combination increases the risk of these adverse
effects. Because ARBs do not affect bradykinin, they are not associated with cough
and have a lower risk of angioedema than ACE inhibitors. Caution should be exer-
cised when ARBs are used in patients with angioedema from ACE inhibitors because
crossreactivity has been reported. Similar to ACE inhibitors, ARBs are contraindicated
in pregnancy.

Angiotensin Receptor–Neprilysin Inhibitor

• Valsartan/Sacubitril is an ARNI approved to reduce the risk of cardiovascular death
and hospitalization for HF in patients with NYHA class II–IV HF and reduced LVEF.
Neprilysin is an enzyme that degrades bradykinin and other endogenous vasodilator and natriuretic
peptides. By reducing neprilysin-mediated breakdown of these compounds, vasodilation, diuresis,
and natriuresis are enhanced, and renin and aldosterone secretion is inhibited.

•In patients with HFrEF and NYHA class II–III symptoms tolerating an ACE inhibitor or
ARB, current guidelines recommend replacing those drugs with the ARNI to further
reduce morbidity and mortality. Discontinue ACE inhibitors 36 hours prior to initiating
the ARNI; no waiting period is needed in patients receiving an ARB.

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Titrate the initial starting dose to the target dose after 2–4 weeks (see Table 9-1).
Closely monitor BP, serum potassium, and renal function after the start of therapy
and after each titration step.
• The most common adverse effects include hypotension, dizziness, hyperkalemia,
worsening renal function, and cough. Angioedema is most common with sacubitril/
valsartan than with enalapril (0.5% vs 0.2%, respectively). Sacubitril/valsartan is
contraindicated in patients with a history of angioedema associated with an ACE
inhibitor or ARB. It is also contraindicated in pregnancy and should not be used
concurrently with ACE inhibitors or other ARBs.

ÿ-Blockers
• ÿ-Blockers antagonize the detrimental effects of the sympathetic nervous systems in
HF and slow disease progression. Clinical trial demonstrated evidence that certain ÿ-
blockers reduce HF mortality, all-cause hospitalizations, and hospitalizations for
worsening HF, among other endpoints.
• The ACC/AHA guidelines recommend use of ÿ-blockers in all stable patients with
HFrEF in the absence of contraindications or a clear history of ÿ-blocker intolerance.
Patients should receive a ÿ-blocker even if symptoms are mild or well controlled with
ACE inhibitor and diuretic therapy. It is not essential that ACE inhibitor doses be
optimized before a ÿ-blocker is started because the addition of a ÿ-blocker is likely to
be of greater benefit than an increase in ACE inhibitor dose.
• ÿ-Blockers are also recommended for asymptomatic persons with a reduced LVEF
(stage B) to decrease the risk of progression to HF.
• Carvedilol, metoprolol succinate (CR/XL), and bisoprolol are the only ÿ-blockers
shown to reduce mortality in large HF trials. Because bisoprolol is not available in the
necessary starting dose of 1.25 mg, the choice is typically limited to either carvedilol
or metoprolol succinate. Target doses are those associated with reductions in
mortality in placebo-controlled clinical trials (Table 9-1).
•Initiate ÿ-blockers in stable patients who have no or minimal evidence of fluid over-
load. Because of their negative inotropic effects, start ÿ-blockers in very low doses
with slow upward dose titration to avoid symptomatic worsening or acute
decompensation. Doses should be doubled no more often than every 2 weeks, as
tolerated, until the target or maximally tolerated dose is reached.
•Inform patients that ÿ-blocker therapy is expected to positively influence disease
progression and survival even if there is little symptomatic improvement. In addition,
dose titration is a long, gradual process; response to therapy may be delayed; and
HF symptoms may actually worsen during the initiation period.
• Adverse effects include bradycardia or heart block, hypotension, fatigue, impaired
glycemic control in diabetic patients, bronchospasm in patients with asthma, and
worsening HF. Absolute contraindications include uncontrolled bronchospastic dis-
ease, symptomatic bradycardia, advanced heart block without a pacemaker, and
acute decompensated HF. However, ÿ-blockers may be tried with caution in patients
with asymptomatic bradycardia, COPD, or well-controlled asthma.

Aldosterone Antagonists
• Spironolactone and eplerenone block mineralocorticoid receptors, the target for
aldosterone. In the kidney, aldosterone antagonists inhibit sodium reabsorption and
potassium excretion. However, diuretic effects with low doses are minimal, suggest-
ing that their therapeutic benefits result from other actions. In the heart, aldosterone
antagonists inhibit cardiac extracellular matrix and collagen deposition, thereby
attenuating cardiac fibrosis and ventricular remodeling. Aldosterone antagonists also
attenuate the systemic proinflammatory state, atherogenesis, and oxidative stress
caused by aldosterone.
• Current guidelines recommend adding a low-dose aldosterone antagonist to standard
therapy to improve symptoms, reduce the risk of HF hospitalization, and increase
survival in select patients provided that serum potassium and renal function can be
carefully monitored. Based on clinical trial data in HFrEF, low-dose aldosterone
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antagonists may be appropriate for: (1) patients with mild to moderately severe HFrEF
(NYHA class II–IV) who are receiving standard therapy, and (2) those with LV
dysfunction and either acute HF or diabetes early after MI.
• Start with low doses (spironolactone 12.5 mg/day or eplerenone 25 mg/day) especially
in older persons and those with diabetes or a creatine clearance <50 mL/
min/1.73m2 (0.48 mL/sec/m2 (Table 9-1).
• Avoid aldosterone antagonists in patients with renal impairment, elevated serum
potassium (>5 mEq/L [mmol/L]), or history of severe hyperkalemia. Spironolactone
also interacts with androgen and progesterone receptors, which may lead to gyneco-
mastia, impotence, and menstrual irregularities in some patients.

Nitrates and Hydralazine

•Isosorbide dinitrate (ISDN) is a venodilator that reduces preload, whereas hydrala-
zine is a direct arterial vasodilator that reduces systemic vascular resistance (SVR)
and increases stroke volume and CO. The beneficial effects of combining a nitrate
with hydralazine extend beyond their complementary hemodynamic actions and are
likely related to attenuating the biochemical processes driving HF progression.
• Guidelines recommend addition of hydralazine/ISDN to self-described African
Americans with HFrEF and NYHA class III–IV symptoms treated with ACE inhibitors
(or ARBs) and ÿ-blockers. The combination can also be useful in patients unable to
tolerate either an ACE inhibitor or ARB because of renal insufficiency, hyperka-lemia,
or hypotension.
• Obstacles to successful therapy with the combination include the need for frequent
dosing (ie, three times daily with the fixed-dose combination product), high frequency
of adverse effects (eg, headache, dizziness, and GI distress), and increased cost for
the fixed-dose combination product.

Ivabradine
•Ivabradine inhibits the If current in the sinoatrial node that is responsible for con-
trolling HR, thereby slowing spontaneous depolarization of the sinus node and
resulting in a dose-dependent slowing of the HR. It does not affect AV conduction,
BP, or myocardial contractility. Elevated resting heart rate (HR) (>70–80 bpm) is an
independent risk factor for adverse HFrEF outcomes, and ÿ-blockers are frequently
underdosed in clinical practice for a variety of reasons. Because of the clear benefits
of ÿ-blockers on mortality, labored should titrate to the maximum tolerated doses
before considering use of ivabradine.
•Ivabradine is indicated to reduce the risk of hospitalization for worsening HF in patients
with LVEF ÿ35% who are in sinus rhythm with resting HR ÿ70 bpm and are either on
a maximally tolerated dose of a ÿ-blocker or have a contraindication to ÿ -blocker use.

• The usual starting dose is 5 mg twice daily with meals (Table 9-1). After 2 weeks of
treatment, if the resting HR is between 50 and 60 bpm, the dose should be continued.
If the HR is >60 bpm, the dose can be increased to the maximum of 7.5 mg twice
daily. If at any point the HR is <50 bpm or the patient has symptomatic bradycardia,
the dose should be reduced by 2.5 mg twice daily; if the patient is only receiving 2.5
mg twice daily, ivabradine should be discontinued.
• The most common adverse effects are bradycardia, atrial fibrillation, and visual
disturbances.

Digoxin
• Although digoxin has positive inotropic effects, its benefits in HF are related to its
neurohormonal effects. It attenuates the excessive sympathetic system nervous
activation in HF and increases parasympathetic activity, thereby decreasing HR and
enhancing diastolic filling. Observational studies of digoxin conducted in the context
of contemporary HF therapy showed either neutral effects or reductions in hospital-
izations and either neutral or detrimental effects of digoxin on mortality.

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• Based on available data, digoxin is not considered a first-line agent in HF, but a trial
may be considered in conjunction with GDMT including ACE inhibitors (or ARBs), ÿ-
blockers, and diuretics in patients with symptomatic HFrEF to improve symptoms and
reduce hospitalizations. Digoxin may also be considered to help control ven-tricular
rate in patients with HFrEF and supraventricular arrhythmias, although ÿ-blockers are
generally more effective rate control agents, especially during exercise.
•In the absence of digoxin toxicity or serious adverse effects, digoxin should be con-
tinued in most patients. Digoxin withdrawal may be considered for asymptomatic
patients who have significant improvement in systolic function with optimal ACE
inhibitor and ÿ-blocker treatment.
• The target serum digoxin concentration for most patients is 0.5–0.9 ng/mL (0.6–1.2
nmol/L). Most patients with normal renal function can achieve this level with a dose of
0.125 mg/day. Patients with decreased renal function, low body weight, advanced age,
or interacting drugs (eg, amiodarone) should receive 0.125 mg every other day.

PHARMACOLOGIC THERAPY FOR HFpEF

• Treatment includes controlling HR and BP, alleviating causes of myocardial ischemia,
reducing volume, and restoring and maintaining sinus rhythm in patients with atrial
fibrillation. Many of the drugs are the same as those used to treat HFrEF (eg, diuret-
ics, ÿ-blockers), but the rationale and dosing may be different.
• A loop or a thiazide diuretic should be considered for patients with volume overload.
Use a loop diuretic for more severe volume overload or inadequate response to a
thiazide. Avoid lowering preload excessively, which may reduce stroke volume and
CO. Start diuretics at low doses to avoid hypotension and fatigue.
• ACE inhibitors may be considered in all patients, especially patients with symptom-atic atherosclerotic
cardiovascular disease or diabetes and one additional risk factor.
• ARBs may be considered in all patients, especially those who are intolerant of ACE
inhibitors.
• Aldosterone antagonists can reduce the risk of hospitalization in patients who do not
have contraindications and are not at risk for hyperkalemia. They may be beneficial for
patients with elevated BNP or NT-proBNP.
• ÿ-Blockers should be considered in patients with one or more of the following conditions:
(1) MI, (2) hypertension, and (3) atrial fibrillation requiring ventricular rate control.
• Nondihydropyridine calcium channel blockers (CCB; diltiazem or verapamil) should
be considered for patients with atrial fibrillation warranting ventricular rate control who
are either intolerant to or have not responded to a ÿ-blocker. A non-dihydropyridine or
dihydropyridine (eg, amlodipine) CCB can be considered for symptom-limiting angina
or hypertension.

TREATMENT OF ACUTE DECOMPENSATED HEART FAILURE (ADHF)

GENERAL APPROACH
• Acute decompensated heart failure involves patients with new or worsening signs or
symptoms (often resulting from volume overload and/or low CO) requiring medical
intervention, such as emergency department visit or hospitalization.
• Goals of Treatment: The overall goals are to relieve symptoms, improve hemodynamic
stability, and reduce short-term mortality so the patient can be discharged in a stable
compensated state on oral drug therapy.
• Consider hospitalization based on clinical findings. Admission to an intensive care unit
(ICU) may be required if the patient experiences hemodynamic instability requiring
frequent monitoring of vital signs, invasive hemodynamic monitoring, or rapid titration
of IV medications with close monitoring.
• Focus the history and physical exam on potential etiologies of ADHF; presence of
precipitating factors (eg, arrhythmias, hypertension, myocardial ischemia or infarction,
anemia, and thyroid disorders); onset, duration, and severity of symptoms; and a
careful medication history.

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Heart Failure | CHAPTER 9

• Symptoms of volume overload include dyspnea, orthopnea, PND, ascites, GI symp-

toms (poor appetite, nausea, early satiety), peripheral edema, and weight gain. Low
output symptoms include altered mental status, fatigue, GI symptoms (similar to volume
overload), and decreased urine output.
• Signs of volume overload include pulmonary crackles, elevated jugular venous pressure,
HJR, S3 gallop, and peripheral edema. Low output signs include tachycar-dia,
hypotension (more commonly) or hypertension, narrow pulse pressure, cool extremities,
pallor, and cachexia.
• Laboratory testing may include BNP or NT-proBNP, thyroid function tests, complete
blood count, cardiac enzymes, and routine serum chemistries (eg, serum creatinine,
liver function tests).
• Ascertain hemodynamic status to guide initial therapy. Patients may be categorized into
one of four hemodynamic subsets based on volume status (euvolemic or “dry” vs
volume overloaded or “wet”) and CO (adequate CO or “warm” vs hypoperfusion or
“cold”) (Fig. 9-2 ).
• Reserve invasive hemodynamic monitoring for patients refractory to initial therapy,
whose volume status is unclear, or who has significant hypotension or worsening renal
function despite appropriate initial therapy.
• Address and correct reversible or treatable causes of decompensation.
• Assess medications being taken prior to admission and determine whether adjustment-
ment or discontinuation is required.
•If fluid retention is evident on physical exam, pursue aggressive diuresis, preferably
with IV diuretics.
•In the absence of cardiogenic shock or symptomatic hypotension, strive to continue all
GDMT for HF. ÿ-blockers may be temporarily held or dose-reduced if recent changes
are responsible for acute decompensation. Other GDMT (ACE inhibitors, ARBs, ARNI,
and aldosterone antagonists) may also need to be temporarily withheld in the presence
of renal dysfunction, with close monitoring of serum potassium. Most patients may
continue to receive digoxin at doses targeting a trough serum concentration of 0.5–0.9
ng/mL (mcg/L; 0.6–1.2 nmol/L).

NONPHARMACOLOGIC THERAPY FOR ADHF

• Place all patients with congestive symptoms on sodium restriction (<2 g daily) and
Consider fluid restriction for refractory symptoms.
• Consider noninvasive ventilation for patients in respiratory distress due to acute
pulmonary edema, particularly those at risk for intubation.
• Provide pharmacologic thromboprophylaxis with unfractionated heparin or low-
molecular-weight heparin for most patients with limited mobility; consider mechanical
thromboprophylaxis with intermittent pneumatic compression devices in patients at high
risk for bleeding.
• Most nonpharmacologic therapies for ADHF are reserved for patients failing pharmaco-
logic therapy. Ultrafiltration and wireless invasive hemodynamic monitoring (W-IHM)
may be used to manage congestive symptoms. Temporary mechanical circulatory
support (MCS) with an intra-aortic balloon pump (IABP), ventricular assist device (VAD),
or extracorporeal membrane oxygenation (ECMO) may be considered for hemodynamic
stabilization until the underlying etiology of cardiac dysfunction resolves or has been
corrected (“bridge to recovery”) or until evaluation for definitive therapy (eg, durable
MCS or cardiac transplantation) can be completed (“bridge to decision”).
IV vasodilators and inotropes may be used with temporary MCS to maximize
hemodynamic and clinical benefits or facilitate device removal. Systemic anticoagulant
therapy is generally required to prevent device thrombosis, regardless of the method selected.
• Durable MCS with temporary device implantation is used for patients awaiting heart
transplantation who are unlikely to survive until a suitable donor is identified (“bridge to
transplantation”). Permanent device implantation is used in patients ineligible for heart
transplantation due to advanced age or comorbid conditions (“destination therapy”).

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106

Subset II (warm and wet)

Subset I
Symptom Persistent
(warm and dry)
relief symptoms
IV loop diuretic
± IV vasodilator

Optimized chronic See Subset I Use adjunct strategies

oral medications to overcome diuretic resistance
Persistent
symptoms

PAC to guide further management

2.2
Cardiac
index
m2 )
min/
(L/

Subset IV
Subset III
Orthostatic (cold and wet)
(cold and dry) No orthostasis
or
PCWPÿ15 mm Hg PCWP 15-18 mm Hg SBP < 90 mm Hg Assess SBP SBPÿ90 mm Hg
Assess volume status ± ± PAC
PAC
IV inotrope No
SBP IV diuretic
SBPÿ90 mm Hg (± vasopressor improvements
IV fluids ± IV vasodilator
<90 mm Hg Assess SBP if needed)
± PAC +

No IV diuretic
IV inotrope ± PAC
improvements
(± vasopressor if needed) IV vasodilator No
No improvements improvements

MCS MCS

18
Pulmonary capillary wedge pressure (mm Hg)

(IV, intravenous; MCS, mechanical circulatory support; PAC, pulmonary artery catheter; PCWP, pulmonary capillary wedge pressure; SBP, systolic BP.)

FIGURE 9-2. General management algorithm for acute decompensated heart failure based on clinical presentation. Patients may be categorized into a hemodynamic subset based on signs and symptoms or invasive
hemodynamic monitoring. Adjunct strategies for overcoming diuretic resistance include increasing the dose of loop diuretic; switching to a continuous infusion; adding a diuretic with an alternative mechanism of action, an IV
vasodilator, or an IV inotrope; and in select patients, adding mechanical circulatory support.
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Heart Failure | CHAPTER 9

• Cardiac transplantation is the best option for patients with irreversible advanced HF.
New surgical strategies such as ventricular aneurysm resection and myocardial cell
transplantation offer additional options for patients ineligible for VAD implantation or
heart transplantation.
PHARMACOLOGIC THERAPY FOR ADHF
Loop Diuretics
• Current guidelines recommend IV loop diuretics (furosemide, bumetanide) as first-
line therapy for ADHF patients with volume overload.
• Bolus administration reduces preload by functional venodilation within 5–15 minutes
and later (>20 minutes) via sodium and water excretion, thereby improving pulmonary
congestion. Although patients with HFrEF can tolerate significant reductions in preload
without compromising stroke volume, excessive diuresis can decrease CO. Excessive
reductions in venous return may also compromise CO in diastolic dysfunction,
intravascular volume depletion, or patients in whom CO is significantly dependent on
adequate filling pressure (ie, preload-dependent). Reflex increases in neurohormonal
activation (ie, elevated renin, norepinephrine, and AVP) may result in arteriolar and
coronary vasoconstriction, tachycardia, and increased myocardial oxygen consumption.

• Use low doses (equivalent to IV furosemide 20–40 mg) initially in ADHF patients who
are naïve to loop diuretics. For patients taking loop diuretics prior to admission, a total
daily dose of 1- to 2.5-times their home dose is recommended. Higher doses are
associated with more rapid relief of congestive symptoms but may also increase the
risk of transient worsening of renal function. Doses may be administered as either an
IV bolus (ie, divided every 12 hours) or continuous IV infusion. Use diuretic therapy
judiciously to obtain the desired improvement in congestive symptoms while avoiding
a reduction in CO, symptomatic hypotension, or worsening renal function.
• Diuretic resistance may be improved by administering larger IV bolus doses,
transitioning from IV bolus to continuous IV infusions, or adding a second diuretic with
a different mechanism of action, such as a distal tubule blocker (eg, oral metolazone,
oral hydrochlorothiazide ). , or IV chlorothiazide). Sequential nephron blockade
with a loop and thiazide-type diuretic should generally be reserved for inpatients who
can be monitored closely for the development of severe electrolyte and intravascular
volume depletion. In the outpatient setting, a very low dose of the thiazide-type diuretic
or infrequent administration (eg, 1–3 times weekly) is recommended.

Vasopressin Antagonists
• Vasopressin receptor antagonists affect one or two AVP (antidiuretic hormone)
receptors, V1A or V2 . Stimulation of V1A receptors (located in vascular smooth
muscle cells and myocardium) results in vasoconstriction, myocyte hypertrophy,
coronary vasoconstriction, and positive inotropic effects. V2 receptors are located in
renal tubules, where they regulate water reabsorption.
ÿ Tolvaptan selectively binds to and inhibits the V2 receptor. It is an oral agent
indicated for hypervolemic and euvolemic hyponatremia in patients with syndrome
of inappropriate antidiuretic hormone (SIADH), cirrhosis, or HF. Tolvaptan is
typically initiated at 15 mg orally daily and then titrated to 30 or 60 mg daily as
needed to resolve hyponatremia. It is a substrate of cytochrome P450-3A4 and is
contraindicated with potent inhibitors of this enzyme. The most common side
effects are dry mouth, thirst, urinary frequency, constipation, and hyperglycemia.
ÿ Conivaptan nonselectively inhibits both the V1A and V2 receptors. It is an IV agent
indicated for hypervolemic and euvolemic hyponatremia due to a variety of causes
but is not indicated for patients with HF.
• Monitor patients closely to avoid an excessively rapid rise in serum sodium that could
cause hypotension or hypovolemia requiring drug discontinuation. Therapy may be
restarted at a lower dose if hyponatremia recurs or persists and adverse effects resolve.

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• The role of vasopressin receptor antagonists in the long-term management of HF is

unclear. In a clinical trial of hospitalized patients with HF, tolvaptan improved
hyponatremia, diuresis, and signs/symptoms of congestion. However, the study failed to
demonstrate improved long-term outcomes, including morbidity and mortality.
Another randomized trial in patients with ADHF found worsening renal function in
significantly more patients receiving tolvaptan than placebo. Overall, these two trials do
not support routine use of tolvaptan in ADHF, and it should be reserved for managing
severe hyponatremia.

Vasodilators
• Venodilators reduce preload by increasing venous capacitance, improving symptoms of
pulmonary congestion in patients with high ventricular filling pressures. Arterial
vasodilators counteract the peripheral vasoconstriction and impaired CO that can result
from activation of the sympathetic nervous system, RAAS, and other neuro-hormonal
mediators in HF. Arterial vasodilators reduce impedance, decrease after-load and
cause reflex improvement in LV performance and increased CO. Mixed vasodilators act
on both arterial resistance and venous capacitance vessels, reducing congestive
symptoms while increasing CO.
•IV vasodilators should be considered before positive inotropic therapy in patients with low CO and
elevated SVR (or elevated BP in those without a pulmonary artery catheter). However, hypotension
may preclude their use in patients with preexisting low BP or SVR.

•IV nitroglycerin is often preferred for preload reduction in ADHF, especially in patients
with pulmonary congestion. It reduces preload and pulmonary capillary wedge pressure
(PCWP) via functional venodilation and mild arterial vasodilation.
In higher doses, nitroglycerin displays potent coronary vasodilating properties and
beneficial effects on myocardial oxygen demand and supply, making it the vasodila-tor
of choice for patients with severe HF and ischemic heart disease.
ÿ Initiate nitroglycerin at 5–10 mcg/min (0.1 mcg/kg/min) and increase every 5–10
minutes as necessary and tolerated. Maintenance doses usually range from 35 to
200 mcg/min (0.5–3 mcg/kg/min). Hypotension and excessive decrease in PCWP
are important dose-limiting side effects. Tolerance to the hemodynamic effects may
develop over 12–72 hours of continuous administration.
• Sodium nitroprusside is a mixed arteriovenous vasodilator that increases cardiac index
(CI) to a similar degree as dobutamine and milrinone despite having no direct inotropic
activity. However, nitroprusside generally produces greater decreases in PCWP, SVR,
and BP.
ÿ Hypotension is an important dose-limiting adverse effect of nitroprusside, and its use
should be primarily reserved for patients with elevated SVR. Close monitoring is
required because even modest HR increases can have adverse consequences in
patients with underlying ischemic heart disease or resting tachycardia.
ÿ Nitroprusside is effective in the short-term management of severe HF in a variety of
settings (eg, acute MI, valvular regurgitation, after coronary bypass surgery, and
ADHF). It does not usually worsen, and may improve, the balance between myo-
cardial oxygen demand and supply. However, an excessive decrease in systemic
arterial pressure can decrease coronary perfusion and worsen ischemia.
ÿ Nitroprusside has a rapid onset and a duration of action <10 minutes, necessitating
continuous IV infusions. Initiate therapy with a low dose (0.1–0.2 mcg/
kg/min) to avoid excessive hypotension, and increase by small increments (0.1–0.2
mcg/kg/min) every 5–10 minutes as tolerated. Usual effective doses range from 0.5
to 3 mcg/kg/min. Taper nitroprusside slowly when transitioning to oral medications to
avoid the rebound phenomenon of reflex neurohormonal activation after abrupt
withdrawal. Nitroprusside-induced cyanide and thio-cyanate toxicity are unlikely
when doses <3 mcg/kg/min are administered for less than 3 days, except in patients
with significant renal impairment (ie, serum creatinine >3 mg/dL [265 ÿmol/L ]).

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Heart Failure | CHAPTER 9

Inotropes
• Prompt correction of low CO in patients with “cold” subsets (III and IV) is required to
restore peripheral tissue perfusion and preserve end-organ function. Although IV
inotropes can improve hypoperfusion by enhancing cardiac contractility, potential
adverse outcomes limit their use to select patients with refractory ADHF. Inotropes
should be considered only as a temporizing measure to maintain end-organ perfu-
sion in patients with cardiogenic shock or severely depressed CO and low systolic BP
(ie, ineligible for IV vasodilators) until definitive therapy can be initiated, as a “bridge”
for patients with advanced HF who are eligible for MCS or cardiac trans-plantation,
or for palliation of symptoms in patients with advanced HF who are ineligible for MCS
or cardiac transplantation.
• Dobutamine and milrinone produce similar hemodynamic effects, but dobutamine
usually causes more pronounced increases in HR, and milrinone is associated with
greater relaxation in arterial smooth muscle.
• Dobutamine is a ÿ1 - and ÿ2 -receptor agonist with some ÿ1 -agonist effects; Its
positive inotropic effects are due to effects on ÿ1 -receptors. Stimulation of cardiac ÿ1
-receptors does not generally produce a significant increase in HR. Modest peripheral
ÿ2 -receptor-mediated vasodilation tends to offset minor ÿ1 -receptor-mediated vaso-
constriction; the net vascular effect is usually vasodilation.
ÿ CI is increased because of inotropic stimulation, arterial vasodilation, and a vari-
able increase in HR. It causes relatively little change in mean arterial pressure
(MAP) compared with the more consistent increases observed with dopamine.
Dobutamine should be considered over milrinone when a significant decrease in
MAP might further compromise hemodynamic function.
ÿ Vasodilation usually reduces PCWP, making dobutamine particularly useful in the
presence of low CI and an elevated LV filling pressure; However, these effects may
be detrimental in the presence of reduced filling pressure.
ÿ Initial doses of 2.5–5 mcg/kg/min may be increased progressively to 20 mcg/kg/min
based on clinical and hemodynamic responses. The dose should be tapered rather
than abruptly discontinued.
ÿ Dobutamine's major adverse effects are tachycardia and ventricular arrhythmias.
Potentially detrimental increases in oxygen consumption have also been observed.
• Milrinone inhibits phosphodiesterase III and produces positive inotropic and arterial
and venous vasodilating effects (an inodilator). It has supplemented use of amri-
none, which has a higher rate of thrombocytopenia.
ÿ During IV administration, milrinone increases stroke volume and CO with mini-mal
change in HR. However, the vasodilating effects may predominate, leading to
decreasing BP and a reflex tachycardia. Milrinone also lowers pulmonary PCWP
by venodilation and is particularly useful in patients with a low CI and elevated LV
filling pressure. However, this decrease in preload can be hazardous for patients
without excessive filling pressure, thus blunting the improvement in CO. Use mil-
rinone cautiously in severely hypotensive HF patients because it does not increase,
and may even decrease, arterial BP.
ÿ Most patients are started on a continuous IV infusion of 0.1–0.3 mcg/kg/min, titrated
to a maximum of 0.75 mcg/kg/min. A loading dose of 50 mcg/kg over 10 minutes
can be given if rapid hemodynamic changes are required, but its use is uncommon
due to an increased risk of hypotension.
ÿ The most notable adverse events are arrhythmia, hypotension, and thrombocyto-
penia. Measure the platelet count before and during therapy.
• Norepinephrine and dopamine have combined inotropic and vasopressor activity.
Although therapies that increase SVR are generally avoided in ADHF, they may be
required in select patients where marked hypotension precludes use of traditional
inotropes (eg, septic shock, refractory cardiogenic shock). These agents are
sometimes combined with traditional inotropes so each drug can be adjusted

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Independently to achieve the desired hemodynamic response, although little data exists
to support that practice.
ÿ Norepinephrine stimulates ÿ1 - and ÿ1 -adrenergic receptors. Stimulation of ÿ1
-receptors in myocardial tissue increases HR, contractility, and therefore CO, but
peripheral ÿ1 -receptor-induced vasoconstriction is the predominant clinical
hemodynamic effect. Lack of affinity for ÿ2 -receptors may be responsible for the
limited effect of norepinephrine on CO.
ÿ Dopamine is an endogenous precursor of norepinephrine that stimulates ÿ1 , ÿ1 , ÿ2 ,
and D1 (vascular dopaminergic) receptors. Positive inotropic effects mediated
primarily by ÿ1 -receptors are prominent with doses of 2–5 mcg/kg/min. The CI is
increased with minimal changes in SVR. At doses between 5 and 10 mcg/kg/min,
chronotropic and ÿ1- mediated vasoconstriction become more prominent and MAP
usually increases as a result of increases in both CI and SVR.
ÿ Studies of low-dose dopamine (2–5 mcg/kg/min) given with IV loop diuret-ics to
enhance diuresis demonstrated no improvements in urine output, renal protection, or
symptom relief, but increased rates of tachycardia. Thus, low-dose dopamine may
not provide any advantages over traditional inotropes in this setting.

EVALUATION OF THERAPEUTIC OUTCOMES

CHRONIC HEART FAILURE
• Ask patients about the presence and severity of symptoms and how symptoms affect
daily activities.
• Evaluate efficacy of diuretic treatment by loss of the signs and symptoms of excess fluid
retention. Focus the physical examination on body weight, extent of JVD, presence of
HJR, and presence and severity of pulmonary congestion (crackles, dyspnea on
exertion, orthopnea, and PND) and peripheral edema.
• Other outcomes are improvement in exercise tolerance and fatigue, decreased noc-
turia, and decreased HR.
• Monitor BP to ensure that symptomatic hypotension does not develop as a result of
drug therapy.
• Body weight is a sensitive marker of fluid loss or retention, and patients should weigh
themselves daily and report changes of 3–5 lb (1.4–2.3 kg) to their healthcare provider
so adjustments can be made in diuretic doses.
• Symptoms may worsen initially on ÿ-blocker therapy, and it may take weeks to
months before patients notice symptomatic improvement.
• Routine monitoring of serum electrolytes (especially potassium and magnesium) and
renal function (BUN, serum creatinine, eGFR) is mandatory in patients with HF.

ACUTE DECOMPENSATED HEART FAILURE

• Assess the efficacy of drug therapy with daily monitoring of weight, strict fluid intake and
output measurements, and HF signs/symptoms. Monitor frequently for electro-lyte
depletion, symptomatic hypotension, and renal dysfunction. Assess vital signs frequently
throughout the day.
• Patients should not be discharged until optimal volume status is achieved, they have been
successfully transitioned from IV to oral diuretics, and IV inotropes and vaso-dilators have been
discontinued for at least 24 hours.
• Optimize GDMT in hemodynamically stable patients without contraindications, including reinitiation of
therapies withheld earlier in the admission. Low-dose ÿ-blockers may be safely initiated at discharge
without increasing the risk of read-mission. Transitioning eligible patients to the ARNI sacubitril/
valsartan may also be considered.

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Heart Failure | CHAPTER 9

• Schedule a follow-up appointment at 7–10 days postdischarge and a nurse visit or

phone call at 3 days for select patients. Also schedule pertinent follow-up labs (eg,
potassium, serum creatinine, INR, serum digoxin concentration).
• All patients should be considered for referral to a formal disease management
program.

See Chapter 35, Chronic Heart Failure, authored by Robert B. Parker, Jean M. Nappi,
and Larisa H. Cavallari, and Chapter 36, Acute Decompensated Heart Failure, authored
by Brent N. Reed and Jo E. Rodgers, for more detailed discussions of these topics.

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