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Heart Failure
Lior Ness
19.2.2009
4th year Medical Student
Sackler Medical School, Tel-Aviv University
Internal Medicine Department
Sheba Medical Center
ISRAEL
Definition
Heart failure is a clinical syndrome that
occurs in patients who develop a
constellation of clinical symptoms
(dyspnea and fatigue) and signs (edema
and rales) that lead to frequent
hospitalizations, a poor quality of life,
and a shortened life expectancy.
In other words…
Heart failure is a condition in
which the heart is unable to pump
blood at an adequate rate or
volume.
Epidemiology
Overall prevalence of HF in developed countries
is 2%, with over 20 million people affected
worldwide.
Prevalence rising with age: 6-10% of people
over 65.
Although the relative incidence of HF is lower in
women than in men, women constitute 50% of
cases because of their longer life expectancy.
Prognosis is poor: 30-40% of patients die within
1 year of diagnosis and 60-70% die within 5
years, mainly from worsening HF or as a sudden
event.
Pathogenesis
Etiologies
Any condition that leads to an alteration in
LV structure or function can predispose a
patients to developing HF.
In most cases, patients remain
asymptomatic following the initial decline
in pumping capacity of the heart.
LV dysfunction is necessary for the
pathogenesis of HF, but not sufficient.
Etiologies
Pathogenesis- compensatory
mechanisms (1)
Renin-Angiotensin-Aldosterone (RAA)
Adrenergic nervous system
Increased myocardial contractility
Vasodilatory molecules: ANP, BNP,
prostaglandins, NO
Pathogenesis- compensatory
mechanisms (2)
LV function is modulated so that the functional
capacity of the patient is preserved. Patients
may remain asymptomatic for a period of years.
At some point, patients become overtly
symptomatic, with a striking increase in
morbidity and mortality.
The exact mechanisms that are responsible for
this transition are not fully understood, but
involve activation of neurohormonal (NE,
angiotensin II), adrenergic and cytokine systems
that lead to a series of adaptive changes within
the myocardium, known as LV remodeling.
LV Remodeling
Myocytes hypertrophy and alterations in the
contractile properties and metabolism.
Progressive loss of mycotes through necrosis
and apoptosis.
ß-adrenergic desensitization.
Reorganization of the extracellular matrix.
LV Remodeling may contribute independently to
the progression of HF due to changes in LV
geometry
Clinical Manifestations
Symptoms
Fatigue
– Mechanism: low cardiac output. Noncardiac
comorbidities (e.g. anemia) also contribute.
Dyspnea
– Mechanism: pulmonary congestion with accumulation
of interstitial or intra-alveolar fluid.
– In early stages, observed only during exertion.
Orthopnea is a later manifestation, often
accompanied by nocturnal cough or paroxysmal
nocturnal dyspnea (PND).
– In advanced HF: Cheyne-Stokes respirations, acute
pulmonary edema.
Symptoms cont.
Gastrointestinal symptoms: anorexia, nausea,
and early satiety associated with abdominal pain
and fullness.
– May be related to edema of the bowel and/or
congested liver.
Cerebral symptoms (confusion, disorientation,
sleep and mood disorders) in severe HF.
Nocturia.
Physical Examination
General Appearance and Vital Signs
– In mild to moderate HF: no distress at rest, but patient
uncomfortable when lying flat for more than few
minutes. In more severe HF, patient must sit upright
and may have labored breathing.
– Blood pressure usually reduced due to LV dysfunction
(but can be normal/high in early stages). Pulse
pressure may be diminished (reduction in stroke
volume).
– Adrenergic activity: sinus tachycardia, peripheral
vasoconstriction and cyanosis.
– With severe chronic HF, there may be marked
cachexia and weight loss.
Physical Examination cont.
JVP
– Increased. In early stages, JVP may be
normal at rest but may become abnormally
elevated with sustained pressure on the
abdomen (positive abdominojugular reflux).
Pulmonary Examination
– When present in patients without concomitant
lung disease, crepitations are specific to HF.
– Pleural effusion.
Physical Examination cont.
Cardiac Examination
– If cardiomegaly present, PMI displaced.
– In some patients S3 is audible, most commonly in
patients with volume overload.
– S4 is not specific but usually present in patients with
diastolic dysfunction.
Abdomen
– Hepatomegaly, ascites.
Extremities
– Peripheral edema (usually absent in patients treated
adequately with diuretics). Edema is symmetric,
dependent and pitting.
Diagnosis of HF
Diagnosis is relatively straightforward when
the patient presents with classic signs and
symptoms; however, the signs and symptoms
of HF are neither specific nor sensitive.
Diagnosis
ECG
– LV hypertrophy, prior MI.
Chest X-ray
– Cardiac size and shape.
Assessment of LV function
– Echocardiogram, MRI (gold standard).
– The most useful index of LV function: Ejection Fraction (EF).
Biomarkers
– BNP, troponin, CRP
Exercise Testing
– Not routinely used for every patient, but useful for assessing the
need for cardiac transplantation.
– Measures peak oxygen uptake (VO2).
Differential Diagnosis
Conditions with circulatory congestion
secondary to abnormal salt and water
retention (e.g. renal failure).
Noncardiac causes of pulmonary edema
(e.g. ARDS).
Treatment
Progression of HF
Stage A: Patients who are at risk for developing HF but
without structural heart disease or symptoms (e.g.
diabetic, hypertensive).
Stage B: Patients who have structural heart disease but
without symptoms of HF (e.g. previous MI).
Stage C: Patients with structural heart disease and
symptoms of HF (dyspnea and fatigue)
Stage D: Patients with refractory HF requiring special
interventions (e.g. cardiat transplantation).
Every effort should be made to prevent HF by
treating the preventable causes (hypertension).
Patients in stages B and C should be treated with
drugs that prevent disease progression.
NYHA Classification
Once patients have developed structural heart disease,
their therapy depends on their NYHA functional
classification.
NYHA Classification – Strategies
Class I (asymptomatic): Slow disease
progression by blocking neurohormonal
systems that lead to LV remodeling.
Class II-IV (symptomatic): Alleviate fluid
retention, lessen disability, and reduce risk
of further disease progression.
– Usually treated with diuretics and
neurohormonal interventions.
Treatment of HF with Depressed
Ejection Fraction (<40%)
Physical activity is beneficial for patients with NYHA
class I-III.
Diet: Sodium restriction is recommended in all patients
with HF.
Diuretics
– Should be initiated in low doses and then carefully titrated
upward to relieve symptoms of fluid overload. Once the
congestion has been relieved, treatment with diuretics should be
continued to prevent recurrence of fluid retention.
– Drug of choice: loop diuretics (fusid). Thiazides less potent and
lose effectiveness in renal insufficiency.
– Adverse effects: electrolyte and volume depletion, azotemia,
increased neurohormonal activation and disease
progression.
Treatment (EF<40%)
Preventing Disease Progression
ACE Inhibitors
– Should be used in both symptomatic and
asymptomatic patients with a depressed EF.
– Stabilize LV remodeling, improve symptoms,
reduce hospitalization and prolong life.
– Adverse effects: Decreased blood
pressure, azotemia, hyperkalemia,
nonproductive cough, angioedema.
Angiotensin Receptor Blockers
– Well tolerated in patients who are intolerant of ACE
inhibitors because of cough, skin rash and
angioedema.
– Should be used in symptomatic and asymptomatic
patients with EF<40%.
– Same benefits as ACEI: Improve LV remodeling and
prolong life.
– Adverse effects: Same as ACEI- low blood
pressure, impairs renal function, potassium
retention.
ß-Blockers
– Interfere with the harmful effects of sustained
activation of the adrenergic nervous system. Most of
the deleterious effect is related to ß1 receptor.
– Indicated for both symptomatic and asymptomatic
patients with EF<40%. Initiated in low doses, then
titrated slowly if well tolerated.
– Adverse effects: Bradycardia, heart blocks,
hypotension (especially in agents that also block
α1), bronchospasm.
Aldosterone Antagonists
– Classified as potassium-sparing diuretics, but have
beneficial effects that are independent of sodium
balance.
– In chronic ACEI therapy, aldosterone levels may
return to levels similar to those before therapy.
– Recommended for patients with NHYA IV or III with
EF<35%, who are receiving standard therapy
(diuretics, ACEI, beta-blockers).
– Adverse effects: hyperkalemia (therefore not
recommended if creatinine>2.5 mg/dl or serum
potassium>5 meq/L), painful gynecomastia in 1015% of patients (eplerenone may be substituted).
Algorithm for Treatment of HF
Anticoagulation and Antiplatelet
Therapy
Patients with HF have an increased risk for arterial or
venous thromboembolic events. The rate of stroke
ranges from 1.3 to 2.4% per year.
Depressed LV function is believed to promote relative
stasis of blood in dilated cardiac chambers with
increased risk of thrombus formation.
Treatment with warfarin (goal INR of 2.0-3.0) is
recommended for patients with HF and CAF or PAF, or
with a history of emboli (including stroke and TIA).
Aspirin is recommended in HF patients with ischemic
heart disease for the prevention of MI.
Management of HF with a
preserved EF (>40-50%)
Pathogenesis of HF with preserved EF not fully
understood. Suggested: diastolic dysfunction,
vascular and ventricular stiffness.
There are no proven pharmacologic or device
therapies.
Treatment should be focused on the underlying
disease process (e.g. MI, hypertension).
Precipitating factors (e.g. tachycardia, AF)
should be treated as quickly as possible.
Dyspnea may be treated by sodium restriction,
nitrates, ACEI, ARBs, and/or beta-blockers.
Acute HF
Acute HF – Precipitating Factors
Factors that may precipitate acute decompensation
in patients with chronic HF:
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–
–
–
–
–
–
–
–
–
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Dietary indiscretion
MI
Arrhythmias (tachy/brady)
Discontinuation of HF therapy
Infection
Anemia
Medications: CCB, beta-blockers, NSAIDs, antiarrythmic agents
(class I agents, sotalol), anti-TNF Abs.
Alcohol consumption
Pregnancy
Worsening hypertension
Acute valvular insufficiency
Management of Acute HF
Stabilizing the hemodynamic derangements that
provoked the symptoms.
Treating reversible factors that precipitated
decompensation (e.g. infection, arrythmias,
dietary indiscretion, PE, IE, environmental
and/or emotional stress, etc.).
Reestablish an effective outpatient medical
regimen that will prevent disease progression
and relapse.
Hemodynamic Derangements in
Acute HF
The two primary hemodynamic determinants of
acute HF are:
– Elevated LV filling pressure (may have signs of fluid
retention).
– Depressed cardiac output (usually accompanied by
an increase in systemic vascular resistance).
These two hemodynamic derangements may
occur singly or together.
The therapeutic approach to treating patients
with acute HF should be tailored to reflect the
patient’s hemodynamic presentation.
Pharmacologic Management of
Acute HF
Vasodilators: Exert dilating effect on arterial
resistance and venous capacitance, which
results in a lowering of LV filling pressure.
Improve CO without increasing heart rate.
Inotropic agents: Stimulate cardiac contractility
as well as peripheral vasodilation. Improve CO
and reduce LV filling pressure.
Vasoconstrictors: Support systemic blood
pressure.
The End