Approach to

Heart Failure

Heart Failure
Heart Failure, is a clinical syndrome in
which an abnormality of cardiac structure
or function is responsible for the inability
of the heart to eject or fill with blood at a
rate commensurate with the requirements
of metabolizing tissues

General Etiologies Of Cardiac

Failure
CORONARY VASCULAR -> ACUTE MI
VALVULAR
-> AORTIC , MITRAL VALVE DISEASE
MYOCARDIAL
-> ISCHEMIC CARDIOMYOPATHY
HYPERTENSION
-> HYPERTENSIVE CRISIS
RHYTHM DISTURBANCES -> TACHYCARDIA ,
INDUCED HF
6. PERICARDIAL
-> TAMPONADE , CONSTRICTION
1.
2.
3.
4.
5.

Underlying cardiac disease

Conditions that
that
depress ventricular function

CAD
C.M.PATHY
HTN
DISEASE
DCM
Valvular heart disease
Congenital heart disease

Conditions
restrict filling

RESTRICTIVE
PERICARDIAL

Precipitating causes
1. Increased salt intake
2. Non compliance with anti CHF
medications
3. Acute myocardial infarction
4. Aggravation of Hypertension
5. Acute arrhythmias
6. Infections and or fever

1.
2.
3.
4.
5.

Pulmonary Embolism
Anemia
Thyrotoxicosis
Pregnancy
Rheumatic, Viral, and Other Forms of
Myocarditis
6. Infective Endocarditis
7. Physical, Environmental, and Emotional
Excesses

Pathogenesis
1. Myocardial cell loss myocyte
hypertrophy and elongation.
2. An increase in ventricular volume (the
Starling effect) helps maintain cardiac
output (CO), but at the cost of increasing
ventricular filling pressures.
3. The increase in diastolic stretch and
pressure produces further damage
stretch-induced myocyte death
(apoptosis)

CARDIACOUTPUT
OUTPUT
CARDIAC
DEC.RENAL
RENALBLD
BLDFLOW
FLOW
DEC.

SYMPATHETICDISCHARGE
DISCHARGE
SYMPATHETIC

RAA.ACTIVATION
ACTIVATION
RAA.

INC.FORCE
INC.FORCE
RATE
RATE
PRELOAD
PRELOAD
AFTERLOAD
AFTERLOAD

REMODELLING

Forms of Cardiac Failure

1.
2.
3.
4.
5.

Systolic and diastolic failure

Low output and high output failure
Acute and chronic heart failure
Backward and forward failure
Left and right heart failure

Approach to the patient

1. RESPIRATORY AND OTHER SYMPTOMS
2. Due to inadequate perfusion of peripheral
tissues
1. Fatigue
2. Dyspnoea

3. Due to elevated intracardiac filling

pressures
1. Orthopnoea
2. PND
3. Peripheral edema

Symptoms of heart failure

1. Respiratory Distress
2. Breathlessness- cardinal manifestation of left
ventricular failure
3. May present with progressively increasing
severity as
1.
2.
3.
4.
5.

exertional dyspnea
orthopnea
paroxysmal nocturnal dyspnea
dyspnea at rest
acute pulmonary edema.

Symptoms.
URINARY SYMPTOMS.
1. Nocturia may occur early in the course of heart
failure.
2. Oliguria is a sign of late cardiac failure.
. CEREBRAL SYMPTOMS.
1. Confusion, impairment of memory, anxiety,
headache, insomnia, bad dreams or nightmares,
and, rarely, psychosis with disorientation,
delirium, and hallucinations.

Symptoms of predominant
right-sided Heart Failure
1. Breathlessness is not very prominent because
pulmonary congestion is usually absent.
2. Congestive hepatomegaly - dull ache or heaviness in
epigastrium.
3. Other gastrointestinal symptoms, including anorexia,
nausea, bloating, a sense of fullness after meals, and
constipation due to congestion of the liver and
gastrointestinal tract.
4. In severe, preterminal heart failure, inadequate bowel
perfusion can cause abdominal pain, distention, and
bloody stools.

Physical examination
1. JVP
2. S3
3. Pulmonary congestion (rales,
dullness over pleural effusion)
4. Peripheral edema
5. Hepatomegaly
6. Ascites

Laboratory Investigations
1.
2.
3.
4.
5.
6.
7.

CBC, ESR
Urine routine
LFT
RFT
CXR
ECHO
Measurement of BNP

BRAIN NATRIURETIC PEPTIDE

(BNP)
Pre pro-BNP is formed in the
ventricles with myocyte stretch
Broken down to N-terminal-pro-BNP
(NT-pro-BNP) and BNP.
Highly accurate for identifying or
excluding HF with high sensitivity
and specificity
BNP - valuable in differentiating
cardiac from pulmonary causes of
dyspnea

Framingham Criteria for Diagnosis of

Congestive Heart Failure
One major +two minor for diagnosis

Major Criteria
1.
2.
3.
4.
5.
6.
7.

Paroxysmal nocturnal dyspnea

Neck vein distention
Rales
Cardiomegaly
Acute pulmonary edema
S3 gallop
Increased venous pressure (>16
cmH2O)
8. Positive hepatojugular reflux
9. Weight loss 4.5 kg over 5 days'

Minor Criteria
1. Extremity edema
2. Night cough
3. Dyspnea on exertion
4. Hepatomegaly
5. Pleural effusion
6. Vital capacity reduced by one-third
from normal
7. Tachycardia (120 bpm)

NYHA GRADING
Class 1 :
Class 2 :
activity
Class 3 :
Class 4 :

no symptoms
symptoms with ordinary
less than ordinary activity
even at rest

Staging of systolic HF
1. STAGE A- ASYMPTOMATIC/ MILD HF NYHA
CLASS 1 / 2
2. STAGE B- MILD /MODERATE HF ,NYHA
CLASS 2 / 3
3. STAGE C- ADVANCED HF , CLASS 3 / 4
4. STAGE D- REFRACTORY HF ,CLASS 3 / 4
5. SUSTAINED DECOMPENSATION,
FREQUENT HOSPITALISATION

Conditions That MIMIC CHF

1. Pulmonary disease
1. Chronic bronchitis
2. Emphysema
3. Asthma

2. Other causes of peripheral edema

1.
2.
3.
4.

Liver disease
Varicose veins
Cyclic edema
Renal dysfunction

General measures
1. Prevent HF
2. Daily measurement of weight
3. Immunization with influenza and
pneumococcal vaccines
4. Education of the patient and family
5. Avoid Excessive alcohol, temperature
extremes, and tiring trips
6. Meals - small in quantity, frequent
7. Reduce sodium intake

Activity
1. Releive anxiety.
2. Physical and emotional rest
3. Anticoagulants, leg exercises,
and elastic stockings.
4. Absolute bed rest is rarely
required
5. Regular isotonic exercise
6. Weight reduction in obese

 Administration of oxygen
Sleep apnoea - nocturnal
continuous positive airway pressure
Dialysis or ultrafiltration in
patients with severe HF and renal
dysfunction
Other mechanical methods theraputic thoracocentesis or
paracentesis .
CORRECTION OF PRECIPITATING FACTORS

Measures for symptom relief

CONTROL OF EXCESSIVE
FLUID
Diet
Diuretics

Thiazide diuretics
Loop diuretics
Metalazone
Potassium sparing
diuretics

Role of diuretics
1. Rapid relief of symptoms
2. Controls fluid retention
3. Appropriate use of diuretics is
the key element in the
success of other drugs

DIURETICS
THIAZIDE DIURETICS -useful alone or in
combination with other diuretics
In chronic mild HF
K+ depletion and metabolic alkalosis
Suited only if GFR >50%of normal

METALAZONE
Site of action and potency similar to the thiazides
Effective in the presence of moderate renal failure
Both metolazone and thiazides potentiate
intravenous
loop diuretics

FUROSEMIDE, BUMETANIDE,
AND TORSEMIDE
Useful in all forms of HF, particularly in
refractory HF and pulmonary edema.
Effective in patients with
hypoalbuminemia, hyponatremia,
hypochloremia, and with reductions in
glomerular filtration rate
The action may be potentiated by I.V.
administration and by the addition of other
diuretics

POTASSIUM-SPARING
DIURETICS
Spironolactone acts by competitive
inhibition of aldosterone
Amiloride and triamterene act
directly on the distal
tubule/collecting duct.
Most effective with loop and/or
thiazide diuretics.
Lower dose of spironolactone (25
mg/d), prolong life in patients with
advanced HF

Prevention of deterioration of cardiac

function or drugs increasing survival

1. Angiotensin converting enzyme

(ACE inhibitors)
2. Angiotensin receptor blockers
3. Aldosterone blockers
4. Beta adrenoceptor blockers

Angiotensin-Converting Enzyme
(ACE) Inhibitors
1. Prevention and treatment of HF at
almost all stages
2. Slows remodeling .
3. Cardiac output rises
4. Pulmonary wedge pressure falls,
5. Afterload is reduced with no or only
mild reduction of arterial pressure.
6. Signs and symptoms of HF are
relieved

1. Enhance exercise performance

2. Reduce long-term mortality .
3. Major effect of ACE inhibitors is on
inhibition of local (tissue) reninangiotensin systems.
4. ACE inhibitor should be maintained
indefinitely.

ACE Inhibitor in cardiac

failure
Name Starting dose Target
Enalapril 1.25-2.5 BD 10 BD
Captopril
6.25-12.5 TID 25-50 TId
Lisinopril 2.5-5 0D 20-35 OD
Ramipril 1.25 -2.5 BD 5 BD

ARB
1. Equally effective
2. ACE inhibitor
intolerance

BETA BLOCKERS
Drug
Start
Target
Carvedilol 3.125 bd
25bd
Bisoprolol
1.25 od
10 od
Metoprolol
12.5 -25 od
200bd
As ADD on therapy with diuretics and ACEI
Improves ejection fraction,exercise
tolerance lowers rate ,dec.myo O2
demand,,reduces arrythmias reverse
LVH,prevents sudden deaths

Use of Beta blockers

1.
2.
3.
4.

Optimise volume status

Start at lowest possible dose
Increase dose gradually
Monitor vital signs ,wt , clinical
profile

Enhancement of Cardiac
contractility
1. Digitalis,digoxin oubain
2. Sympatho mimetic
amines
3. Phosphodiesterase
inhibitors

When should Digoxin be

used

DIGOXIN
1. Positive inotropic response
2. Inhibit Na+, K+-ATPase
3. Effective in systolic HF complicated by
atrial flutter and fibrillation and a rapid
ventricular rate
4. Does not improve survival in patients with
systolic HF and sinus rhythm, it reduces
symptoms of HF
5. No value in diastolic HF.

Sympathomimetic
Amines
1. Dopamine and dobutamine
,dopexamine
2. Act on -adrenergic receptors
3. Improve myocardial contractility
4. In severe, acute HF
5. Constant intravenous infusion
6. Can be given for several days
7. Used in refractory HF as a bridge
to cardiac transplantation.
8. Downregulation of adrenergic
receptors

Phosphodiesterase
Inhibitors
1. Amrinone,milrinone,enoximone,pir
oximone,fenoximone
2. Inhibit phosphodiesterase III
3. Positive inotropic and vasodilator
actions
4. Administered intravenously
5. Reverse the major hemodynamic
abnormalities associated with HF

Vasodilators
1. Useful in severe, acute HF with significant
systemic vasoconstriction despite ACE inhibitor
therapy.
2. Rapid onset and brief duration of action
3. Sodium nitroprusside
4. Intravenous nitroglycerin 20micg/min max
400micg/min
5. Nesiritide iv bolus 2micg/kg+0.01micg/kg/min
6. Combination of hydralazine and isosorbide
dinitrate - for chronic oral administration

Nesiritide, a recombinant
analog of BNP
1. The newest therapeutic option for ADHF.
2. Increase natriuresis, diuresis, and cardiac index
3. Reduce pulmonary capillary wedge pressure,
pulmonary artery pressure, pulmonary vascular
resistance, and systemic blood pressure in a
dose-dependent manner.
4. Reversal of the deleterious neurohormonal
response associated,with HF
5. Reduces levels of endothelin 1, aldosterone,and
norepinephrine.

 Nesiritide is more effective than

nitroglycerin in producing rapid and
significant reduction of LV filling
pressures
Does not require ICU admission or
invasive monitoring .
Lower incidence of tachycardia and
proarrhythmic effects.
Lessen the need for supportive
therapies such as diuretics

Survival benefit of different

drugs
Those which reduce MORTALITY
Those which Increase
MORTALITY
Those without any proved
influence on MORTALITY

Reduce mortality
1. Beta Blockers
2. A.C.E. Inhibitors
3. Angiotensin Receptor
Blockers
4. Spironolactone
5. Amiodarone

Drugs increasing Mortality

1. Inotropes&Inotropic
dilators
2. Antiarrythmics except

1. betablockers&Amiodarone

3. Calcium Channelblockers
4. High dose Digoxin

Those without any proved

influence on MORTALITY
Diuretics
Digoxin(low dose)
Nitrate

LVEF <40 %

Assess volume status

Fluid retention +

No fluid retention

Diuretic titrate to euvolemic

ACE 1

Beta blockers

VENTRICULAR
RESYNCHRONIZATION
1. Intraventricular conduction is depressed
in about one-fourth of patients with
chronic HF
2. Resynchronization with a device that
has three pacing leads (right atrium,
right ventricle, and cardiac vein, which
provides left ventricular stimulation)
improve performance in patients with HF
3. Increase ejection fraction

MANAGEMENT OF
ARRHYTHMIAS
1. Premature ventricular contractions
and episodes of asymptomatic
ventricular tachycardia are common
in advanced HF
2. VT/VF is responsible for about onehalf of all deaths
3. Correction of electrolyte and acidbase disturbances

Amiodarone
1. Amiodarone, a class III
antiarrhythmicis the drug of
choice for patients with HF and
atrial fibrillation.
2. Implantable automatic defibrillator
prevent sudden deaths

Anticoagulants
1. Increased risk of pulmonary emboli
secondary to venous thrombosis and of
systemic emboli secondary to
intracardiac thrombi
2. Patients with HF and atrial fibrillation,
previous venous thrombosis, and
pulmonary or systemic emboli are at
high risk
3. Heparin followed by warfarin

Management of Diastolic HF
1.
2.
3.
4.
5.
6.
7.
8.
9.

HTN regression of LVH important ARB,ACE

Myocardial ischemia.. Bblockers ,CCB,nitrates
Chronic AF. restore sinus rythmn,rate control
Beta blocker slow rate ,reduce O2 demand,lower
BP,regress LVH
CCB has lusiotropic effect (relaxation enhancing effect)
ACE inh. Effect uncertain ARB use regress LVH
Exercise conditioning.. improves diastolic function
,dynamic isotonic exercise ideal
Better Prognosis
Bad prognosis-Older age ,males ,lower
ej.fraction,ass,CAD,DM,impaired renal function

Management Of ADHF

Administration of oxygen
Morphine sulfate
Mechanical ventilation is indicated
A sitting position improves pulmonary
function.
Placing the patient on strict bed rest and
reducing pain and anxiety decrease cardiac
workload.

1. Intravenous inotropes and vasodilators - The

combination of an intravenously administered
vasodilator such as nitroglycerin, niseritide, or
of a phosphodiesterase inhibitor together with
a sympathomimetic amine
2. Hemodynamic monitoring cvc,swan ganz
catheter,O2 saturation
3. Extracorporeal ultrafiltration and
hemofiltration-Acute hemodialysis and
ultrafiltration may be effective, especially in
the patient with significant renal dysfunction
and diuretic resistance ,removes i.v fluid

1. Mechanical circulatory supports

2.
Devices
1. Counter pulsation device(Intra
aortic baloon pump and non
invasive counter pulsation)
2. Cardiopulmonary assist devices
3. Left ventricular assist devices

 In hospitalized patients with refractory HF,

therapy to be guided by hemodynamic
measurements by a balloon flotation
(Swan-Ganz) catheter
The goal is to achieve pulmonary capillary
wedge pressure of 15 to 18 mmHg
Right atrial pressure of 5 to 8 mmHg
Cardiac index >2.2 L/min per m2
Systemic vascular resistance of 800 to
1200 dyne s/cm5.

SURGICAL THERAPY
CARDIAC TRANSPLANTATION best
predictor peak O2 consumption with
maximal exercise (VO2max)NI
>20ml/kg/min,<10ml/kg/min
transplantation ideal
Novel surgeries
Ventricular remodelling surgeries
Dynamic cardiomyoplasty
Mitral valve repair

NEWER Rx MODALITIES FOR ADHF

1. BALOON COUNTER PULSATION
INTRAAORTIC BALOON PUMP
2. VAD PULSATILE LOW FLOW VAD
3. PACING BIVENTRICULAR PACING ,
AV SEQUENTIAL PACING

NEWER DRUGS
B N P analogue
Nesiritide

Endopeptidase inhibitor(ACE+neutral
peptidases)
Omapatrilat

Calcium Sensitiser
Pimobendan,Levosibendan
LEVOSIBENDAN is a novel agent with
inotropic properties developed
specifically for the management of
ADHF.
It acts by sensitizing troponin C to
calcium

Endothelin receptor antagonist

BOSENTAN
TEZOZENTAN

Effective in acute coronary

syndromes, acute renal failure and
acute HF.
Indirectly improve contractility while
decreasing pulmonary capillary
wedge pressure.

 VASOPRESSIN ANTAGONISTS (V2 RA)

Tolvaptan, Lixiraptan ,Coniraptan
CAN BE USED AS ADJUVANT
HF

to DIURETIC IN ADVANCED

ENOXIMONE TYPE 3 PDEI

PA Pr. MONITORING REQUIRED

LV FILLING PRESSURE > 15 mm Hg
IDEAL INOTROPE FOR PATIENT ON

BLOCKERS

PROGNOSIS
1. Depends primarily on the nature of the
underlying heart disease
2. Presence or absence of a precipitating
factor
3. Prognosis can be estimated by observing
the response to treatment.
4. When patients can be rendered free of
congestion, survival may be 80% at two
years.

1. High BUN (>43 mg/dL) is the best

single predictor of inhospital
mortality
2. Severely depressed ejection
fraction<15%
3. Inability to walk on level at normal
pace>3min
4. Low SBP (<115 mm Hg)
5. High serum creatinine (SCr) levels
(>2.75 mg/dL).
6. Elevations in circulating levels of Btype natriuretic peptide (BNP)

When all available

therapeutic measures have
been exhausted, comfort
care, with continued
infusions of inotropic
agents, diuretics, and the
administration of
anxiolytics and analgesics
should be considered.