Congestive heart failure

1 MAGDI AWAD SASI HEART FAILURE 2013
Heart Failure
MAGDI AWAD SASI 2013

DEFINITION
Heart (or cardiac) failure: pathophysiological state in which the heart is
unable to pump blood at a rate commensurate with the requirements of
the metabolizing tissues or can do so only from an elevated filling
pressure
According to AHA,
HF is a clinical syndrome including circulatory congestion or inadequate
tissue perfusion , due to abnormal heart function and associated
neurohormonal abnormalities.
An inadequate or decreased cardiac output which causes an increase in
the blood volume within the vascular system. The resulting congestion
within the venous system interferes with the movement of body fluids,
resulting in fluid accumulation in the tissue spaces, causing edema
Frequency : United States
• More than 3 million people have congestive heart failure (CHF), and more
than 400,000 new patients present yearly. The prevalence rate is 1-2%.
Race
Blacks are 1.5 times more likely to die of CHF than whites are.
Nevertheless, black patients appear to have similar or lower in-hospital
mortality rates than white patients.
Sex
Prevalence is greater in males than in females in patients aged 40-75 yrs.
No sex predilection is noted among patients older than 75 years.
Age
Prevalence of CHF increases with increasing age and affects about 10% of
the population older than 75 years

Mortality/Morbidity
Approximately 30-40% of patients with congestive heart failure (CHF) are
hospitalized every year. CHF is the leading diagnosis-related group (DRG)
among hospitalized patients older than 65 years. 35% will die within one
year of diagnosis. Less than 50% of patients with HF have typical physical
signs. Less than 50% of patients being correctly identified during the initial
consultation. 50% readmission rate within 6 months
50% of HF patients will die 5 years after the diagnosis
The most common cause of death is progressive heart failure, but sudden
death may account for up to 45% of all deaths.
Patients with coexisting insulin-dependent diabetes mellitus have a
significantly increased mortality rate.
Cardiac Physiology
(remember this?)
• CO = SV x HR
• HR: parasympathetic and
sympathetic tone
• SV: preload, afterload,
contractility
Preload
• Def: Passive stretch of muscle prior to contraction
• Measurement: Swan-Ganz
– LVEDP( venous return)
• Really a function of diastole

• Affected by compliance
– Low compliance = higher LVEDP with lower LVEDV
Afterload
• Def: Force opposing/stretching muscle after contraction begins
• Measurement: SVR
Contractility
• Def: Normal ability of the muscle to contract at a given force for
a given stretch, independent of preload or afterload forces
• In other words:
– How healthy is your heart muscle?
• Ischemia,infarction, Hypertrophy (?), Muscle loss
Pathophysiology
• Hemodynamic changes
• Neurohormonal changes
• Cellular changes
1.Hemodynamic changes:
• HF can be secondary to systolic dysfunction or diastolic dysfunction
• 2. Cellular changes
• Changes in Ca+2
handling
• Changes in adrenergic receptors:
Slight in α1 receptors

β1 receptors desensitization followed by down regulation
• Changes in contractile proteins
• Program cell death (Apoptosis)
• Increase amount of fibrous tissue
• 3. Neurohormonal changes
Neurohormonal changes
N/H changes Favorable effect Unfavorable effect
Sympathetic activity HR , contractility,
vasoconst. Venous
return,
filling
Arteriolar constriction
After load workload
O2 consumption
Renin-Angiotensin –
Aldosterone
Salt & water retention
Venous Return
Vasoconstriction
after load
Vasopressin Same effect Same effect
interleukins &TNF- May have roles in myocyte
hypertrophy
Apoptosis
Endothelin Vasoconstriction VR After load
Classifying Heart Failure
• Forward Vs Backward
• Rt. Vs Lt. sided HF
• Acute Vs Chronic HF
• Low Vs High output HF
• Systolic Vs Diastolic HF

• A etiology It is a common end point for many diseases of cardiovascular system
1. Vascular –
Ischemic heart disease,
myocardial infarction
2. Valvular –
stenosis/regurgitation(
RHD, infective
endocarditis)
3. Preesure- hypertension
4.Muscle-
cardiomyopathy
5. Rhythm- atrial
fibrillation
Symptoms:
Left ventricular failure-
The patient present with chest symptoms which may delay the diagnosis and
keep the patient to seek chest consultants advice.
Failure of forward flow from left ventricle into the aorta result into pulmonary
congestion with chest symptoms.
Since the left ventricle does not empty completely, it cannot accept blood
returning from the lungs via the pulmonary veins. The pulmonary veins become
engorged and fluid seeps out through the veins and collects in the lungs.
LVF can be acute or chronic depending on the underlying cause of heart disease
LVF= CHEST SYMTOMS= D/D OF ALL LUNG DISEASES= CHEST FINDING

LVF symptoms are:
Dyspnea at rest
Dyspnea upon exertion: This has been found to be the most sensitive
symptom reported, yet the specificity for dyspnea is less than 60%.
Orthopnea and paroxysmal nocturnal dyspnea (PND): These symptoms
are observed; however, the sensitivity for orthopnea and PND is only 20-
30%.
Cough: Cough that produces pink, frothy sputum is highly suggestive of
congestive heart failure (CHF).The sputum is whitish , soap like , watery.
Wheezing= new onset of wheezing above age of 60 years or wheezing in
elder diabetic or wheezing all of a sudden in HTN patient is cardiac
asthma until prove other wise.
Palpitation in arrhythmia
Chest pain or tightness especially if the cause is vascular(IHD/ACS).
Non specific symptoms of low COP
Malaise, Weakness,Light headedness, fatigue, dizziness ,sweating ,lose of effort.

Right ventricular heart failure
The patient present with abdominal symptoms which may delay the diagnosis
and keep the patient to seek gastroenterologist advice.
Failure of forward flow from right ventricle into the pulmonary artery results
into systemic congestion with abdominal symptoms.
Failure of the right ventricle to maintain a normal output of blood.
Since the right ventricle does not empty completely, it cannot fully accept blood
returning from the body. Pressure builds in the veins of the body causing fluid to
seep out and collect in the cells of the body – especially the extremities.
Engorgement of the systemic veins produces pitting edema, enlargement of the
liver, and ascites.

RVF can be acute or chronic depending on the underlying cause of heart disease
RVF= ABDOMENAL SYMTOMS= D/DOF ABDOMENAL DISEASES= ABD FINDING.
Right-sided or right ventricular (RV) heart failure usually occurs as a result of
left-sided failure. When the left ventricle fails, increased fluid pressure is, in
effect, transferred back through the lungs, ultimately damaging the heart's right
side. When the right side loses pumping power, blood backs up in the body's
veins. This usually causes swelling in the legs and ankles.
RVF symptoms are:
Abdominal distention
Right hypochondrial pain
Epigastric fullness, early satiety , nausea , vomiting(stomach congestion)
Change of bowel habit –constipation, diarrhea, malabsorption
Bilateral leg swelling
Yellowish coloration of sclera
Change of urine frequency and colour
These symptoms are caused by internal abdominal organs congestion
And can be mistaken for local abdominal pathology.
RVF is caused by:
1. Left ventricular failure - most common cause- mitral stenosis
2. Pulmonary hypertension caused by chronic lung disease
(cor pulmonale)
3. Cardimyopathies and
myocarditis

SIGNS:
General appearance
Patients with mild heart failure appear to be in no distress after a
few minutes of rest, but they may be obviously dyspneic during and
immediately after moderate activity. Patients with LV failure may
be dyspneic when lying flat without elevation of the head for more
than a few minutes. Those with severe heart failure appear anxious
and may exhibit signs of air hunger in this position.
Patients with recent onset of heart failure are generally well
nourished, but those with chronic severe heart failure are often
malnourished and sometimes even cachectic.
Chronic marked elevation of systemic venous pressure may produce
exophthalmos and severe tricuspid regurgitation and may lead to
visible pulsation of the eyes and of the neck veins.
Central cyanosis, icterus, and malar flush may be evident in patients
with severe heart failure.
In mild or moderate heart failure, stroke volume is normal at rest;
in severe heart failure, it is reduced, as reflected by a diminished
pulse pressure and a dusky discoloration of the skin.
With very severe heart failure, particularly if cardiac output has
declined acutely, systolic arterial pressure may be reduced. The
pulse may be weak, rapid, and thready; the proportional pulse
pressure (pulse pressure/systolic pressure) may be markedly
reduced. The proportional pulse pressure correlates reasonably
well with cardiac output.
Evidence of increased adrenergic activity
Increased adrenergic activity is manifested by tachycardia,
diaphoresis, pallor, peripheral cyanosis with pallor and coldness of
the extremities, and obvious distention of the peripheral veins
secondary to venoconstriction.
Diastolic arterial pressure may be slightly elevated.
Pulmonary rales =LVF
Rales heard over the lung bases( bilateral basal end inspiratory) are
characteristic of heart failure of at least moderate severity.
The absence of rales certainly does not exclude elevation of
pulmonary capillary pressure due to LV failure.

Protodiastolic (S3) gallop: This is the earliest cardiac physical finding in
decompensated heart failure in the absence of severe mitral or tricuspid
regurgitation or left-to-right shunts.
LVF=CHEST-B/L BASAL INSPIRATORY CREPITATION + HEART-S3
Systemic venous hypertension: This is manifested by jugular venous
distention. Normally, jugular venous pressure declines with respiration;
however, it increases in patients with heart failure, a finding known as the
Kussmaul sign. This reflects an increase in right atrial pressure and
therefore right-sided heart failure.
Hepatojugular reflux: This represents distension of the jugular vein
induced by applying manual pressure over the liver. The patient's body
should be positioned at a 45 º angle. This is found in patients with
elevated left-sided filling pressures and reflects elevated capillary wedge
pressure and left-sided heart failure.
Edema
Bilateral pitting pedal odema.
Usually, a substantial gain of extracellular fluid volume (ie, a
minimum of 5 L in adults) must occur before peripheral edema is
manifested.
Edema, in the absence of dyspnea or other signs of LV or RV failure,
is not solely indicative of heart failure and can be observed in many
other conditions, including chronic venous insufficiency, nephrotic
syndrome, or other syndromes of hypoproteinemia or osmotic
imbalance.
Hepatomegaly
Hepatomegaly is prominent in patients with chronic right-sided
heart failure, but it may occur rapidly in acute heart failure.
When occurring acutely, the liver is usually tender.
In patients with considerable tricuspid regurgitation, a prominent
systolic pulsation of the liver, attributable to an enlarged right atrial
V wave, is often noted. A presystolic pulsation of the liver,
attributable to an enlarged right atrial A wave, can occur in
tricuspid stenosis, constrictive pericarditis, restrictive
cardiomyopathy involving the RV, and pulmonary hypertension
(primary or secondary).

Hydrothorax (pleural effusion)
Hydrothorax is most commonly observed in patients with
hypertension involving both systemic and pulmonary systems.
Hydrothorax is usually bilateral, although when unilateral, it is
usually confined to the right side of the chest.
When hydrothorax develops, dyspnea usually intensifies because of
further reductions in vital capacity.
Ascites
This finding occurs in patients with increased pressure in the
hepatic veins and in the veins draining into the peritoneum.
Ascites usually reflects long-standing systemic venous
hypertension.
Pulsus alternans ( one strong and one weak beat)
Pulsus alternans occurs most commonly in heart failure due to increased
resistance to LV ejection, as occurs in hypertension, aortic stenosis,
coronary atherosclerosis, and dilated cardiomyopathy.
It is usually associated with an S3 gallop, signifies advanced myocardial
disease, and often disappears with treatment of heart failure.
Accentuation of P2 heart sound, S3 gallop, and systolic murmurs
This accentuation is a cardinal sign of increased pulmonary artery
pressure. It disappears or improves after treatment of heart failure.
Mitral and tricuspid regurgitation murmurs are often present in
patients with decompensated heart failure because of ventricular
dilatation. These murmurs often disappear or diminish when
compensation is restored. Note that correlation between the
intensity of the murmur of mitral regurgitation and its significance
in patients with heart failure is poor. Severe mitral regurgitation
may be accompanied by soft murmur.
The presence of an S3 gallop in adults is important, pathologic, and
often the most apparent finding on cardiac auscultation in patients
with significant heart failure.
Cardiac cachexia
Cardiac cachexia is found in long-standing heart failure, particularly
of the RV, because of anorexia from hepatic and intestinal
congestion and sometimes because of digitalis toxicity.
Occasionally, impaired intestinal absorption of fat and (rarely)
protein-losing enteropathy occur.

Left heart failure
IHD, Myocarditis,
Valvular heart diseases
Forward failure Backward failure
↓ cardiac output
Tissue anoxia
↓ renal perfusion
Activation of RAAS
PULMONARY
CONGESTION and
OEDEMA
Na+, H2O retention
Residual blood in left ventricle
 Left atrial pressure and volume
 Pressure in pulmonary venous circulation
Pulmonary arterial hypertension
 Right ventricular pressure
SYSTEMIC VENOUS
CONGESTION and
PERIPHERAL OEDEMA
Right heart failure
Right side valvular disease
Rt side myocardial disease
Pulmonary hypertension

Precipitating Factors
• Infection Sodium Intake
• Medications!!! Anemia
• Thyroid disorders Endocarditis
• Pulm Embolus Noncompliance
• Arrhythmia Myocardial Infarction
• Stress reaction
Diagnosis of CHF / Routine Tests:
CBC count INVESIVE
Electrolytes 1. Exercise stress test
Renal function tests 2. Cardiac catheterization
Liver function tests 3. Holter monitor
B-type natriuretic peptide
ECG
Chest x-ray
Echocardiogram
CXR
Cardiomegaly
Vascular redistribution
Kerley B lines
Interstitial edema
Peri-bronchial “cuffing”
Effusions

Chest radiographs in patients with abrupt onset are usually helpful but can be
limited because a delay of as long as 12 hours is possible from the onset of
dyspnea due to acute heart failure to the development of classic abnormal
findings on radiographs.
Classic radiographic findings demonstrate cardiomegaly (in patients with
underlying CHF) and alveolar edema with pleural effusions and bilateral
infiltrates in a butterfly pattern. The other signs are loss of sharp definition of
pulmonary vasculature, haziness of hilar shadows, and thickening of
interlobular septa (Kerley B lines).
In long standing biventricular chronic heart failure, chest radiographs may only
show cardiomegaly without alveolar edema or pleural effusions due to
adaptive lung mechanism with increased arterial vasoconstriction and
lymphatic drainage.

Electrocardiography
o The presence of left atrial enlargement and LV hypertrophy is
sensitive (although nonspecific) for chronic LV dysfunction.
o ECG may suggest an acute tachyarrhythmia or bradyarrhythmia.
o ECG may aid in the diagnosis of acute myocardial ischemia or
infarction as the cause of heart failure or may suggest the likelihood
of prior myocardial infarction or presence of coronary artery
disease as the cause of heart failure.
o ECG is of limited help when an acute valvular abnormality or LV
systolic dysfunction is considered to be the cause of heart failure;
however, the presence of left bundle branch block (LBBB) on an
ECG is a strong marker for diminished LV systolic function
Echocardiogram
Chamber enlargement
Wall motion abnormalities
Diminished ejection fraction
Possible LVH
Possible valvular problems
Assess diastolic dysfunction

Heart disease
(any)
Hypertension
Diabetes,
Hypercholesterolemia
Asymptomatic
LV dysfunction
Systolic / Diastolic
Marked symptoms
at rest despite
max. therapy
Dyspnea, Fatigue
Reduced exercise
tolerance
Stages in the Evolution of Heart Failure
A
B
C
D
AHA guidelines 2001
Treatment Goals
• Improve symptoms
A. Enhance well-being and quality of life
B. Increase exercise tolerance
• Improve survival
A. Prevent progressive heart failure
B. Prevent sudden death
C. Prevent thromboembolic episodes

• Treatment ::
• Oxygen – nasal, BiPAP, intubation
• Fluid Balance
Restrict fluid- 1000ml daily/ salt intake
Monitor Input/Outputs and daily weight
Dialysis if needed -Critical renal failure patients
Aspirin 75mg
 Promoting Rest and Activity
 Bed rest or limited activity may be necessary during the acute
phase
 Provide an overbed table close to the patient to allow resting the
head and arms
 Use pillows for added support.
 Gradual ambulation is encouraged to prevent risk of venous
thrombosis and embolism due to prolonged immobility
 Activities should progress through dangling, sitting up on a chair
and then walking in increased distances under close supervision.
 Assess for signs of activity intolerance (dyspnea, fatigue and
increased pulse rate that does not stabilize readily)
 Providing Skin Care
 Edematous skin is poorly nourished and susceptible to pressure
sores
 Change position at frequent intervals
 Assess the sacral area regularly
 Use protective devices to prevent pressure sores
 Promoting Elimination
 Advise to avoid straining at defecation which involves Valsalva
manoeuvre.
 Administer laxative as ordered
 Encourage use of bedside commode

Preload Reduction
– Loop diuretics Lasix 20-200mg IV (q 6-8 hours)
– Nitrates -Nitroglycerin IV:10-200 mcg/min
– ACEi / ARB Captopril 6.25-50mg PO q8h
Enalapril 2.5-20mg PO BID
Afterload Reduction
– IV NTG, Nitroprusside
– Hydralazine 10-100mg PO q6-8 h
– ACE-I / ARB
Ionotropic Support
– Dopamine / Dobutamine 500mg in 250cc D5W
3-10 cg/kg/min

– Amrinone / Milrinone n Digoxin (chronic)
– Mechanical (ABP) Cardiogenic shock unresponsive to above tx
A.-----------Diuretics
• volume overload , sodium overload , preload reduction
Advantages
• Highly effective in most classes
• Essential with fluid retention
• Well tolerated, simple to use
Disadvantages
• Electrolyte abnormalities Na, k ,Ca ,Mg
• Hypovolemia, hypotension, renal dysfunction
• Activation of neurohormaonal system
AIM----Elimination of symptoms and/or signs of congestion
• Avoid volume depletion
A. Postural hypotension B. Increase in heart rate
C. Increase in BUN/Cr D. Neuroendocrine activation
Thiazide Diuretics-----Hydrochlorothiazide, Chlorthalidone , Metolazone
Loop Diuretics----------Furosemide , Torsemide
Potassium Sparing Diuretics---Spironolactone , Triamterene , Amiloride
Spironolactone :
Aldosterone inhibition minimize potassium loss, prevent sodium and water
retention, endothelial dysfunction and myocardial fibrosis.

B-------------ACE Inhibitors
ACE inhibitors should be the initial treatment for heart failure
• Improve hemodynamic status
• Attenuate neurohumoral abnormalities
• Improve symptoms, left ventricular ejection fraction .
• Reduce incidence of hospitization
• Slow progression
• Reduce mortality
Neurohormonal Changes
• Decreased angiotensin II.
• Reduction in arterial resistance (afterload).

• Reduction in venous tension (preload).
• Inhibition of cardiac and vascular remodeling .
• Increased bradykinin
• Decreased or no change in aldosterone
• Decreased norepinephrine
Reduction in Sudden Death/Potential Mechanisms
• Increase in serum/total body potassium
• Decreased adrenergic stimulation
• Reduced heart size and decrease in ventricular hypertrophy
• Prevention of myocardial ischemia
• Prevention of progressive myocardial damage
FDA Approved
• Captopril ,Enalapril ,Lisinopril ,Quinapril ,Trandolapril ,Fosinopril
Adverse effects :
 Dry irritating persistent cough
 Hyperkalemia
 Angioedema
 Fetal toxicity

CHF: ACE Inhibitor Doseages
Captopril
Enalapril
Lisinipril
Quinapril
• Start: 6.25 bid/tid
• Usual: 6.25-50 bid/tid
• Start: 2.5 qd/bid
• Usual: 2.5-10 bid
• Start: 2.5-5 qd
• Usual: 5-20 qd
• Start: 5 bid
• Usual 10-20 bid
C---------------Beta Blockers
• Primary mechanism is inhibition of down regulation of beta receptors
• Additional mechanisms
A. Restore receptor density
B.Protect against cardiotoxicity of catecholeamines
C. Improve systolic/diastolic function in ischemic myocardium
• First Generation: Beta 1 and Beta 2
Propranolol/Timolol
• Second Generation: Beta 1
Metoprolol/Atenolol
• Third Generation: Vasodilating Properties
Carvedilol
Improve symptoms and clinical class

• Degree of benefit appears to relate to degree of disability before
treatment
• Should be used in all stable Class II/III patients unless contraindicated
• Treatment should not be initiated in patients with acutely
decompensated CHF
• Clinical response may take 2 to 3 months
Risks of Treatment
• Hypotension Fluid retention and worsening CHF
• Bradycardia and heart block

CHF: Beta Blockers
• Carvedilol
• Metoprolol
• Bisoprolol
• Start: 3.125 mg bid
• Usual: 25 mg bid
• Start: 12.5-25 mg qd
• Usual: 50-100 mg bid
• Start: 1.25 mg qd
• Usual: 5-10 mg qd
 Start at low dose and monitor for bradycardia
 Carvedilol and Metoprolol are the most commonly used for CCF amongst
beta blockers
D------------Angiotensin Receptor AT-1 blockers (ARB) :
Losartan, Irbesartan, Candesartan
 Competitive antagonists of Angiotensin II (AT-1).
 No inhibition of ACE or Cough.

 E--------------Vasodilators :
 Isosorbide dinitrate and hydralazine also used specially in patients who
cannot tolerate ACE inhibitors.
 Amlodipine and prazosin are other vasodilators can be used in CCF.

F-------Cardiac glycosides : Digoxin :
 Inhibition of Na/K ATPase pump increase intracellular sodium
concentration – eventually increase cytosolic calcium.
 It restores the vagal tone and abolishes the sympathetic over activity.
 Has positive inotropic (strengthens force of cardiac contractility) and
negative chronotropic effects (decreases heart rate.
 Increase the refractoriness of AV node thus decrease ventricular response
to atrial rate.

 Digoxin is used as a first-line drug in patients with congestive heart failure
who are in atrial fibrillation.
Adverse effects / Precautions :
 Nausea, vomiting, gynecomastia, visual disturbances and psychosis.
 Ventricular bigeminy, AV block and bradycardia.
 Antidote for Toxicity: Digibind
 Nursing Responsibilities
Assess heart rate before administration; if below 60
bpm or above 120 bpm, withhold the drug.
Monitor serum potassium
Assess for signs of Digitalis toxicity
- Bradycardia
- GI manifestations (anorexia, nausea, vomiting and
diarrhea)
- Dysrrhythmias
- Altered visual perceptions
- In males: gynecomastia, decreased libido and
impotence
 Amiodarone and verapamil can increase the plasma concentration of
digoxin by inhibiting its excretion
IN DIASTOLIC FAILURE;
USE B-BLOCKER, ACE-I , CALCIUM CHANNEL BLOCKER RATE LIMITING
• Difficult to treat
• Diuretics for volume overload. Avoid volume depletion
• Prevent tachycardia
• Rate-limiting calcium channel blockers first choice
• Beta 1 beta blockers second choice

ADVERSE PROGNOSTIC MARKERS IN CHRONIC HEART FAILURE
• Old Age,
• Severity of heart failure (NYHA class)
• Left ventricular dysfunction,
• Diabetes Mellitus,
• Raised creatinine,
• Hyponatremia , Hypoalbuminaemia,Anaemia
• Presence of arrhythmia : AF / VT
Causes of Mortality in Heart Failure
• Pump failure
• Arrhythmia
• Severe Anaemia
• Associated serious co-morbidities i.e. Renal failure
Cardiac Inotropes =
• Dopamine acts at a variety of receptors (dose dependant)
• Rapid elimination- can only be administered as a continuous infusion
Dobutamine
• Stimulates beta-adrenergic receptors and produces a positive inotropic
response
• Unlike the vasoconstriction seen with high doses of dopamine,
dobutamine produces a mild vasodilatation .

PDE Phosphodiesterase inhibitors
• Inamrinone (amrinone) and Milrinone (bipyridines)
• Acts by inhibiting the enzyme Phosphodiesterase
• Thus lead to increase of intracellular concentrations of cAMP
• cAMP is responsible for the conversion of inactive protein kinase to active
form
• Protein kinases are responsible for phosphorylation of Ca channels
• Thus causing increased Ca entry into the cell.
MECHANISM OF ACTION:
• Increase myocardial contractility by increasing the Ca influx during AP
• Also have vasodilating effect
• Selective for PDE isoenzyme-3 (found in cardiac and smooth muscle)
ADVERSE RECTIONS
• Inamrinone: nausea, vomiting, arrhythmias, thrombocytopenia and liver
enzyme changes
• Withdrawn in some countries
• Milrinone: arrhythmias, less likely to cause other ADR
Niseritide
• Brain (B-type) natriuretic peptide (BNP) is secreted constitutively by
ventricular myocytes in response to stretch
• BNP binds to receptors in the vasculature, kidney, and other organs,
producing potent vasodilation with rapid onset and offset of action by
increasing levels of cGMP

• Niseritide is recombinant human BNP approved for treatment of acute
decompensated CHF.
• It reduces systemic and pulmonary vascular resistances, causing an
indirect increase in cardiac output and diuresis.
• Effective in HF because cause reduction in preload and afterload
• ADR- hypotension
OTHERS;
Implantable cardioverter-defibrillator
Pacemakers, Biventricular pacemaker
Heart transplant
Cardiac Resynchronisation Therapy

Congestive heart failure

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