HEART FAILURE

Presented by,
Dr. CAROLYNE JOUTE
 OUTLINE
-Definition
-Key Concepts

-Epidemiology,Risk factors,Prognosis,Etiology

-Criteria of HF,Classification

-Symptoms

-Physical Examination

-Diagnosis

-Management
 INTRODUCTION
WHAT IS HEART FAILURE?

A complex clinical syndrome that results from

structural or functional impairment of
ventricular filling or ejection of blood, which in
turns leads to the cardinal symptoms of
dyspnea, fatigue and signs of HF.
HF Key Concepts
Cardiac output (CO) = Stroke Volume (SV) x Heart Rate (HR)

SV= EDV – ESV .

It is determined by preload, afterload and myocardial contractility

Ejection Fraction (EF): One of the measurements used by physicians

to assess how well a patient’s heart is functioning “Ejection” refers
to the amount of blood that is pumped out of the heart’s main
pumping chamber during each heartbeat “Fraction” refers to the
fact that, even in a healthy heart, some blood always remains
within this chamber after each heartbeat.

An ejection fraction is a percentage of the blood within the chamber

that is pumped out with every heartbeat
Normal EF = 55 to 75 percent
Epidemiology
 In India the prevalence of HF is about 1% of
the population or about 8-10 million
individuals. The estimated mortality
attributable is about 0.1- 0.16 million
individual/year.
 As worldwide more than 20 million people
are affected. The overall prevalence in adult
population in developed countries is 2%.
RISK FACTORS
1)Primary Risk Factors:
Coronary Artery Disease
Advancing age

2)Contributing risk factors:

HTN
DM
obesity
valvular heart disease
hypervolemia
tobacco use
smoking
PROGNOSIS
 Despite many recent advances in the evaluation and
management of HF, the development of symptomatic HF
still carries a poor prognosis.

 Community-based studies indicate that 30–40% of

patients die within 1 year of diagnosis and 60–70% die
within 5 years.

 Although it is difficult to predict prognosis in an

individual, patients with symptoms at rest (New York
Heart Association [NYHA] class IV) have a 30–70% annual
mortality rate, whereas patients with symptoms with
moderate activity (NYHA class II) have an annual
mortality rate of 5–10%.
PATHOPHYSIOLOGY
 HF begins after an index event produces an initial
decline in the heart’s pumping capacity. After this
event,a variety of compensatory mechanisms are
activated including the adrenergic nervous system.
The renin angiotensin aldosterone system and the
cytokine system.In the short term, this system are
able to restore cardiovascular function to a normal
homeostatic range with the result that the patient
remains asymptomatic. However,with time,the
sustained activation of this systems can lead to
secondary end organ damage within the ventricle wih
worsening left ventricular remodelling and
subsequent cardiac decompensaton.
 SYMPTOMS OF HF
1.RESPIRATORY DISTRESS:

a)EXERTIONAL DYSPNEA: seen in early HF, it may simply appear to be an

aggravation of the breathlessness that occurs in normal subjects during
activity.As LV failure advances,the intensity of exercise resulting in
breathlessness declines progressively.

b)ORTHOPNEA: dyspnea occuring in the recumbent position,usually a later

manifestation of HF than is exertional dyspnea. It occurs due to redistribution
of fluid from the abdomen and lower extremities into the chest in lying
position with a resultant increase in pulmonary capillary pressure. Orthopnea
is generally relieved by sitting upright or sleeping with additional pillows.

c)PAROXYSMAL NOCTURNAL DYSPNEA: refers to acute episodes of severe

SOB and coughing that generally occurs at night and awaken the patient from
sleep, usually 1-3 hrs after the patient retires. PND may manifest as coughing
or wheezing possibly because of increased pressure in the bronchial arteries
leading to increased airway resistance.
DIFFERENTIATION BETWEEN CARDIAC AND
PULMONARY DYSPNEA

Patient with COPD may also waken at night with

dyspnea,but this is usually associated with sputum
production and the dyspnea is relieved after patients rid
themselves of secretions by coughing rather than
specifically by sitting up.When the dyspnea arises after
a history of intensified cough and expectoration,it is
usually primarily pulmonary in origin.

Acute cardiac asthma usually occurs in patients who

have obvious clinical evidence of heart disease and
maybe further differentiated from acute bronchial
asthma by diaphoresis and bubblier airway sounds and
the more occurrence of cyanosis.
 The difficulty in distinguishing between pulmonary and cardiac
dyspnea may be compounded by the coexistence of disease
involving both organ system.Thus,patients with history of chronic
bronchitis or asthma who develops LV failure tends to develop
particularly severe bronchoconstriction and wheezing in
association with bouts of PND and pulmonary edema. Airway
obstruction and dyspnea that responds to bronchodilators or
smoking cessation favor a pulmonary origin of the dyspnea,
while the responds to these manifestations to diuretics supports
HF as the cause of dyspnea.

 Pulmonary function testing should be carried out in patients in

whom the etiology of dyspnea is unclear despite detailed clinical
evaluation.The result may be helpful in determining whether
dyspnea is produced by heart disease,lung disease, a
combination of the two, or neither.
OTHER SYMPTOMS:
Gastrointestinal symptoms:
-Anorexia
-nausea
-early satiety associated with abdominal pain and fullness are common
complaints and maybe related to edema of the bowel wall and/or a
congested liver.
-Congestion of the liver and stretching of its capsule may lead to right
upper quadrant pain.

Cerebral symptoms
-confusion
-disorientation
-sleep and mood disturbances may be observed in patients with
severe HF,particularly elderly patients with cerebral atherosclerosis
and reduced cerebral perfusion.Nocturia is common in HF and may
contribute to insomnia.
PHYSICAL EXAMINATIONS
 1.GENERAL APPEARANCE AND VITAL SIGNS:In mild or moderately severe
HF,the patients appear to be in no distress at rest except for feeling
uncomfortable when lying flat for more than a few mins. In more severe HF, the
patient may have labored breathing,may not be able to finish a sentence
because of SOB. Systolic BP may be Normal or high in early HF,low in severe
HF. PR diminished reflecting a reduction in stroke volume.Peripheral
vasoconstriction leading to cool peripheral extremities and cyanosis of the lips
and nail beds due to excessive adrenergic activity.

 2.HEPATOJUGULAR REFLEX: In the early stage of HF,JVP may be normal at

rest but may become abnormally elevated with sustain pressure in the
RUQ(hepatojugular reflex)

 3.PULMONARY EXAMINATION:Pulmonary crackles (rales or

crepitations)result from the transudation of fluid from the intravasacular space
into the alveoli. PLEF result from the elevation of pleural capillary pressure and
resulting transudation of fluid into the pleural cavities. Tachypnea, B/L fine
basal crepitation and rhonchi may be present due to Pul.edema. Sometimes
signs of P/E may be present
 4.CARDIAC EXAMINATION:Cardiac enlargement may
be seen. S1 maybe diminished in intensity,3rd and 4th
HS are often audible. Pansystolic murmur maybe heard
due to incompetance of mitral and tricuspid valve due
to dilatation of ventricles.

 5.ABDOMEN AND EXTREMITIES: Liver may be

enlarged and tender due to congestion, Ascites may be
present. Jaundice and peripheral edema may also be
present.

 6.CARDIAC CACHEXIA: With severe chronic HF,there

may be marked weight loss and cachexia.
DIAGNOSIS
1. ROUTINE LAB TESTING:
CBC,SE,BUN,Creatinine,hepatic enzyme and uninalysis. Selected patients should
have assessment for DM,Dyslipidemia and thyroid abnormalities.

2.ECG: to assess cardiac rhythm and determine the presence of LV hypertrophy

or a prior MI. It may also show conduction defects and electrolyte imbalance.

3.CXR:provides useful information about cardiac shape and sizes as well as the
state of pulmonary vasculature and identify non cardiac causes of the patient’s
symptoms. Cardiomegaly ( C:T ratio > 0.5 and especially >0.60 is a strong
indicator of HF)

4.ASSESSMENT OF LV FUNCTION: 2D Echo/Doppler which can provide a

semiquantitative assessment of LV size and function as well as the presence or
absence of valvular and regional wall motion abnormalities.

5.BIOMARKERS : BNP and N terminal pro BNP which are released from the
failing heart are relatively sensitive markers for the presence of HF. Atrial
Natriuretic Peptide(ANP) and Brain Natriuretic Peptide (BNP) are elevated in HF.
TREATMENT
General measures for the management of HF:
1) Diet:Good general nutrition and weight
reduction for the obese. Avoidance of high
salt foods specially for patients with CHF
2) Alcohol: Moderation or elimination of
alcohol consumption. Alcohol induced
cardomyopathy requires abstinence.
3) Smoking cessation
4) Exercise
5) Influenza and pneumococcal vaccination
Heart Failure Emergency Management

U Upright Position
N Nitrates
L Lasix
O Oxygen
A ACE, ARBs, Aldactone, Amiodarone
D Digoxin, Dobutamine, Dopamine
M Morphine Sulfate
E Extremities Down
MANAGEMENT OF HF
 Heart Failure Stage A
At Risk Of Developing Heart Failure but no structural heart disease yet:
- Adequate BP control
- Adequate Diabetes control
- Weight reduction
- Quit smoking
- Avoid cardiotoxins
- Lipid management
- Atrial fibrillation management

 Heart Failure Stage B

Structural Heart Disease Without Overt Symptoms
Care measures as in Stage A along with:
-Should be on ACE-I
–Add beta blockers
–Spironolactone – if LVEF <40%
-Surgical consultation for coronary artery revascularization and valve
repair/replacement (as appropriate)
Heart Failure Stage C
Structural Heart Disease With Overt Symptoms

Nonpharmacological Interventions
-Therapeutic life style changes:Diet- low salt, low fat, rich in
fruit and veggie, increase fiber, water intake limited to 1.5 liters
-Smoking cessation
-Activity & exercise
-Duration of activity: Exercise training and rehab atleast 30
min aerobic exercise/brisk walking with 5 days and ideally 7
days a week
– Benefits: improve HRQOL (Health related quality of life)
increase in functional status, improve exercise capacity and
reduce hospitalization and mortality, improve endothelial
function and improve O2 extraction from peripheral tissue
 Heart Failure Stage C

Pharmacological Interventions
– All measures of stage A and B

Diuretics
– Furosimide (20-40mg once or twice)
– Hydroclorothiazide (25mg once or twice)
– Metolazone (2.5-5mg OD )
– Spironolactone (12.5-25 once or twice)

• Aim of diuretic therapy on outpatient is to decrease weight 0.5-

1kg daily with adequate diuresis and adjust the dose accordingly
until evidence of fluid retention resolved
– Then daily wt and adjust the dose accordingly
Heart Failure Stage C Pharmacological
Interventions
1.ACE Inhibitors
Captopril: 6.25mg thrice till 50mg thrice a day
Enalapril : 2.5mg twice to 1020mg twice a day
Lisinopril: 2.5-5mg once to 2040mg once a day
Ramipril: 1.25-2.5mg once till 10mg once a day
C/I – Cr >3mg/dl, angioedema, pregnant, hypotension
(SBP<80mmHg), B/L RAS, inc. K(>5mg/dl)

Initiation: start low dose – if tolerated then gradual increase in few

days to weeks to target dose or max tolerable dose. – Renal function
monitoring before starting, 1-2weeks after and periodically thereafter
and after changing dose
2.Angiotensin Receptor Blockers
-When ACEI intolerant or alternative to ACEI
-Can be substituted to ACEI with
angioedema history but with caution (pt can
develop angioedema with ARB as well)
-Losartan: 25-50mg once till 50-150mg
once a day
-Valsartan: 20-40mg twice till 160mg
-Same initiation and monitoring as ACEI
-Titration by doubling the dose
3.Beta Blockers
-Bisoprolol: 1.25-2.5mg once till 10mg
-Carvedilol: 3.125 twice till 50mg
-Metoprolol Succinate: 12.5 once till 200mg
once
Abrupt withdrawal avoided

4.Aldosterone Receptor Antagonists

-Spironolactone 12.525mg once till 50mg daily
5. Digoxin
-No loading required
–usual dose 0.125-0.25mg daily (low dose
0.125mg alternate day if >70yrs, CKD, Low lean
body mass

6. Hydralazine Nitrate Combination

Indication: NYHA III-IV, HFrEF on ACEI and BB
Bildil (37.5mg hydralazine and 20mg ISDN) start
one tab TID to increase till 2tab TID
If given separately then both at least TID
 Heart Failure Stage C
Device Therapy
1.Implantable Cardioverter Defibrillator (ICD) –
Nonischemic or ischemic heart disease (at least 40 days
post-MI) with LVEF of ≤35% with NYHA class II or III
symptoms or NYHA 1 with EF ≤30% on chronic medical
therapy, who have reasonable expectation of meaningful
survival for more than 1 year

2.Cardiac Resynchronization Therapy (CRT) –

Indicated for patients who have LVEF of 35% or less,
sinus rhythm, left bundle-branch block (LBBB) with a QRS
duration of 150 ms or greater, and NYHA class II and III.
 Heart Failure Stage D
-All the measures of Stage A, B & C
-Until definitive therapy [e.g., coronary
revascularization, Mechanical circulatory
support, heart transplantation or resolution of
the acute precipitating problem], patients
with cardiogenic shock should receive
temporary intravenous inotropic support to
maintain systemic perfusion and preserve
end-organ performance.
 Heart Failure Stage D
-Mechanical Circulatory Support
1.Intraaortic balloon pump (IABP) therapy
– Used for cardiogenic shock
– Allows heart to rest

2.Ventricular assist devices (VADs)

– Takes over pumping for the ventricles
– Used as a bridge to transplant
3.Destination therapy-permanent, implantable VAD
4.Cardiomyoplasty- wrap latissimus dorsi around heart
5.Ventricular reduction -ventricular wall resected
6.Transplant/Artificial Heart
Take Home Message
-HF is common problem in elderly and having prognosis worse
than Ca Lung
-It is clinical diagnosis supplemented by lab test and echo
-Echo can suggest the etiology of heart failure
-Diuretics are for acute relief and also for chronic management
of fluid overload
-Look for the precipitating event for acute decompensation
-ACE inhibitors/ARB, Beta blockers, Spironolactone improve
prognosis in patient with reduced ejection fraction
-Maintain patient on 2- to 3-g sodium diet. Follow daily weight
and determine target/ideal weight, which is not the dry weight
- In order to prevent worsening azotemia and adjust the dose
of diuretic accordingly
-Heart transplantation is for end stage heart failure
THANK YOU!
