heart failure mahesh ppt.pptx

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Heart Failure
Dr.V.Mahesh
Themost common reason for hospitalization in adults >65 years old.

• Heart Failure- Clinical syndrome … can result from
any structural or functional cardiac disorder that impairs
ability of ventricle to fill with or eject blood

z Heart Failure
Definition
• It is the pathophysiological process in which the heart as a
pump is unable to meet the metabolic requirements of the
tissue for oxygen and substrates despite the venous return
to heart is either normal or increased

z
HF is a clinical syndrome characterized by typical symptoms (e.g.
breathlessness, ankle swelling and fatigue) that may be accompanied by
signs (e.g., elevated jugular venous pressure, pulmonary crackles and
peripheral oedema) caused by a structural and/or functional cardiac
abnormality, resulting in a reduced cardiac output and/ or elevated
intracardiac pressures at rest or during stress.1
1.ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2016.
2.Dickstein K et al. Eur Heart J 2008;29:2388–442
2016 ESC HF

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HF is a clinical syndrome with
symptoms and or signs
caused by a structural and/or
functional cardiac abnormality
and corroborated by elevated
natriuretic peptide levels and
or objective evidence of
pulmonary or systemic
congestion.
2021 Update
J Cardiac Fail 2021;00:127)

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Introduction
Heart Failure is increasing in epidemic proportions across the world
including the developing countries like India.
Prevalence of HF to be increased by 46% globally by 2030 as per
ACC/AHA 2021 statistics.
The incidence of HF in patients more than 45 years is 6.0-7.9/1000
person years, while in >65 it is 20/1000 person years
One in 6 patients with HFREF develop worsening HF within 18 months of
the diagnosis.
The 30- day admission rate is approximately 56%.

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Heart Failure
Key Concepts
• Cardiac output (CO) = Stroke Volume (SV) x Heart Rate (HR)
– Becomes insufficient to meet metabolic needs of body
• SV – determined by preload, afterload and myocardial
contractility
• Ejection Fraction (EF) (need to understand)
• Classifications HF
–
–
–
Systolic failure – decrease contractility
Diastolic failure – decrease filling
Mixed

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Etiology
Cardiac performance is depends on
fouressential components:
⚫Preload
⚫Afterload
⚫Contractilityof the muscle
⚫Heartrate

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• Volume of blood in
ventricles
at end diastole
• Depends on venous return
• Depends on compliance
Preload Afterload
• Force needed to eject blood
into circulation
• Depends upon arterial BP,
pulmonary artery pressure
• Valvular disease
increases afterload
Factors Effecting Heart Pump Effectiveness

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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 percentageof the blood within the
chamber that is pumped out with every heartbeat
Normal EF = 55 to 65 percent

90ml/140ml = 64% (EF 55-65% normal)

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Keys To Understanding HF
•
•
•
All organs (liver, lungs, legs, etc.) return blood to heart When heart
begins to fail/ weaken unable to pump blood
Forward fluid backs up Increase pressure within all organs
Organ response
–
– LUNGS: congested increase effort to breathe fluid starts to escape into
alveoli (pulmonary edema) fluid interferes with O2 exchange (hypoxia)
aggravates shortness of breath
Shortness of breath during exertion may be early symptoms
progresses later require extra pillows at night to breathe (orthopnea) and
experience "P.N.D." or paroxysmal nocturnal dyspnea

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• LEGS, ANKLES, FEET: blood from feet and legs back-up of
fluid and pressure in these areas, as heart unable to pump blood
as promptly as received increase fluid within feet and legs
(pedal/dependent edema) and increase in weight
Keys To Understanding HF

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Clinical classification of Cardiac Failure:
According to the position
• Backward failure
• Forward failure
According to the location of heart failure
• Leftventricularfailure
• rightventricularfailure
• Biventricularfailure(Total Heart failure)
According to thecardiac output
• Highoutput failure
• lowoutputfailure
According to the function impaired
• Systolic failure
• Diastolic failure 10

z Heart Failure
Etiology
• Systolic Failure - most common
– Hallmark finding: Decrease in left ventricular ejection
fraction <40% (EF)
• Due to
– Impaired contractile function (e.g., MI)
– Increased afterload (e.g., hypertension)
– Cardiomyopathy
– Mechanical abnormalities (e.g., valve disease)

z Heart Failure
Etiology
Diastolic failure
– Impaired ability of ventricles to relax and fill during
diastole decrease stroke volume and CO
– Diagnosis based on presence of pulmonary congestion,
pulmonary hypertension, ventricular hypertrophy
– Normal ejection fraction (EF)- Know why!
Not have much blood to eject

z Heart Failure
Etiology
• Mixed systolic and diastolic failure
– Seen in disease states such as dilated cardiomyopathy (DCM)
– Poor EFs (<35%)
– High pulmonary pressures
• Biventricular failure
– Both ventricles may be dilated and have poor filling and
emptying capacity

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Systolic
Dysfunction
Diastolic
Dysfunction
Ventriclescannot pump
effectively
ventricles cannot relax
and fill during diastole
2
4

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Systolicand diastolic heartcomparewith normal heart
2
5

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High out put failure: It occurs when the body need
excess oxygen. The heart increases out put but is still unable
to meet body’s needs.
2
6
It iLow out put failure: It is the condition when the
heart is unable to pump an adequate supply of blood to the
body.
• Low output failure results in Hypoperfused tissue cells.
• It occurs when the myocardium is so damaged that it cannot
maintain adequate cardiac output.
• Right and left sided cardiac failure are sometimes referred to
as low output failure.

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2021
Update
New classification of HF according to LVEF

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Pathophysiology of cardiac
failure:
2
8
• Neurohumoral orextrinsic compensation involves
two major mechanisms:
Thesympathetic nervoussystem
Renin-angiotensinaldosterone
⚫The most important intrinsiccompensatory
mechanism is Myocardial Hypertrophy or
Ventricular Remodeling.

z Heart Failure
Pathophysiology
A.Cardiac compensatory mechanisms
1. Tachycardia
2. Ventricular dilation - Frank Starling’s law
3. Myocardial hypertrophy

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B. Homeostatic Compensatory Mechanisms
Activation of Sympathetic Nervous System (First line)
1. In vascular system resulting in vasoconstriction
(What effect on afterload?)
2. Kidneys
i. Decrease renal perfusion Renin angiotensin release
ii. Aldosterone release Na and H2O retention
3. Liver
i. Stores venous volume causing ascites, hepatomegaly
Heart Failure
Pathophysiology

z Heart Failure
Pathophysiology
Counter Regulatory Response
• Increased Na… increases release of Anti diuretic hormone (ADH)
• Release of atrial natriuretic factor (ANP) and BNP…..
Increases Na and H20 excretion
– Thus Prevents severe cardiac decompensation

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Saltand waterretention
Due to CO & RBF RAA activation(renin
angiotensinaldosterone activation)
Sympatheticactivation
Causes salt and waterretention
Angiotensin
Aldosterone
via renal tubules
Both try tocompensate the low CO & low BP
But itcan worsen thevenous pressure(preload)
More fluid accumulation in the interstitium
Worsens the signs of heart failure
3
2

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Heart Failure
Pathophysiology
– Neurohormonal responses: Endothelin - stimulated by ADH,
catecholamines, and angiotensin II
• Arterial vasoconstriction
• Increase in cardiac contractility
• Hypertrophy

z Heart Failure
Pathophysiology
– Neurohormonal responses: Proinflammatory cytokines
(e.g., tumor necrosis factor)
• Released by cardiac myocytes in response to cardiac injury
• Depress cardiac function cardiac hypertrophy, contractile
dysfunction, and myocyte cell death

z Heart Failure
Pathophysiology
– Neurohormonal responses: Over time systemic inflammatory response
results
• Cardiac wasting
• Muscle myopathy
• Fatigue

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Neurohormonal changes
N/H changes Favorable effect Unfavor. effect
 Sympathetic activity
 HR , contractility, vasoconst. 
 V return,
 filling
Arteriolar constriction 
After load  workload
 O2 consumption
 Renin-Angiotensin –
aldosterone
Salt & water retention VR Vasoconstriction 
 after load
 Vasopressin Same effect Same effect
 interleukins &TNF May have roles in myocyte
hypertrophy
Apoptosis
Endothelin
Vasoconstriction VR  After load

z Heart Failure
Pathophysiology
reduce
• Promote venous and arterial vasodilation,
preload and afterload
• Prolonged HF depletion of these factors
– Natriuretic peptides: atrial natriuretic peptide (ANP) and
b-type natriuretic peptide (BNP)
• Released in response to increase in atrial volume and
ventricular pressure

Cardiac failure
Reduced CO Ses
cardiac filling
Renin pressure
Sympathetic
NS activation
Angiotension I
vasoconstriction
Angiotension II
Na & Water
retention
Aldosterone
Cardiac remodeling
3
8

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•
Consequences of compensatory mechanisms
• Ventricular dilation: Enlargement of heart chambers elevated left ventricular pressure
initially effective adaptive mechanism
then mechanism inadequate cardiac output decrease
• Frank-Starling law: Initially increase venous return results in increase in force of
contraction later increase ventricular filling and myocardial stretch eventually results
in ineffective contraction
• Hypertrophy: Increase in muscle mass and cardiac wall thickness in response to chronic
dilation heart muscle poor contractility, increase in oxygen needs, poor coronary
artery circulation, prone to ventricular dysrhythmias (sudden cardiac death)
Heart Failure
Pathophysiology

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Heart Failure
Pathophysiology
• Ventricular remodeling/ cardiac remodeling
– Refers to the changes in size, shape, structure and physiology of the heart after injury
to the myocardium

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Ventricularremodeling:
4
1
It is the most important intrinsiccompensatory
mechanism referred as cardiac remodeling
It is the processof progressiveof ventricularsize,
shape and function owing to the influence of
Mechanical, Neurohumoral and possibly genetic
factors in clinical conditions including
• Myocardial infraction
• Cardiomyopathy
• Hypertension
• Valvular heartdisease
Hall marks are: Hypertrophy, loss of myocytes and
interstitial fibrosis.

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Ventricular remodeling in diastole &systole
4
2

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End
Result
FLUID OVERLOAD Acute Decompensated Heart Failure
/Pulmonary Edema
Medical Emergency!!

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Heart Failure
Classification Systems
• New York Heart Association (NYHA) Functional
Classification of HF
– Classes I to IV
• ACC/AHA Stages of HF (newer)
– Stages A to D

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Heart Failure
Classification Systems

NY ASSN Funct Class
ACC/AHA
Stages

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Heart
Failure
Risk Factors
• Primary risk factors
– Coronary artery disease (CAD)
– Advancing age
• Contributing risk factors
– Hypertension
– Diabetes
– Tobacco use
– Obesity
– High serum cholesterol
– African American descent
– Valvular heart disease
– Hypervolemia

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1. Impaired cardiac function
• Coronary heart disease
• Cardiomyopathies
• Rheumatic fever
• Endocarditis
2. Increased cardiac workload
• Hypertension
• Valvular disorders
• Anemias
• Congenital heart defects
3. Acute non-cardiac
conditions
• Volume overload
• Hyperthyroid, Fever,infection
Heart Failure
Causes

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1. Systolic versus Diastolic
– Systolic - loss of contractility get decease
CO
– Diastolic - decreased filling or preload
2. Left sided versus Right sided
– Left ventricle – lungs congested
– Right ventricle – peripheral edema
1. High output vs Low output
– Hypermetabolic state
1. Acute versus Chronic
– Acute MI
– Chronic Cardiomyopathy
Heart
Failure
Causes

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• Signs and symptoms
– Dyspnea
– Orthopnea &
PND ??
– Cheyne Stokes
– Fatigue
– Anxiety
– Rales
• Orthopnea: dyspnea on lying flat - due to increased
distribution of blood to the pulmonary circulation while
recumbent
Heart Failure
Symptoms

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Paroxysmal Nocturnal
Dyspnoea
•
•
•
•
Attacks of severe shortness of breath and coughing that
generally occur at night
It usually awakens the person from sleep, and may be quite
frightening
Cause:
– Caused in part by the depression of the respiratory center
during sleep, which may reduce arterial oxygen tension,
particularly in patients with reduced pulmonary
compliance
– Also, in the horizontal position there is redistribution of
blood volume from the lower extremities and splanchnic
beds to the lungs
Little effect in normal individuals, but in patients with failing
left ventricle, there is a significant reduction in vital capacity

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Heart Failure
Clinical Manifestations
• Acute decompensated heart failure (ADHF)
Pulmonary edema, often life-threatening
• Early
– Increase in the respiratory rate
–Decrease in PaO2(hypoxia)
• Later
– Tachypnea
– Respiratory acidosis

Acute Decompensated Heart Failure
(ADHF)
Clinical Manifestations
Physical findings
•
•
•
•
•
•
Orthopnea
Dyspnea, Tachypnea
Use of accessory muscles of
respiration
Cyanosis
Cool and clammy skin
S3 gallop rhythm
•
•
•
Physical findings
• Cough with frothy, blood-
tinged sputum
Breath sounds: Crackles,
wheezes, rhonchi
Tachycardia
Hypotension or
hypertension

Person Literally Drowning In
Secretions
Immediate Action Needed

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Right Heart
Failure
• Signs and Symptoms
– Fatigue, weakness, lethargy
– weight gain
– Increase abdominal girth
– Anorexia
– Right upper quadrant pain
– elevated neck veins
– Hepatomegaly
– May not see signs of LVF

zWhat is present in this extremity, common to right sided HF?

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Can You Have RVF Without LVF?
• What is this called?
COR PULMONALE

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Heart Failure
Complications
• Pleural effusion
• Atrial fibrillation (most common dysrhythmia)
– Loss of atrial contraction (kick) – necessary for 20-
25% of cardiac output
• Reduce CO by 20% to 25%
– Promotes thrombus/embolus formation
• Increase risk for stroke

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Heart Failure
Complications
• High risk of fatal dysrhythmias (e.g., sudden cardiac death,
ventricular tachycardia) with HF and an EF <35%
•
•
HF lead to severe hepatomegaly, especially with RV
failure
– Fibrosis and cirrhosis (cardiac cirrhosis) - develop
over time
Renal insufficiency or failure (cardiorenal syndrome)

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Heart Failure
Initial Evaluation
Primary goal - Determine underlying cause
• Thorough history and physical examination – to identify cardiac
and noncardiac disorders or behaviors that might cause or
accelerate the development or progression of HF
• Volume status and vital signs should be assessed

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Heart Failure
Diagnostic Tests
Initial Lab workup includes
blood count
electrolytes
calcium and
1. ECG
2. Chest X ray
3. Complete
(CBC)
4. Urinalysis
5. Serum
(including
magnesium)
6. Blood
(BUN)
urea nitrogen
and serum
creatinine (Cr)
7. Glucose
8. Fasting lipid profile (FLP)
9. liver function tests (LFT)
peptide
10. Thyroid-stimulating
hormone (TSH)
11. Cardiac Troponins
12. Beta naturetic
(BNP)
13. Arterial Blood gas (ABG)

z Chest xray
Normal Pulmonary edema

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• 2-dimensional echocardiogram (2-D echo) with
Doppler should be performed during initial
evaluation of patients presenting with HF to assess
ventricular function, size, wall thickness, wall
motion, and valve function
Heart Failure
Diagnostic Tests

z Heart Failure
Diagnostic Studies
• Invasive hemodynamic monitoring
– Can be useful for carefully selected patients with acute HF who
have persistent symptoms despite empiric adjustment of standard
therapies and
a. Whose fluid status, perfusion, or systemic or pulmonary vascular
resistance is uncertain
•
b. Whose systolic pressure remains low, or is associated with
symptoms, despite initial therapy
c. Whose renal function is worsening with therapy
d. Who require parenteral vasoactive agents
Coronary angiography if ischemia is likely cause of heart
failure

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Heart Failure
Emergency Management
U
N
Upright Position
Nitrates
L
O
A
D
Lasix
Oxygen
ACE, ARBs, Aldactone, Amiodarone
Digoxin, Dobutamine, Dopamine
M
E
Morphine Sulfate
Extremities Down

z 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

z 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)

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Nonpharmacological Interventions
•
•
Salt :3 gm for stage A&B and <1.5 gm for stage C&D
BMI: 30-34.9kg/m2 (grade 1 obesity) lowest mortality –
weight U-shaped mortality curve (cardiac cachexia)
– daily weight monitoring – same time with same clothing
– Weight gain of 3 lb (1.5 kg) over 2 days or a 3- to 5-lb
(2.5 kg) gain over a week – report to health care
provider
Heart Failure
Stage B

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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: increase in functional status, improve
Heart Failure
Stage C
exercise capacity and reduce hospitalization and mortality,
improve endothelial function and improve O2 extraction from
peripheral tissue

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• 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

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Heart Failure
Stage C
Pharmacological Interventions
ACE Inhibitors
•
•
•
•
•
Capotopril: 6.25mg thrice till
50mg thrice a day
Enalapril : 2.5mg twice to 10-
20mg twice a day
Lisinopril: 2.5-5mg once to 20-
40mg 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
ACE induced cough – 20%

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• When ACEI intolerant or
•
•
alternative to ACEI
AT 1 receptor blocker
Can be substituted to ACEI with
angioedema
caution (pt
history but with
can develop
angioedema with ARB as well)
•
•
•
•
Losartan: 25-50mg once till 50-
150mg once a day
Valsartan: 20-40mg twice till
160mg twice
Same initiation and monitoring as
ACEI
Titration by doubling the dose
Heart Failure
Stage C
Angiotensin Receptor Blockers

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To all pt with LV dysfunction
•
• Start early when Symptoms
improved
Caution: Can worsen heart failure
START LOW AND GO SLOW
•
•
• Start in low dose even during
hospitalization (careful in pt require
inotropic support) gradually increase
dose in weeks duration and try to
reach target dose
1.25-2.5mg once till
3.125 twice till 50mg
• Bisoprolol:
10mg once
• Carvedilol:
twice
• Metoprolol Succinate: 12.5 once till
200mg once
•
•
•
Continue even Sx not improved
Abrupt withdrawal avoided
S/E: fluid retention and worsening
HF, slow heart rate, fatigue, blocks,
hypotension (minimize by different
dosing timings of BB and ACEI)
Heart Failure
Stage C
Beta Blockers

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• Indications: NYHA
≤35%, no C/I (GFR
II-IV,
>30,
2.5mg/dl male and 2.0mg/dl
female, K<5mg/dl
• 12.5-
•
Dosing: Spironolactone
25mg once till 50mg daily
Monitoring:
–
– stop all K supplements, check K+ and
Cr 2-3 days after starting then one
week and every month for 3 months
and every 3 month & when clinically
indicated .
Cycle restarted after changing dose of
ARA or ACEI
•
EF • High K containing food: Prunes,
Cr: banana, salmon fish, dark green
leafy vegetables, mushrooms,
yogurt, white beans and dried
apricot
S/E: Increase K+(10-15%),
gynecomastia
Heart Failure
Stage C
Aldosterone Receptor Antagonists

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•
•
•
•
•
•
Only decrease frequency of hospitalizations, Symptoms and
HRQOL
Don’t stop digoxin if patient is not on ACEI or BB, but try to initiate
them
No loading required – usual dose 0.125-0.25mg daily (low dose
0.125mg alternate day if >70yrs, CKD, Low lean body mass
0.5-0.9 ng/dl plasma conc. (narrow therapeutic range)
S/E: Nausea, vomiting and diarrhea, visual disturbances (yellow-green
halos and problems with color perception), supraventricular and ventricular
arrhythmias
Heart Failure
Stage C
Digoxin
No mortality benefit

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Therapeutic uses of
digoxin
Heart failure with atrial fibrillation (use onlywhen
diuretics and ACEI have failed to control the
symptoms
Mild symptoms
Acute heart failure
Slow loading dose
Rapid Digitalization
Treatmentof atrial arrhythmia( atrial fibrillation &
flutter)
8
6

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•
•
•
Heart Failure
Stage C
Hydralazine Nitrate Combination
Indication: African-American origin, 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

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•
Heart Failure
Stage C
Drugs not to be used:
– Statins (no benefit – unless there is ischemic etiology)
– CCB (except Amlodipine)
– NSAIDS
– Thiozolidinidinones
– Most anti arrhythmics drugs (except Amiodarone, dofelitide)
– Nutritional Supplements
– Hormonal therapy

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Pharmacologic Treatment for Stage C
Heart Failure Stage C
NYHA Class I – IV
Treatment:
For NYHA class II - IV patients .
Provided estimated creatinine
> 30 mL/ min and K + <5.0 mEq /dL
For persistentlysymptomatic
African Americans ,
NYHA class III -IV
Class I , LOE A
ACEI or ARB AND
Beta Blocker
Class I , LOE C
Loop Diuretics
Class I , LOE A
Hydral-Nitrates
Class I , LOE A
Aldosterone
Antagonist
Add
Ad
d
A
d
d
For all volume overload ,
NYHA class II - IV patients

ACEI- Angiotensin-converting enzyme inhibitor, ARB-Angiotensin receptor blockers
Sabe MA, et al. Cleveland Clinic J of Medicine 2015;82(10):693-701.
• A novel treatment,
Sacubitril/Valsartan), has
shown great promise to
change HF’s poor
outcomes.
• Sac/Val not only blocks
the renin angiotensin
system, but also enhances
the activity of vasoactive
substances such as the
natriuretic peptides and
bradykinin

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•
•
Heart Failure
Stage C
 Device Therapy
 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
 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, III, or ambulatory IV symptoms on GDMT

ARNI is preferred choice as
foundational therapy along with
beta blocker & Diuretics
Because of new evidence, ARNI
is now also recommended in
newly diagnosed, ACEi/ARB naïve
patients
Clinicians should aim to achieve optimal GDMT within 3 to
6 months of an initial diagnosis of
Treatment
Algorithm

z Heart Failure
Stage D
ClinicalEventsandFindingsUsefulforIdentifyingPatientsWith Advanced HF
1. Repeated (≥2) hospitalizations or ED visits for HF in the past year
2. Progressive deterioration in renal function (e.g., rise in BUN and creatinine)
3. Weight loss without other cause (e.g., cardiac cachexia)
4. Intolerance to ACE inhibitors due to hypotension and/or worsening renal function
5. Intolerance to beta blockers due to worsening HF or hypotension
6. Frequent systolic blood pressure <90 mm Hg
7. Persistent dyspnea with dressing or bathing requiring rest
8. Inability to walk 1 block on the level ground due to dyspnea or fatigue
9. Recent need to escalate diuretics to maintain volume status, often reaching daily
furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone
therapy
10. Progressive decline in serum sodium, usually to <133 mEq/L
11. Frequent ICD shocks

z
•
•
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
intravenous inotropic support to
receive
maintain
temporary
systemic
perfusion and preserve end-organ performance.
Heart Failure
Stage D

z Heart Failure
Stage D
•
•
•
•
•
•
Mechanical Circulatory Support
Intraaortic balloon pump (IABP) therapy
– Used for cardiogenic shock
– Allows heart to rest
Ventricular assist devices (VADs)
– Takes over pumping for the ventricles
– Used as a bridge to transplant
Destination therapy-permanent, implantable VAD
Cardiomyoplasty- wrap latissimus dorsi around heart
Ventricular reduction -ventricular wall resected
Transplant/Artificial Heart

z Left Ventricular Assist Devices (LVAD)
The Jarvik 2000
The Jarvik-7
The World's First Artificial Heart

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Transcutaneous Ventricular Assist
Device

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Implantable Ventricular
Assist Device

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Stage A
At high risk for developing heart
failure. Includes people with:
•Hypertension
•Diabetes mellitus
•CAD (including heart attack)
•History of cardiotoxic drug
therapy
•History of alcohol abuse
•History of rheumatic fever
•Family history of CMP
or illicit
•Exercise regularly
•Quit smoking
•Treat hypertension
•Treat lipid disorders
•Discourage alcohol
drug use
•If previous heart attack/ current
diabetes mellitus or HTN, use
ACE-I
Stage B
•Those diagnosed with “systolic”
heart failure- have never had
symptoms of heart failure
(usually by finding an ejection
fraction of less than 40% on
echocardiogram
•Care measures in Stage A +
•Should be on ACE-I
•Add beta -blockers
•Surgical consultation for
coronary artery revascularization
and valve repair/replacement (as
appropriate
Heart
Failure
Therapies

z
Stage C
Patients with known heart
failure with current or prior
symptoms.
Symptoms include: SOB,
fatigue, Reduced exercise
intolerance
All care measures from Stage
A apply, ACE-I and beta-
blockers should be used +
Diuretics, Digoxin,
Dietary sodium
restriction
Weight monitoring,
Fluid restriction
Withdrawal drugs that
worsen condition
Maybe Spironolactone
therapy
Heart Failure
Therapies

z
Stage D
Presence of advanced
symptoms, after assuring
optimized medical care
All therapies -Stages A, B
and C + evaluation
for:Cardiac transplantation,
VADs, surgical options,
research therapies,
Continuous intravenous
inotropic infusions/ End-of-
life care
Heart Failure
Therapies

z
SBP Admission and early post-discharge SBP inversely correlates
with post-discharge mortality
Coronary artery disease
(CAD)
Troponin release
Extent and severity of CAD appears to be a predictor of poor
prognosis
Results in a 3-fold increase in in-hospital mortality and
rehospitalization rate, a 2-fold increase in post-discharge
mortality
Increase in QRS duration occurs in approximately 40% of
Ventricular dyssynchrony patients with reduced systolic function and is a strong predictor of
early and late post-discharge mortality and rehospitalization
Renal impairment
Worsening renal function during hospitalization or soon after
discharge is associated with an increase in in-hospital and post-
discharge mortality
Heart Failure
Prognostic Factors

z
Hyponatremia
Defined as serum sodium < 135 mmol/l, occurs in approximately
25% of patients, and is associated with a 2- to 3-fold increase in
post-discharge mortality
of discharge
Clinical congestion at time An important predictor of post-discharge mortality and morbidity
EF
Similar early post-discharge event rates and mortality between
reduced and preserved EF
BNP/NT-proBNP
Elevated natriuretic peptides associated with increased resource
utilization and mortality
Functional capacity at
time of discharge
Pre-discharge functional capacity, defined by the 6-min walk test,
is emerging as an important predictor of post-discharge outcomes
Heart Failure
Prognostic Factors

z
Take Home
Message
•
•
•
•
•
•
Heart failure is common problem in elderly and having prognosis
worse then Carcinoma 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

z
•
•
•
•
•
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
Use Digoxin in most symptomatic heart failure
Encourage exercise training
Consider a cardiology consultation in patients who fail to improve
Heart transplantation is for end stage heart failure
Take Home
Message

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