Heart Failure

Presented by:
Dr Kukoyi Babatunde
House Officer
Sacred Heart Hospital, Lantoro

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Outline

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Objectives
Definition
Epidemiology
Relevant Anatomy and Physiology
Classification
Pathogenesis
Clinical Features
Investigations
Differential Diagnosis
Management
Prognosis
Prevention
Conclusion
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Objectives

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To improve the
understanding the basic
mechanism of progression of
heart failure
To enumerate the required
investigations in heart failure
and their importance
To highlight treatment
modalities and algorithm for
instituting treatment

Definition
Heart failure can be defined as a
condition in which the heart is unable
to pump blood at a rate that meets
the requirements of metabolizing
tissues, or can only do so at filling
pressures that are higher than
normal.

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Epidemiology
More than 20 million people have heart failure
worldwide
The overall prevalence of HF in the adult
population in developed countries is 2%. HF
prevalence follows an exponential pattern, rising
with age, and affects 610% of people over age
65
The lifetime risk of developing HF is one in five
in adults over 40yrs
Every year in the USA, more than 550,000
individuals are diagnosed with HF and nearly
300,000 deaths annually are directly attributable
to HF
HF has accounted for 34 of 303 (11.2%) recorded
admissions to the Medical ward of SHHL this year
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Epidemiology
In industrialized countries, coronary artery disease
(CAD) has become the predominant cause in men and
women and is responsible for 6075% of cases of HF
Very little is known about the prevalence or risk of
developing HF in emerging nations because of the
lack of population-based studies in those countries
However in a recent study known as the Subsaharan
Survey of acute heart failure conducted between
2007 and 2010, heart failure was most commonly due
to hypertension and rheumatic heart disease.
Ischemic heart disease was not found to be a
common cause of AHF

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Relevant Anatomy and

Definitions Physiology

- Stroke Volume: Amount of blood pumped out

of each ventricle per heartbeat. (about
70mls in an average resting heart)
- Cardiac Output: The amount of blood
pumped by the heart per minute (5L/min)
- Preload: Refers to the degree to which the
heart muscle is stretched before contraction
i.e end diastolic volume
- Afterload: Resistance against which blood is
expelled
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Relevant Anatomy and

Phyisology
Ejection Fraction: Fraction of blood that is
pumped out of the ventricle during systole to the
volume of blood in the ventricle at the end of
diastole
Frank Starling Law of the Heart: Energy of
contraction is proportional to the initial length of
cardiac muscle fibre
S1: Closure of mitral and tricuspid valves
S2: Closure of aortic and pulmonary valves
S3: Rapid ventricular filling
S4: Atrial contraction against stiff ventricles
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Relevant Anatomy and

Physiology

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Relevant Anatomy and

Physiology

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Relevant Anatomy and

Physiology

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Classification of Heart
Failure
1. Systolic and Diastolic heart failure
. Systolic heart failure: Inability of the ventricle to
contract well leading to reduction in Cardiac
output
. Diastolic heart failure: Inability of the ventricles
to relax normally leading to increased filling
pressure
2. Left sided, Right sided heart failure and
biventricular heart failure
3. Acute Heart failure and Chronic heart failure
4. High output and low output heart failure

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NYHA Classification according to severity

Class I: Patients with cardiac disease but
without resulting limitation of physical activity
Class II: Patients with cardiac disease resulting
in slight limitation of physical activity
Class III: Patients with cardiac disease
resulting in marked limitation of physical
activity
Class IV: Patients with cardiac disease
resulting in inability to carry on any physical
activity without discomfort
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Aetiology

Major Causes
Ischemic heart disease
Cardiomyopathies
Hypertension

Other Causes
Valvular heart disease Mitral, tricuspid, aortic
Congenital heart disease ASD, VSD
Alcohol and drugs Chemotherapeutic drugs eg Imatinib
High output states Anemia, Thyrotoxicosis, Pagets
disease, Hemochromatosis
Pulmonary hypertension and embolism
Infections Chagas Disease, Rheumatic heart disease
Arrhythmias
Pericardial disease Constrictive pericarditis, Pericardial
effusion
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Pathogenesis
an index event either damages the heart
muscle, with a resultant loss of functioning
cardiac myocytes, or, alternatively, disrupts
the ability of the myocardium to generate
force, thereby preventing the heart from
contracting normally
Regardless of the nature of the inciting event,
the feature that is common to each of these
index events is that they all in some manner
produce a decline in the pumping capacity of
the heart
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Pathogenesis

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Pathogenesis
The heart is able to adapt to reduced myocardial
contractility or increased hemodynamic burden by
several neurohumoral compensatory mechanisms.
(1)release of the neurotransmitter norepinephrine by
the sympathetic nervous system
(2)activation of the renin-angiotensin-aldosterone
system, and
(3) release of vasodilatory molecules, including the
atrial and brain natriuretic peptides (ANP and
BNPatrial natriuretic peptide (ANP).
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Pathogenesis
These ultimately lead to Left
Ventricular remodeling which include
1. Ventricular dilatation and wall
thinning
2. Myocyte hypertrophy, necrosis and
apoptosis
3. Increased collagen synthesis
4. Alterations in contractile properties
of the myocytes
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Clinical Features

Symptoms
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnea
Cough
Easy fatigability
Limb swelling, abdominal swelling or generalized body
swelling
Anorexia, nausea, and early satiety
confusion, disorientation, and sleep and mood disturbances
Weight loss
Yellowish discoloration of the eyes

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Signs (Examination findings)

General Examination
Cyanosis
Peripheral edema
Jaundice
Chronic ill look

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Systemic Examination

Cardiovascular System
- Pulse: Sinus tachycardia, diminished pulse pressure
- B.P: Systolic B.P may be normal/high in early HF, but it
generally is reduced in advanced HF
- JVP: Normal in early HF but abnormally elevated in advanced HF
- Heart:
Displaced apex beat
Heaving apical impulse/ Right parasternal heave
S3 or S4 may be present
Murmurs may also be present
Respiratory system
- Obvious respiratory distress
- Crepitations (rales) can be heard especially at the bases of the
lungs
Abdominal examination
- Tender hepatomegaly
- Ascites

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Investigations

Laboratory Investigations
Full Blood Count
E/U/Cr
Fasting blood glucose
Retroviral screening
Fasting lipid profile
BNP
Liver function tests

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Investigations
Radiological investigations
- Chest X-ray
- ECG
-Echocardiogram
-Coronary angiography
-Endomyocardial biopsy

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Framingham Criteria for CCF

Major Criteria
Paroxysmal Nocturnal Dyspnoea
Crepitations
S3 gallop
Cardiomegaly
Increased central venous pressure
Weight loss 4.5kg in 5days in response to treatment
Neck vein distention
Acute pulmonary edema
Hepatojugular reflux

Minor Criteria
- Bilateral ankle edema
- Dyspnoea on exertion
- Tachycardia
- Decrease in vital capacity
- Nocturnal cough
- Hepatomegaly
- Pleural effusion
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Differential diagnosis

Renal failure
Liver disease
Acute bronchial asthma
Pulmonary tuberculosis
Acute Respiratory distress syndrome

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Management of Acute Heart Failure

This is an emergency, usually manifests as acute pulmonary
edema presenting with dyspnea, orthopnoea cough
productive of frothy sputum
Important steps in management include
- Admit patient
- Place in cardiac position
- Administer 100% Oxygen
- Intravenous Furosemide 40-80mg
- IV Diamorphine 2.5mg- 5mg slowly
- Glyceryl trinitrate spray 2 puffs or GTN tablets (2 0.3mg tabs)
- If patient is worsening, repeat IV Furosemide 40-80mg
- For systolic BP less than 100mmHg, manage as Cardiogenic
Shock

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Management of Chronic Heart

Failure
Lifestyle Modification
Pharmacological Therapy
Non Pharmacological (Surgical
therapy)

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Lifestyle Modification
Patient education Avoidance of exacerbating
factors eg NSAIDs, CCBs and antiarrhythmics
Optimize weight (BMI)
Salt restriction
Smoking cessation
Alcohol reduction/ cessation
Physical activity
Fluid restriction
Sexual activity
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Pharmacological Therapy
Drugs that improve symptoms
Drugs that reduce mortality (prevent disease
progression)
A. Diuretics
-. Loop Diuretics e.g Furosemide, Bumetanide, Torsemide
-. Thiazides e.g Hydrochlorthiazide, Metolazone
-. Aldosterone antagonists eg Spironolactone, Eplerenone
They improve symptoms of heart failure particularly
congestive symptoms and signs of elevated filling
pressure

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Phamacological Therapy
B. ACE-inhibitors e.g Lisinopril, Enalapril
They prevent or stabilize cardiac remodeling
Useful in both symptomatic and
asymptomatic patients
Reduces mortality due to HF
C. B-blockers eg Carvedilol, Metoprolol
beta blockers reverse the process of LV
remodeling, improve patient symptoms,
prevent hospitalization, and reduce mortality
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Pharmacological Therapy
D. Digoxin
It helps symptoms of heart failure.
Indicated in patients with atrial
fibrillation and heart failure and in
those with depressed ejection fraction.
E. Vasodilators
Hydralazine + Isosorbide dinitrate can
be given to patients intolerant of
ACEi/ARBs.
Reduces mortality in black patients
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Other Medications
Anticoagulants
Statins
Antiplatelets

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Non Pharmacological
Therapy
Revascularization procedures
Biventricular pacemaker or
implantable cardioverterdefibrillator
Left ventricular assistive devices
Cardiac Transplantation

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Refractory/Intractable heart
failure
Persistence of symptoms that limit daily life
(NYHA III or IV) despite optimal previous
treatment with drugs of proven efficacy for the
condition.
- Reassess the cause
- Reassess the drugs- compliance and dosage
- Strict bed rest, Na and fluid restriction,
diuretics
- Opiates and IV nitrates
- IV inotropes are given in extreme conditions
- Consider for Cardiac transplant
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- Palliative care may be necessary

Prognosis
Mortality following hospitalization for patients
with heart failure is 10.4% at 30 days, 22% at 1
year, and 42.3% at 5 years
Each rehospitalization increases mortality by
about 20-22%.
Mortality is greater than 50% for patients with
NYHA class IV.
Heart failure associated with acute MI has an
inpatient mortality of 20-40%
Mortality approaches 80% in patients who are
also hypotensive (eg, cardiogenic shock)
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Prevention of Heart Failure

Primary prevention
- Involves preventing the development of causal heart
disease and preventing the progression of established
cardiac disease to heart failure.
- The role of smoking, cholesterol, sedentary lifestyle
- Antihypertensive therapy
- Improved socioeconomic conditions and antimicrobial
therapy
- ACE inhibitor therapy has been shown to reduce the
risk of developing heart failure and to improve survival.
Secondary Prevention
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Tertiary Prevention

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Conclusion
Heart failure is a relatively common
condition especially in our
environment.
Early recognition of risk factors and
appropriate treatment by physicians
would help to both prevent and
reduce the morbidity and mortality
from the disease.
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References
The Causes, Treatment, and Outcome of Acute
Heart Failure in 1006 Africans From 9 Countries:
Results of the Sub-Saharan Africa Survey of Heart
Failure
Bui, AL; Horwich, TB; Fonarow, GC (January
2011). Epidemiology and Risk profile of heart
failure Nature Reviews Cardiology8(1): 3041.
Concise Guide to the Management of heart failure
WHO/CGC Task force on heart failure education
Harrisons Principle of Internal Medicine 18th
Edition
Kumar & Clarks Clinical Medicine
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Review of Medical Physiology William F Ganong 43

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