The document provides an extensive overview of heart failure, including its definition, epidemiology, classification, clinical features, etiology, prognosis, and therapy. It discusses the types of heart failure—acute, chronic, systolic, diastolic, high-output, and low-output—along with their causes and diagnostic approaches. It also outlines management strategies, including lifestyle changes and pharmacological treatments based on the severity of the condition.

1. CARDIOLOGY
Cardiology lecture 2 :- Heart Failure
Date:- 15/09/2020
Prepared by
Dr Guled Mohamud Nur
(GMN@N)
MBBS

2. OVERVIEW
 Heart failure is inability of the heart to
maintain adequate cardiac output to
meet the demands of the body is known
as cardiac failure.
 It can result from any structural or
functional cardiac disorder.

3. Epidemiology
 The prevalence of heart failure is 1–2% of the
adult population in developed countries and
rises to ≥ 10% in persons of 70 years or older.
 The lifetime risk of developing heart failure is
estimated to be 20% for all persons older than
40 years.
 In the USA, approximately 5.1 million have
heart failure that leads to 27100 deaths per
year.

4. Clinical features
Typical symptoms
 breathlessness at rest or on exercise,
fatigue, tiredness, ankle oedema
Typical signs
 tachycardia, tachypnoea, pulmonary
rales, pleural effusion, raised jugular
venous pressure, peripheral oedema,
hepatomegaly.

5. Clinical features
Objective evidence of a structural or
functional abnormality of the heart at rest
 cardiomegaly, third heart sound, cardiac
murmurs, abnormality on the
echocardiogram, such as reduced LVEF
or valve disease or other structural
disorder, raised natriuretic peptide
concentration.

6. Classification of the
heart failure

7. Classification
The heart failure may be classified in
several ways
 Acute versus chronic heart failure
 Left versus right and biventricular failure
 Systolic versus diastolic failure
 Low output versus high output failure

8. Acute versus chronic heart
failure
Acute heart failure
 Heart failure developing suddenly in hours
or days in a previously asymptomatic
patient is called acute heart failure.
Chronic heart failure
 Heart failure developing gradually is
chronic heart failure.

9. Systolic versus diastolic failure
 In majority of patients heart failure is due to
combined systolic and diastolic dysfunction.
 Heart failure with reduced ejection fraction
(<40%) (HFrEF), Also referred to as systolic HF.
 Heart failure may develop as a result of impaired
myocardium contraction (systolic dysfunction).
 Heart failure with preserved ejection fraction
(>40%) (HFpEF), Also referred to as diastolic HF.
 Heart failure may develop due to poor
ventricular filling caused by impaired ventricular
relaxation.

10. Left versus right and
biventricular failure
Left heart failure
 refers to predominant congestion of the pulmonary
veins with fluid retention and pulmonary oedema.
Right heart failure
 refers to congestion of the systemic veins with fluid
retention and peripheral oedema.
 These conditions may coexist, and the most
common cause of right ventricular failure is raised
pulmonary artery pressure due to left ventricular
failure.

11. Low output versus high output
failure
High-output heart failure
 refers to the syndrome caused by circulatory
high-output conditions, such as anaemia,
thyrotoxicosis, septicaemia, arteriovenous shunts,
liver failure, Paget’s disease, and beriberi.
Low output failure
 Low cardiac output at rest or during exertion
characterizes heart failure caused by common
conditions such as congenital, valvular,
rheumatic, hypertensive, coronary and
cardiomyopathic.

12. Etiology
 Hypertension and coronary artery disease
are the commonest causes of heart
failure in industrialized countries whereas,
in underdeveloped countries, other
causes, such as infectious diseases, are
more important.
 Valvular heart disease , cardiomyopathies
,and congenital heart disease are also
important causes.

13. Etiology
 Patients with diabetes mellitus have a four
times higher risk for heart failure and higher
mortality compared to non–diabetics.
 Alcohol is a direct myocardial toxin and a
reversible cause of heart failure.
 Tobacco and cocaine increase the risk for
CAD, which can lead to heart failure.
 Both hyperthyroidism and hypothyroidism
can be reversible causes of heart failure.

14. etiology
 Pulmonary arterial hypertension may lead to RV
failure.
 Male sex , less education , physical inactivity , and
overweight have also been identified as independent
risk factors for CHF.
 Obstructive sleep apnoea is associated with
hypertension and a higher incidence of heart failure.
 Patients with metabolic syndrome,
hypertriglyceridaemia, low HDL, hypertension, and
fasting hyperglycaemia) are at higher risk of
cardiovascular disease and heart failure.
 HIV infection is also an important cause of left or
biventricular dysfunction.

15. Presentation
 Presenting symptoms of heart failure, such as
dyspnoea, exercise intolerance , and fatigue,
are non-specific and mimicked by many other
conditions, especially in the elderly.
 Several classification schemes (the most
popular being by the New York Heart
Association (NYHA), Canadian Cardiovascular
Society (CCS), have been presented for a
semi-quantitative assessment of symptom
severity.

16. Presentation
 Orthopnoea , dyspnoea that occurs in the
recumbent position, is a later manifestation.
 It may also be seen in patients with COPD
and abdominal obesity or ascites.
 Paroxysmal nocturnal dyspnoea refers to
acute episodes of dyspnoea and coughing
that occur at night and awaken the patient.
It is relatively specific for heart failure.

17. Presentation
 Pulmonary oedema may develop in
acute exacerbations of heart failure.
Minor episodes of haemoptysis may
represent transient, exercise-induced
pulmonary oedema.
 Cardiac asthma refers to wheezing due to
bronchospasm or increased pressure in
the bronchial arteries.

18. Presentation
 Altered mental status may reflect hypoperfusion.
 Anorexia or nausea and right upper quadrant pain
and ascites reflect bowel and liver congestion.
 Ankle oedema may be caused by heart or renal
failure and pericardial constriction, particularly
with elevated JVP, chronic venous insufficiency,
calcium channel blockers, IVC obstruction,
prolonged air travel, idiopathic, liver congestion
and hypoalbuminaemia, secondary
hyperaldosteronism.

19. Presentation
 Unilateral ankle oedema may be due to
venous thrombosis, lymphatic obstruction,
and saphenous vein harvesting for CABG.
 Young patients may be not edematous
despite intravascular volume overload.
 In obese patients and elderly patients,
edema may reflect peripheral rather than
cardiac causes.

20. Physical examination
 Physical signs are also non-specific:
 Sinus tachycardia or AF in 30% of patients with
advanced disease
 Tachypnea
 Raised jugular venous pulse
 Third heart sound (S 3 )
 Basal pulmonary rales
 Peripheral oedema with ankle swelling and
hepatomegaly.
 Systolic murmurs may be present

21. NYHA functional
classification
NYHA (New york heart
association)

22. NYHA functional classification
Class I
 Patients with cardiac disease but no resulting limitation
of physical activity.
 Ordinary physical activity does not cause undue
fatigue, palpitation, dyspnoea, or anginal pain.
Class II
 Patients with cardiac disease resulting in slight limitation
of physical activity.
 Comfortable at rest, but ordinary physical activity results
in fatigue, palpitation, dyspnoea, or anginal pain.
 By limiting activity, patients still able to lead a normal
social life.

23. NYHA functional classification
Class III
 Patients with cardiac disease resulting in
marked limitation of physical activity.
 Comfortable at rest, but less-than-ordinary
physical activity results in fatigue,
palpitation, dyspnoea, or anginal pain.
 Patients unable to do any housework.

24. NYHA functional classification
Class IV
 Patients with cardiac disease resulting in inability
to carry out any physical activity without
symptoms.
 Dyspnoea or angina may be present, even at rest.
 Comfortable at rest, but less-than-ordinary
physical activity results in fatigue, palpitation,
dyspnoea, or anginal pain.
 Patients incapacitated and virtually confined to
bed or a chair.

25. ACC/AHA stages of
heart failure
ACC ( American college of
cardiology )
AHA (American heart association)

26. ACC/AHA stages of heart failure
Stage A
 At high risk for developing heart failure. No
identifi ed structural or functional
abnormality; no signs or symptoms.
Stage B
 Developed structural heart disease that is
strongly associated with the development
of heart failure but without signs or
symptoms.

27. ACC/AHA stages of heart failure
Stage C
 Symptomatic heart failure associated with
underlying structural heart disease.
Stage D
 Advanced structural heart disease and
marked symptoms of heart failure at rest
despite maximal medical therapy.

28. Investigations
 Complete blood count (CBC), blood urea
nitrogen and creatinine, glucose and HbA1c,
serum electrolytes, liver function tests, lipid
profile, and thyroid function tests are taken
routinely.
 Natriuretic peptide ( BNP ) and its precursor N
terminal pro-BNP are sensitive and specific
 This peptide is raised with advanced age,
female sex, and renal insufficiency and
lowered with obesity.

29. Investigations
 Other biomarkers In ambulatory chronic
heart failure patients, such as high-sensitivity
C-reactive protein, B-type natriuretic peptide.
 Screening for haemochromatosis, sleep-
disturbed breathing, HIV, rheumatological
diseases, amyloidosis, or
phaeochromocytoma is also undertaken
when there is a clinical suspicion of these
diseases.

30. Investigations
ECG
 Left ventricular hypertrophy, atrial enlargement,
previous myocardial infarction, active ischaemia,
conduction abnormalities, and arrhythmias may be
present. An entirely normal ECG makes the
diagnosis of systolic dysfunction unlikely (<10%).
Chest radiography
 may reveal cardiomegaly and/or pulmonary
congestion (Kerley B lines and interstitial oedema
with upper lobe blood diversion).
 Pleural effusions may be present, with biventricular
failure.

31. Investigations
 Echocardiography (key investigation)
 echo, may provide important information
about ventricular dimensions, extent of
systolic dysfunction, whether dysfunction is
global or segmental, the status of valves,
and estimates of pulmonary artery
pressure.
 MRI provides the most accurate estimate
of ventricular structure and function.

32. Investigations
 Holter monitoring may be considered in
patients who are being investigated for
ventricular arrhythmias.
 Coronary angiography is indicated when the
patient has angina or coronary artery disease
is suspected.
 Cardiac catheterization may also be needed
when echocardiography is insufficient to
define the severity of valve disease and/or
pulmonary pressures.

33. Prognosis
 Conditions associated with a poor
prognosis in heart failure are as age,
aetiology, NYHA class, LVEF, key co-
morbidities (renal dysfunction, diabetes,
anaemia, hyperuricaemia), and plasma
natriuretic peptide concentration.

34. Therapy
General measures
 Patients with heart failure should be enrolled in a
multidisciplinary care management programme
to reduce the risk of heart failure hospitalization.
 Regular aerobic exercise is beneficial for patients
with stable, non-decompensated heart failure
 REST: bed rest reduces the demands of the heart,
therefore beneficial. Head of the patient should
be proposed up to reduce lung congestion.
 Sexual activity is not advised for patients with
decompensated or advanced (NYHA class III or
IV) heart failure.

35. Therapy
General measures
 Salt restriction is usually advisable,
especially in patients with stages C and D.
 Fluid restriction to 1.5–2 L/day may be
considered only in patients with severe
symptoms and hyponatraemia.
 Weight loss is initially advisable in patients
with coronary artery disease.

36. Therapy
General measures
 Alcohol, Smoking cessation, avoidance of
high altitude (>1500 m), and vaccination
against influenza and pneumococcus are
recommended.
 Contraception with combined hormonal
contraceptives is contraindicated due to
fluid retention and increased thrombotic
risk.

37. Therapy
General measures
 Non-steroidal antiinflammatory drugs
(including COX-2 inhibitors) as well as
corticosteroids and herbal preparations
(licorice, ginseng, ma huang) cause salt
and water retention and should be used
with much caution.
 Tricyclic antidepressants are
contraindicated due to pro-arrhythmic
potential.

38. Stages in the
development of HF and
recommended therapy
by stage.

39. STAGE A
 At high risk for HF but without structural heart disease
of symptoms of HF.
 e.g., Patients with:
 HTN, Atherosclerotic disease, DM, Obesity,
Metabolic syndrome, or Patients using cardiotoxins,
With family history of cardiomyopathy.
Therapy
 Goals:- Heart healthy lifestyle, Prevent vascular,
coronary disease Prevent LV structural abnormalities
Drugs
 ACEI or ARB in appropriate patients for vascular
disease or DM, Statins as appropriate

40. STAGE B
 Structural heart disease but without signs or symptoms of
HF.
 e.g., Patients with:
 Previous MI, LV remodeling including, LVH and low EF,
and Asymptomatic valvular disease.
Therapy
 Goals:- Prevent HF symptoms, Prevent further cardiac,
remodeling.
Drugs
 ACEI or ARB is appropriate
 Beta blockers as appropriate
In selected patients
 ICD, Revascularization or valvular surgery as appropriate.

41. STAGE C
 Structural heart disease with prior or current
symptoms of HF.
 e.g., Patients with:
 Known structural heart disease and HF signs
and symptoms.
HFpEF: Therapy
 Goals:- Control symptoms, Improve HRQOL
(health related quality of life), Prevent
hospitalization, and Prevent mortality
 Strategies:- Identification of comorbidities

42. STAGE C
Treatment
 Diuresis to relieve symptoms of congestion
 Follow guideline driven indications for
comorbidities
 e.g., HTN, AF, CAD, DM
 Revascularization or valvular surgery as
appropriate.

43. STAGE C
HFrEF:Therapy
 Goals:- Control symptoms, Patient education,
Prevent hospitalization, and Prevent mortality
Drugs for routine use
 Diuretics for fluid retention
 ACEI or ARB
 Beta blockers
 Aldosterone antagonists

44. STAGE C
Drugs for use in selected patients
 Hydralazine/isosorbide dinitrate
 ACEI and ARB
 Digoxin
selected patients
 CRT (cardiac resynchronization therapy)
 ICD (implantable cardioverter-defibrillator)
 Revascularization or valvular surgery as
appropriate.

45. STAGE D
Refractory HF
e.g., Patients with:
 Marked HF symptoms at rest, Recurrent
hospitalizations, and Patients despite GDMT
(guideline-directed medical therapy)
THERAPY
 Goals:- Control symptoms, Improve
HRQOL, Reduce hospital readmissions,
Establish patient’s end of life goals.

46. STAGE D
Refractory HF
Options
 Advanced care measures
 Heart transplant
 Chronic inotropes
 Temporary or permanent MCS (mechanical
circulatory support)
 Experimental surgery or drugs
 Palliative care and hospice
 ICD deactivation

47. Control of congestive heart
failure
Reduction of cardiac workload
 Physical and emotianal rest, 1-2 weeks in
symptomatic cardiac failure.
 Small but frequent meals
 Weight loss by reducing calories intake
 Use vasodilators
Control of excessive retention of salt and water
 Decreased intake, low salt diet
 Increased excretion, diuretics

48. Control of congestive heart
failure
Enhancement of myocardium contractility
 Use digitalis
 Use dopamine and dobutamine

49. Drug management of
the heart failure

50. Diuretics
 Loop diuretics, e.g. frusemide (lasix)
 Potassium sparing diuretics e.g. spirolactone
(aldactone)
 Thiazide diuretics e.g. hydrochlorothiazide
 Diuretics are the most effective means of
providing symptomatic relief to patient with
moderate to severe congestive heart failure.
 Loop diuretics is most effective in severe
heart failure.

51. Diuretics
 In acute conditions, diuretics should be given iv
because they may not be absorbed
adequately due to congestion in the gut.
 Frusemide is given in the dosage of 20-320 mg
daily preferably in two or more divided doses.
 In severe renal insufficiency, larger doses of
frusemide such as 500 mg may be required.
 Patient with refrectory edema may respond to
combination of frusemide and thiazide such as
metolazone.

52. Angiotensin converting enzyme
(ACE) inhibitors
 ACE inhibitors should be considered as a part
of the initial therapy of the cardiac failure.
 All patient of cardiac failure should be on ACE
inhibitors if there is no contraindication.
 Prognosis is markedly improved and
development of heart failure is slowed with the
use of ACE inhibitors.
 e.g. captopril, enalapril, ramipril, and lisinopril.

53. Spirolactone
 Spirolactone (aldactone) is a specific
competitive antagonist to aldosterone.
 Along with its effect of potassium sparing
diuretics, it inhibits myocardium
remodeling and fibrosis and should be
given in severe heart failure.

54. Angiotensin receptors blockers
 These agents as effective as ACE inhibitors
in the management of cardiac failure.
 The advantage is that they do not cause
cough and skin rash.
 E.g. Losartan, valsartan

55. Vasodilators
Nitrates
 Are not used routinely in heart failure
 Long acting nitrates such as isosorbide
nitrate may be given if paroxysmal
noctural dyspnea in uncontrolled.
 Nitrates are mainly used in acute heart
failure, in acute cardiogenic pulmonary
edema, acute decompensated of chronic
heart failure.

56. Vasodilators
Hydralazine
 Combination of oral hydralazine and oral
nitrates is an alternative to ACE inhibitors for the
treatment of cardiac failure in patients who do
not tolerate ACE inhibitors.
Nesiritide
 This new agent is a recombinant form of human
brain natriuretic peptide and is a potent
vasodilator that reduces ventricular filling
pressure and improve cardiac output.

57. Digitals
 Digoxin is a positive inotropic agent and is
the first line therapy in patients with hear
failure associated with atrial fibrallation.
Dosage : Initial dose (digitalization)
 rapid digitalization (duration 24 hours)
 single dose of 0.5 mg IV over 10-20 minutes
followed by additional 0.25 mg IV every 6
hours to maximum of 1mg in 24 hours.

58. Digitals
Dosage : Slow digitalization (duration 1
week)
 Single oral dose of 0.5 mg for 3 days
followed by maintenance dose (0.15-0.5
mg daily).
 Antacids and broad spectrum oral
antibiotics decrease the absorption of
digoxin.

59. Role of the beta-blockers
 Although beta-blockers have traditionally
been considered contraindicated in cardiac
failure, however, there is now strong evidence
that these agents have important beneficial
effect.
 First trial was done non cardioselective beta-
blocker (carvedilol) but later trial with
metaprolol and bisoprolol, also proved 30-35%
reduction in mortality as well as reduced
hospitalizations.

60. Non pharmacological
treatment of heart
failure

61. Coronary revascularization
 Since underlying coronary artery disease is
the cause of heart failure in the majority
of patients, coronary revascularization
may improve symptoms and prevent
progression if there is evidence of
ischemia.

62. Biventricular pacing
 In patients with heart failure and bundle
branch block and functional class III heart
failure, cardiac conduction abnormalities
can trigger mechanical dys-synchrony of
ventricular contraction impairing cardiac
performance.
 In these patients biventricular pacing in both
right and left ventricle produce improvement
in symptoms and exercise tolerance.

63. Implantable cardio-verter
defibrillator (ICD)
 Patients with sustained episodes of
ventricular tachycardia should be receive
implantable cardioverter defibrillator
(ICD).

64. Left ventricular assist devices
(LVAD)
 There is pump like devices that receive
blood and pump with pressure working
like ventricles.
 They are required in severe heart failure
when the pumpimg function of ventricles
is severely impaired.
 These devices are very expensive

65. Surgical treatment
cardiac transplantation
 Patient with severe heart failure and
limited life expectancy are considered
candidates for heart transplantation.
 One year survival rate after
transplantation exceeds 80-90% and five
year survival rates above 70%

66. Reference By
Clinical Cardiology
Current Practice Guidelines