CHRONIC HEART FAILURE

Definition: Chronic heart failure (CHF) is a clinical syndrome that occurs as a

result of structural or functional changes in the heart that impair the ability of the
ventricle to fill with blood and / or “expel” it.
Congestive heart failure (CHF): a clinical syndrome in which the heart is unable to
pump enough blood to meet the metabolic needs of the body; characterized by
ventricular dysfunction that results in low cardiac output
Systolic dysfunction: CHF with reduced stroke volume and ejection fraction (EF)
Diastolic dysfunction: CHF with reduced stroke volume and preserved ejection
fraction
Right heart failure (RHF): CHF due to right ventricular dysfunction; characterized
by backward heart failure
Left heart failure (LHF): CHF due to left ventricular dysfunction; characterized by
forward heart failure
Biventricular (global) CHF: CHF in which both the left and right ventricle are
affected, resulting in simultaneous backward and forward CHF
Chronic compensated CHF: clinically compensated CHF; the patient has signs of
CHF on echocardiography but is asymptomatic or symptomatic and stable (see
“Diagnostics” below)
Acute decompensated CHF: sudden deterioration of CHF or new onset of severe
CHF due to an acute cardiac condition (e.g., myocardial infarction)

Etiology - The main diseases leading to CHF:

1. Coronary heart disease
2. Arterial hypertension
3. Dilated cardiomyopathy
4. Heart defects
The three major causes of heart failure are coronary artery disease, hypertension,
and diabetes mellitus. Patients typically have multiple risk factors that contribute to
the development of CHF.
Pathogenesis: two links are involved
1) central - reduction of cardiac output,
2) peripheral:
a) arterial spasm (increase in afterload),
b) stagnation in the veins (increased preload).
The following mechanisms play a role in pathogenesis:
1. Sympathoadrenal system.
2. Renin-angiotensin system.
3. Aldosterone system.

Cardiac output, which is stroke volume times heart rate, is determined by three
factors: preload, afterload, and ventricular contractility.

Preload - The extent to which heart muscle fibers are stretched before the onset of
systole. Preload is directly related to end-diastolic pressure and end-diastolic volume.

Afterload - The force against which the ventricle contracts to eject blood during
systole. Afterload is primarily determined by the blood pressure in the aorta, which is
influenced by total peripheral resistance.

Underlying mechanism of reduced cardiac output

1. Systolic ventricular dysfunction (most common) due to:

 Reduced contractility: Damage and loss of myocytes reduce ventricular
contractility and stroke volume.
 Increased afterload: increase in mean aortic pressure, outflow obstruction
 Increased preload: ventricular volume overload
 Cardiac arrhythmias
 High-output conditions (see “High-output heart failure” below)

2. Diastolic ventricular dysfunction due to:

 Decreased ventricular compliance: increased stiffness or impaired relaxation of
the ventricle → reduced ventricular filling and
increased diastolic pressure → decreased cardiac output
 Increased afterload: increase in pulmonary artery pressure
 Increased preload: ventricular volume overload

Consequences of systolic and diastolic dysfunction

 Forward failure: reduced cardiac output → poor organ perfusion → organ

dysfunction (e.g., hypotension, renal dysfunction)
 Backward failure
  Increased left-ventricular volume and pressure → backup of blood into lungs →
increased pulmonary capillary pressure → cardiogenic pulmonary edema
 Reduced cardiac output → systemic venous congestion → edema and
progressive congestion of internal organs
 Resulting macroscopic findings: nutmeg liver

Compensation mechanisms

 Aim: maintain cardiac output if stroke volume is reduced

 ↑ Adrenergic activity → increase in heart rate, blood pressure, and ventricular
contractility
 Increase of renin-angiotensin-aldosterone system activity (RAAS): activated
following decrease in renal perfusion secondary to reduction of stroke
volume and cardiac output
 ↑ Angiotensin II secretion → vasoconstriction → ↑ systemic blood pressure
→ ↑ afterload
 Kidney: vasoconstriction of the efferent arterioles and, to a lesser degree,
the afferent arterioles → ↓ net renal blood flow and ↑ intraglomerular pressure
to maintain GFR
 ↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload
 Brain natriuretic peptide (BNP): ventricular myocyte hormone released in
response to increased ventricular filling and stretching
 ↑ Intracellular smooth
muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary
wedge pressure

CHF is characterized by reduced cardiac output that results in venous congestion and
poor systemic perfusion!
Stages

NYHA functional classification

The NYHA (New York Heart Association) functional classification system is used to assess the
patient's functional capacities (i.e., limitations of physical activity and symptoms) and has
prognostic value.
NYHA Characteristics
class
Class I No limitations of physical activity; no symptoms of CHF
Class II Slight limitations of moderate or prolonged physical activity (e.g., symptoms after
climbing 2 flights of stairs or heavy lifting); comfortable at rest
Class III Marked limitations of physical activity (symptoms during daily activities like
dressing, walking across rooms); comfortable only at rest
Class IV Confined to bed, discomfort during any form of physical activity; symptoms present
at rest

General features of heart failure

- Nocturia (In the supine position, cardiac output increases and renal
vasoconstriction decreases, leading to an increase in filtered urine and nocturia.)
- Fatigue
- Tachycardia, various arrhythmias (Due to an increase in sympathetic tone)
- Heart sounds: S3/S4 gallop (An S3 gallop indicates rapid ventricular filling,
while an S4 gallop indicates ventricular hypertrophy (reduced compliance). Other
heart sounds may indicate valvular disease as a potential cause of CHF.)
- Pulsus alternans - A physical finding characterized by alternating strong and
weak pulses (with a regular pulse rhythm) caused by alterations in cardiac output.
Associated with left ventricular failure and cardiac tamponade.

Clinical features of left-sided heart failure

Pulmonary symptoms dominate
 Dyspnea , orthopnea
 Pulmonary edema in severe cases or acute decompensated heart failure (see
below)
 Bilateral basilar rales may be audible on auscultation
  Paroxysmal nocturnal dyspnea: nocturnal bouts of coughing and acute
shortness of breath
 Cardiac asthma: increased pressure in the bronchial arteries results in airway
compression, leading to bronchospasm
 Laterally displaced apical heart beat (precordial palpation beyond the
midclavicular line)
 Forward failure: cool extremities, cerebral and renal dysfunction, sweating
(NYHA IV)

Clinical features of right-sided heart failure

Symptoms of fluid retention (backward failure) dominate

 Peripheral pitting edema

 Signs of increased central venous pressure (CVP)
- Jugular venous distention: visible jugular venous congestion , also seen in
biventricular heart failure
- Hepatojugular reflux: jugular venous congestion induced by exerting
manual pressure over the patient's liver → ↑ volume load on the right side of
the heart → right heart is unable to pump additional blood volume → visible
jugular venous distention persists for several seconds
 Hepatic venous congestion
- Hepatosplenomegaly
- Abdominal pain (Caused by stretching of the liver capsule)
- Jaundice
- Ascites
 Congestion of other organs, e.g., congestive gastritis or gastropathy (nausea,
loss of appetite), renal congestion
!!! In clinical practice, biventricular heart failure with features of left and right
heart failure is more likely than isolated failure of one ventricle!
Diagnostics
Heart failure is primarily a clinical diagnosis. Laboratory tests and imaging tests, including a
chest x-ray and echocardiogram, are useful for evaluating the severity and cause of the
condition.

Diagnostic approach
1. Medical history, including preexisting conditions and history of alcohol and
recreational or prescribed drug use
2. Initial evaluation involves a range of routine laboratory tests and a test for BNP
level, ECG, and chest x-ray.
3. Echocardiography is the gold standard tool for assessing cardiac morphology
and function, as well as investigating the underlying cause of CHF.
4. Other procedures (exercise testing, angiography) may be required for further
investigation.
Initial evaluation
Laboratory analysis
 Elevated BNP and NT-pro BNP (Brain natriuretic peptide (half-life: 4–8
hours) and its precursor N-terminal pro-B-type BNP (half-life 2–3 days) are
hormones that are produced by the cardiac ventricles. BNP is a systemic
vasodilator and diuretic. The level of BNP is proportional to ventricular
volume and pressure overload.)
High levels of BNP in patients with classic symptoms of CHF confirm the
diagnosis (high predictive index). [22]
CHF unlikely CHF likely
BNP (pg/mL) < 100 > 500
NT-pro BNP (pg/mL) < 300 > 450

 Elevated atrial natriuretic peptide (ANP):

 Complete blood count: may show anemia
 Serum electrolyte levels: hyponatremia → indicates a poor prognosis
 Kidney function tests: ↑ creatinine, ↓ sodium
 Urine analysis: rule out concurrent renal impairment
 Fasting glucose: to screen for diabetes mellitus, which is a common
comorbidity
 Fasting lipid profile: to detect dyslipidemia associated with a higher
cardiovascular risk

Electrocardiogram (ECG)
ECG abnormalities in CHF are common, but are mostly nonspecific and
nondiagnostic.
- Signs of left ventricular hypertrophy
↑ QRS voltage (in the left chest leads and limb leads I and aVL) → positive
Sokolow-Lyon index
↑ QRS duration (incomplete or complete left bundle branch block)
 Left axis deviation
- Assessment of prior or concurrent heart conditions
Previous or acute MI: see ECG changes in STEMI
Arrhythmias (e.g., atrial fibrillation, ventricular arrhythmias, sinus
tachycardia or bradycardia, AV block)
- Signs of pericardial effusion and tamponade: low voltage ECG

Chest x-ray
Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF
from pulmonary disease
Signs of cardiomegaly
Cardiac-to-thoracic width ratio > 0.5 (The ratio is calculated by dividing the cardiac
diameter by the thoracic diameter on the same horizontal level in posteroanterior (PA) view.)

Boot-shaped heart on PA view (due to right ventricular enlargement)

Assess pulmonary congestion (see x-ray findings in pulmonary congestion)

Transthoracic echocardiogram
Gold standard for evaluating patients with heart failure
Assess ventricular function and hemodynamics
Atrial and ventricular size
 Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates
cardiac hypertrophy
 Systolic function: left ventricular ejection fraction
-Normal EF: > 55%
-Reduced EF: 30–44%
-Extremely reduced EF: < 30%
 Diastolic function (diastolic filling, ventricle dilation)
Investigate etiology
Valvular heart disease
Wall motion abnormalities (indicate prior or acute MI)
Right ventricular strain
Tissue Doppler: ↑ PCWP in left-sided heart failure
PCWP - (Pulmonary capillary wedge pressure ) An indirect measure of left atrial pressure.
Measured by advancing a balloon catheter into a small pulmonary artery and then inflating the
catheter. The PCWP is then measured distal to the inflated balloon. Normal: 4–12 mm Hg.

Further tests
 Cardiac stress test (exercise tolerance test): to assess the functional impairment due to
CHF or other conditions (particularly CHD!)
 Radionuclide ventriculography : indicated to assess left ventricular volume and ejection
fraction (LVEF)
 Cardiac MRI: particularly useful for assessing cardiac morphology and function
 Cardiac size and volumes, wall thickness, valvular defects, wall motion abnormalities
 Coronary angiography (left heart catheterization): indicated to detect/confirm CHD and
possible percutaneous coronary intervention
 Right heart catheterization: if pulmonary hypertension is suspected, to assess the
severity of systolic dysfunction, and/or to differentiate between types of shock
 SvO2: will be low in decompensated heart failure
 Endomyocardial biopsy: may be performed if a specific diagnosis is suspected in
patients with rapidly progressive clinical CHF or in case the results would alter the
management of the patient, e.g., in amyloidosis

Treatment
General measures
 Lifestyle modifications
 Salt restriction (< 3 g/day)
 Fluid restriction in patients with edema and/or hyponatremia
 Weight loss and exercise
 Cessation of smoking and alcohol consumption
 Immunization: pneumococcal vaccine and seasonal influenza vaccine
 Patient education
 Self-monitoring and symptom recognition
 Daily weight check
  Weight gain > 2 kg within 3 days: consult the doctor
 Monitoring of potential side effects (e.g., hypotension caused by ACE
inhibitors, hyperkalemia caused by aldosterone-antagonists,
sensitivity to sunlight caused by amiodarone)
 Treat any underlying conditions and contributing comorbidities.

1. ACE inhibitors (Enalapril - 5-20 mg x 2 times a day; Lisinopril - 5-20 mg x 2

times a day)
2. In case of intolerance to ACE inhibitors: Angiotensin II receptor blockers
(Candesartan - 4-32 mg x 1 time a day; Losartan - 50-100 mg / day x 1-2 times a
day)
3. Beta - blockers (Bisoprolol - initial dose - 1.25-2.5 mg / day, maximum dose -
10 mg / day; Metoprolol - initial dose - 12.5-25.0 mg / day, maximum dose - 150
mg / day)
4. Loop and thiazide diuretics (furosemide - 40 mg - inside or in / in; maximum
daily dose - 600 mg; torasemide - 5-10mg / day; Hydrochlorothiazide - inside 25-
50 mg / day; maximum daily dose - 200 mg )
5. Antagonists of aldosterone (spironolactone (veroshpiron) - 25 mg / day by
mouth; eplerenone - 25 mg / day)
6. Cardiac glycosides (Digoxin - 0.125-0.25 mg / day)
7. Other treatment methods (Ultrafiltration, myocardial revascularization,
resynchronization therapy, defibrillator implantation, mechanical assistive devices,
heart transplantation)

Prognosis - depends on the severity of the underlying disease and functional class.
Class I, Class II - relatively favorable,
Class III - serious
Class IV - unfavorable.