2. objectives
To define HF
To classify HF
To discuss clinical presentation and complications of HF
To discuss examination and investigations
To discuss management of HF
3. DEFN
Heart failure is defined as the pathophysiologic state in
which impaired cardiac function is unable to maintain an
adequate circulation for the metabolic needs of the tissues
of the body.
It may be acute or chronic.
The term congestive heart failure(CHF) is used for the
chronic form of heart failure in which the patient has
evidence of congestion of peripheral circulation and of
lungs.
CHF is the end-result of various forms of serious heart
diseases.
4. CAUSES OF HEART FAILURE
Intrinsic pump failure. (weakening of heart muscle) due to
Ischemic heart disease, myocarditis, metabolic disorders,
fibrillations, flutter)
Increased workload which increases myocardial demand. May be
pressure load (systemic/pulmonary arterial HTN, valvular stenosis,
lung diseases) or volume load(valvular insufficiency, severe
aenemia, thyrotoxicosis, arteriovenous shunts, hypoxia in lung
disease)
Impaired filling of cardiac chambers (cardiac tamponade,
constrictive pericarditis)
5. CAUSES
Systolic dysfunction (EF<40%). –ischemia, HTN, drugs(anthracyclines,
cyclophosphamide)
Diastolic dysfunction – massive Left ventricular hypertrophy, myocardial
fibrosis, amyloid deposition, constrictive pericarditis and restrictive
cardiomyopathy. – common in elderly women and diabetics
Valve dysfunction – endocarditis (viral, bacterial rheumatic heart disease,
calcifications)
Fluid or pressure overload in a normal heart
Increased demand e.g. hyperthyroidism and anaemia
6. Types of heart failure
Acute or chronic
Right sided or left sided
Forward or backward
HF with reduced EF and HF with reserved EF, MID range
7. Acute vs chronic heart failure
Acute Chronic
Sudden and rapid onset
No oedema but has hypotension
Can occur in large MI, valvular
rupture, cardiac tamponade, massive
pulmonary embolism, acute viral
myocarditis, acute bacterial toxaemia
Slow dev’t
Has oedema
Develops compensatory mechanisms
like tachycardia, cardiac dilation,
hypertrophy to maintain CO
May be due to myocardial ischemia
from atherosclerotic coronary artery
disease; multivalvular heart disease,
systemic HTN; chronic lung disease.
8. Left Vs Right sided HF
Left Right
Due to stress on left heart chambers
Causes are; systemic HTN, mitral or
aortic Valvular stenosis; Ischemic heart
disease; myocarditis; restrictive
pericarditis
Pulmonary congestion(dyspnea);
reduced tissue perfusion(kidney, brain,
skeletal muscles)
More as consequence of left sided HF
Also due to intrinsic lung disease
,Pulmonary or tricuspid valvular
disease, Pulmonary HTN 2 to
thromboembolism, Myocardial
disease, Congenital heart disease(left-
right shunt)
Present systemic venous
congestion(edema), cyanosis, coldness
of extremities
9. Backward Vs Forward HF
Backward Forward
The ventricles fail to eject blood
normally so there is increase in end-
diastolic volume and increase in atrial
volume and pressure that is
transmitted to backward to the veins.
Manifestations result from failure of
heart to pump blood causing
hypoperfusion of tissues like kidney
which activates the RAAS
10. Presentation:
Infants and young children
Respiratory distress with rapid respiration, cyanosis,
wheezing, subcostal, intercostal, and sternal recession
Rapid pulse, gallop rhythm, excessive sweating
Tender hepatomegaly
Difficulty with feeding
Cardiomegaly
11. Presentation
Older children and adults
Palpitations, shortness of breath, exercise intolerance
Fatigue, orthopnea, exertional dyspnoea, wheezing
Rapid pulse, gallop rhythm
Raised jugular venous pressure (JVP)
Dependent oedema, enlarged tender liver
Basal(fine) crepitations only in inspiration course r in both esp in
pneumonia
17. Management of heart failure
Bed rest with head of bed elevated
Prop up patient in sitting position
Reduce salt intake and limit fluid intake(1-1.5L/day)
Surgery e.g. coronary artery bypass, valve repair/replacement, heart
transplant
Medical devices e.g. VADs, Implantable cardioverter-defibrillators (ICDs),
Cardiac resynchronization therapy (CRT), or biventricular pacing
Manage other underlying causes accordingly
18. Drugs used
ACE inhibitors ; inhibit formation of angiotensin ll and diminish the
inactivation of bradykinin e.g. captopril, fosinopril, enalapril
Dose; enalopril(2.5mg once daily), captopril(6.25-12.5mg 8-12hourly)
Contraidicated in pregnancy
Angiotensin receptor blockers ; competitive antagonists of angiotensin ll type
l receptor e.g. valsartan, losartan. (Are contra indicated in pregnancy)
Aldosterone antagonists; e.g. spironolactone, eplerenone. Indicated in
patients with severe HFrEF
Dose; spirinolactone(25-50mg/day) k+ greater than 5(contraindicated)
all Prolong survival
19. Drugs cont’d…
Beta- blockers e.g. bisoprolol, carvedilol, metoprolol succinate. Decrease
HR, remodelling and cell death
Dose: carvedilol (3.125mg 12hourly)
Diuretics; reduce pulmonary congestion and peripheral oedema (reduce
orthopnea and PND). loop diuretics (furosemide) are commonly used
Dose; furosemide (20-40mg oral/IV 12hourly)
Positive Inotropic drugs e.g. digoxin. Low drug concentrations are used
in severe HFrEF
Dose; 125-250microgram/daily
Vaso dilators e.g. nitrates and venodilators e.g. hydralazine or
hydralazine/isosorbide dinitrate.
20. Order of therapy
Loop duiretics
ACE inhibitors/ARBs and beta-blockers
Digoxin,spironolactone,hydralazine/isosorbide dinitrate
Management of chronic heart failure
• Periodic monitoring of body weight, BP, respiratory rate and O2
saturation
• Salt and fluid restriction
• Limit alcohol intake
• Regular exercise within limits of symptoms
• Continued treatment with medicines listed above
21. Refernces:
Uganda clinical guidelines 2016.
Davidsons Principles and Practice of Medicine, 22nd edition, pg
Harsh Mohan - Textbook of Pathology, 6th Edition
Editor's Notes
Presenting complaint
Review of other systems
Medical history
Socio– family history
Examinations (cvs, rs, cns)