In the fetus, the ductus arteriosus links the pulmonary artery with the aorta. At this time, the pressure in the pulmonary circulation is greater than in the systemic circulation to that blood flows from right to left i.e. from the pulmonary artery into the aorta.

After birth, the ductus close in response to the raised pO2 in the blood and the fibroses up and becomes the ligamentum arteriosus. The ductus may, however, fail to close and this is termed patent ductus arteriosus. This is the 3rd commonest forms of congenital heart disease after ventricular septal defects and atrial septal defects. Like these conditions, it is associated with a left to right shunt (because of the relatively high pressures in the systemic circulation). The magnitude of the shunt will depend on the diameter of the ductus. With time, as a result of the increased blood flow to the lungs, pulmonary hypertension may develop and if the pressure becomes great enough the shunt will reverse becoming right to left (as in the fetus).

This failure to close is common in premature infants when the ductus will usually, in the end, close spontaneously, in the end. Patent ducts arteriosus is commoner in babies with, e.g., Down’s syndrome and congenital rubella. In term infants, it rarely closes on its own. Treatment may be by instilling prostaglandin inhibitors, which cause contraction, or by surgery. Infective endocarditis may develop in untreated cases.

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Please note that I made these for my own use but thought they may be useful to others!

Cardiac Pathology

 

Divided into diseases of the:

1. Coronary arteries
2. Endocardium (including valves)
3. Myocardium (including congenital heart disease)
4. Pericardium

 

1. Coronary arteries

 

Any vascular disease can involve these (e.g. vasculitis) but atheroma is the important one.

Clinically: angina, unstable angina and myocardial infarction (due to superimposed thrombosis secondary to ulceration or fissuring).

 

Left coronary artery >

• anterior descending > anterior septum and wall of left ventricle
• circumflex branch > lateral wall of left ventricle

 

Right coronary artery > posterior septum and wall of left ventricle

 

Distribution of infarction:

1. Subendocardial infarction due to severe, generalized disease.
2. Focal due to blockage of a major artery.

 

 Complications of myocardial infraction:

 

Minutes:

Arrhythmias: ventricular fibrillation / heart block

Acute cardiac failure / cardiogenic shock

 

Days:

Thromboses:

• Mural (over the infract) which may be followed by systemic embolisation
• Atrial thrombus (due to atrial fibrillation)
• (DVT which may be followed by pulmonary embolization)

 

Week:

Rupture (due to softening of muscle):

• Myocardium (leading to cardiac tamponade and death)
• Papillary muscle (mitral incompetence)
• Septum (left to right shunt)

 

Pericarditis

 

Weeks:

• Chronic cardiac failure.
• Immune pericarditis (Desslers’s syndrome)

 

Months:

Cardiac aneurysm (due to fibrosis)

 

At any time:

Another infarct

 

1. B) Myocardium

 

Myocarditis

Causes:

Infectious:

• Viral e.g. Coxsackie
• Bacterial e.g. Borrelia (Lyme Disease)

 

Toxic: e.g. Diphtheria

 

Immunological e.g. Rheumatic fever

 

Cardiomyopathy:

Definition: Heart muscle disease not due to ischaemia, hypertension, valvular disease or inflammation

 

1. Dilated cardiomyopathy: end stage of the above (which has burnt out), alcohol or pregnancy
2. Hypertrophic cardiomyopathy: autosomal dominant
3. Restrictive cardiomyopathy: endomyocardial, fibro-elastosis, amyloid, haemochromtosis

 

Rheumatic fever

Preceded by streptococcal sore throat.

Type 2 hypersensitivity reaction (antibodies to streptococci cross react with antibodies to myocardium.

 

Clinical features

• General: fever etc.
• Skin: nodules
• CNS: chorea
• Heart:
• Pericarditis
• Myocarditis (Aschoff bodies- collections of macrophages)
• Endocarditis including valves – may lead to chronic valve disease (see below)

 

Congenital Heart Disease

 

Risk factors: e.g. Down’s syndrome, rubella, thalidomide

 

1. Left to right shunts e.g. atrial or ventricular septal defects ( if untreated may reverse
2. Right to left shunt “ Cyanotic”

e.g. Tetralogy of Fallot:

• large ventricular septal defect
• pulmonary stenosis

3)  overriding of the aorta

4)  right ventricular hypertrophy

 

 

1. C) Endocardium

 

Valve disease

 

Mitral valve:

 

Leads to dilation and hypertrophy of the left atrium

In incompetence there is, also, dilatation of the left ventricle

 

Incompetence:

• Post -inflammation: rheumatic fever
• Infective endocarditis
• Left ventricular failure
• Myocardial infarction
• “Floppy mitral valve syndrome”

 

Stenosis:

• Post-inflammation: rheumatic fever

 

Complications:

• Atrial fibrillation
• Infective endocarditis

 

 

Aortic valve:

 

Stenosis:

• Age related calcification
• Calcification of abnormal valve:

Congenital bicuspid

Post -inflammation: rheumatic fever

 

Leads to marked cardiac hypertrophy and the risk of sudden death

 

Incompetence

• Post -inflammation: rheumatic fever
• Infective endocarditis
• Dilatation of valve ring e.g. Marfan’s syndrome

 

Leads to dilatation and hypertrophy

 

 

Infective endocarditis

 

Vegetations form on the valves

 

1. Acute:

Pathogenic organism (e.g. staphylococcus aureus) and normal valve

 

2. Subacute:

Less pathogenic organism (e.g. streptococcus viridans, from the mouth, or enterococci, from the gut) and an abnormal valve

 

 

Complications:

• Systemic features: Fever etc.
• Embolisation of vegetations

Infected infarcts in the brain or kidneys

Splinter haemorrhages

 

 

Other causes of valve vegetations

e.g. marantic in patients with cancer

 

 

1. D) Pericardium

 

Classified according to appearance

1. Fibrinous e.g. myocardial infarction
2. Serous e.g. rheumatic fever
3. Purulent e.g. bacterial infection
4. Haemorrhagic e.g. traumatic, tumour
5. Fibrotic +/- calcification (chronic) = constrictive pericarditis g. TB

 

 

Pericardial haemorrhage:

1. Myocardial infarction
2. Dissecting aortic aneurysm

 

Read Some Notes on Cardiac Pathology in full