This is a practical approach to the description of heart failure as well as the approach to the management of the same condition.

1. HEART FAILURE
DR KD DELE
DEPT OF FAMILY MEDICINE DORA NGINZA HOSPITAL

2. DEFINITION
• Heart failure is “a complex clinical syndrome that can result from any
structural or functional cardiac disorder that impairs the ability of the
ventricle to fill with or eject blood.” (AHA/ACC)
• Heart failure can be defined as an abnormality of cardiac structure or
function leading to failure of the heart to deliver oxygen at a rate
commensurate with the requirements of the metabolizing tissues (despite
normal filling pressures or only at the expense of increased filling pressures).
American Heart Association (AHA) and the American College of Cardiology (ACC),

3. INTRODUCTION
• HF is a silently progressive condition.
• HF is increasing in prevalence.
• Prevalence of HF increases with age, to up to about 90.1 in 1000 among patients
over 85 years.
• Many of the symptoms of HF are non-specific.
• HF has a large impact on quality of life, including physical activities and
psychological distress. Comorbidities impact prognosis in patients with HF.
• HF places a significant physical and emotional burden on the caregiver.

4. INTRODUCTION
• Heart failure accounts for 5% of admissions to hospital medical wards.
• Mean length of hospital stay increases with each rehospitalisation for HF
• HF severity can be classified based on structure and damage to heart
(ACC/AHA) or based on symptoms or physical activity (NYHA).
• There are many causes of HF that result in ventricular remodelling, reduction of
the left ventricular ejection fraction, and neurohumoral imbalance.
• The prognosis of heart failure has improved recent years, but the mortality rate
is still high with approximately 50% of patients dead at 5 years.

5. THE BURDEN OF HEART FAILURE
• NUMBER of PATIENTS: 21 MILLION adults worldwide are living with heart failure.This
number is expected to rise
• ECONOMIC BURDEN: In 2012, the overall worldwide cost of heart failure was nearly
$108 BILLION
• MORTALITY: 50% of heart failure patients die within 5 years from diagnosis
• REHOSPITALISATION: Heart failure is the NUMBER 1 cause of hospitalisation for
patients aged >65 years
• COMORBIDITIES: The vast majority of heart failure patients has 3 or more
comorbidities

6. EFFECTS ON QUALITY OF LIFE
• Patients with HF commonly report psychological distress, including:
• depression
• hostility and anxiety
• limitation in their activities of daily living
• disruption of work roles and social interaction with friends and family
• reduced sexual activity and satisfaction

7. The Sub-Saharan Africa Survey of Heart
Failure (THESUS-HF)
1006 patients presenting with AHF in 9
African countries
Mean age was 52.3 years, 51%were women
Mean left ventricular ejection fraction was
39.5%
Most commonly due to hypertension 45.4%
Rheumatic heart disease14.3%
Ischemic heart disease 7.7%
The median hospital stay was 7 days
in-hospital mortality of 4.2%.
Estimated 180-day mortality was 17.8%
Comorbidities
Renal dysfunction gfr<30): 7.7%
Diabetes mellitus: 11.4%
Anaemia (hb <10 g/dL): 15.2%
Atrial fibrillation 18.3%
HIV: 13%
Most patients were treated with renin-
angiotensin system blockers but not β-
blockers at discharge. Hydralazine
hydrochloride and nitrates were rarely used.
Damasceno A1, et al (2012).The causes, treatment, and outcome of acute heart failure in 1006 Africans
from 9 countries.Arch Intern Med. 2012 Oct 8;172(18):1386-94

8. AETIOLOGY

9. AETIOLOGY OF HEART FAILURE
• The Main causes of Heart Failure are:
• Ischaemic heart disease (35–40%)
• Cardiomyopathy (dilated) (30–34%)
• Hypertension (15–20%)
• Also: Valvular heart disease and diabetes mellitus.
CURRENT Diagnosis & Treatment in Family Medicine 3RD Edition. By Jeannette E. South-Paul and Samuel C.
Matheny

10. AETIOLOGY OF HEART FAILURE
MYOCARDIAL DISEASE
• Coronary artery disease
• Hypertension
• Cardiomyopathy
VALVULAR HEART DISEASE
• Mitral
• Aortic
• Tricuspid
• Pulmonary

11. AETIOLOGY OF HEART FAILURE
ARRHYTHMIA
• Tachyarrhythmia
• Atrial
• Ventricular
• Bradyarrhythmia
• Sinus node dysfunction
OTHERS
CONDUCTION DISORDERS
(arrhyt..)
• Atrioventricular block
CONGENITAL HEART DISEASE

12. AETIOLOGY OF HEART FAILURE
VOLUME OVERLOAD
• Renal failure
• Iatrogenic (e.g. post-operative
fluid infusion
HIGH OUTPUT STATES
• Anaemia
• Sepsis
• Thyrotoxicosis
• Paget‘s disease
• Arteriovenous fistula

13. AETIOLOGY OF HEART FAILURE
ENDOCARDIAL DISEASE
• With/without hypereosinophilia
• Endomyocardial fibrosis (EMF –
restrictive cardiomyopathies)
PERICARDIAL DISEASE
• Constrictive pericarditis
• Pericardial effusion

14. Main causes for heart
failure:
Hypertensive heart
disease (35 %),
Ischaemic heart
disease (20 %),
Dilated
cardiomyopathy (15 %),
Rheumatic valvular
heart disease (7 %)
1,294 outpatients
Nigeria
(383 patients),
South Africa
(169 patients),
Sudan
(501 patients),
Uganda
(151 patients),
Mozambique
(90 patients)
Participants from Africa:
younger,
lower literacy levels
less likely to have health/
medication insurance
Less likely to be on beta-
blockers
most likely to be in
NYHA class IV.
(compared with
participants from other
regions)
Dokainish H,Teo K, Zhu J et al. Heart failure in Africa,Asia, the Middle East and South America: the INTER-
CHF study. Int J Cardiol. 2016;204:133–41. doi: 10.1016

15. PATHOPHYSIOLOGY

16. DESCRIPTIVE TERMS
• Related to Ejection Fraction: HFrEF (reduced ejection fraction: EF<40%)
HFmEF (mildly impaired EF – EF 40-49%)
HFpEF (preserved EF – EF ≥50%)
• Related to time-course: New onset, transient, chronic
• Related to progression: Acute, stable, worsening/decompensating
• Related to location: Left heart, right heart, combined/congestive
• Half of patients with heart failure will have preserved EF

17. THE ACC/AHA STAGES OF HEART FAILURE
(BASED ON STRUCTURE & DAMAGE TOTHE HEART)
ACC/AHA Stage Symptoms
A At high risk for heart failure but without structural heart disease or
symptoms of heart failure.
B (Development of) Structural heart disease but without signs or symptoms
of heart failure.
C Structural heart disease with prior or current symptoms of heart failure.
(i.e. Symptomatic HF with underlying structural heart disease)
D Refractory heart failure requiring specialized interventions. (Advanced
structural disease. Marked symptoms of HF at rest despite maximal medical
therapy)

18. NYHA FUNCTIONAL CLASSIFICATION
(BASED ON SYMPTOMS & PHYSICAL ACTIVITIES)
NYHA Class
Class I (Mild) No limitation of physical activity.
Ordinary physical activity does not cause undue fatigue, palpitation,
dyspnoea.
Class II (Mild) Slight limitation of physical activity.
Comfortable at rest.
Ordinary physical activity results in fatigue, palpitation, dyspnoea
Class III (Moderate) Marked limitation of physical activity.
Comfortable at rest.
Less than ordinary activity causes fatigue, palpitation, or dyspnoea.
Class IV (Severe) Unable to carry on any physical activity without discomfort.
Symptoms of heart failure at rest.
If any physical activity is undertaken, discomfort increases.

19. PATHOPHYSIOLOGY:
PATHOPHYSIOLOGICAL CHANGES IN HEART FAILURE
When the heart fails,
considerable changes – both
structural and functional –
occur to the heart and
peripheral vascular system
in response to the
haemodynamic changes
associated with heart failure
These include:
Ventricular dilatation
Myocyte hypertrophy
Increased collagen synthesis
Altered myosin gene
expression
Altered sarcoplasmic Ca2+-
ATPase density
IncreasedANP secretion
Salt and water retention
Sympathetic stimulation
Peripheral vasoconstriction
These physiological changes
are compensatory
and maintain cardiac output
and peripheral perfusion.
However, as heart failure
progresses,
these mechanisms
are overwhelmed and
become pathophysiological.

20. PATHOPHYSIOLOGY:
PATHOPHYSIOLOGICAL CHANGES IN HEART FAILURE
The purpose of
compensation is to: maintain
blood pressure and tissue
perfusion.
The loss of beneficial
compensatory mechanisms…
Leads to development of
cardiac decompensation.
These lead to:
Pathological peripheral
vasoconstriction
and sodium retention in
heart failure
by activation of
the renin–angiotensin–
aldosterone system
Main Factors involved are:
Venous return (preload)
Outflow resistance (afterload)
Myocardial deterioration /
contractility (inotropic state)
Neurohormonal and sympathetic
system activation – leads to salt
and water retention
Neurohormones:norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines, act both in an
indirect and in a directly toxic fashion to maintain the vicious cycle

22. NATURAL HISTORY OF HF:
THE CARDIOVASCULAR CONTINUUM
Risk Factors:
Environmental
determinants
Cardiovascular
risk factors
Genetic
determinants
Sedentary lifestyle
Vascular&
Myocardial
Remodelling:
LVH
CAD / Ischemia /
Infarction
Microcirculatory
disturbances
Diastolic
dysfunction
Systolic
dysfunction
Diastolic Heart
Failure
Systolic
Heart Failure
vs congestive
HF is a silently progressing disease
We begin to look at the disorder at the end of its natural history - that is too late!

23. SIGNS & SYMPTOMS

24. SIGNS & SYMPTOMS
• A high index of suspicion is necessary to diagnose the syndrome of heart
failure early in its clinical presentation, because it is frequently manifested
by nonspecific signs and symptoms.
• A prompt diagnosis allows for early treatment with therapies proven to
delay the progression of heart failure and improve quality of life.

25. SYMPTOMS AND SIGNS OF HF
SYMPTOMS
• SYMPTOMS:TYPICAL
• Breathlessness/Dyspnoea
• Orthopnoea
• Paroxysmal nocturnal dyspnoea
• Reduces exercise tolerance
• Fatigue, tiredness and increased time to
recover after exercise
• Ankle swelling/ fluid retention
• Nonspecific symptoms include
• chronic non-productive cough,
• wheezing, and
• nocturia.
• Right ventricular failure :
• right upper quadrant pain 20 to
hepatic congestion and
• peripheral oedema.

26. SYMPTOMS AND SIGNS OF HF
The absence of dyspnoea on
exertion essentially rules
out the presence of heart
failure due to left ventricular
dysfunction in a
predominantly symptomatic
population with a reported
100% sensitivity.
• Paroxysmal nocturnal
dyspnoea (PND) has the
highest specificity of any
symptom for heart failure.
• Likewise, if PND,
orthopnoea, or edema is
not present, the likelihood
of heart failure decreases.
• a detailed history and
review of symptoms
remain the best approach
in identifying the cause of
heart failure and assessing
response to therapy..

27. SYMPTOMS AND SIGNS OF HF
SIGNS
• SIGNS: COMMON
• Third heart sound (gallop rhythm)
• Laterally displaced apex beat
• Cardiac murmur
• Elevated jugular venous pressure
• Hepatojugular reflux
Gallop rhythm (S3 +/- S4) and
displacement of cardiac apex have
been found to be specific
predictors of left ventricular
dysfunction.

28. COMORBIDITIES IN HF
• Comorbidities impact prognosis in patients with HF
• Why comorbidities are relevant in HF:
• Comorbidities may affect the use of treatments for HF
• Drugs used to treat comorbidities may cause worsening of HF
• Drugs used to treat HF and comorbidities may interact and reduce patient
adherence
• Most comorbidities are associated with worse clinical status and are
predictors of poor prognosis in HF

29. COMORBIDITIES IN HF
• Most patients with heart failure patients have about 3 or more comorbidities
• Comorbidities in patients with HF include the following:
Hypertension
Angina
Renal dysfunction
Diabetes mellitus
Hyperlipidaemia
Obesity
COPD
Anaemia
Sleep disturbance
Depression
Gout
Cachexia
Iron deficiency
Cancer

30. DIAGNOSIS OF HF

31. PRINCIPLES OF DIAGNOSIS OF HF
• Consider: Medical history, signs, symptoms
• Confirm: Natriuretic peptides, Echocardiography
• Assess clinical phenotype: HFrEF vs. HFpEF
• Assess aetiology:Angiography, cMRI, Biopsy
• Risk stratification
• Workup for targeted therapies

32. DIAGNOSIS OF HF (ESC)

33. DIAGNOSIS OF HF
• Adequate diagnosis of HF includes screening for cardiac dysfunction in patients at risk,
confirming the clinical suspicion with objective diagnostic measures, and identifying the
underlying phenotype and aetiology.
• The HF diagnosis should be considered at all levels of care, to guide management
decisions.
• Measuring natriuretic peptide levels can help diagnosis.A normal natriuretic peptide level
in an untreated patient virtually excludes significant cardiac disease, making an
echocardiogram unnecessary.

34. ELECTROCARDIOGRAPHY
• Normal ECG = left ventricular systolic
dysfunction unlikely (94% sensitivity)
• Left bundle branch block, (poor
prognostic indicator)
• Atrial fibrillation (predictor of heart
failure in a pt with SOB)
• new T-wave changes (predictor of heart
failure in a pt with SOB)
• Left ventricular hypertrophy
• Evidence of MI
• Any abnormal ECG finding (may
indicate need for echocardiography
tor/o structural abnormality or
possible infiltrative processes)
• Can detect arrhythmias once heart
failure

35. BETA-TYPE NATRIURETIC PEPTIDE (BNP)
Particular relevance of BNP
include:
• diagnosis
• staging
• risk stratification
• monitor/titrate therapy
• admission/discharge
decisions:
• > rule out symptomatic LV
dysfunction
The likelihood of heart failure
increases with BNP levels
greater than 100 pg/mL:
Less than 100 pg/mL:
Negative predictive value high
excluding the diagnosis of
heart failure
consider alternate
diagnoses.
100-400 pg/mL:
Increased likelihood of heart failure;
history, physical examination,and
other tests are required to improve
the probability of the diagnosis.
Greater than 400 pg/mL
Diagnosis of heart failure is highly
likely.
BNP levels are not recommended to
screen or monitor heart failure.
A normal beta-type natriuretic peptide level in an untreated patient virtually excludes significant
cardiac disease.

36. IMAGING STUDIES
Chest Radiography
Venous congestion,
interstitial oedema,
Alveolar oedema,
Cardiomegaly CTR > 50%
Pleural effusion
Hilar haze
Redistribution – upper
lobe pulmonary vein
dilation
Cardiac Doppler
Echocardiography
Left ventricular function
(ejection fraction)
diastolic function
various causes of heart
failure
segmental wall motion
abnormalities
myocardial ischemia etc
Cardiac
Catheterization
For patients with new-
onset heart failure of
uncertain aetiology,
LVSD
strong suspicion of
ischemic myocardium /
abnormalities seen on
non-invasive testing such
as echocardiography or
nuclear imaging)

37. CXR CHANGES IN HF

38. ECHO: NVS DILATED/POOR CONTRACTILITY

39. ECG IN HF
Heart failure patients had
• significant prolonged QRS duration,
• prolonged QT duration,
• significant ECG evidence of prior
myocardial ischaemia,
• intraventricular conduction disorder,
abnormal axis,
• ventricular hypertrophy and
• atrial fibrillation.
They also found myocardial ischaemia,
intraventricular conduction disorder,
atrioventricular disorder, abnormal axis,
atrial enlargement, ventricular
hypertrophy, ventricular arrhythmia and
atrial fibrillation as a predictive model.
All 733 patients attending the rapid
access clinic for possible heart failure in
StVincent’s University Hospital, Dublin,
from the period of 2000 till 2012
S James et al, (2015). 22 Role of 12-lead electrocardiography in predicting heart failure in the community.
https://heart.bmj.com/content/101/Suppl_5/A12.1

40. Mant J et al (2009). Systematic review and individual patient data meta-analysis of diagnosis of heart failure,
with modelling of implications of different diagnostic strategies in primary care. Health Technol Assess. 2009
Dyspnoea : high sensitivity (89%)
History of myocardial infarction (89%)
Orthopnoea (89%)
Oedema (72%)
Elevated jugular venous pressure (70%)
cardiomegaly (85%)
added heart sounds (99%)
lung crepitations (81%)
hepatomegaly (97%)
They however all have low sensitivity for
HF: Eg 11% for added heart sounds, 51%
for dyspnoea, and 53% for pedal oedema
Electrocardiography (ECG),
B-type natriuretic peptides (BNP) and
N-terminal pro-B-type natriuretic peptides
(NT-proBNP)
all had high sensitivities (89%, 93% and 93%
respectively)
Chest X-ray was moderately specific (76-
83%) but insensitive (67-68%).
BNP was more accurate than ECG. diagnostic
odds ratio of ECG/BNP of 0.32

41. DIAGNOSIS
• The diagnosis of heart failure can pose significant challenges in Africa due to lack
of access to appropriate diagnostics.
• Internationally, the minimum approach to the diagnosis of HF are clinical history
and examination, and chest X-ray… +/- ECG depending on availability.
• while objective measurements of cardiac function, such as echocardiography, are
now essential parts of diagnosis eg in European and North American guidelines

42. DIFFERENTIAL DIAGNOSIS
CARDIAC include:
arrhythmia,
anginal / CAD
valvular heart disease
cardiac shunt
OTHERS include:
Anaemia,
Thyrotoxicosis,
Carbon monoxide
poisoning,
NON-CARDIAC include:
Asthma,
COPD,
Infection,
Interstitial lung disease,
Pulmonary embolism,
Obstructive sleep apnoea,
Severe obesity causing
hypoventilation syndrome.

43. TREATMENT

44. TREATMENT OF HF
TREATMENT OBJECTIVES:
Prognosis:
Reduce mortality
Morbidity:
relieve symptoms
Improve QoL
Eliminate oedema and fluid
retention
Increase exercise capacity
Reduce fatigue and breathless
Reduce need for hospitalisation
Provide end of life/hospice care
Prevention:
Occurrence of myocardial
damage
Progression of myocardial
damage
Remodelling of myocardium
Reoccurrence of symptoms
and fluid accumulation
Hospitalization

45. TREATMENT OF HF
• The World Health Organization has targeted that medicines to prevent
recurrent cardiovascular disease be available in 80 % of communities and
used by 50 % of eligible individuals by 2025.
• Four key cardiovascular medications identified are: aspirin, statin,
angiotensin-converting enzyme (ACE) inhibitor and beta-blockers, and
furosemide for symptomatic relief.

46. ACC/AHA GUIDELINES RECOMMEND INCREMENTAL
ADDITION OFTREATMENTS AS HF PROGRESSES

47. TREATMENT OF HF
TREATMENT OPTIONS FOR CHRONIC HF

48. ADDING THERAPIES IS ADDING LIFE
Fonarow GC et al. J Am Heart Assoc 2012;1:16-26
This study examined the individual and incremental clinical effectiveness of guideline-recommended
therapies for patients with HF and reduced LVEF.

49. ADDING THERAPIES IS ADDING LIFE
Fonarow GC et al. J Am Heart Assoc 2012;1:16-26

50. TREATMENT OF HF
Diuretics
The most commonly
prescribed class of
agent
To control sodium and
water retention
To relieve
breathlessness and
oedema
ACE inhibitors
Used in 61% of patients
with HF
Used in almost 80% of
those with HFrEF
Captopril was
prescribed at much
lower doses compared
to others like enalapril
Beta-blockers
Less widely used
overall 37% in patients
with HF
Used in 49% of patients
with HFrEF
Examples: atenolol,
carvedilol

51. DIURETICS
• Patients with heart failure who present with common congestive symptoms
(pulmonary and peripheral oedema) are given a diuretic to manage fluid
retention and achieve and maintain a euvolemic state.
• Loop diuretics are the treatment of choice because they increase sodium
excretion 20%-25% and substantially enhance free water clearance.
• To minimize the risk of over and under-diuresis, the diuretic response should
guide the dosage of loop diuretics with dose increases until a response is
achieved

52. ACE INHIBITORS
• ACEIs are prescribed to all patients with symptomatic heart failure unless
contraindicated
• ACEIs have proven benefit in alleviating heart failure symptoms, reducing
hospitalization, and improving survival.
• Cont5raindication to ACEi = ARBs (Angiotensin II Receptor Blockers)

53. Β-BLOCKERS
• In patients with NYHA class II or III heart failure, the β-blockers [bisoprolol, metoprolol
succinate – sustained release, and carvedilol have been shown to improve mortality and
event-free survival.
• These benefits are in addition to ACEI therapy and support the use of β-blockers as part of
standard therapy in these patients.
• Because β-blockers may cause a 4- to 10-week increase in symptoms before improvement is
noted, therapy should be initiated when patients have no or minimal evidence of fluid
retention.
• Relative contraindications include bradycardia, hypotension, hypoperfusion, severe peripheral
vascular disease, atrioventricular block, severe COPD, or a history of asthma

54. OTHERS
• Aldosterone antagonists— e.g. aldosterone antagonists spironolactone and
eplerenone. For selected patients with moderately severe to severe symptoms
who are difficult to control (NYHA class III with decompensations or class IV).
Action: Blocks Blocks neuro-hormal activation and controls volume. SE =
hyperkalaemia, especially when used with ACEI
• Angiotensin II receptor blockers—ARBs have been shown to be nearly as
effective as, but not superior to,ACEIs as first-line therapy for symptomatic heart
failure.
• Digoxin—Digoxin therapy is only indicated to reduce hospitalizations in
patients with uncontrolled symptomatic heart failure or as a ventricular rate
control agent if a patient has a known arrhythmia.

55. OTHERS…
• Hydralazine and nitrates—The combination is a reasonable treatment in patients,
who have persistent heart failure symptoms with standard therapy
• Anticoagulation—It is well established that patients with heart failure are at an
increased risk of thrombosis from blood stasis in dilated hypokinetic cardiac chambers
and peripheral blood vessels.Warfarin in individualized patients
• Implantable devices—implantable cardioverter-defibrillators (ICDs) for secondary
prevention of sudden cardiac death in patients with symptomatic heart failure. ICDs are
recommended for patients with NYHA class II or III heart failure, a left ventricular
ejection fraction less than 35%, and a reasonable 1-year survival with no recent MI
(within 40 days).

56. THANKYOU FORYOUR
TIME