The document provides a comprehensive overview of heart failure, including its definition, common causes, types, pathophysiology, risk factors, signs and symptoms, diagnosis, and treatment options. It emphasizes that heart failure is a significant clinical syndrome affecting millions worldwide, primarily driven by conditions like coronary artery disease and hypertension. The management involves correcting underlying issues, nonpharmacologic therapies, and a range of medications, along with emphasizing the importance of early diagnosis and clinical evaluation.
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Introduction
Definiton:
Aclinical syndrome resulting from any structural or
functional cardiac defect
The heart is unable to pump sufficiently to maintain blood
flow to meet the body's needs
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Introduction
The mostcommon causes of heart failure are
coronary artery disease, high blood pressure, and
diabetes.
HF is diagnosed on the presence of characteristic
signs and symptoms and not on the basis of any
diagnostic tests
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Introduction
Heart failureis a common, costly, and potentially fatal
condition.
In 2015 it affected about 40 million people globally.
Overall around 2% of adults have heart failure and in those
over the age of 65, this increases to 6–10%.
In the year after diagnosis the risk of death is about 35%
after which it decreases to below 10% each year.
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Types of HF
According to cardiac output:
a. Low-Output Heart Failure
b. High-Output Heart Failure
According to anatomical side
a. Left side heart failure
b. Right side heart failure
According to onset
a. Acute heart failure
b. Chronic heart failure
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Pathophysiology of HF
Pump fails → decreased stroke volume /CO.
Compensatory mechanisms kick in to increase CO
SNS stimulation → release of epinephrine/nor-
epinephrine
o Increase HR
o Increase contractility
o Peripheral vasoconstriction (increases afterload)
Myocardial hypertrophy: walls of heart thicken to
provide more muscle mass → stronger contractions
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Pathophysiology of HF
Hormonal response:
↓ renal perfusion interpreted by juxtaglomerular
apparatus as hypovolemia. Thus: Kidneys release
renin, which stimulates conversion of antiotensin I →
angiotensin II, which causes:
o Aldosterone release → Na retention and water
retention (via ADH secretion)
o Peripheral vasoconstriction
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Pathophysiology of HF
Compensatory mechanisms may restore CO to near-
normal.
But, if excessive the compensatory mechanisms can
worsen heart failure because:
Vasoconstriction:
o ↑ the resistance against which heart has to pump (i.e.,
↑ afterload), and may therefore ↓ CO
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Pathophysiology of HF
Na and water retention:
o ↑ fluid volume, which ↑ preload. If too much
“stretch” (d/t too much fluid) → ↓ strength of
contraction and ↓ CO
Excessive tachycardia → ↓ diastolic filling time →
↓ventricular filling → ↓ SV and CO
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C/P of HF
Symptoms
Left Heart Failure:
o Dyspnea on exertion
o Dyspnea at rest
o Orthpnea
o Paroxysmal nocturnal dyspnea (PND)
o Fatigue, inability to exercise
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C/P of HF
Symptoms
Right Heart Failure:
o Swelling of feet, hands
o Abdominal distention/fullness
o Right upper quadrant pain
o Early satiety
o Weight loss (cardiac cachexia)
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C/P of HF
Signs
Left Heart Failure:
o Rales
o Pleural effusions
o Displaced apical impulse
o Tachycardia, LVS3, murmur of MR(mitral regurge)
o Narrow pulse pressure
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C/P of HF
Signs
Right Heart Failure:
o Edema of lower extremities
o Elevated JVP(jugular vein pressure)/+
HJR(hepatojugular reflux)
o RVS3, murmur of TR(tricuspid regurge)
o Hepatomegaly, RUQ(right upper quadrant) tenderness
o Ascites - Pleural effusions
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Classification of HF
New York Heart Association (NYHA)
Class I : symptoms of HF only at levels that would
limit normal individuals.
Class II : symptoms of HF with ordinary exertion
Class III : symptoms of HF on less than ordinary
exertion
Class IV : symptoms of HF at rest
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Classification of HF
American College of Cardiology and the American
Heart Association(ACC/AHA) Guidelines
Stage A : High risk of HF, without structural heart
disease or symptoms
Stage B : Heart disease with asymptomatic left
ventricular dysfunction
Stage C : Prior or current symptoms of HF
Stage D : Advanced heart disease and severely
symptomatic or refractory HF
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Investigation
I. LAB
A) Nonspecific
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
Viral studies (If viral myocarditis suspected)
Others
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Investigation
I. LAB
B) Specific
BNP:
o With chronic heart failure, atrial myocytes secrete
increase amounts of atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) in response to high atrial
and ventricular filling pressures
o Promotes vasodilation, diuresis and natriuresis
o Usually is > 400 pg/mL in patients with dyspnea due to
heart failure.
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Investigation
III. Cardiac testing
ECG:
o May show specific cause of heart failure e.g Ischemic
heart disease
ECHO:
o Left ventricular ejection fraction
o Structural/valvular abnormalities
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Investigation
III. Cardiac testing
Exercise Testing
o Should be part of initial evaluation of all patients with
CHF.
Coronary arteriography
o Should be performed in patients presenting with heart
failure who have angina or significant ischemia
o Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic pressure.
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Diagnosis of HF
HF should be suspected on the basis of clinical
presentation and radiographic findings.
It’s a clinical diagnosis. There is no diagnostic test!
Depressed ventricular EF should be confirmed with
echocardiography, or cardiac catheterization with left
ventriculography.
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Treatment
Management of Chronicheart failure:
General measures
Correct underlying cause
Remove precipitating cause
Prevention of deterioration of cardiac function
Control of congestive HF state
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Treatment
Nonpharmacologic therapy:
Exercisetraining:
o for stable HF patients increased exercise capacity,
decreased hospitalization rate, increased quality
of life, decreased symptoms.
Weight loss in obese patients
Dietary Na restriction
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Treatment
Nonpharmacologic therapy:
Fluidand free water restriction especially if
hyponatremic
Minimize medications known to have deleterious
effects on heart failure (negative inotrops, NSAIDs,
over-the-counter stimulants)
Oxygen
Fluid removal (dialysis, thoracentesis, paracentesis)
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Medical Treatment
Order ofdrug therapy
o Loop diuretics
o ACE inhibitor (or ARB if not tolerated)
o Beta blockers
o Digoxin
o Hydralazine, Nitrate
o Potassium sparing diuretics
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Medical Treatment
Diuretics
A. Loopdiuretics
Furosemide, buteminide
For Fluid control, and to help relieve symptoms
B. Potassium-sparing diuretics
Spironolactone, eplerenone
Help enhance diuresis
Maintain potassium
Shown to improve survival in CHF
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Medical Treatment
ACE Inhibitor
Improve survival in patients with all severities of heart
failure.
Begin therapy low and titrate up as possible:
o Enalapril
o Captopril
o Lisinopril
If cannot tolerate, may try ARB
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Medical Treatment
Beta Blockertherapy
Certain Beta blockers (carvedilol, metoprolol,
bisoprolol) can improve overall survival in NYHA
class II to III HF, probably in class IV.
Contraindicated:
o Heart rate <60 bpm
o Symptomatic bradycardia
o Signs of peripheral hypoperfusion
o COPD, asthma
o Prolonged PR interval, 2nd or 3rd degree heart block
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Medical Treatment
Hydralazine plusNitrates
Hydralazine + Isosorbide dinitrate
can be useful to reduce morbidity or mortality in
patients with current or prior symptomatic HF who
cannot be given an ACE inhibitor or ARB
Recommended for African Americans with NYHA
class III–IV
Decreased mortality, lower rates of hospitalization, and
improvement in quality of life.
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Medical Treatment
Digoxin
Givento patients with HF to control symptoms such as
fatigue, dyspnea, exercise intolerance
Digoxin can be used in HF patients with atrial
fibrillation to help rate control
Shown to significantly reduce hospitalization for heart
failure, but no benefit in terms of overall mortality.
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Medical Treatment
Other importantmedication
Statin therapy:
recommended in CHF for the secondary prevention of
cardiovascular disease.
Benefits:
o Improved LVEF(left ventricular ejection fraction)
o Reversal of ventricular remodeling
o Reduction in inflammatory markers e.g CRP
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Medical Treatment
Meds toAVOID in heart failure
NSAIDS
o Can cause worsening of pre-existing HF
Thiazolidinediones
o Cause fluid retention that can exacerbate HF
Metformin
o increased risk of potentially lactic acidosis
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Implantable Cardioverter-
Defibrillators forHF
Sustained ventricular
tachycardia is
associated with sudden
cardiac death in HF.
About one-third of
mortality in HF is due
to sudden cardiac
death.
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Acute Decompensated HF
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.
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Acute Decompensated HF
Causes:
Acute MI
o Rupture of chordae tendinae/acute mitral valve
insufficiency
Volume Overload
o Transfusions, IV fluids
o Non-compliance with diuretics, diet (high salt intake)
Worsening valvular defect
o Aortic stenosis
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Acute Decompensated HF
Clinical manifestations:
Signs
o Tachypnea
o Tachycardia
o Hypertension/Hypotension
o Crackles on lung exam
o Increased JVD(jagular venous distension)
o S3, S4 or new murmur