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
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.
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
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.
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
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.
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
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.
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
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.
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
