Heart Failure
DR ST DODIYI-MANUEL
Outline
Introduction
Aetiology
Pathophysiology
Clinical features
Investigation
Treatment
Prognosis
Conclusion
Introduction
Heart failure is a clinical syndrome due to a
structural and or functional cardiac disorder
that results in impaired ability of the heart to
function as a pump to meet the physiologic
demands of the body.
Introduction
Heart failure is a clinical syndrome consisting of
cardinal symptoms ( breathlessness, ankle swelling
and fatigue) that may be accompanied by signs( eg
elevated jugular venous pressure, pulmonary crackles
and peripheral edema) that is due to a structural
and or functional abnormality in the heart that
results in elevated intracardiac pressures and /or
inadequate cardiac output at rest and or during
exercise.
Heart failure(HF) is defined as a clinical syndrome
with symptoms and/or signs caused by a structural
and/or functional cardiac abnormality and
corroborated by elevated natriuretic peptide
levels and/or objective evidence of pulmonary
or systemic congestion.
introduction
The incidence of HF increases with age.
It is commoner in blacks than in Caucasians.
It accounts for 3 – 7% of hospital admissions in
Africa.
Aetiology
COMMON CAUSES
Hypertension
Rheumatic heart disease
Cardiomyopathy ( Dilated)
Aetiology
LESS COMMON CAUSES
Ischemic heart disease
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Constrictive pericarditis
Pericardial effusion
Cor pulmonale
Fluid overload
Myocarditis
Risk factors
Arrhythmias – atrial fibrillation
Infections - Pneumonia, Infective endocarditis
Anaemia
Thyrotoxicosis
Pulmonary embolism
Pregnancy
Drugs – poor drug adherence
ingestion of steriods, NSAIDS
Classification
1. Based on onset- Acute/ Chronic heart failure
2. Based on anatomical location- left/ right/
biventricular heart failure
3. Based on Phenotypes- HFrEF < 40%, HFmrEF 41 -
49%. HFpEF ≥ 50%
4.High output/Low output failure
5.Based on the New York heart association
Class I: No limitation of physical activity
Class II: Slight limitation of physical activity
Class III: Marked limitation of physical activity
Class IV: Symptoms occur even at rest; discomfort with
any physical activity
6. American heart association classification
Stage A: High risk of heart failure but no structural heart
disease or symptoms of heart failure
Stage B: Structural heart disease but no symptoms of heart
failure
Stage C: Structural heart disease and symptoms of heart
failure
Stage D: Refractory heart failure requiring specialized
interventions
OTHER CLASSIFICATIONS
6. KILLIP Classification in myocardial infarction
Killip class 1 – individuals with no clinical signs of heart
failure
Killip class II – individuals with rales or crackles in the lung,
S3 gallop, and elevated JVP
Killip class III- individuals with frank acute pulmonary edema
Killip class IV- individuals in cardiogenic shock or
hypotension(SBP < 90mmHg) &evidence of low C.O.
(oliguria, cyanosis or impaired mental status)
Pathophysiology
Initially these mechanisms are able to restore the
heart function to normal.
However with sustained activation of these systems,
end organ damage within the ventricles occurs with
subsequent decompensation.
Pathophysiologic changes
Ventricular dilatation
Myocyte hypertrophy
Activation of renin angiotensin aldosterone
system(RAAS)
Activation of the sympathetic nervous system
Release of BNP, ANP
Release of anti diuretic hormone(ADH)
Release of endothelin & NO
Frank starlings law suggests that as diastolic volume
increases and cardiac myocytes stretch the cardiac
output increases proportionately.
This continues until it exceeds its elastic limit when
further stretches in the cardiac myocyte only brings
about a progressive decline in cardiac output.
RAAS
↓Renal perfusion →Renin
↓
Angiotensinogen → Angiotensin 1
ACE ↓
Angiotensin II
↙ ↘
Vasoconstriction Aldosterone
↓
Na + H₂O
retention, cardiac
remodeling, fibrosis, apoptosis
Activation of sympathetic nervous
system
↓CO ↓BP → ↓Baroreceptor activity
↓
↓Inhibition of VMC
↓
↑VMC activity
↓
Release of cathecholamines (NE,E)
↙ ↘
vasoconstriction ↑ Heart rate
Release of ANP & BNP
Atrial natriuretic peptide
Released from atrial myocytes in response to stretch
It induces diuresis & vasodilatation
Suppresses RAAS but in HF renal response to ANP is poor
Brain natriuretic peptide
Released mainly from ventricles
Similar action to ANP
Has great diagnostic & prognostic value
ARNI
Neprilysin breaks down
vasoactive peptides
angiotensin 1, ii
bradykinin
natriuretic peptides
Release of ADH
↓Blood volume
↑ECF osmolarity
Activation of osmoreceptors in hypothalamus
Release of ADH from post pituitary
↑Reabsorption of water@ DCT & collecting ducts
Release of endothelin and nitric
oxide
Endothelin
Potent vasoconstrictor released from endothelium in HF in response to
hypoxia cathecholamines & angiotensin
Nitric oxide (EDRF)
Potent vasodilator released from endothelium
Its effect is blunted in HF
Pathophysiology
Heart failure begins after an index event produces an
initial decline in the hearts pumping ability.
Following this decline various compensatory
mechanisms are activated, including the renin
angiotensin aldosterone system, the sympathetic
nervous system etc.
Clinical features
Exertional dyspnea and/or dyspnea at rest
Orthopnea
Chest pain/pressure and palpitations
Tachycardia
Fatigue and weakness
Nocturia and oliguria
Clinical features
Anorexia, weight loss, nausea
Exophthalmos and/or visible pulsation of eyes
Distention of neck veins
Weak, rapid and thready pulse
Rales, wheezing
S3 gallop and/or pulsus alternans
Increased intensity of P 2 heart sound
Hepatojugular reflux
Ascites, hepatomegaly, and/or anasarca
Central or peripheral cyanosis, pallor
STAND UP AND
STRETCH.
TOO EARLY TO
SLEEP
Investigations
Chest radiograph- Alveolar edema
Kerly B lines
Cardiomegaly
Upper lobe Diversion
Pleural Effusion
Electrocardiogram - Arrhythmias, LVH/RVH, Atrial enlargement
Echocardiography- confirm diagnosis, identify the cause, thrombi,
Investigations
N terminal pro B- type natriuretic peptide
B- type natriuretic peptide
Full blood count
Renal and liver function test
Electrolyte levels
Fasting lipid profile
Thyroid function test
Urinalysis
Iron studies
AIM OF TREATMENT
To relieve symptoms.
Treat underlying causes and precipitants.
To retard the progression of the disease.
To prevent complications/co morbidities
Treatment
NON PHARMACOLOGIC THERAPY
Stop smoking
Reduction in alcohol consumption
Diet rich in fruits & vegetables
Increased physical activity
Reduced dietary sodium
Treatment
Loop diuretics – Frusemide, bumetamide
S/E- hypokalaemia,hyperuricaemia,glucose intolerance,myalgia,
ototoxicity
Thiazide diuretics – hydrochlorothiazide, bendroflumethiazide
S/E hyperuricaemia, hyponatraemia. Glucose intolerance
Aldosterone antagonists– Spirinolactone, eplerenone (no
gynaecomastia )
S/E hyperkalaemia, gynaecomastia
Angiotensin converting enzyme inhibitors ACEIs- Lisinopril,
enalapril, ramipril, perindopril
S/E cough, hypotension, hyperkalaemia, angioedema
Angiotensin 2 receptor blockers(ARB) – Losartan, valsartan,
telmisartan, olmesartan
S/E hyperkalaemia, hypotension, angioedema
Betablockers – bisoprolol, atenolol, metoprolol, carvedilol
S/E bradycardia, airway obstruction
Angiotensin receptor Neprilysin inhibitor
Sacubitril/Valsartan – PARADIGM HF Study
Used in HFrEF patients in NYHA-II- IV, allow 36hrs wash out in patients
ACEI/ARB
C/I – Severe liver disease, pregnancy, angioedema to ACEI/ARB
S/E- Hyperkalaemia, renal impairement, hypotension, angioedema
DRUG TREATMENT CONT.
CARDIAC GLYCOSIDES– Digoxin (foxglove plant)
S/E arrhythmias ,heartblock, confusion, insomnia, agitation, xanthopsia,
delirium, nausea
VASODILATORS AND NITRATES- hydralazine and isosorbide dinitrate
Used in patients allergic to ACEI/ARB
S/E hypotension
Treatment
PHARMACOTHERAPY
Inotropic agents- dopamine, dobutamine
Anticoagulants- heparin,
I(f) inhibitors- Ivabradin
Sodium glucose transporter inhibitors- inhibit renal tubular glucose
reabsorption without insulin release- Canagliflozin,
dapagliflozin,empagliflozin
Non pharmacological therapy
Ventricular assist devices
Biventricular pacing - CRT
Implantable cardioverter defibrillator
Continuous flow pumps- Impella CP
Cardiac transplantation
Cardiac resynchronization syndrome/
biventricular pacing
Presence of sinus rhythm
Class II, III, or ambulatory class IV symptom despite good medical
therapy
LVEF less than or equal to 35%
QRS more than 150ms (especially if left bundle branch block
morphology is present)
DUAL CHAMBER PACING
ICD
IMPLANTABLE CARDIOVERTER
DEFIBRILLATOR: RECOMMENDATIONS
Secondary prevention (cardiac arrest survivors of
VT/ventricular fibrillation [VF], hemodynamically unstable
sustained VT)
Structural heart disease and sustained VT, whether
hemodynamically stable or unstable
Syncope of undetermined origin with hemodynamically
significant sustained VT or VF induced at electro physiologic
study
LVEF less than or equal to 35% at least 40 days after MI and
NYHA functional class ll or lll
LVEF less than 30% at least 40 days after MI and NYHA
functional class l
LVEFless than or equal to 35% despite
medical therapy in patient with non
ischaemic cardiomyopathy and NYHA
functional class ll and lll
Nonsustained VT caused by prior MI,
LVEF less than 40%, and inducible VF or
sustained VT at electrophysiologic study
MGT OF ACUTE PULMONARY EDEMA
Admit patient
Sit patient upright/in cardiac position
Give 60 – 100% oxygen
Diamorphine 2.5 – 5mg IV slowly
IV Frusemide 80mg
ACEI/ARA
Aldosterone antagonists
Digoxin
Anticoagulation – heparin to prevent DVT
THANK YOU
