Summary
Medicine Cardiovascular Pathology Summary
- Course
- Medicine (SCMD3000)
- Institution
- University Of The Witwatersrand (wits)
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CVS BlockPathology Summary
Chaandanee Bhayroo
1420214
GEMP 1
,Pathology of Heart Failure
1) Failure of the pump – systolic (empty) / diastolic (relax) dysfunction
2) Obstruction to flow – prevent valve opening = increased chamber pressure
3) Regurgitation – allows back flow
4) Shunted flow - defects
5) Disorders of cardiac conduction - arrhythmias
6) Rupture of the heart / major vessels – loss of continuity
Results in CONGESTIVE HEART FAILURE
• Pathophysiological state resulting from impaired cardiac function which renders the heart
unable to maintain an output sufficient for the metabolic requirements of the tissues and
organs of the body at rest
• Characterised by decreased cardiac output and the damming of blood back into the
venous system
Compensatory Mechanisms
• Frank-Starling Mechanism
o Increase EDV = dilate heart = increase myofiber stretching = contract more forcibly =
increases CO
• Neurohormonal Activation
o Release NA
o Increases HR
o Activates RAAS = increase sodium and water retention = increase vascular tone
o Release atrial natriuretic peptide = balance RAAS
• Myocardial structural changes
o Increase in size = hypertrophy
Decompensated Heart Failure
With time, the failing muscle is no longer able to propel sufficient blood to meet the needs of the
body
Left-sided Heart Failure
• Ischaemic heart disease
• Systemic hypertension
• Mitral or aortic valve disease
• Primary disease of the myocardium
Morphology
• Left ventricular hypertrophy
• Left ventricular dilatation
• Raised lung pressure = congestion and pulmonary oedema = RBCs leak into alveolar spaces =
phagocytosed by macrophages = heart failure cells
• Decreased renal perfusion
• Expansion of blood volume
• Cerebral hypoxia – irritability, restlessness, coma
, Clinical Features
• Dyspnoea on exertion
• Orthopnoea
• Cardiomegaly
• Tachycardia
• Decreased renal perfusion
Right Heart Failure
Consequence of left heart failure
May also be isolated due to pulmonary hypertension = cor pulmonale
Morphology
• Enlarged and congested liver (centrilobular) = cardiac cirrhosis
• Portal hypertension and splenomegaly
• Systemic venous congestion = transudate effusion
• Peripheral/ pre-sacral (bedridden)/ anasarca (massive generalised) oedema
Clinical features
• Little respiratory symptoms
• Hepatomegaly
• Peripheral oedema
• Effusions
• Ascites
, Myocarditis
• An inflammatory process resulting in injury to cardiac myocytes
• May lead to cardiac failure, arrhythmias, or sudden death
• Occurs at any age
• Infants, pregnant and immunosuppressed most vulnerable
Clinical Features
• Asymptomatic
• Mild ECG changes
• Heart failure
• Recover without sequelae
Etiological agents
1. Infectious – Coxsackie virus A and B (most common) – directly activates immune response
2. Non-infectious – immune mediated diseases, drugs, transplant rejections, rheumatic fever,
sarcoidosis
Pathogenesis
1. Specific agent evokes cell mediate immune response
a. Viral = lymphocytes and macrophages
b. Drugs/hypersensitivity = eosinophils
2. Immune cells damage the cardiac myocyte
Acute Myocarditis
• Macroscopically, the heart is dilated, pale and mottled with scattered interstitial
haemorrhages. Endocardial thrombi
• Microscopically, there is focal necrosis, interstitial oedema, inflammatory cells
A) Lymphocytes + macrophages = viral
B) Eosinophils = hypersensitivity
reaction / drug induced
C) Giant cells = granulomatous
D) Organism infiltrates myocardium =
shagus disease
Chronic Myocarditis
• Macroscopically, heart is firm, large with foci or interstitial
fibrosis. Endocardial mural thrombi
• Microscopically, myocardial fibres are hypertrophied.
Occasional residual inflammatory cells
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