3. The condition in which an abnormality of cardiac
structure or function is responsible for the
inability of the heart to fill with or eject blood at
a rate commensurate with the requirements of
the metabolizing tissues.”
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
4. 1. Systolic versus Diastolic
2. Low-output versus High-output
3. Right-sided versus Left-sided
4. Acute versus Chronic
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
5. Systolic Heart Failure = The principle abnormaility
is the inability of the ventricle to contract
normally and expel sufficient blood
Diastolic Heart Failure = The principle abnormality
is the inability of the ventricle to relax and fill
normally
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
6. Low-Output Heart Failure = Occurs in patients with a
primary abnormality in the heart’s ability to discharge
enough blood/nutrients to the arterial system
High-output Heart Failure = Occurs in patients with
reduced systemic vascular resistance. Etiologies
include hyperthyroidism, severe Anemia, AV fistula,
pregnancy and beriberi
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
8. Baroreceptor mediated increase in sympathetic
tone in heart failure results in tachycardia,
arterial and venous constriction
Increased local and circulating concentrations of
norepinephrine cause myocyte hypertrophy
and apoptosis
Via renal venoconstriction the sympathetic
nervous system stimulates the renin-
angiotensin-aldosterone system
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
9. 1. Angiotensin II promotes cardiac remodeling
2. Angiotensin II causes arterial
vasoconstriction increasing afterload
3. Angiotensin increases aldosterone secretion
and proximal tubular sodium transport
4. Aldosterone also promotes cardiac
remodeling
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
10. 1. Activation of carotid baroreceptors results in
sympathetic stimulation of the supraoptic and
paraventricular nuclei in the hypothalamus
which results in the release of vasopressin
2. Vasopressin is an antidiuretic agent and causes
free water retention
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
12. Hypertensive heart
disease
Ischemic Heart
Disease
Cardiomyopathies
(dilated, hypertrophic,
and restrictive.
Pericardial disease
(tamponade,
constriction.
Valvular Heart
disease.
Arrythmias
High output causes
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
13. 1. Infection
2. Arrhythmias
3. Physical, Dietary, Fluid, Environmental, and Emotional Excesses
4. Myocardial Infarction
5. Pulmonary Embolism
6. Anemia
7. Thyrotoxicosis and Pregnancy
8. Aggravation of Hypertension
9. Rheumatic, Viral, or Other Forms of Myocarditis
10. Infective Endocarditis
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
14. 1. Dyspnea
2. cough
3. Orthopnea
4. Paroxysmal Nocturnal Dyspnea
5. Cheyne-Stokes respiration
6. Fatigue and weakness
7. Anorexia and nausea associated with abdominal pain
and fullness
8. Nocturia
9. Confusion, difficulty in concentration, memory
impairment, headache, insomnia, anxiety
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
17. Major Criteria ( CRAP-PINS)
1. Cardiomegaly
2. Rales
3. Acute pulmonary edema
4. PND
5. Positive hepato Jugular
reflex HJR
6. Increased venous pressure
7. Neck vein
8. S3 gallop
Minor Criteria ( Enehpvt)
1. Extremity edema
2. Night cough
3. Exertional dyspnea
4. Hepatomegaly
5. Pleural effusion
6. Vital capacity reduced by
1/3 from normal
7. Tachycardia ≥120 bpm
1major+2minor=Dx
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
18. 1. Class I: symptomatic only with greater than
ordinary activity
2. Class II: symptomatic with ordinary activity
3. Class III: symptomatic with minimal activity
4. Class IV: symptomatic at rest
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
19. 1. Chest Xray = Cardiomegaly, pulmonary vascular
congestion, pleural effusions, Kerley B lines
2. ECG = Will aid in evaluating for ischemia, or
structural changes in heart,arrythmias,chamber
enlargement.
3. Echocardiogram = Will aid in determining
underlying etiology and severity of ventricular
systolic and/or diastolic dysfunction.
4. Labs: BUN, Cr, Na, abnormal LFTs, CBC,
cardiac enzymes.
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
22. Avoid overtreatment: Hypovolemia
CO impaired renal function
weakness and lethargy
Thiazide Diuretics
Reduce reabsorption of Na+
and Cl- in distal convoluted
tubule (H2O follows salt)
Watch out for K+ depletion and
metabolic alkalosis
Use by themselves for mild HF
or in combination w/ other
drugs for severe HF
Loop Diuretics
Reversibly inhibit
reabsorption of Na+, K+,
and Cl- in the thick
ascending loop of Henle.
Metabolic alkalosis and
hypokalemia
Useful for all forms of HF
Potassium-Sparing Diuretics
Block exchange between
Na+ and both K+ and H+ in
distal tubules and cortical
collecting ducts Na+
diuresis and K+ retention
Weak, not good as sole
agents
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
23. Thiazide and Loop diuretics provide symptomatic
relief but there is no known mortality benefit
Spironolactone does have a mortality benefit
although it is a weak diuretic; In RALES trial
published in NEJM in 1999 a 30% decrease in
mortality was noted in Class III or IV heart failure
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
24. Chronic activation of renin-angiotensin-aldosterone system in
HF causes:
1. Ventricular remodeling
2. Further deterioration of cardiac function
3. Potentially fatal arrhythmias
ACEI
Produce vasodilation (limit angiotensin II-mediated vasoconstriction)
aldosterone sodium retension
Inhibit degredation of bradykinins bradykinin levels synthesis
of prostaglandins and NO
Careful: may induce hypotension! Start slowly.
Watch for azotemia, K+, cough, angioedema
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
25. If a patient can not tolerate an ACE-I or ARB secondary to
azotemia, hyperkalemia or cough hydralazine + nitrates
should be used as a 25% decrease in mortality was
shown with these drugs in the V-HeFT trial published in
the NEJM.
1. Arteriodilators (e.g. hydralazine afterload
2. Venodilators (e.g. nitrates) preload
3. Combination of these maximal benefit
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
26. CHF chronically catecholamines and
sympathetic nervous system progressive
myocaridal damage LV function and LV
dilation
-blockers EF (will transiently ) LV size
and mass
Contraindicated in decompensated CHF
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
27. Metoprolol bisoprolol and carvedilol have been
shown to improve survival in patients with heart
failure.
Carvedilol also is an alpha receptor blocker and
thus causes mild vasodilation. It is the most
studied drug and preferred B blocker in heart
failure patients.
Must be titrated very carefully and is
contraindicated in decompensated CHF
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
28. Increases myocardial contractility
No mortality benefit but decreases hospital
admissions for CHF
No use in diastolic heart failure, hypertophic
cardiomyopathy
Prefered in systolic HF
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
29. Inotropic agent
Electrophysiologic effects: enhanced cardiac
parasympathetic tone delayed AV conduction and
sinus node automaticity
intracellular Ca+ and Na+ may myocyte excitability and
ventricular arrhythmias
Reduces symptoms and hospitalizations but not mortality
Check blood levels after 7-14 days and monitor for digoxin
toxicity
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
30. 1. Discuss pathogenesis of ascites in ccf
2. Clinical presentation of left heart failure
3. Action of digoxin and its symptoms of toxicity
4. Management of acute heart failure
5. Contraindications of ACEI
6. Outline management of heart failure.
mwebazavictor1997@gmail.com DR
MWEBAZA VICTOR
