1. CARDIAC
FAILURE
(HEART
FAILURE)

2. Cont.
Definition
 A complex clinical syn resulting from any
structural or functional cardiac disorder that
impairs the ability of the ventricle to fill with or
eject blood

3. Cont.
AETIOLOGY OF CARDIAC FAILURE
 The causes of cardiac failure include: -
 Pump failure
 Pressure overload
 Volume overload
 Multifactorial

4. Cont.
Pump failure
 Myocardial weakness e.g. myocardial
infarction, ,myocardial infections, nutritional,
cardiomyopathy, physical agents
 Cardiac arrhythmias
 Reduced or poor myocardial response
 Multiple factors

5. Cont.
Pressure overload
 This is a situation where there is
increased resistance to the expulsion of
blood from the ventricles or inflow of blood
into ventricles.
 Left ventricle – aortic stenosis, systemic
hypertension
 Right ventricle – mitral stenosis, pulmonary
hypertension, lung disease

6. Cont.
Volume overload
 This occurs when the ventricles are required
to expel more than the normal amount of
blood
Incompetent valves (regurgitation)
High output states
Hypoxia
Arteriolar-venous shunts
Multifactorial- This involves a combination of
the above-mentioned factors.

7. Causes of hf
• Ischemic heart disease – 40 percent
• Dilated cardiomyopathy – 32 percent
• Primary valvular heart disease – 12 percent
• Hypertensive heart disease – 11 percent
• Other – 5 percent
Uptodate13.5version
Italian registry-
6200pts

8. Cont.
CHRONIC HEART FAILURE
LEFT VENTRICULAR FAILURE (LVF)
 The left ventricle is more commonly
affected than the right ventricle.
 Left ventricular failure leads to right
ventricular failure then total heart failure
(CCF).

9. Cont.
Pathology
 The left ventricle fails to expel all the blood it
receives hence contains an increasing volume of
blood at the end of systole (increased diastolic
volume).
 Accumulation of the residual blood and the
incoming blood during systole causes dilatation of
the ventricle with further increase in inadequacy of
contraction.
 Ventricular dilation leads to stretching of valve
rings (mitral 10cm) causing Mitral incompetence
(Mitral Regurgitation - MR)

10. Cont.
 With mitral regurgitation some blood expelled
during systole passes through the valve to the
left atria increasing pressure here (left atria)
and this leads to venous congestion in the
pulmonary system causing oedema of the
lungs (pulmonary oedema)
 Pulmonary congestion leads to shortness of
breath, orthopnoea, PND and haemoptysis.
 This retrograde loss of blood through the
leaking valve further compromises the
ventricular output.

11. Cont.
RIGHT VENTRICULAR FAILURE (RVF)
 RVF usually combined with LVF and pure
RVF occurs in few instances.
 RVF is usually caused by left ventricular
failure (LVF).
 When caused by pulmonary diseases it is
described as the heart of pulmonary
disease (cor pulmonale).

12. Cont.
Pathology
 Left ventricular failure causes increased
left atrial pressure which increases the
workload on the right ventricle leading to
right ventricular hypertrophy and
eventually failure.
 The failing right ventricle is unable to
expel all the blood received hence
becomes dilated.

13. Cont.
 The dilatation results in the stretching of the
Tricuspid valve ring leading to Tricuspid
regurgitation and blood accumulates in the right
atrium, systemic and portal venous systems
leading to systemic venous congestion and
causing oedema.
 There is increased diastolic volume which
causes visceral congestion and effusions,
peripheral congestion and oedema (stasis,
pitting oedema and distended neck veins).

14. Cont.
Classification of severity
• Class I
– No limitation of physical activity and No
symptoms with ordinary exertion
• Class II
– Slight limitation of physical activity and Ordinary
activity causes symptoms

15. Cont.
• Class III
– Marked limitation of physical activity and Less
than ordinary activity causes
symptoms Asymptomatic at rest
• Class IV
– Inability to carry out any physical activity without
discomfort and Symptoms at rest

16. Cont.
 Primary /precipitating factors
– Infection
– Anemia
– Pregnancy
– Thyrotoxicosis
– Arrhythmias

17. Cont.
– Infective endocardiatis
– MI
– PTE
– HTN
– Myocardiatis –viral&rheumatic

18. Cont.
Presentation
 Dyspnoea
 Orthopnoea
 PND
 Cardiac asthma
 Acute pulmonary edema
 Fatigue
 ABD sym - Anorexia, nausea, abdominal pain and
fullness.
 Cerebral sym - confusion, difficulty in concentration,
impairment of memory, headache, insomnia, noctuniria
and anxiety

19. Cont.
Physical findings
 Tachycardia
 High diastolic BP & occasional decrease in
systolic BP (decapitated BP)
 Jugular venuos distension
 Displaced and sustained apical impulses
 Third heart sound – low pitched sound that is heard
during rapid filling of ventricle
 Hydrothorax and Ascites
 Cardiac edema- pretibial region and ankles,
sacral, arms and face though rare

20. Cont.
 Congestive Hepatomegaly.
 Jaundice.
 Cardiac Cachexia-serious weight loss.
 Other Manifestations-extremities may be cold,
pale, and diaphoretic., Urine flow is
depressed, prerenal azotemia may be present,
long-standing severe HF, impotence and
depression are common.

21. PERICARDITIS
 Inflammation of the pericardium
Aetiology
 Acute Infections
 Bacterial
 Pyogenic cocci - Strep pyogenes, Strep pneumoniae,
Staph aureus
 Tuberculosis
 Viral – Echovirus, Coxasackie virus
 Protozoal/Parasitic – amoebiasis, toxoplasmosis,
ecchninococcal
 Fungal - Histoplasmosis (H. capsulatum),
Actinomycosis

22. Cont.
 Myocardial infarction – as a result of
autoimmune hypersensitivity reaction
triggered by injury to the heart muscle.
 In association with connective tissue
disorders
 S.L.E
 Rheumatoid arthritis
 Acute rheumatic fever
 Polyarteritis nodosa

23. Cont.
 Metabolic – uraemia and hypothyroidism
 Neoplastic – primary and secondary
 Physical agents – radiation, blunt trauma
 Heamorrhage
 Trauma
 Drug induced

24. Cont.
1. ACUTE PERICARDITIS
 Acute pericarditis is an acute inflammatory
process of the pericardium involving the serosal
lining of the pericardium.
 There is: -
 Active hyperaemia
 Inflammatory oedema
 Leucocyte emigration
 Exudate accumulates in the pericardial sac with
fibrin deposition on the surface giving the “bread
and butter” appearance.

25. Cont.
Pathology
 The diagnostic feature at autopsy is
usually the “bread and butter” appearance
 The exudate first appears around the
great vessels at the base of the heart as
opaque, dull and roughened layer.
 If this exudate becomes abundant it forms
a rough fibrinous covering over the heart
which gives the heart irregular projections

26. Cont.
 The effusion can be: -
 Serous
 Acute rheumatism, myocardial infarction
 Haemorrhagic
 Tuberculosis, uraemia, infective microbes, secondary
metastatic tumour
 Purulent (suppuration)
 Septic pericarditis, pyogenic pericarditis

27. Cont.
2. CHRONIC PERICARDITIS
 Chronic pericarditis results from inadequately
treated bacterial pericarditis especially TB
A. TB Pericarditis
 Follows chronic pulmonary tuberculosis
 The presumed route of infection is by lymphatic or
extension from the infected pleura.
 The exudate formed is: -
 Turbid or blood stained
 Tubercles are visible on pericardial surface
 Calcification may lead to constrictive pericarditis

28. Cont.
B. Constrictive Pericarditis
 Evident by the obliteration of the
pericardial sac by the thick layer of dense
fibrous tissue
 Seen in:-
 Pyogenic pericarditis
 Tuberculosis
 Rheumatoid arthritis

29. Cont.
C. Hydropericardium
 Accumulation of clear transudate or clear
fluid
 Seen in conditions of generalized oedema
 The pericardial surfaces are smooth and
shinny in appearance

30. Cont.
D. Haemopericardium
 Heamorrhage into the pericardial sac
 Results from: -
 Rupture of the heart secondary to infarction
 Rupture of aortic aneurysm
 Stab wounds on the heart and great vessels
 Its rapid development leads to cardiac
tamponade

31. Cont.
PRESENTATION OF PERICARDITIS
 CCF
 Low stroke volume
 Pericardial Effusion
 Occurs when an inflammatory exudate
collects in the closed pericardium
 May give rise to mechanical embarrassment
of the circulation by reducing ventricular
filling leading to cardiac tamponade.

32. Cont.
INVESTIGATIONS
 Chest X-ray
 ECG
 Echocardiography

33. DISORDERS OF THE
MYOCARDIUM
Disorders of the Myocardium
 Myocardial Ischaemia
 Angina Pectoris
 Myocardial infarction
 Cardiomyopathy
 Dilated (Congestive) Cardiomyopathy
 Hypertrophy cardiomyopathy
 Restrictive cardiomyopathy

34. Cont.
 Myocarditis
 Miscellaneous
 Fatty infiltration
 Fatty change
 Atrophy

35. Cont.
1.CARDIOMYOPATHIES
 Cardiomyopathy is a term indicating disease of the
cardiac muscle.
 It can be divided into primary cardiomyopathy where
the cause is unknown and secondary cardiomyopathy
where the cause is known.
CLASSIFICATION
 Dilated (Congestive) cardiomyopathy – there is
ventricular dilatation
 Hypertrophic cardiomyopathy – myocardial
hypertrophy
 Restrictive cardiomyopathy – impaired ventricular
filling

36. Cont.
A. DILATED CARDIOMYOPATHY (DCM)
 Dilated cardiomyopathy is characterized by
gradual four chamber hypertrophy and
dilatation resulting in gradual progressive
cardiac failure.
 Because of dilatation of the chambers and the
ensuing heart failure DCM is also called
congestive cardiomyopathy.
 Patients with DCM present with unexplained
heart failure usually between the ages of 30 –
60 years.

37. Cont.
Causes
 The cause is unknown but associated factors
include:
 Familial (autosomal dominant)
 Viral infection – Coxsackie’s virus , HIV
 Alcohol toxicity (chronic alcoholism)
 Peripartum

38. Cont.
Pathology
Macroscopy
 Cardiomegally
 Dilatation of the heart chambers
 Thickening of ventricular walls
 Thrombosis (mural)

39. Cont.
Microscopy
 Hypertrophy of heart muscle cells
 Degenerative changes
 Cellular infiltration with mononuclear
inflammatory cells
Clinical Features
 Congestive cardiac failure
 Cardiac arrhythmias
 Embolism

40. Cont.
Investigations
 Chest X-ray – cardiac enlargement
 ECG – diffuse non-specific ST segment and T
wave abnormalities
 Echocardiogram – dilatation of the left
ventricle and/or right ventricle with poor global
contraction

41. Cont.
B. HYPERTROPHIC CARDIOMYOPATHY
(HCM)
 Hypertrophic cardiomyopathy is an inherited
disorder of the heart muscle characterized by
a variable hypertrophy of the right ventricle
without a cardiac or systemic cause.
 It exhibits massively thickened inter-ventricular
septum that results in distorted ventricular
contraction with abnormal valve movement
during systole.
 Mitral stenosis may be present.

42. Cont.
Causes
 Familial (autosomal dominant)
 Collagen disease/storage disease
 Increased circulating catecholamines
 Infants of diabetic mothers

43. Cont.
Pathology
Macroscopy
 Cardiomegally
 Asymmetrical septal hypertrophy – more
thickening of the septum than left ventricular
wall
 Left ventricle cavity is compressed into a
banana-like configuration
 Thickening of the basal septum at the level of
the mitral valve results in obstruction

44. Cont.
Microscopy
 Myocardial cell disorganization
 Hypertrophy of muscle cell with large
prominent nuclei.
 Replacement fibrosis

45. Cont.
Clinical Features
 Cardiac arrhythmias
 Cardiac failure
 Sudden death
 Syncope
 Dyspnoea
 Chest pain

46. Cont.
Investigations
 Chest X-ray
 ECG – is diagnostic as it shows ventricular
hypertrophy
 Genetic analysis

47. Cont.
C. Restrictive Cardiomyopathy
 This is a form of cardiomyopathy characterized
by restriction in ventricular filling due to
reduction in the volume of the ventricle.
 The myocardium does not relax properly in
diastole as it is restricted resulting in reduced
ventricular filling and hence reduced cardiac
output.
 The restriction stems from fibrosis of the
ventricular muscle.

48. Cont.
Causes/associated conditions
 Idiopathic/Familial
 Amyloidosis
 Sarcoidosis
 Loeffler’s endocarditis
 Endomyocardial fibrosis

49. Cont.
Clinical Features
 Dyspnoea
 Fatigue
 Embolic features
 Features of constrictive pericarditis
 A high JVP with diastolic collapse – Friedreich’s
sign
 Elevation of venous pressure with inspiration –
Kussmaul’s sign
 Cardiomegally
 Third or fourth heart sound

50. Cont.
Investigations
 Chest X-ray – confirms enlarged heart
 ECG – low voltage and ST segment and T
wave abnormalities
 Echocardiogram – asymmetrical myocardial
thickening, impaired ventricular filling
 Endomyocardial biopsy

51. Cont.
2. MYOCARDITIS
Definition: Myocarditis is an inflammatory
lesion of the myocardium
Aetiology
 Infections
 Viruses
 Coxsackie Group A, B, Echovirus type 8
,Infleunza ,Adenoviruses ,Polio ,HIV

52. Cont.
 Bacterial toxins/bacteria
 Staphylococcus ,Syphilis ,Streptococcus
,Diptheriae
 Protozoal - Trypanosomiasis (T. cruzi – Chaga’s
disease)
 Parasites - Trichinosis spiralis and
Toxoplasmosis
 Fungal -Candida albicans, Aspergillus

53. Cont.
 Poisons and chemicals - Drugs - cytotoxics –
daunorubicin; Alcohol
 Physical agents - severe hypothermia, irradiation
 Hypersensitivity reactions/connective tissues
disorders
 Rheumatic fever,
 Rheumatoid arthritis
 S.L.E
 Endocrine/metabolic disorders - Diabetes mellitus,
hypothyroidism, hyperthyroidism
 Idiopathic

54. Cont.
Features
 Acute unexplained heart failure
 Cardiac Arrthymias
 Chest pain
 Gallop rhythm
 Cardiac enlargement