Heart Failure
DEFINITIONS
o
HF is a complex clinical syndrome caused by inability of the
heart to pump sufficient blood to meet the body’s metabolic
needs
o
HF is a complex clinical syndrome caused by any structural or
functional cardiac disorder that impairs the ability of the
ventricle to fill with or eject blood.
 HF
can result from any disorder that reduces ventricular
filling (diastolic dysfunction) and/or myocardial contractility
(systolic dysfunction)

Congestive HF is a term that is sometimes used, and may
describe acute or chronic HF with evidence of volume
overload.

Heart failure is called congestive HF when fluid builds up in
various parts of the body, i.e. it is often used as one of the
common symptoms (swelling or water retention)
Classification
1. Based on the location of the deficit: predominantly left
ventricular, right ventricular or biventricular
2. Depending on the time of onset: acute or chronic
Classification
3. Clinically, based on the functional status of heart:
a. HF with Preserved EF (HFpEF): Patients usually have LVEF ≥50%
a. HF with Reduced EF (HFrEF): Patients with a clinical diagnosis of HF
and LVEF ≤40%
c. HF with mid-range EF (HFmEF): Patients with LVEF between 41% to
49% represent a ‘grey area’ and subcategorized as borderline HFmEF
Ejection Fraction (EF)
is the fraction of blood
pumped out of the
ventricle with each beat
Left ventricular ejection fraction (LVEF) is the central measure of left
ventricular systolic function.
LVEF is the fraction of chamber volume ejected in systole (stroke
volume) in relation to the volume of the blood in the ventricle at the
end of diastole (end-diastolic volume).
The simplest classification as per American College of Cardiology
(ACC) that is used clinically as follows:

Hyperdynamic = LVEF greater than 70%

Normal = LVEF 50% to 70% (midpoint 60%)

Mild dysfunction = LVEF 40% to 49% (midpoint 45%)

Moderate dysfunction = LVEF 30% to 39% (midpoint 35%)

Severe dysfunction = LVEF less than 30%
 HFpEF
o
Defined as an LVEF of 50% or greater
o
Accounts for about 50% (highly variable) of patients with HF
o
Normal wall motion
o
In patients with HFpEF who are mostly females and older
adults EF is usually more than 50%
 HFpEF
o
the volume of the left-ventricular (LV) cavity is typically
normal, but the LV wall is thickened and stiff; hence, the
ratio of LV mass/end-diastolic volume is high .
 HFrEF
o
Defined as a clinical diagnosis of HF and an LVEF of 40% or
less
o
Dilated ventricle
o
in patients with HFrEF, the LV cavity is typically dilated, and
the ratio of LV mass/end-diastolic volume is either normal or
reduced.
As far as treatment and outcome are concerned, Patients with
HFrEF respond favorably to the standard pharmacological
treatment regimen and demonstrate better prognosis.
Patients with HFpEF have not been shown to respond to
standard pharmacological treatments, except for nitrates, and
therefore, have a poor prognosis, especially during the
decompensated phase of HF
Common precipitating factors that may cause a previously
compensated HF patient to decompensate include:
- myocardial ischemia and
-pulmonary infections
- nonadherence with diet or drug therapy
- inappropriate medication use.
Drugs may precipitate or exacerbate HF because of their
negative inotropic, cardiotoxic, or sodium- and waterretaining properties.
Etiology
•
Hypertension
•
Peripartum cardiomyopathy
•
Valvular heart disease
•
Tachycardia induced cardiomyopathy
•
Metabolic causes e.g. obesity
•
Endocrine disorders (e.g. DM and hyper/hypothyroidism)
•
Toxins (e.g. alcohol, cocaine, cobalt, iron secondary to transfusion)
Etiology
•
Nutritional deficiency (e.g. thiamine and L-carnitine deficiency)
•
Medications (e.g. anthracyclines, trastuzumab, amphetamines,
and anabolic steroids)
•
High-output conditions (e.g. anemia and Paget disease)
•
Myocarditis due to viruses, HIV/AIDS, medications (e.g. antibiotics,
chlorthalidone and methyldopa)
Etiology
•
Connective tissue disorders (e.g. SLE, rheumatoid arthritis, and
scleroderma)
•
Infiltrative disorders (e.g. amyloidosis, sarcoidosis, and
hemochromatosis)
•
Stress cardiomyopathy especially in post-menopausal women.
 CAD, hypertension, valvular heart disease, and myocarditis are the
most common causes of chronic HF
Clinical Presentation

Patient presentation may range from asymptomatic to cardiogenic
shock

Symptoms & signs (Common):
- Dyspnea (particularly on exertion)
- fatigue (which lead to exercise intolerance)
- Orthopnea
- Raised jugular venous pressure (jugular venous distention)
- Pulmonary congestion and peripheral edema
(due to fluid overload)
Clinical Presentation

Symptoms & signs (Common):
- paroxysmal nocturnal dyspnea
- Basal crepitations
- Tachycardia
- nocturnal dyspnea
- tachypnea
- cough
Clinical Presentation

Other symptoms & signs:
- Nonspecific symptoms may include fatigue, nocturia,
hemoptysis, abdominal pain, anorexia, nausea, bloating, ascites,
poor appetite, mental status changes, and weight gain
Clinical Presentation and Diagnosis

Physical examination findings:
- pulmonary crackles
- S3 gallop (Third Heart Sound), cool extremities
- Cheyne–Stokes respiration
- tachycardia
- narrow pulse pressure
- cardiomegaly
- symptoms of pulmonary edema (extreme breathlessness and
anxiety, sometimes with coughing and pink, frothy sputum)
- peripheral edema
- jugular venous distention (Raised jugular venous pressure)
- hepatojugular reflux
- hepatomegaly
Diagnosis

Patient’s history

physical examination to determine the presence of clinical
symptoms and signs

laboratory tests
Diagnosis

Laboratory Tests:
- Natriuretic peptide:
B-type natriuretic peptide (BNP) greater than 100 pg/mL (>100 ng/L)
N-terminal pro-B-type natriuretic peptide (NT-proBNP) >400 pg/mL
* Both natriuretic peptide biomarkers have been used increasingly to establish the
presence and severity of HF.
* This natriuretic peptide level is raised with advanced age, female sex, and renal failure,
anemia, pulmonary diseases (pneumonia, apnoea , OSA), sever burns, cardiac surgery and
lowered with obesity.
Diagnosis

Laboratory Tests:
- Cardiac troponins: its conc. may be elevated in the setting of chronic
or acute decompensated HF, suggesting myocyte injury or necrosis.
* Elevations in either troponin I or T levels in the setting of acute HF are of prognostic
significance and must be interpreted in the clinical context.
- Serum creatinine: may be increased owing to hypoperfusion;
preexisting renal dysfunction can contribute to volume overload
- Complete blood count: useful to determine if HF is due to reduced
oxygen-carrying capacity
Diagnosis

Other Tests:
- Chest x-ray: useful for detection of cardiac enlargement, pulmonary edema, and pleural
effusions
- Echocardiogram (cardiac ultrasound imaging technique): provides immediate
information on chamber volumes, ventricular systolic and diastolic function, wall
thickness, valve function and pulmonary hypertension, and ejection fraction.
Transthoracic echocardiography establishes HF phenotype (i.e., HFrEF vs. HFpEF or
HFmrEF).
- Electrocardiogram (ECG): may be normal or could show numerous abnormalities
including acute ST-T–wave changes from myocardial ischemia, atrial fibrillation,
bradycardia, and LV hypertrophy
Classification of Heart Failure

Patients with HF can be classified according to severity of
symptoms by using the New York Heart Association (NYHA)
Functional Classification System OR the American College of
Cardiology and American Heart Association (ACC/AHA)

NYHA classification is based on the patient’s activity level and
exercise tolerance
Classification of Heart Failure
New York Heart
Association (NYHA)
American College of
Cardiology and American
Heart Association
(ACC/AHA)
It is based on symptoms and exercise capacity
It is more recent classification
It ranges from Class I to class IV
It is based on structural changes and symptoms.
It ranges from stage A to stage D. All patients with overt
HF are in stages C and D.
Class I with no limitations of physical activity,
while Class IV, symptoms of HF are present at
rest
Stage A is patients at high risk for HF, while Stage B
describes patients with no signs or symptoms of HF, but
with structural changes associated with the development of
the disease.
Classification of Heart Failure
NYHA functional classification
ACC/AHA stages of HF
(based on symptoms or physical activity)
(based on structure and damage to heart)
None
Stage A
At high risk for HF, but without
structural or functional abnormality
No signs or symptoms of HF
Class I
Asymptomatic HF; no limitations in physical
activity (e.g. walking or climbing stairs) caused by
HF symptoms
Stage B
Structural heart disease but without
signs or symptoms of HF (e.g. undue
fatigue, palpitation or dyspnoea)
Class I
No limitations in physical activity caused by HF
symptoms
Stage C
Structural heart disease with prior or
current symptoms of HF
Class II
Slight limitation of physical activity (climbing
stairs or walking uphill); asymptomatic at rest, but
symptoms of HF (dyspnoea, fatigue, palpitation, or
anginal pain) with normal level of activity
Class III Marked limitations in physical activity because of
HF symptoms; asymptomatic at rest
Class IV Symptoms of HF at rest or unable to carry out any
physical activity
(restricting walking distance and
limiting climbing to one flight of
stairs)
Classification of Heart Failure
NYHA functional classification
ACC/AHA stages of HF
(based on symptoms or physical activity)
(based on structure and damage to heart)
Class IV Symptoms of HF at rest
Stage D
Refractory HF requiring specialized
interventions
Comorbidities in HF
Gout
Hyperlipidaemia
Iron deficiency
COPD
Comorbidities in
patients with HF
HTN
Angina
Renal
dysfunction
Diabetes mellitus
Anaemia
Cachexia
Obesity
Depression
Sleep disturbance
Cancer
Treatment of HF
HF is a chronic condition and for patients their quality of life and
ability to continue with normal daily activities is important


Aims of treatment are:
- to relieve/control symptoms,
- to slow disease progression,
- to prevent or minimize hospitalizations,
- to improve quality of life, and
- prolong survival
The main treatments are:
- healthy lifestyle changes
- medication
- devices implanted in the chest to control the heart rhythm
- surgery
Nonpharmacologic Interventions
Lifestyle changes
Stop smoking
Increase physical activity—with guidance.
Weight loss in obese patients
Healthy diet—reduce salt intake (<2 gm/day), aim for five
portions of fruit or vegetables per day and low saturated fat intake
Fluid restriction
Fluid restriction: to avoid fluid overload, patients are usually
encouraged to limit the amount of fluid consumed per day
(max. 2 L/day from all sources)
 Non-surgical
devices
- Implantable cardiac defibrillators are used to prevent sudden
cardiac death
- Cardiac resynchronization devices can be used to improve the
pumping function

Revascularization (Coronary revascularisation)
If heart failure is due to reversible ischaemic disease, percutaneous
coronary intervention or coronary artery bypass grafting
revascularization procedures may improve myocardial function

Heart transplant
Certain patients with severe HF may meet the criteria to be
considered for a heart transplant after all other pharmacological and
nonpharmacological options
Cardiac transplantation is the best therapeutic option for patients with
chronic irreversible NYHA class IV HF, with a 10-year survival of
~50% in well-selected patients
Pharmacologic Interventions
ACE inhibitors, ARBs, beta-blockers, or
diuretics have all been shown effective in
management of HF
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Diuretics
- Indicated inpatients with evidence of fluid retention
- Short-term (days) benefits: decreased jugular venous distension,
pulmonary congestion, and peripheral edema
- Intermediate-term (weeks to months) benefits: decreased daily
symptoms, increased exercise tolerance
- Long-term (months to years) benefits : No benefit on mortality
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Diuretics
- Start with a low initial dose and then double the dose and titrate
according to the patient’s weight as needed.
- Loop diuretics are preferred because of their greater diuretic
capabilities; loop diuretics also retain efficacy with decreased renal
function
- Monitor and replace K and magnesium as needed, especially with loop
diuretics
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 ACEI (or ARB)
- ARB used in patients with cough and angioedema due to ACEI
 β-blocker
- It is recommended for all patients with stable, symptomatic HF (NYHA functional class
II to IV) to reduce the risk of HF hospitalization and death.
- Beta-blockers and ACE inhibitors are complementary and can be started together once
the diagnosis of HFrEF has been made (add to existing ACE inhibitor therapy (at least at
a low dose) when HF symptoms are stable and patients are euvolemic)
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Mineralocorticoid/Aldosterone receptor antagonists (MRA)
Add MRAs (e.g., spironolactone or eplerenone) to ACEIs (or ARB) and β-blockers is
recommended in patients with NYHA functional class II to IV HF who have LVEF ≤35%
to reduce morbidity and mortality
 Ivabradine for persistently symptomatic HF with sinus rhythm,
LVEF ≤35% and a resting heart rate ≥70 beats/min
It is a new therapeutic agent (approved by the FDA in 2015) that selectively inhibits the If
current in the sinus node (sinoatrial node), providing heart rate reduction.
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Angiotensin receptor-neprilysin inhibitor (ARNI)
(sacubitril/valsartan) for a patient on ACEI (or ARB) for chronic
NYHA functional class II/III symptoms
- It is novel therapy approved by the U.S. FDA in 2015
- It now receives for NYHA functional class II/III patients who have been stable on a
prior regimen of ACE inhibitor or ARB
- Benefits: decreased composite endpoint of death from CV causes or hospitalization for
HF, decreased mortality and hospitalization for HF
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Angiotensin receptor-neprilysin inhibitor (ARNI)
(sacubitril/valsartan)
Maintenance dose:
- Double the dose every 2–4 weeks to a target dose of sacubitril 97 mg/valsartan 103 mg
twice daily, as tolerated.
- If switching from an ACE inhibitor, allow a 36-hour washout period before initiating
sacubitril/valsartan.
Pharmacological treatment of HF with
reduced/preserved EF

HFrEF
 Angiotensin receptor-neprilysin inhibitor (ARNI)
(sacubitril/valsartan)
Monitoring:
- Monitor renal function and K 1–2 weeks after initiating therapy or increasing the dose,
especially in high-risk patients (e.g., preexisting hypotension, DM, K supplements,
azotemia).
- Monitor fluid status because patients may require a dose reduction in diuretic therapy.
Pharmacological treatment of HF with
reduced/preserved EF
 Implantable cardioverter-defibrillator (ICD) therapy
Primary prevention for (LVEF ≤ 35%, NYHA functional class II-III) or (NYHA
functional class II, LVEF≤ 30%) and secondary prevention
ICD is recommended in patients with LVEF ≤35% despite >3 months of treatment with
optimal pharmacological therapy to reduce the risk of sudden death.
 cardiac resynchronization therapy (CRT)
NYHA functional class II-IV HF, LVEF ≤ 35%, left bundle branch block (LBBB) with
QRS ≥150 ms

HFpEF
 Diuretics for volume control, high BP management, relief of
ischemia
Pharmacological
treatment of HF with
Pharmacologic
Interventions
reduced/preserved EF

A combination of ACEI, ARB, beta blockade, and spironolactone has
been successfully tried

In patients resistant to loop diuretics (1st line therapy in patients with
fluid retention), a thiazide may be added in combination
Pharmacologic Interventions

ACE inhibitors
- Patients with heart failure may have increased plasma angiotensin
II. So, ACEI block conversion of angiotensin I to angiotensin II.
- Angiotensin II causes vasoconstriction, remodelling of the heart,
and stimulates aldosterone release causing sodium and water
retention.
- Enalapril, captopril, and lisinopril have been mostly studied in
CHF trials and ramipril and trandolapril in post-MI trials
Pharmacologic Interventions

ACE inhibitors
- Benefits: decreased mortality, decreased hospitalizations,
symptom improvement, improved clinical status
- Start low and double the dose every 1–4 weeks to target dose
- Monitor SCr and K for 1–2 weeks after initiating therapy or
increasing the dose, especially in high-risk patients (preexisting
hypotension, DM, K supplements, azotemia).
Pharmacologic Interventions

ACE inhibitors
- Contraindications to the use of ACEI/ARB are bilateral renal
stenosis, serum potassium >5 mmol/L, and serum creatinine >2.5
mg/dL (relative contraindication)
* If creatinine rises above 3 mg/dL or K >5.5 mmol/L, the dose of ACEI
should be halved.
* With values >3.5 mg/dL creatinine or >6 mmol/L K, ACEI should be
stopped.
Pharmacologic Interventions

Beta-blockers
- β-blockers block the effect of the sympathetic nervous system, which is
activated in HF, reducing pre-load and afterload resulting in an increased in
cardiac output
-Benefits: slow disease progression, decreased mortality, hospitalizations,
improve symptoms and clinical status
- Only bisoprolol, carvedilol, and metoprolol succinate are recommended in
HFrEF.
Pharmacologic Interventions

Beta-blockers
- Beta-blockers should not be prescribed without diuretics in patients with current
or recent history of fluid retention.
- Start low and increase (double) the dose every 2 weeks (or slower, if needed) to
target dose. Aim to achieve target dose in 8–12 weeks
- Monitor BP, HR, and symptoms of hypotension or bradycardia (monitor in 1–2
weeks)
- If hypotension alone is the problem, try reducing the ACE inhibitor (or another
antihypertensive) first or scheduling one agent at bedtime and one in the morning.
- Do not increase ß-blocker dose during episodes of fluid retention after therapy
initiation or dose titration.
Pharmacologic Interventions

Beta-blockers
- Contraindications to the use of beta blockers are severe asthma,
second- or third-degree AV block, sick sinus syndrome (bradycardia
<50 bpm) without permanent pacing, phaeochromocytoma or cocaine
use (unopposed alpha receptors causing vasoconstriction).
Pharmacologic Interventions

Diuretics—symptom control: They are used for the symptomatic
treatment of fluid retention and overload in HF

The aim of treatment with diuretics is to maintain patients at their
‘dry weight’ and prevent sudden increase in fluid retention and
symptoms of fluid overload

First line is Loop diuretics (e.g. furosemide and bumetanide)
because they are most effective (especially in pulmonary oedema)
Pharmacologic Interventions
Diuretics

Thiazide diuretics produce a more sustained, gradual diuresis and
are used to treat fluid retention in mild heart failure (e.g. peripheral
oedema)

Over-diuresis should be avoided as this may lead to renal
impairment
Pharmacologic Interventions
Diuretics
 ADRs of duiretics: renal failure, hypotension, hyponatraemia,
hypokalaemia, fatigue, and gout. Hypokalaemia should be treated by
using a potassium-sparing diuretic (e.g. amiloride) or potassium
supplementation

Maintenance of potassium levels is important to reduce the risk of
cardiac arrhythmias

Serum electrolytes, renal function, and weight should be monitored
regularly during treatment especially after any increase in diuretic
dosage
Pharmacologic Interventions

Aldosterone receptor antagonists (ARAs):
- they reduce sodium and water retention
- aldosterone has a number of non-renal
effects such as stimulating myocardial fibrosis and remodelling,
endothelial dysfunction, and cardiac excitability, which are important
in the pathophysiology of HF
Pharmacologic Interventions

Aldosterone receptor antagonists (ARAs):
- Recommended in patients with NYHA class II–IV with an LVEF of 35% or
less to reduce morbidity and mortality unless a contraindication exists.
- Patients with NYHA class II should have a history of CV hospitalization or
elevated brain natriuretic peptide (BNP) levels
- Benefits of spironolactone in NYHA class III and IV HF: decreased mortality,
hospitalizations, and improved symptoms
Pharmacologic Interventions

Aldosterone receptor antagonists (ARAs):
- Benefits of eplerenone in NYHA class II HF: decreased composite endpoint of
death from CV causes or hospitalization from HF, decreased death from CV
causes, decreased hospitalizations for HF, decreased mortality
- Benefits of eplerenone in left ventricular dysfunction after MI: decreased
mortality, decreased composite endpoint of death from CV causes or
hospitalization for CV events
Pharmacologic Interventions

Aldosterone receptor antagonists:
- Spironolactone
* It is licensed for use in severe HF.
* It may cause painful gynaecomastia in men.
* Renal function and serum potassium levels must be closely
monitored due to the risk of hyperkalaemia, especially when these
agents are used together with an ACE or ARB.
- Eplerenone is used in post-MI HF and moderate HF (class II)
Pharmacologic Interventions

Aldosterone receptor antagonists (ARAs):
considerations:
- it Should be added to ACE inhibitor (or ARB) and β-blocker therapy
- SCr should be less than 2.5 mg/dL for men and less than 2.0 mg/dL in women
(or estimated glomerular filtration rate greater than 30 mL/minute/1.73 m2), and
K should be less than or equal to 5.0 mEq/L.
Pharmacologic Interventions

Aldosterone receptor antagonists (ARAs):
Monitoring:
- K and SCr within 2–3 days, again at 7 days after starting therapy, monthly for
first 3 months, and every 3 months thereafter. If the dose of ACE inhibitor or
ARB is increased, restart monitoring.
- Decrease dose by 50% or discontinue if K is greater than 5.5 mEq/L.
- Gynecomastia: eplerenone can be considered as an alternative to
spironolactone if gynecomastia is present.
Pharmacologic Interventions

Aldosterone receptor antagonists:
- Contraindications to aldosterone antagonists are
hyperkalaemia (K >5 mmol/L), creatinine >2.5 mg/dL, and
concomitant use of a combination of ACE and ARB.
Pharmacologic Interventions

Angiotensin II receptor antagonists
- ARBs used in patients who are intolerant of ACE inhibitors, e.g.
develop cough or angioedema
- ARBs are less strong in reduce morbidity and mortality in HF
than ACE inhibitors or aldosterone receptor antagonists
Pharmacologic Interventions

Nitrates and Hydralazine:
- Nitrate (e.g. ISDN) and hydralazine can be add to standard treatment
with an ACE inhibitor, β-blocker, and/or aldosterone antagonist and
diuretic
- Recommended
in addition to ACE inhibitors and β-blockers to reduce
morbidity and mortality
Pharmacologic Interventions

Nitrates and Hydralazine:
- This combination may be poorly tolerated due to dizziness and headache
- This combination is considered as an alternative for ACE inhibitors or
aldosterone antagonists in patients with in renal impairment
- Hydralazine and isosorbide dinitrate (combination drug) (specifically
benefits African Americans with HF)
Pharmacologic Interventions

Nitrates and Hydralazine:
- Benefits: decreased mortality, reduced pulmonary congestion and
improved exercise tolerance
- Dosing:
Fixed-dose (hydralazine 37.5 mg plus isosorbide dinitrate 20 mg) starting at
1 tablet three times daily with a goal dose of 2 tablets three times daily
Hydralazine 75 to 300 mg daily in 3 or 4 divided doses; isosorbide dinitrate
60–120 mg daily in 3 or 4 divided doses
Pharmacologic Interventions

Digoxin:
- It can be beneficial in decreasing hospitalizations in patients with
HFrEF; should be added after guideline-directed medical therapy
- It is used to treat AF associated with HF
- Benefits: Improved symptoms and exercise tolerance, decreased
hospitalizations
- It increase in cardiac output, improvement in HF symptoms and
a decreased rate of HF hospitalizations.
- It increases the strength of heart muscle contractions and slow the
heartbeat
Pharmacologic Interventions

Digoxin:
- Digoxin should be used together with standard HF therapies
(ACE inhibitors, β-blockers, and diuretics) in patients with
symptomatic HF to reduce hospitalizations.
- Dosing: for most patients, 0.125 mg/day
- considerations:
- No indication to load patients with digoxin in the setting of HF
- Avoid abrupt discontinuation; can precipitate clinical deterioration
Pharmacologic Interventions

Digoxin:
- Monitoring
- Serum concentrations should be less than 1 ng/mL; in general,
concentrations of 0.5–0.9 ng/mL are suggested.
- Minimizes the risk of adverse effects and ventricular arrhythmias
associated with increased concentrations.
- Risk of toxicity increases with age and renal impairment.
Pharmacologic Interventions

Digoxin:
- Monitoring
- Risk of toxicity increases in the presence of hypokalemia,
hypomagnesemia, or hypercalcemia.
- Signs of toxicity generally include nausea, vomiting, vision changes.
- SCr should be monitored because the drug is primarily cleared renally.
Pharmacologic Interventions

Digoxin:
- Hypokalaemia can increase sensitivity to digoxin
- Patients should be monitored for bradycardia (signs of toxicity)
- Drug interactions:
(1) Clarithromycin, erythromycin
(2) Amiodarone
(3) Dronedarone
(4) Itraconazole, posaconazole
(5) Cyclosporine, tacrolimus
(6) Verapamil
Pharmacologic Interventions

If Channel Blocker:
- Ivabradine selectively inhibits the If current in the sinus node,
slowing the HR and reducing myocardial oxygen demand
- it is used for patients in sinus rhythm.
- It has been approved for use in stable HF patients who have a left
ventricular EF of <35%, and a HR of 75 b/m or greater despite
standard treatment or in patients who are unable to tolerate βblockers
Pharmacologic Interventions

If Channel Blocker:
Ivabradine:
- Benefits: decreased mortality and hospitalization
- Monitoring: Assess HR and rhythm for bradycardia, and AF after 2 weeks of
therapy initiation or modification
Pharmacologic Interventions

Calcium Channel Blocker:
- Amlodipine should be considered for the treatment of comorbid
hypertension and/or angina in patients with heart failure, but
verapamil, diltiazem or short acting dihydropyridine agents should
be avoided.

Amiodarone:
- Patients taking amiodarone should have a routine 6-monthly
clinical review, including liver and thyroid function test
Pharmacologic Interventions

Anticoagulants and Antiplatelets
- Patients with HF are at an increased risk of thromboembolic
events. However, the role of antiplatelets and anticoagulants remains
debatable due to a lack of prospective clinical trials.
- Aspirin (75–150 mg once daily) should be prescribed for patients
with the combination of heart failure and atherosclerotic arterial
disease (including coronary heart disease).
Pharmacologic Interventions
 Inotropic
agents:
- Intravenous inotropic agents (such as dobutamine) should only be
considered for the short-term treatment of acute decompensation of
chronic heart failure.
- It used to restore organ perfusion and reduce congestion in patients
with HF with reduced ejection fraction, so as to increase in cardiac
output and reduce neuro-humoral activation.
Acute heart failure
(AHF)
Pharmacologic Interventions

Acute heart failure (AHF)

AHF is a life-threatening medical condition

Treatment of AHF targets relief of congestion and optimization of
cardiac output

Oral or IV diuretics, IV vasodilators (e.g. nitroglycerin, nitroprusside,
isosorbide dinitrate), and, when appropriate, inotropes (e.g. digoxin,
dopamine), based on presenting hemodynamics.

Current treatment strategies in AHF target improving hemodynamics
while preserving organ function.
Pharmacologic Interventions

Acute heart failure

Hospitalisation (admit the patient in the telemetry bed or in ICU)


Oxygen (SaO2 <90%), ventilation
IV diuretic
- IV loop diuretics are recommended for all patients with AHF admitted with
signs/symptoms of fluid overload to improve symptoms (e.g. IV bolus doses of
furosemide (40-80mg) and repeated as necessary)
Pharmacologic Interventions


Acute heart failure
Vasodilators
- Vasodilators (e.g. nitroglycerin, nitroprusside, isosorbide dinitrate) are especially
useful in patients with hypertensive AHF
- They should be avoided in patients with SBP <90 mmHg (or with symptomatic
hypotension).

Inotropes
- inotropes/vasopressors (e.g. dobutamine, dopamine, levosimendan,
norepinephrine, epinephrine) should be reserved for patients with a severe reduction
in cardiac output resulting in compromised vital organ perfusion, which occurs most
often in hypotensive AHF (SBP <90 mmHg)
- Inotropic agents are not recommended in cases of hypotensive AHF where the
underlying cause is hypovolaemia or other potentially correctable factors before
elimination of these causes.
Pharmacologic Interventions


Acute heart failure
Opiates
- Opiates relieve dyspnoea and anxiety in patients with severe dyspnoea
- In AHF, routine use of opiates is not recommended and they may only be
cautiously considered in patients with severe dyspnoea, mostly with pulmonary
oedema.

Other agents for acute control of the ventricular rate in patients with
AF
- Digoxin and/or beta-blockers should be considered as the 1st line therapy
- Amiodarone may be considered