Heart Failure

WARMADEWA SCHOOL MEDICINE

A.A. Gede Budhitresna MD,PhD,FINASIM

The most common reason for

adults >65 years

hospitalization in

Heart Failure
Results from any
structural or functional
abnormality that
impairs the ability of
the ventricle to eject
blood (Systolic Heart
Failure) or to fill with
blood (Diastolic Heart
Failure).

Definition-Heart Failure (HF)

Key Concepts
CO = SV x HR-becomes insufficient to
meet metabolic needs of body
SV- determined by preload, afterload and
myocardial contractility
EF< 40% (need to understand)
Classifications HF
Systolic failure- dec. contractility
Diastolic failure- dec. filling
Mixed

Heart Failure

The Vicious Cycle of Congestive Heart

Failure

LV Dysfunction causes
Decreased cardiac output

Decreased Blood Pressure and

Decreased Renal perfusion

Stimulates the Release

of renin, Which allows
conversion of
Angiotensin
to Angiotensin II.
Angiotensin II stimulates
Aldosterone secretion which
causes retention of
Na+ and Water,
increasing filling pressure

 Main causes
Ischemic heart disease, Cardiomyopathy, Hypertension
Other causes: Valvular heart disease, Congenital
heart
disease, Alcohol and drugs, Hyperdynamic circulation
(anaemia, thyrotoxicosis, haemochromatosis, Paget's
disease), Right heart failure (RV infarct, pulmonary
hypertension, pulmonary embolism, cor pulmonale
(COPD)), Arrhythmia and Pericardial disease.

 Impaired cardiac contractility as in

myocardial infarction and
cardiomyopathy
Ventricular outflow obstruction
(pressure overload) as in hypertension
and aortic stenosis
Impaired ventricular fillings as in mitral
stenosis and constrictive pericarditis
Volume overload as in mitral
regurgitation

 Infections
Arrhythmias
Physical, Dietary, Fluid, Environmental, and Emotional
Excesses.
Myocardial infarction
Pulmonary embolism
Anemia
Thyrotoxicosis and pregnancy
Aggravation of hypertension
Rheumatic, Viral, and Other Forms of Myocarditis
Infective endocarditis

The heart depends on a number of adaptive mechanisms

for maintenance of its pumping function:
1- The Frank Starling mechanism (cardiac dilatation)
2- Myocardial hypertrophy
3- Increased release of catecholamines, activation
of renin-angiotensin-aldosteron system and other
Neurohumoral adjustments
N.B.: These effects are compensatory at first, then they are
overwhelmed and become pathophysiological

PATHOPHYSIOLOGICAL CHANGES

Ventricular dilatation
Myocyte hypertrophy
Increased collagen synthesis
Altered myosin gene expression
Altered sarcoplasmic Ca2+-ATPase density
Increased ANP secretion
Salt and water retention
Sympathetic stimulation
Peripheral vasoconstriction

Neurohormonal changes
N/H changes

Sympathetic activity

Renin-Angiotensin

Favorable effect

Unfavor. effect

HR , contractility,

Arteriolar constriction

vasoconst. V return,

After load workload

filling

O2 consumption

Salt & water retention

VR

Vasoconstriction

Vasopressin

Same effect

Same effect

interleukins &TNF

May have roles in myocyte

hypertrophy

Apoptosis

Vasoconstriction VR

After load

after load

Aldosterone

Endothelin

Types of Heart Failure

Low-Output Heart Failure
Systolic Heart Failure:
decreased cardiac output
Decreased Left ventricular ejection fraction
Diastolic Heart Failure:
Elevated Left and Right ventricular end-diastolic pressures
May have normal LVEF

High-Output Heart Failure

Seen with peripheral shunting, low-systemic vascular
resistance, hyperthryoidism, beri-beri, carcinoid, anemia
Often have normal cardiac output

Right-Ventricular Failure
Seen with pulmonary hypertension, large RV infarctions.

Causes of Low-Output Heart

Failure
Systolic Dysfunction

Coronary Artery Disease

Idiopathic dilated cardiomyopathy (DCM)
50% idiopathic (at least 25% familial)
9 % mycoarditis (viral)
Ischemic heart disease, perpartum,
hypertension, HIV, connective tissue
disease, substance abuse, doxorubicin
Hypertension
Valvular Heart Disease

Diastolic Dysfunction

Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy (HCM)
Restrictive cardiomyopathy

Can You Have RVF Without LVF?

What is this called?

COR PULMONALE

18

Clinical Presentation of Heart

Failure
Due to excess fluid accumulation:

Dyspnea (most sensitive symptom)

Edema
Hepatic congestion
Ascites
Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)

Due to reduction in cardiac ouput:

Fatigue (especially with exertion
Weakness

Physical Examination in Heart

Failure
S3 gallop
Low sensitivity, but highly specific
Cool, pale, cyanotic extremities
Have sinus tachycardia, diaphoresis and peripheral
vasoconstriction
Crackles or decreased breath sounds at bases (effusions) on lung
exam
Elevated jugular venous pressure
Lower extremity edema
Ascites
Hepatomegaly
Splenomegaly
Displaced PMI
Apical impulse that is laterally displaced past the midclavicular
line is usually indicative of left ventricular enlargement>

21

Measuring Jugular Venous

Pressure

Lab Analysis in Heart Failure

CBC

Since anemia can exacerbate heart failure

Serum electrolytes and creatinine
before starting high dose diuretics
Fasting Blood glucose
To evaluate for possible diabetes mellitus
Thyroid function tests
Since thyrotoxicosis can result in A. Fib,
and hypothyroidism can results in HF.
Iron studies
To screen for hereditary hemochromatosis as cause of heart
failure.
ANA
To evaluate for possible lupus
Viral studies
If viral mycocarditis suspected

Laboratory Analysis (cont.)

BNP
With chronic heart failure, atrial
mycotes secrete increase amounts of
atrial natriuretic peptide (ANP) and
brain natriuretic pepetide (BNP) in
response to high atrial and
ventricular filling pressures
Usually is > 400 pg/mL in patients
with dyspnea due to heart failure.

Chest X-ray in Heart

Failure
Cardiomegaly
Cephalization of the pulmonary
vessels
Kerley B-lines
Pleural effusions

Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and

function of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to
causes that inc. pressure or volume overload as in Heart failure

American Heart Assn-Media files Animations

Pulmonary vessel congestion

Pulmonary Edema due to

Heart Failure

Kerley B lines

Cardiac Testing in Heart

Failure
Electrocardiogram:
May show specific cause of heart failure:
Ischemic heart disease
Dilated cardiomyopathy: first degree AV block, LBBB, Left
anterior fascicular block
Amyloidosis: pseudo-infarction pattern
Idiopathic dilated cardiomyopathy: LVH

Echocardiogram:
Left ventricular ejection fraction
Structural/valvular abnormalities

Further Cardiac Testing in

Heart Failure
Exercise Testing
Should be part of initial evaluation of all patients with CHF.

Coronary arteriography
Should be performed in patients presenting with heart failure
who have angina or significant ischemia
Reasonable in patients who have chest pain that may or
may not be cardiac in origin, in whom cardiac anatomy is not
known, and in patients with known or suspected coronary
artery disease who do not have angina.
Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic pressure.

Further testing in Heart

Failure
Endomyocardial biopsy
Not frequently used
Really only useful in cases such as viral-induced
cardiomyopathy

Ventricular remodeling

Heart Failure
Classification Systems
New York Heart Association Functional
Classification of HF
Classes I to IV

ACC/AHA Stages of HF (newer)

Stages A to D

STAGE

DISABILITY

CLASS 1
MILD

No symptoms Can perform ordinary

activities without any limitations

CLASS 2
MILD

Mild symptoms - occasional

swelling Somewhat limited in ability to
exercise or do other strenuous activities

CLASS 3

Noticeable limitations in ability to

exercise or participate in mildly strenuous
activities
Comfortable only at rest

MODERATE
CLASS 4 SEVERE

Unable to do any physical activity without

discomfort Some HF symptoms at rest
36

Chronic Treatment of Systolic

Heart Failure
Correction of systemic factors

Thyroid dysfunction
Infections
Uncontrolled diabetes
Hypertension

Lifestyle modification
Lower salt intake
Alcohol cessation
Medication compliance

Maximize medications
Discontinue drugs that may contribute to heart failure (NSAIDS,
antiarrhythmics, calcium channel blockers)

Order of Therapy
1.
2.
3.
4.
5.
6.

Loop diuretics
ACE inhibitor (or ARB if not tolerated)
Beta blockers
Digoxin
Hydralazine, Nitrate
Potassium sparing diuretics

Diuretics
Loop diuretics
Furosemide, buteminide
For Fluid control, and to help relieve symptoms

Potassium-sparing diuretics

Spironolactone, eplerenone
Help enhance diuresis
Maintain potassium
Shown to improve survival in CHF

ACE Inhibitor
Improve survival in patients with all
severities of heart failure.
Begin therapy low and titrate up as possible:
Enalapril 2.5 mg po BID
Captopril 6.25 mg po TID
Lisinopril 5 mg po QDaily

If cannot tolerate, may try ARB (angiotensin

receptor blocker)

ACE Inhibitors for CCF

Beta Blocker therapy

Certain Beta blockers (carvedilol, metoprolol,
bisoprolol) can improve overall and event free
survival in NYHA class II to III HF, probably in class
IV.
Contraindicated:

Heart rate <60 bpm

Symptomatic bradycardia
Signs of peripheral hypoperfusion
COPD, asthma
PR interval > 0.24 sec, 2nd or 3rd degree block

Beta blockers in CCF

Hydralazine plus Nitrates

Dosing:
Hydralazine
Started at 25 mg po TID, titrated up to 100 mg po TID

Isosorbide dinitrate
Started at 40 mg po TID/QID

Decreased mortality, lower rates of

hospitalization, and improvement in
quality of life.

Digoxin
Given to patients with HF to control
symptoms such as fatigue, dyspnea,
exercise intolerance
Shown to significantly reduce
hospitalization for heart failure, but no
benefit in terms of overall mortality.

DIGOXIN cont.
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.

DIGOXIN cont.
Cardiac glycosides : Digoxin
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.

DIGOXIN cont.
Digoxin : Adverse effects /
Precautions :
Nausea, vomiting, gynecomastia,
visual disturbances and psychosis.
Ventricular bigeminy, AV block and
bradycardia.
Amiodarone and verapamil can
increase the plasma concentration of
digoxin by inhibiting its excretion.

DIGOXIN cont.
Digoxin toxicity treatment:
Toxicity can be treated with higher
than normal doses of potassium.
Digoxin antibody (digibind) is used
specifically to treat life-threatening
digoxin overdose.

Other important medication in Heart

Failure -- Statins
Statin therapy is recommended in CHF for the
secondary prevention of cardiovascular
disease.
Some studies have shown a possible benefit
specifically in HF with statin therapy
Improved LVEF
Reversal of ventricular remodeling
Reduction in inflammatory markers (CRP, IL6, TNF-alphaII)

Meds to AVOID in heart failure

NSAIDS
Can cause worsening of preexisting HF

Thiazolidinediones
Include rosiglitazone (Avandia), and pioglitazone
(Actos)
Cause fluid retention that can exacerbate HF

Metformin
People with HF who take it are at increased risk of
potentially lethic lactic acidosis

Implantable CardioverterDefibrillators for HF

Sustained ventricular
tachycardia is associated with
sudden cardiac death in HF.
About one-third of mortality in
HF is due to sudden cardiac
death.
Patients with ischemic or
nonischemic cardiomyopathy,
NYHA class II to III HF, and
LVEF 35% have a
significant survival benefit
from an implantable
cardioverter-defibrillator (ICD)
for the primary prevention of
SCD.

Left ventricular assist

device

Management of Refractory Heart

Failure
Inotropic drugs:
Dobutamine, dopamine, milrinone, nitroprusside,
nitroglycerin

Mechanical circulatory support:

Intraaortic balloon pump
Left ventricular assist device (LVAD)

Cardiac Transplantation
A history of multiple hospitalizations for HF
Escalation in the intensity of medical therapy
A reproducable peak oxygen consumption with
maximal exercise (VO2max) of < 14 mL/kg per min.
(normal is 20 mL/kg per min. or more) is relative
indication, while a VO2max < 10 mL/kg per min is a
stronger indication.

Intraaortic balloon pump

IABP Machine

Acute Decompensated Heart

Failure
Cardiogenic pulmonary edema is a
common and sometimes fatal cause
of acute respiratory distress.
Characterized by the transudation of
excess fluid into the lungs
secondary to an increase in left atrial
and subsequently pulmonary venous
and pulmonary capillary pressures.

Acute Decompensaated Heart

Failure (cont.)
Causes:
Acute MI
Rupture of chordae tendinae/acute mitral valve
insufficiency

Volume Overload
Transfusions, IV fluids
Non-compliance with diuretics, diet (high salt
intake)

Worsening valvular defect

Aortic stenosis

Decompensated Heart Failure

Symptoms
Severe dyspnea
Cough

Clinical Findings

Tachypnea
Tachycardia
Hypertension/Hypotension
Crackles on lung exam
Increased JVD
S3, S4 or new murmur

Labs/Studies in Acute
Decompensated Heart Failure
Chemistry, CBC
EKG
Chest X-ray
May consider cardiac enzymes
2D-Echo

Decompensated Heart Failure

Treatment
Strict Is and Os, daily weights
Oxygen, mechanical ventilation if needed
Loop diuretics (Lasix!)
Morphine
Vasodilator therapy (nitroglycerin)
Nesiritide (BNP) can help in acute
setting, for short term therapy

Heart Failure
Complications
Pleural effusion
Atrial fibrillation (most common
dysrhythmia)
Loss of atrial contraction (kick) -reduce CO
by 10% to 20%
Promotes thrombus/embolus formation inc.
risk for stroke
Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants

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 - develop over time
Renal insufficiency or failure

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 >
Inc. pressure within all organs.
Organ response
LUNGS: congested > stiffer , inc effort to breathe; fluid starts to escape into
alveoli; fluid interferes with O2 exchange, aggravates shortness of breath.

Shortness of breath during exertion, may be early symptoms > progresses > later
require extra pillows at night to breathe > experience "P.N.D." or paroxysmal
nocturnal dyspnea .
Pulmonary edema
Legs, ankles, feet- blood from feet and legs > back-up of fluid and pressure in these
areas, heart unable to pump blood as promptly as received > inc. fluid within feet
and legs causes fluid to "seep" out of blood vessels ; inc. weight

In God we
trust,
everything
else should be
based on
evidence

THANK
YOU
(Claude Organ)

agbudhitresna@yahoo.com