This document provides an overview of heart failure (HF), also known as congestive heart failure. It defines HF as a state where the heart cannot pump enough blood to meet metabolic demands, resulting in organ hypoperfusion. Common causes include cardiomyopathies, myocardial infarction, and ischemic heart disease. Symptoms include edema, shortness of breath, fatigue, and reduced exercise tolerance. Treatment focuses on reducing preload and afterload through diuretics, vasodilators, and renin-angiotensin system inhibitors to decrease workload on the heart.

1. Heart Failure/ CCF/ CHF
Prepared by:
Kopila Mugrati
MSN.

2. Definition
• Heart failure is a physiologic state in which the
heart cannot pump enough blood to meet the
metabolic needs of the body. (oxygen
consumption) resulting in hypoperfusion of the
tissue, followed by pulmonary and systemic venous
congestion.

3. • It is clinical syndrome manifested by volume
overload, inadequate tissue perfusion, poor
exercise tolerance.
• Due to vascular congestion during heart failure, it
often called as congestive heart failure.

4. • Is also known as chronic heart failure, cardiac
decompensation, cardiac insufficiency, and
ventricular failure

5. Incidence :
• Affects at least 26 million people worldwide and is
increasing
• Affects about 5 million people every year in US
• Affects both males and females, mortality is higher
among females.
• Leading cause of hospitalization in older patients.

6. Etiology & Risk factors
Extrinsic
factors
Intrinsic
factors
Due to
Caused by
conditions
that weaken
or damage the
myocardium.

7. Intrinsic factors
• Cardiomyopathies
• MI
• Myocarditis
• Ischemic heart diseases
• Pericarditis
• Cardiac tamponade

8. Extrinsic factors
• Drug toxicity
• Arrythmias
• Metabolic/ respiratory acidosis
• AV shunts
• Pulmonary embolism
• anaemia

9. Causes:
1. Abnormal muscle function
MI
Myocarditis
Cardiomyopathy
Ventricular aneurysm
Long term alcohol consumption
Coronary heart disease
Metabolic heart disease
Endocrine heart disease

10. 2. Increase in preload:
Regurgitatio
n of mitral
or tricuspid
valve
Hypervolemi
a
Congenital
defects
Ventricular
septal
defects
(VSD)
Atrial septal
defect
Patent
ductus
arteriosus

11. 3.Limited ventricular filling:
Mitral or tricuspid stenosis
Cardiac tamponade
Constrictive pericarditis
Hypertrophic obstructive cardiomyopathies

12. 4.Increase in afterload:
Hypertension
Pulmonary
or aortic
stenosis
Peripheral
vascular
resistance

13. Functional classification of heart failure

14. Pathophysiology
• Due to etiological factors
• Decrease in pumping action of the heart
• Stimulates the compensatory mechanism
a. Ventricular dilation
b. Increased sympathetic nervous system stimulation
c. Renin angiotensin system activation
d. Remodeling
e. Sustained neurohormonal activities

15. Continue..
• Increase in HR
• Increase in myocardial oxygen use
• Increase in cardiac output
• Increase preload increase afterload
• Congestive heart failure

16. 1.Increased sympathetic nervous system
stimulation
Further contraction of ventricles
Epinephrine and norepinephrine release
Vasoconstriction of arterioles
Causes increase in rate and force of contraction of ventricles
Stimulation of SNS
Decrease in BP
Due to decreased cardiac output

17. 2. Renin angiotensin system activation
Leads to increase in BP
Further causes vasoconstriction
Stimulates secretion of aldosterone by adrenal gland
Stimulate thirst center in brain
Angiotensin II causes vasoconstriction and constricts renal arterioles
Converts Angiotensin I to AngiotensinII
Acts on angiotensinogen ( which is released by liver)
Renal juxtaglomerular cells release Rennin
Decrease in BP

18. 3. Ventricular dilation
Leading to hypoxia of heart, decrease in contraction.
If stretched beyond certain point, becomes ineffective
( Starling's law)
Dilation causes increase in preload
Ventricular dilation refers to lengthening of muscle fibers of heart
chambers.

19. 4. Remodeling
Over time changes in structure, function of myocardial cells takes
place known as remodeling.
Increased wall thickness reduces wall stress
Occurs due to hypertrophy of myocardial cells and sustained
neurohormonal activation
Remodeling takes place during decompensated heart failure

20. 5. Sustained neurohormonal activation
• Remodeling occurs
• Stimulates neurohormonal activity

21. Continue..
If the compensatory mechanism fails
Blood in left ventricle increases
Leads to more work load in heart
Leads to hypertrophy of chambers
Cannot receive blood from pulmonary veins
Leads to increase in left atrial pressure
And finally causes pulmonary edema

23. Clinical manifestations:
• Shortness of breath often with activities or while lying flat
• Weakness and fatigue
• Awakening short of breath at night
• Need for increased pillows at night – helps lungs drain of
excess fluid
• Coughing or wheezing
• Swelling of feet and legs or other “dependent” areas
• Anorexia/loss of appetite • Weight gain
• Fatigue Activity decrease Cough (especially supine)
Edema Shortness of breath

24. Types of heart failure
Left ventricular
failure
Right ventricular
failure
Backward Vs
Forward
High output Vs
low output

26. Left heart Failure
• Left heart failure occurs when the output of the left
ventricle is less than the total volume of blood received
from the right side of the heart via pulmonary
circulation.
• Results in congested pulmonary circuit with blood that
cannot be moved forward and the systemic blood
pressure falls.

27. Causes of left heart failure
• Myocardial infarction
• Systemic hypertension
• Aortic stenosis
• Cardiomyopathy

28. Pathophysiology of LVF
Backward effect:
Due to ventricular failure of inability to pump
Decrease emptying of left ventricle
Increase volume &end diastolic pressure
Increase volume in pulmonary veins& pressure
Increase volume in pulmonary capillary bed
Transudation of fluid from capillaries to alveoli
Filling of alveolar space
Leading to pulmonary edema

29. Forward effect
Increase blood volume and BP
Increase extracellular fluid volume
Increase secretion of sodium and water retention
Increase reabsorption of Na+ and H2O, vasoconstriction
Decrease blood flow to kidneys and glands
Decrease body tissue perfusion
Decrease in cardiac output

30. Clinical manifestations of LHF
• Dyspnea ( more in case of ventricular failure)
• Exertional Dyspnea
• Pulmonary congestion
• Orthopnea (due to increase in amount of blood returning from
lower extremities to heart and lungs)

31. Continue..
• Paroxysmal nocturnal dyspnea (PND: frightening sensation
of suffocation)
• Labored and wheezing respiration
• Cheyne- Strokes respiration (due to prolonged circulation
time between pul. Circulation and central nervous system)

32. Continue..
• Cough (very common in LVF: frothy, blood-tinged sputum)
• Cerebral hypoxia (causing confusion, restlessness, impaired
memory etc..)
• Fatigue and muscular weakness
• Slow removal of metabolic wastes
• Disturbed sleep and rest
• Nocturia
• Later when cardiac output declines, leads to oliguria.

33. Complications of LVF
• Acute pulmonary edema
• Death due to suffocation

34. DIAGNOSTIC EVALUATION
Physical Examination/ History collection
• Bilateral crackles on auscultation.
• Inspection and palpation of precordium reveals enlarged or displaced apical
pulse.
• S3 or S4 may be heard as early finding.
• Blood tests- Like LFT, KFT & TSH, A blood test to check for a chemical called
N-terminal pro-B-type natriuretic peptide (NT-proBNP) may help in diagnosing
heart failure. are peptide (small proteins) that are either hormones or part of
the peptide. They are continually produced in small quantities in the heart and
released in larger quantities when the heart senses that it needs to work
harder.

35. • Chest X-ray- heart may appear enlarged and
fluid buildup may be visible in your lungs.
• Electrocardiogram (ECG)
• Echocardiogram
• Stress test- measure how heart and blood vessels
respond to exertion.
• Cardiac computerized tomography (CT) scan or
magnetic resonance imaging (MRI).
• Coronary angiogram
• Myocardial biopsy

36. Right ventricular failure
• Right heart failure occurs when the output of the
right ventricle is less than the input from the
systemic venous circuit which results in congestion
of venous circuit and decreased output to lungs.

37. Causes of RHF/RVF
• Left heart failure
• Pulmonary embolism
• COPD
• Congenital heart diseases
• Pulmonary hypertension

38. Backward effect
Peripheral edema, dependent edema, generalized edema
Increased pressure at capillary line
Increased volume in distendable organs(liver, spleen)
Increased volume in systemic venous circulation
Increased volume and pressure in the greater veins
Increase volume and pressure
Increase volume and end diastolic pressure
Decrease emptying of rt ventricle

39. Clinical manifestations
• Peripheral edema& dependent edemas
• Venous congestion of organs
• Hepatomegaly
• Abdominal pain due to Hepatomegaly
• Discomfort
• Constant aching or a sharp pain in rt upper quadrant
• Anoxia leading to necrosis of lobules of liver (cardiac
cirrhosis)
• Ascites, jaundice
• Anorexia, nausea, bloating

40. Continue..
• Cardiac cachexia (marked wasting of tissue mass)
• Anasarca
• Cynosis of nail beds
• Anxious, depressed, fear
• Insomnia
Complication:
Death

41. DIAGNOSTIC EVALUATION (RHF)
Physical Examination/ History collection
• Serum BPN: Brain natriuretic peptide (BNP) test is a
blood test that measures levels of a protein called BPN that
is made by heart and blood vessels. BNP levels are higher
than normal when heart failure occurs.
• S3 or S4 may be heard as early finding.
• Blood tests- Like LFT, KFT & TSH, BUN

42. continue…
• Chest X-ray- heart may appear enlarged cardiac
silhouette and congestion of lungs.
• Electrocardiogram (ECG)
• Echocardiogram with doppler flow studies
• Stress test- measure how heart and blood vessels
respond to exertion.
• ABG ( respiratory alkalosis)
• Cardiac computerized tomography (CT) scan or
magnetic resonance imaging (MRI).
• Coronary angiogram
• Myocardial biopsy

43. Management
1. Reduce myocardial workload:
• Diuretics are the mainstay of treatment in patients
with volume overload. Diuretics act to decrease
sodium reabsorption at various sites within the
nephrons, thereby enhancing sodium and water
loss.
• Vasodilators. IV nitroglycerin is a vasodilator that
reduces circulating blood volume. It also improves
coronary artery circulation by dilating the coronary
arteries. Therefore nitroglycerin reduces preload,
slightly reduces afterload (in high doses), and
increases myocardial oxygen supply. When titrating
IV nitroglycerin, monitor BP frequently (every 5 to
10 minutes) to avoid symptomatic hypotension.

44. Continue..
• Sodium nitroprusside (Nipride) is a potent IV vasodilator
that reduces both preload and afterload.
• Morphine. Morphine sulfate reduces preload and
afterload.
• Positive Inotropes. Inotropic therapy increases myocardial
contractility. Drugs include β-adrenergic agonists (e.g.,
dopamine [Intropin], dobutamine [Dobutrex], epinephrine,
norepinephrine [Levophed]), the phosphodiesterase
inhibitor milrinone (Primacor), and digitalis.

45. DRUG THERAPY
• Heart Failure Drug Mechanism of Action
• Diuretics:
• Loop Diuretics • Decrease fluid volume
• Decrease preload
• Decrease pulmonary venous pressure
• Relieve symptoms of heart failure
(e.g., edema) • furosemide (Lasix), bumetanide (Bumex)
• Thiazide Diuretics*
• hydrochlorothiazide (HCTZ)
• metolazone (Zaroxolyn)
• Potassium-Sparing Diuretics
• spironolactone (Aldactone)
• eplerenone (Inspra)

46. • Renin-Angiotensin-Aldosterone System Inhibitors:
ACE Inhibitors
• captopril (Capoten)
• benazepril (Lotensin)
• enalapril (Vasotec)
Angiotensin II Receptor Blockers
• losartan (Cozaar)
• valsartan (Diovan)

47. Drugs
• Renin-Angiotensin-
Aldosterone System
Inhibitors: ACE Inhibitors
• captopril (Capoten)
• benazepril (Lotensin)
• enalapril (Vasotec)
Angiotensin II Receptor
Blockers
• losartan (Cozaar)
• valsartan (Diovan)
Action
• Dilate venules and
arterioles
• Improve renal blood flow
• Decrease fluid volume
• Relieve symptoms of
heart failure
• Promote reverse
remodeling
• Decrease morbidity and
mortality

48. • Vasodilators:
• hydralazine
(Apresoline)*
• isosorbide dinitrate/
hydralazine (BiDil)*
• nitrates (e.g.,
nitroglycerin [Nitro-Bid],
isosorbide dinitrate
[Isordil])
• nesiritide (Natrecor)†
• nitroprusside (Nipride)†
• Reduce cardiac afterload,
leading to increased CO
• Dilate the arterioles of
the kidneys, leading to
increased renal perfusion
and fluid loss
• Decrease BP
• Decrease preload
• Relieve symptoms of
heart failure (e.g., dyspnea)

49. • β-Adrenergic Blockers*
• metoprolol (Toprol XL)
• bisoprolol (Zebeta) •
carvedilol (Coreg)
Positive Inotropes β-
Adrenergic Agonists†
• dopamine (Intropin)
• dobutamine (Dobutrex)
Phosphodiesterase
Inhibitor†
• milrinone (Primacor)
Digitalis Glycoside*
• digoxin (Lanoxin)
Continue..
• Morphine
• Antidysrhythmic Drugs
• Anticoagulants

50. 2. Elevate client's head
3. Reduce fluid retention
4. Improve ventricular pump performance
5. Supplement with oxygen
6. Control dysrhythmias
7.Reduce stress and risk of injury

51. Surgical management
• Ventricular assist devices
• Heart transplantation
• cardiomyoplasty

52. Thank you!