Heart failure guidelines

Etiopathogenesis, classification,
guidelines and management of
Heart failure
Chair Person: DR. BASAVARAJ BALIGAR MD, DM ( Cardiology)
Student: Dr Chethan T L

Definition:
• Heart failure is defined as a complex clinical syndrome that results
from structural or functional impairment of ventricular filling or
ejection of blood, which in turn leads to cardinal symptoms of
dyspnoea, fatigue and signs of heart failure, namely edema and rales.

Classification of Heart failure:
Heart failure with reduced ejection fraction( HFrEF)(<40%)
Heart failure with preserved ejection fraction( HFpEF) (> 40-50%)

Pathophysiology of Heart failure:
• HF is a progressive disorder that is initiated after an index event
either damages the heart muscle, with a resultant loss of functioning
cardiac myocytes, or alternatively, disrupts the ability of myocardium
to generate force, there by preventing the heart to contract normally.
• The index event may have an abrupt onset as in MI or gradual onset
as in case of hemodynamic pressure or volume overloading or it may
be hereditary as in case of some cardiomyopathes.

• The index event may have an abrupt onset as in MI or gradual onset
as in case of hemodynamic pressure or volume overloading or it may
be hereditary as in case of some cardiomyopathes.
• In most instances , patient remain asymptomatic or minimally
symptomatic after the initial decline in pumping capacity of the heart
or develop symptoms only after dysfunction has been developed for
sometime.

Pathogenesis of heart failure :

Activation of compensatory mechanisms:

Effect of sympathetic system:
Tachycar
dia
Activati
on of
RAAS
vasocon
striction
Aldostero
ne and
AVP
secretion

• SYMPATHETIC NERVOUS SYSTEM
RENIN----------- ANGIOTENSIN II
-------------ALDOSTERONE DIRECT ACTION
ON PCT
ACTIVATION OF
THIRST CENTER
REALEASE OF
AVP
WATER RE
ABSORPTION
SODIUM RE
ABSORPTION

Offsetting of compensatory mechanisms:
• Nueropeptides prostaglandins E2 and I2( vasodilation
and reduction secretion of renin).
ANP and BNP released in response to stretch of
myocardium( vasodilation and reduces
renin and aldosterone)
Over time these effects gets blunted and there is un opposed action of
RAAS system.

LV remodelling:
1. myocyte hypertrophy
2. Alteration in the contractile property of the myocytes
3. Progressive loss myocytes through necrosis, apoptosis.
4. Beta- adrenergic desensitization.
5. Re organisation of the extracellular matrix with dissolution of the
organised structural collagen matrix that doesnot provide structural
support to the myocytes.

• LV remodelling also leads to
1. Hypo perfusion of the sub endocardium leading to further more
worsening of cardiac output.
2. Increased oxidative stress leading to activation of free activation
which further damages the myocytes.

Clinical manifestations :
• Symptoms and signs:
1.Fatigue and shortness of breath are the most cardinal features of heart
failure.
2.Orthopnea
3.Paroxysmal nocturnal dyspnea.( PND)
4.Cheyne – stokes respiration.
5.Nocturia
6. diminished exercise capacity
7. Edema ( of the extremities or scrotum or else where)

• Increasing abdominal girth or bloating
• Abdominal pain( particularly if confined to the right upper quadrant)
• loss of appetite or early satiety
• somnolence or diminished mental acuity

Physical findings in Heart failure:
• Tachycardia
• Narrow pulse pressure or thready pulse
• Pulsus alternans
• Tachypnoea
• Cool extremities
• Elevated jugular venous pressure
• Dullness and diminished breath sounds at one or both lung bases
• Rales , rhonchi, or wheezes

• Sustained apical impulse
• Parasternal lift
• S3 and S4 heart sounds
• Tricuspid or migtral regurgitant murmur
• Hepatomegaly and ascites
• Presacral edema
• Anasarca
• Pedal edema

Diagnosis:
• Routine laboratory testing
• Electro cardiogram
• Chest X ray
• Assesment of LV function: most useful investigation will be 2D echo
which gives information about the LV size and function, also gives about the
valvular or regional wall motion abnormalities( indicative of
a prior MI).
• MRI imaging which gives assessment of LV mass and volume.
now , is considered as gold standard for assessing LV mass and volume.

• Biomarkers:
• Circulating levels of natriuretic peptides, are useful and important
adjunctive tools in the diagnosis of heart failure.
• Both B type natriuretric peptides( BNP) and N terminal pro BNP are
realeased from the failing heart are sensitive markers of HFrEF also ,
they are elevated in HFpEF but slightly less in amount.
• They also give information about the disease severity and prognosis.

Management of heart failure:
• Heart failure may present with many of different phenotypes like
a) chronic heart failure with reduced ejection fraction
b) chronic heart failure with pressrved ejection fraction.
c) acute de compensated heart failure.
d) advanced heart failure.

Acute decompensated heart failure:
• ADHF is a heterogenous syndrome with interrelated abnormalities
like decreased cardiac performance, renal dysfunction and alteration
in the vascular compliance.

ADHF can present as:
• A) decompensated heart failure( 76%)
• B) acute hypertensive heart failure( 20%)
• C) cardiogenic shock( 4%)

Volume management:
Intravenous diuretic agents
 Loop diuretics are the primary pharmacologic agents for treatment of volume
overload in patients with AHF
 Typically produce rapid symptom relief in most patients.
This group of agents (furosemide, torsemide, bumetanide, and ethacrynic acid) can
lead to excretion of up to 25% of the filtered sodium.
 intravenous administration avoids variable bioavailability and allows for rapid
onset of action (typically within 30 to 60 minutes).

Loop diuretic resistant:
One of the inherent limitations of diuretics is that they achieve water loss
via excretion of solute at the expense of glomerular filtration. which in turn
activates a set of homeostatic mechanisms that ultimately limit their
effectiveness.
In normal subjects, the magnitude of natriuresis after a given dose of
diuretic declines over time as a result of the so-called braking
phenomenon.

A patient with HF may be considered to be resistant to diuretic drugs
when moderate doses of a loop diuretic do not achieve the desired
reduction in extracellular fluid volume.
In outpatients, a common and useful method for treating the diuretic-
resistant patient is to administer two classes of diuretic concurrently.

The combination of loop and distal collecting tubule diuretics has
been shown to be effective through several mechanisms.
One is that distal collecting tubule diuretics have longer half-lives
than loop diuretics and may thus prevent or attenuate postdiuretic
NaCl retention.

• A second mechanism by which distal collecting tubule diuretics
potentiate the effects of loop diuretics is by inhibiting Na+ transport
along the proximal tubule.
• In so far as most thiazide diuretics also inhibit carbonic anhydrase, as
well as by inhibiting NaCl transport along the distal renal tubule.

Vascular therapy:
• In the absence of hypotension, vasodilators can be used as first-line agents
in combination with diuretics in the management of patients with AHF to
improve congestive symptoms
Vasodilators can be classified as
(1) predominantly venous dilators, with consequent reduction in preload;
(2) arterial dilators, leading to a decrease in afterload; and
(3) balanced vasodilators, other with combined action on both the venous
and the arterial system.

Currently available vasodilators include the
Organic nitrates (nitroglycerin [NTG] and isosorbide dinitrate)
Sodium nitroprusside (SNP)
Nesiritide.
 All of these drugs act by activating soluble guanylate cyclase (sGC) in
the smooth muscle cells, leading to higher intracellular concentrations
of cyclic guanosine monophosphate (cGMP) and consequent vessel
relaxation.

Nitrates:
• These agents are potent venodilators, producing rapid decreases in
pulmonary venous and ventricular filling pressures and improvement
in pulmonary congestion, dyspnea, and myocardial oxygen demand
at low doses.
• At slightly higher doses and in the presence of vasoconstriction,
nitrates also are arteriolar vasodilators, reducing afterload and
increasing cardiac output.

Nesiritide:
• Nesiritide (recombinant human B-type [brain] natriuretic peptide) is
identical to endogenous BNP and causes potent vasodilation in the
venous and arterial vasculatures, resulting in significant reductions in
venous and ventricular filling pressures and mild increases in cardiac
output.

• Recombinant human relaxin-2 , or serelaxin , is a peptide upregulated
in pregnancy and examined in ADHF patients with a normal or
elevated blood pressure.
Newer vasodilators

• A study conducted , relaxin in acute acute heart failure ( RELAX-AHF)
trial, serelaxin improved dyspnoea, reduced signs and symptoms of
congestion and was associated with less early worsening of heart failure.
• Urodilatin, a modified version of pro–atrial natriuretic peptide (pro-
ANP), is a 32-amino-acid hormone, synthesized and secreted from the
distal tubules of the kidney that regulates renal sodium absorption and
water homeostasis via binding to NPR1 receptors and increasing
intracellular cGMP levels

Soluble Guanylate Cyclase Activators
• Cinaciguat is the first compound in a new class of vasodilators. The mechanism of
action of these compounds is similar to that of organic nitrates (and their end
product nitric oxide [NO]), because both classes of drugs activate the soluble
form of guanylate cyclase (sGC) in smooth muscle cells, thereby leading to the
synthesis of cGMP and subsequent vasodilation.

Ionotropic therapy:
• DOBUTAMINE( sympathomimetic amines)
 Dobutamine is the most commonly used positive inotrope.
 Doses of 1 to 2 µg/kg/min, although higher doses (5 to 10 µg/ kg/min)
may be necessary for those with more profound hypoperfusion.
The lowest effective dose of dobutamine should be used, supported by
continuous blood pressure and rhythm monitoring.

• Dopamine
Low-dose dopamine (≤2 µg/kg/min) has been proposed to cause
selective dilation of renal, splanchnic, and cerebral arteries, potentially
increasing renal blood flow in a selective manner, as well as promoting
natriuresis through direct distal tubular effects.

• Intermediate-dose dopamine (2 to 10 µg/kg/min) results in enhanced
norepinephrine release, stimulating cardiac receptors with an increase
in inotropy and mild stimulation of peripheral vasoconstricting
receptors.
• Because the positive inotropic effect is largely dependent on
myocardial catecholamine stores, which often are depleted in patients
with advanced heart failure, dopamine is a poor inotrope in patients
with severe systolic dysfunction.

• High-dose dopamine (10 to 20 µg/kg/min) causes peripheral and
pulmonary artery vasoconstriction, mediated by direct agonist effects
on alpha1-adrenergic receptors. These doses carry a significant risk of
precipitating limb and end-organ ischemia and should be used
cautiously.

Arginine Vasopressin Antagonists:
 Arginine vasopressin (AVP), also known as antidiuretic hormone, is the main
regulator of plasma osmolality.
 Vasopressin levels are inappropriately high in both acute and chronic forms
of heart failure and are thought to have a major role in the pathophysiology
of this disorder.
 Currently available vasopressin antagonists are tolvaptan (an oral, selective
V2 receptor antagonist) and conivaptan (a V1a/V2 receptor antagonist for
intravenous use).

• Levosimendan is a calcium sensitizer that provides positive ionotropic
activity.
• They are also phosphor diesterase inhibitors which has vasodilator
property and hence makes this drug unsuitable in the states with low
output and hypotension.
• Omecamtiv mecarbil, is a selective myosin activator that prolongs the
duration of ejection period but does not increase the force of
contraction hence , its usage is under trial.

Istaroxime,
• Istaroxime, the prototype of a new class of drugs, exerts its actions on
the myocyte in two ways:
(1) through stimulation of the membrane bound sodium-potassium
adenosine triphosphatase (Na+,K+-ATPase)
and (2) by enhancing the activity of the sarcoendoplasmic reticulum
Ca2+-ATPase type 2a (SERCA-2a).
These distinct mechanisms result respectively, increased cytosolic
calcium accumulation during systole, with positive inotropic effects,
and rapid sequestration of cytosolic calcium into the sarcoplasmic
reticulum during diastole, leading to an enhanced lusitropic effect.

• Stresscopin, or urocortin 2, is a member of the urocortin family, a
recently discovered group of peptide hormones of the corticotropin
releasing factor (CRF) family. They bind with strong affinity to the
corticotropin-releasing hormone receptor type 2 (CRH-R2), which is
highly expressed in the myocardium and in the vascular endothelium.

Other Nonpharmacologic Therapies
Ultrafiltration
Peripheral ultrafiltration is an available modality to remove sodium and
water in hospitalized patients with heart failure.
The theoretical advantage of ultrafiltration is the removal of isotonic
fluid, resulting in greater and more reliable salt removal, potentially
without the neurohormonal activation seen with diuretics.
Around 300-500/ hr is the rate of ultra filtration recommended in case of
diuretic resistant heart failure.

Heart failure with reduced ejection fraction:
NUERO HORMONAL ANTAGONISM:
• ACE inhibitors .
• ARB
• Beta blockers
• Aldosterone antagonists
• Direct renin inhibitors.
• ARNI’s.

ACE INHIBITORS
• They are the most important class of drugs used in nuero hormonal
antagonism and preventing LV remodelling in HFrEF.
• How ever patients on ACE inhibitors may develop angio edema and
cough and hence in those cases ARB’s can be used.

Beta blockers:
• Three beta blockers have been shown to be effective in reducing the risk of
death in patients with chronic HF:
• Bisoprolol
• Metoprolol succinate both competitively block the beta1 receptor,
• Carvedilol competitively blocks the alpha1, beta1, and beta2 receptors.

• Although a number of potential benefits may be obtained by blocking all
three receptors, most of the deleterious effects of sympathetic
activation are mediated by the beta1 adrenergic receptor.
• When given in concert with ACE inhibitors, beta blockers reverse the
process of LV remodelling, ameliorate patient symptoms, prevent
hospitalization, and prolong life.
• Therefore beta blockers are indicated for patients with symptomatic or
asymptomatic HF and a depressed EF to below 40%.

Aldosterone antagonists:
• Elevated aldosterone levels in HFrEF, promote sodium retention and
electrolyte imbalance and endothelial dysfunction and may directly
contribute to myocardial fibrosis.
• Eplerenone and spironolactone are the drugs which are used and
have shown improment in mortality and hospiizilations.

Novel neurohormonal antagonism:
• More recently, an ARB ( valsartan) with endopeptidase inhibitor(
sacubitril), has shown a survival benefit in a large trial when
compared with ACEI alone.
• This drug referred to angiotensin receptor-neprolysin inhibitor is has
largely considered in place where only ACEI are used.

•Heart rate modification:
• IVABRADINE, an inhibitor of funny current in the sino atrial node, slows
the heart rate with negative inotropic effect.
• American college of cardiology suggests that ivabradine should be used
only in cases when ACEI and other neurohormonal antagonists are used
but still being symptomatic and whose heart rate is > 70/ min.

Digoxin:
• Digoxin should be considered in patients who have symptomatic LV
dysfunction along with atrial fibrillation
( OR)
Who have signs and symptoms of heart failure even when on
treatment with ACE inhibitors and Beta- blockers .

Other agents used in HFrEF:
• Statins are used in treatment of HF in the back ground setting of
coronary artery disease.
• Anti coagulation and anti platelet therapy is generally not adviced,
how ever aspirin is given in cases ischemic cardiomyopathy.
• Treatment with long chain omega – 3 polysaturated fatty acids, has
been shown to be associated modestly improvement in clinical
outcomes with patients with HFrEF.

Anti platelet and anti coagulant therapy:
Patients with chronic HF with permanent/persistent/paroxysmal atrial
fibrillation and an additional risk factor for cardioembolic stroke (history of
hypertension, diabetes mellitus, previous stroke or transient ischemic attack, or
≥ 75 years of age) should receive chronic anticoagulant therapy.

Chronic anticoagulation is reasonable for patients with chronic HF who
have permanent/persistent/paroxysmal atrial fibrillation but no
additional risk factor for cardioembolic stroke.
No benefit Anticoagulation is not recommended in patients with
chronic HFrEF without atrial fibrillation, a previous thromboembolic
event, or a cardioembolic source.

Heart failure with preserved ejection fraction:
• GENERAL PRINCIPLES
• Therapeutic targets in HFpEF include control of congestion,
stabilization of heart rate and blood pressure, and efforts at
improving exercise tolerance.

Heart failure with reduced ejection fraction
management:
• Treatment of acute factors:
1) reduction of congestive state.
2) controlling of blood pressure.
3)controlling tachycardia.
4) Management of sleep apnoea.
5) Treatment of myocardial ischemia.

• ACE inhibitors and ARB are not effective in acute management except for
in prevention.
• Aldosterone antagonistas are also ineffective in the treatment.
• Calcium channel blockers and beta blockers are of no use unless in
preventing tachycardia.
• ARNI’s are shown effective in aneoilirating symptoms of heart failure.

• Patients with HFrEF ( < 40%) commonly exhibit sleep disordred breathing.
• Either they exhibit CSA( central sleep apnoea) or OSA ( obstructive sleep
apnoea)
• CSA is also known as chyene stokes breathing is a form of periodic
breathing with in which central apnoea and hypopnoea alternate with
hyperventilation.
• CPAP is the mainstay of the treatment for these conditions along with
strict adherence to medications.

Cardiac resynchronisation therapy:
• CARDIAC RESYNCHRONIZATION THERAPY
• Nonsynchronous contraction between the walls of the left ventricle
(intraventricular) or between the ventricular chambers
(interventricular) impairs systolic function, decreases mechanical
efficiency of contraction, and adversely affects ventricular filling.
• Mechanical dyssynchrony results in an increase in wall stress and
worsens functional mitral regurgitation.

• The single most important association of extent of dyssynchrony is a
widened QRS interval on the surface electrocardiogram, particularly
in the presence of a left bundle branch block pattern.
• Most benefit in mildly symptomatic HFrEF patients accrues from
applying this therapy in those with a QRS width of >149 ms and a left
bundle branch block pattern.

• SUDDEN CARDIAC DEATH PREVENTION IN HEART FAILURE :
• SCD due to ventricular arrhythmias is the mode of death in
approximately half of patients with heart failure and is particularly
proportionally prevalent in HFrEF patients with early stages of the
disease.
• Patients who survive an episode of SCD are considered to be at very high
risk and qualify for placement of an implantable cardioverter-
defibrillator (ICD).

• Although primary prevention is challenging, the degree of residual left
ventricular dysfunction despite optimal medical therapy (≤35%) to allow
for adequate remodeling and the underlying etiology (post–myocardial
infarction or ischemic cardiomyopathy) are the two single most important
risk markers for stratification of need and benefit.

• Currently, patients with NYHA class II or III symptoms of heart failure
and an LVEF <35%, irrespective of etiology of heart failure, are
appropriate candidates for ICD prophylactic therapy. In patients with
a myocardial infarction and optimal medical therapy with residual
LVEF ≤30% (even when asymptomatic), placement of an ICD is
appropriate.

Referrences:
• Harrison textbook of internal medicine, 20th edition.
• Braunwald’s textbook of heart diseases.
• Hurst’s manual of cardiology.

Heart failure guidelines

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Heart failure guidelines