Heart failure, particularly congestive heart failure (CHF), is a progressive condition resulting from systolic or diastolic dysfunction due to various causes, including ischemic heart disease and hypertension. It can lead to inadequate cardiac output and increased venous congestion, affecting the left, right, or both sides of the heart, often resulting in symptoms such as dyspnea and cardiomegaly. Treatment focuses on correcting underlying causes, managing volume overload and improving myocardial contractility through pharmacologic agents and cardiac therapies.

1. HEART FAILURE

2. • Congestive heart failure (CHF), is the common
end point for many forms of cardiac disease.
• Progressive condition with a poor prognosis.

3. • Heart failure may result from systolic or
diastolic dysfunction.
• Systolic dysfunction results from inadequate
myocardial contractile function-
• Ischemic heart disease
• Hypertension.

4. • Diastolic dysfunction refers to an inability of
the heart to adequately relax and fill-
• Massive left ventricular hypertrophy
• Myocardial fibrosis
• Amyloid deposition
• Constrictive pericarditis.

5. • One half of CHF cases are attributable to
diastolic dysfunction.
• Greater frequency seen in older adults,
diabetic patients, and women.
• Heart failure may also be caused by valve
dysfunction (e.g., due to endocarditis) or
following rapid increases in blood volume or
blood pressure.

6. • Failing heart can no longer efficiently pump
blood Increase in end-diastolic ventricular
volumes  increased end-diastolic
pressures elevated venous pressures.
• Inadequate cardiac output—forward failure.
• Increased congestion of the venous circulation
—backward failure

7. Compensatory mechanism
• Frank-Starling mechanism-
• Increased end-diastolic filling volumes dilate
the heart.
• Increased cardiac myofiber stretching.
• Lengthened fibers contract more forcibly.
• Increasing cardiac output.

8. • If the dilated ventricle is able to maintain
cardiac output by this meansCompensated
heart failure.
• With time, the failing muscle is no longer able
to propel sufficient blood to meet the needs
of the body Decompensated heart failure

9. • Activation of neurohumoral systems-
• Release of the neurotransmitter
norepinephrine  increases heart rate and
myocardial contractility and vascular resistance.
• Activation of the renin-angiotensin-aldosterone
system water and salt retention (augmenting
circulatory volume) and increases vascular
tone.

10. • Release of atrial natriuretic peptide balance
the renin-angiotensin-aldosterone system
through diuresis and vascular smooth muscle
relaxation.

11. • Myocardial structural changes, including
augmented muscle mass-
• Cardiac myocytes adapt to increased workload
by assembling new sarcomeres.
• Myocyte enlargement (hypertrophy).

12. • In pressure overload states (e.g., hypertension
or valvular stenosis)-
• New sarcomeres tend to be added parallel to
the long axis of the myocytes, adjacent to
existing sarcomeres.
• Growing muscle fiber diameter thus results in
concentric hypertrophy Ventricular wall
thickness increases without an increase in the
size of the chamber.

13. • In volume overload states (e.g., valvular
regurgitation or shunts)-
• New sarcomeres are added in series with existing
sarcomeres.
• Muscle fiber length increases.
• Ventricle tends to dilate and wall thickness can
be increased, normal, or decreased.
• Heart weight—rather than wall thickness—is the
best measure of hypertrophy.

14. Compensatory hypertrophy
• The oxygen requirements of hypertrophic
myocardium are amplified owing to increased
myocardial cell mass.
• Capillary bed does not expand in step with the
increased myocardial oxygen demands.
• Myocardium becomes vulnerable to ischemic
injury.

15. • Pathologic compensatory cardiac hypertrophy
is correlated with increased mortality
• Cardiac hypertrophy is an independent risk
factor for sudden cardiac death.

16. • Volume-loaded hypertrophy induced by
regular aerobic exercise (physiologic
hypertrophy) is accompanied by an increase in
capillary density, with decreased resting heart
rate and blood pressure.
• These physiologic adaptations reduce overall
cardiovascular morbidity and mortality.

17. • In comparison, static exercise (weight lifting)
is associated with pressure hypertrophy and
may not have the same beneficial effects.
• Heart failure can affect predominantly the left
or the right side of the heart or may involve
both sides.

18. Left-Sided Heart Failure
• Causes-
• Ischemic heart disease (IHD)
• Systemic hypertension
• Mitral or aortic valve disease
• Primary diseases of the myocardium
(amyloidosis).

19. MORPHOLOGY
• Heart-
• Gross:- cardiac findings depend on the underlying
disease process
• Myocardial infarction or valvular deformities may be
present.
• Left ventricle usually is hypertrophied and can be
dilated, sometimes massively.
• Result in mitral insufficiency and left atrial enlargement.
• Increased incidence of atrial fibrillation.

21. Microscopic changes
Nonspecific
Myocyte
hypertrophy with
interstitial fibrosis of
variable severity.
Superimposed on
this background may
be other lesions that
contribute to the
development of
heart failure (e.g.
recent or old
myocardial
infarction).

22. Lungs
In acute heart failure-
Rising pressure in the pulmonary veins transmitted back to the capillaries
and arteries of the lungs.
Increase in hydrostatic pressure in the venules of the visceral pleura.
Results in congestion and edema as well as pleural effusion

23. • GROSS-
• The lungs are heavy and boggy.
• Microscopically-
• Perivascular and interstitial transudates
• Alveolar septal edema
• Accumulation of edema fluid in the alveolar
spaces.

24. Chronic heart failure
Red cells extravasate from the leaky capillaries into alveolar spaces.
Phagocytosed by macrophages.
Breakdown of red cells and hemoglobin Appearance of hemosiderin-laden alveolar
macrophages—heart failure cells.

25. Clinical Features
• Dyspnea (shortness of breath) on exertion
• Cough
• Dyspnea when recumbent (orthopnea)
• Paroxysmal nocturnal dyspnea
• Cardiomegaly
• Tachycardia
• Third heart sound (S3)
• Fine rales at the lung bases

26. • Mitral regurgitation
• Systolic murmu
• Atrial fibrillation- “irregularly irregular”
heartbeat
• Strokes and manifestations of infarction in
other organs.
•

27. • Diminished cardiac output leads to decreased
renal perfusion.
• Triggers the renin-angiotensin-aldosterone
axis
• Increasing intravascular volume and pressures
• Prerenal azotemia

28. • Diminished cerebral perfusion may manifest
as hypoxic encephalopathy
• Irritability, diminished cognition, and
restlessness that can progress to stupor and
coma.

29. Treatment
• Correcting the underlying cause- A valvular
defect or inadequate cardiac perfusion.
• Salt restriction
• Pharmacologic agents that variously reduce
volume overload (e.g., diuretics)
• Increase myocardial contractility (“positive
inotropes”)
• Reduce afterload (adren ergic blockade or
inhibitors of angiotensin-converting enzymes)

30. • Cardiac resynchronization therapy-
• Exogenous pacing of both the right and left
ventricles
• Cardiac contractility modulation (exogenous
stimulation of cardiac muscle)

31. Right-Sided Heart Failure
• Consequence of left-sided heart failure.
• Any pressure increase in the pulmonary
circulation produces an increased burden on
the right side of the heart.
• Isolated right-sided heart failure is infrequent.
• Occurs in patients with disorders affecting the
lungs; hence it is often referred to as cor
pulmonale.

32. • Besides parenchymal lung diseases, cor
pulmonale also may arise secondary to
disorders that affect the pulmonary
vasculature-
• Primary pulmonary hypertension
• Recurrent pulmonary thromboembolism
• Pulmonary vasoconstriction (obstructive sleep
apnea).

33. • The common feature of these disorders is pulmonary
hypertension.
• Results in hypertrophy and dilation of the right side of
the heart.
• In cor pulmonale, myocardial hypertrophy and
dilation are confined to the right ventricle and atrium.
• Bulging of the ventricular septum to the left.
• Reduce cardiac output by causing outflow tract
obstruction.

34. MORPHOLOGY
• Liver and Portal System-
• The liver usually is increased in size and weight
(congestive hepatomegaly).
• Cut section: Prominent passive congestion, a pattern
referred to as nutmeg liver
• Congested centrilobular areas are surrounded by
peripheral paler, noncongested parenchyma.
• Left-sided heart failure- Severe central hypoxia
produces centrilobular necrosis in addition to the
sinusoidal congestion.

35. • Long-standing severe right-sided heart failure-
• Central areas can become fibrotic, creating so-called
cardiac cirrhosis.
• Elevated pressure in the portal vein and its tributaries
(portal hypertension), with vascular congestion
producing a tense, enlarged spleen (congestive
splenomegaly).
• If severe, chronic passive congestion and edema of
the bowel wall may interfere with absorption of
nutrients and medications.

36. • Pleural, Pericardial, and Peritoneal Spaces.
• Systemic venous congestion due to right-sided
heart failure can lead to transudates (effusions)
in the pleural and pericardial spaces.
• A combination of hepatic congestion (with or
without diminished albumin synthesis) and
portal hypertension can lead to peritoneal
transudates (ascites).

37. • Subcutaneous Tissues-
• Edema of dependent portions of the body,
especially the feet and lower legs, is a
hallmark of right sided CHF.
• In chronically bedridden patients, the edema
may be primarily presacral.

38. Clinical Features
• Hepatic and splenic enlargement, peripheral
edema, pleural effusion, and ascites.
• Venous congestion and hypoxia of the kidneys
and brain produce deficits comparable to
those caused by the hypoperfusion of left-
sided heart failure.

39. • Cardiac decompensation- Biventricular CHF,
features of both right-sided and left-sided
heart failure.
• Patients may become frankly cyanotic and
acidotic.
• Consequence of decreased tissue perfusion
• Resulting from both diminished cardiac output
and increasing congestion.