This document discusses congestive heart failure (CHF), including its definition, causes, pathophysiology, clinical manifestations, diagnosis, and management. CHF is characterized by inadequate systemic perfusion due to cardiac abnormalities. The most common cause is left ventricular systolic dysfunction. Clinical manifestations include dyspnea, edema, fatigue, and reduced exercise tolerance. Diagnosis involves imaging, labs, and assessing symptoms according to the NYHA classification system. Management focuses on controlling congestion with diuretics, enhancing contractility with drugs like digoxin, preventing worsening with ACE inhibitors and beta blockers, and treating the underlying cause.

1. Congestive Heart Failure
Dr Muxyi

2. 2. Congestive Heart Failure
Learning objectives: at the end of this lesson the student will
be able to :
1. Define congestive heart failure.
2. List the etiologic agents of congestive heart failure.
3. Understand the Epidemiology of congestive heart failure.
4. Describe the pathophysiology of congestive heart failure.
5. Identify the clinical manifestation of congestive heart
failure.
6. Understand the diagnostic approach of congestive heart
failure.
7. Manage patients with congestive heart failure.
8. Design strategies for prevention of congestive heart failure.

3. Definition:
Heart failure is a clinical syndrome characterized
by inadequate systemic perfusion to meet the
body's metabolic demands as a result of
abnormalities of cardiac structure or function.
This may be further subdivided into either
systolic or diastolic heart failure.
• Systolic heart failure: there is reduced cardiac
contractility
• Diastolic heart failure there is impaired
cardiac relaxation and abnormal ventricular
filling.

4. • The body, sensing inadequate organ
perfusion, activates multiple systemic
neurohormonal pathways which compensate
initially by redistributing blood flow to vital
organs but later exacerbate the patient's
symptoms and lead to clinical deterioration.

5. Etiology:
The most common cause of heart failure is left
ventricular systolic dysfunction (about 60% to
70% of patients). The following are some of the
underlying causes of heart failure .
1) Decreased contractile function
A. Valvular heart disease
B. Coronary Heart Disease : Myocardial ischemia
C. Myocardial Disease : Cadiomyopathy , Myocarditis
2) Increased after load
a. Acute systemic hypertension

6. 3) Abnormalities in preload
A. Excessive preload
B. Reduced preload
4) Reduced compliance states: Constrictive
pericarditis , Restrictive cardiomyopathy

7. Precipitating factors for heart failure:
• These are relatively acute disturbances that
place an additional load on a myocardium that
is chronically and excessively burdened.
• In compensated state patients are
asymptomatic; however as patients have
little additional reserve, they become
symptomatic in the presence of these
precipitating factors.

8. • Knowing the precipitating factors is
important because most of the time they
are treatable and the cardiac function
improves when these precipitating factors are
treated or avoided.
• The most important precipitating factors may
be represented with the mnemonic, HEART
FAILES

9. HEART FAILES
• H- Hypertension (systemic)
• E- Endocarditis (infections)
• A- Anemia
• R- Rheumatic fever and myocarditis
• T- Thyrotoxicosis and pregnancy
• F- Fever (infections)
• A- Arrhythmia
• I- infarction (myocardial)
• L- Lung infection
• E- Embolism (pulmonary)
• S- Stress (emotional, physical, environment, dietary, fluid
excess)

10. Pathophysiology
In left ventricular systolic dysfunction, regardless
of the etiology, cardiac output is low and
pulmonary pressures are high, leading to
pulmonary congestion. As a result, a series of
adaptive mechanisms are activated. Initially,
as a direct result of inadequate cardiac output
and systemic perfusion, the body activates
several neurohormonal pathways in order to
increase circulating blood volume.

11. • With continuous neurohormonal stimulation,
the left ventricle undergoes remodeling with
left ventricular dilatation and hypertrophy,
such that stroke volume is increased without
an actual increase in ejection fraction. This is
achieved by myocyte hypertrophy and
elongation. However, left ventricular chamber
dilatation causes increased wall tension,
worsens subendocardial myocardial perfusion,
and may provoke ischemia in patients with
coronary atherosclerosis.

12. • Furthermore, left ventricular chamber
dilatation may cause separation of the mitral
leaflets and mitral regurgitation with
worsening of pulmonary congestion.
Enhanced neurohormonal stimulation of the
myocardium also causes apoptosis, or
programmed cell death, leading to worsening
of ventricular contractility.

13. Villa Somalia
White house

14. Clinical Manifestations
1. Progressive dyspnea which initially occurs with
exertion and later occurs at rest.
• Dyspnea on exertion has been found to be the
most sensitive complaint, yet the specificity for
dyspnea is less than 60%.
2. Orthopnea and paroxysmal nocturnal dyspnea (PND)
are more specific symptoms;
however, sensitivity for orthopnea and PND is only 20-
30%.
3. Cough productive of pink, frothy sputum is highly
suggestive of CHF. Wheezing may also occur.
4. Peripheral edema and ascites
5. Nonspecific complaints include the following: easy
fatigability , light headedness , malaise anxiety
abdominal pain , nausea etc

15. • Past medical history may include the
following: rheumatic fever , alcohol use,
hypertension , angina , previous history of
myocardial infarction and familial history of
heart disease

16. Physical findings:
• Tachycardia and Tachypnea and signs of respiratory
distress including use of accessory muscles of
respiration
• Jugular venous distention (JVD) frequently is present
and engorged neck veins
• Pulsus alternans (alternating weak and strong pulse
indicative of depressed left ventricle[LV] function
• Wheezing or rales may be heard on lung auscultation
and there may be bilateral basal dullness.
• Apical impulse frequently is displaced laterally
• Cardiac auscultation may reveal aortic or mitral
valvular abnormalities, S3 or S4.

17. • Skin may be diaphoretic or cold, gray, and
cyanotic
• Lower extremity edema also may be noted,
especially in the subacute process.
• New York Heart Association Heart Failure
Classification scheme is used to assess the
severity of a patient's functional limitations
and correlates fairly well with cardiovascular
prognosis.

18. Table III -2-1: New York Heart Association Heart
Failure Symptom Classification System
Grade Symptoms
I No symptom limitation with ordinary physical activity
II
Ordinary physical activity somewhat limited by dyspnea (i.e.,
long distance walking, climbing 2 flights of stairs)
III
Exercise limited by dyspnea at mild workloads (i.e., short
distance walking, climbing one flight of stairs)
IV Dyspnea at rest or with very little exertion

19. Diagnostic Workup
1. Chest x-ray: the main findings are cardiomegally,
pulmonary edema, and pleural effusion.
2. Echocardiography: may help identify valvular
abnormalities, ventricular dysfunction, cardiac
temponade, pericardial constriction, and pulmonary
embolus.
3. Electrocardiogram (ECG): is a nonspecific tool but may
be useful in diagnosing concomitant cardiac ischemia,
prior myocardial infarction (MI), cardiac dysrhythmias,
chronic hypertension, and other causes of left ventricular
hypertrophy.
4. Other laboratory tests : Hemoglobin, Urinalysis, BUN,
Creatinine

21. Management of Heart Failure
Principles of management
1. Identify and treat the precipitating factors
2. Control the congestive state
3. Improve myocardial performance
4.Prevention of deterioration of myocardial
function (slowing progression of heart failure )
5. Treat the underlying cause

22. A. General measures :
Dietary sodium restriction should be implemented in all
patients with congestive heart failure to < 3 g/d.
Activity and life style modification :
 Meals should be small in quantity but more frequent.
 Reduce anxiety and emotional stress
 Avoid excess physical exertion ( NB exercise may be
advised within the limit of the patient’s cardiac
function )
 Weight loss in encouraged in obese patients.
 Cessation of smoking
 Avoid other CVD risk factors

23. B. Control of the Congestive state
Diuretics: are useful in relieving congestion and
reduce or prevent edema.
• Most patients with heart failure have some
degree of symptomatic congestion and benefit
from diuretic therapy.
• Usually a loop diuretic is required, with the
addition of a Thiazide diuretic in patients
refractory to the loop diuretic alone.
1. Furosomide: Initial dose 20-40 mg PO 1-2 X
daily or 20 mg IV Maximum dose 400 mg PO/day
or 80 mg IV /day
2. Hydrochlorothiazide: Initial dose 25 mg
PO/day Maximum dose 100 mg PO/day

24. • N.B . Loop and thiazide diuretics are useful for
symptomatic relief; however they have not been
shown to improve survival.
Side effects : Azotemia, hypokalemia,
metabolic alkalosis and elevation of
neurohormones
3. Spirinolactone: is an aldosterone inhibitor,
reduces mortality in patients with advanced
heart failure. This drug should be reserved for
patients with moderately severe or severe heart
failure ( class IV symptoms )
Initial dose: 25 mg PO/day or every other day
Maximum dose: 50 mg PO BID or higher

25. Side effects
Hyperkalemia is common so monitoring K+
the serum potassium level is essential. As a
result, this drug should not be used in
patients with a creatinine above 2.5 mg/dl.
Gynecomastia in men is the other side effect
of this drug.

26. C. Enhancement of Myocardial
contractility :
1) Digoxin: is a drug which has :
• Inotropic effect and acts by inhibiting the
Na+-K+ ATPase and increase intracellular
calcium. This increases myocardial contractility.
•Neurohormonal modulation of centrally mediated
parasympathomimetic and sympatholytic activity.
By doing so it blocks the AV node and delays
AV conduction.
Initial dose : 0.125 mg PO/day
Maximum dose : 0.25 mg PO/day

27. The use of digoxin can improve symptoms, reduce the
duration and the need for hospitalization in patients
with heart failure,, but has no effect on long term
survival.
♦ Digoxin is renally excreted and so dose adjustment is
necessary in renal failure.
♦ A low dose of the drug (0.125 mg daily) should be
prescribed, especially in women.
♦ Digoxin use is recommended for patients with left
ventricular systolic dysfunction, particularly if they
have atrial fibrillation.
♦ It is relatively contraindicated in some cardiac disease
 Cardiac outflow obstruction in MS (in the absence of
atrial fibrillation )
 Corpulmonale

28. Because of it narrow window of safety, digoxin is
associated with different Side effects
including:
GI : anorexia , nausea, vomiting , weight loss
Neuralgia, delirium
Yellow vision
Gynecomastia
Arrhythmias of different types

29. 2) Vasodilators: may be useful in patients with
severe acute heart failure who demonstrate
systemic vasoconstriction despite ACE inhibitor
therapy. Through vasodilatation they reduce the
peripheral resistance and after load and improve
cardiac performance.
Hydralazine:
Initial dose: 25 mg PO TID
Maximum dose: 150 mg PO QID.
Isosorbide dinitrate: Initial dose 10 mg PO TID
Maximum dose: 80 mg PO TID
♦ Hydralazine and nitrates in combination are
effective afterload reducing agents used in ACE-
intolerant patients.

30. D. Prevention of deterioration of
Myocardial function :
The following drugs prevent deterioration in myocardial
function by inhibiting the neurohumeral mechanism which
causes cardiac remodelling and progression of heart failure.
1) Angiotensin Converting Enzyme (ACE) Inhibitors
Afterload reduction and neurohormonal modulation with ACE
inhibitors ( e.g. Captopril, Enalapril, etc) have been shown
to improve mortality, symptoms, and hospitalizations. The
dose of ACE inhibitors should be titrated to the maximum
that can be tolerated symptomatically or the target dose. .
Initial dose: Captopril 6.25 mg PO/day or every other day
Enalapril 2.5 mg PO BID
Maximum dose: Captopril 50-100 mg PO QID
Enalapril 10- 20 mg PO BID

31. 2) Angiotensin-II Receptor
blocker- These drugs are
useful in patients who cannot
tolerate ACE inhibitors due to
different side effects like
cough angioedema and
lukopenia.
Lasortan: Dose: - 25-50 mg once
0r twice daily
3) Beta Adrenorecepter blockers
Administration of these drugs with
gradually increasing dose has
been reported to improve
symptoms of heart failure, the
need for hospitalization and
reduce mortality. They are
indicated to moderately severe
heart failure.
• They are not indicated in
unstable heart failure ,
hopotensive states , severe fluid
overload , sinus bradycardia , AV
block and asthma.
Metoprololol: Initial dose 6.25
mg PO BID Maximum dose: 75
mg PO BID