Flashcards in Cardiovascular Pathology Deck (25):
What are the two types of heart disease?
Primary- heart disease causes effects on other body systems.
Secondary- A systemic disease results in secondary effects on the circulatory system.
How can heart disease be clinically apparent?
1) predominantly cardiac signs e.g. syncope or exercise intolerance
2) signs related to other changes in organs e.g. respiratory distress
How can heart disease be clinically non-apparent?
1) depends on siting, extent and duration of the lesion
2) The CVS will compensate for a long time and so chronic disease can develop asymptomatically and then suddenly manifest as acute CV disease.
What are the different pathophysiological effects than are seen in heart disease?
Left side- pulmonary congestion/oedema and decreased CO.
Right side- excessive right atrial pressure and systemic venous congestion.
What is the response of the heart to failure?
Cardiomyocytes cannot undergo hyperplasia so they undergo hypertrophy. This results in increased preload or afterload.
Increased Preload- increased volume of blood entering the heart during diastole (volume overload)
Increased Afterload- increased resistance against which the heart must pump during systole (pressure overload)
What happens in response to acute increase in preload?
The heart dilates to accommodate extra blood so force of contraction, SV and CO increase.
What happens in response to chronic increase in preload or afterload?
The myocardium undergoes hypertrophy and this can be concentric or eccentric.
What is concentric hypertrophy?
Increase in the mass of the ventricle, the wall becomes thicker. There is either no change or a decrease in EDV. This is due to increased afterload (pressure overload).
What is eccentric hypertrophy?
There is an increase in the mass of the ventricle, the wall becomes longer and the chamber dilates= increase in EDV. (wall can look thinner due to increase in length), this is due to increased preload. (volume overload)
Why do compensatory mechanisms eventually fail?
During prolonged hypertrophy, the capillary density cannot keep up with the increased myofibre size (ratio is no longer 1:1) so the cardiomyocytes are further from their blood supply= hypoxia and degeneration. Fibrous tissue takes its place- it cannot expand and contract like the myocytes = bad
How do congenital defects arise?
Genetic- inherited: through genome of sperm or ova
Acquired: genomic defect arising in the fertilised zygote
Environmental: Infections (viral in early pregnancy)
Physical (hypoxia, hyperthermia)
Nutrition (vit a deficiency)
What are the three classes of congenital defects?
Septal defects- chamber development/partitioning= SHUNTS
Abnormalities in the great vessels and their origins- SHUNTS or vascular abnormalities
Abnormalities of valve formation- DYSPLASIAS
How does and atrial defect arise?
There is a persistent foramen ovale between the atria. (can still be there in two weeks in calves and foals).
Can be a failure of fusion of the atrial septum= S-shaped connection between the atria- closed by atrial pressure= not significant
How does a ventricular defect arise?
Can occur on its own or with other conditions (teratology of fallot). Seen in cattle, sheep, pigs and cats.
Defect is high in the septum below the aortic valve behind the main LAV valve cusp and below the RAV due to failure of closing of the inter-ventricular septum.
What does a ventricular defect cause?
Causes shunting of blood from L to R, so oxygenated and de oxygenated blood mixes and there is an increase in right ventricular preload with pulmonary overperfusion
How does the truncus arteriosus develop normally?
The ascending aorta and pulmonary artery develop from a spiral partitioning of the truncus arteriosus. It depends on the correct alignment of the spiral partitioned truncus arteriosus with the semilunar endocardial cushions.
What are the three anomalies can arise from defects of the truncus arteriosus?
1) transposition defects of the roots of the great vessels- dextro-rotation of the aorta
2) persistent truncus arteriosus- failure of the spiral partitioning of the truncus arteriosus into the aorta and pulmonary artery so both ventricles empty into the same vessel.
3) semilunar valve stenosis- formation of a fibrous band in the outflow tract beneath the valve or valve cusp distortion and stenosis.
Normally either the aortic or pulmonic valve and the ventricle affected will show hypertrophy due to increased afterload.
What is Eisenmenger's Syndrome?
it happens due to PDA which causes hyperperfusion of the pulmonary vasculature. It causes fibrosis in the pulmonary vessels which increase their resistance, if this resistance becomes higher than the systemic circulation then 'shunt reversal' occurs. The blood flows from the pulmonary artery into the aorta via the PDA `rather than aorta to pulm. a.
What is persistent right aortic arch?
A vascular ring forms between the ligamentous arteriosus (arch L6) and the root of the aorta (L4).
What are anomalous subclavian arteries?
Can be combined with a persistent right aortic arch, the subclavian arteries originate from the aortic arch.
Remember double aortic arch!
What is atrioventricular valvular dysplasia and what are the two forms?
The AV valves fail to form properly and incompetence occurs- cardiac dilation and failure. It is the left AV valve that is normally affected.
1) web-like valve formations with no clear leaflets
2) short chorda tendinae with small papillary muscle masses
What is coarctation of the aorta?
narrowing of the ascending aorta (bovine)
What is ectopia cordis?
The normal heart is situated outside of the thoracic cavity- cattle and pigs.
What is endocardial fibro-elastosis?
young dogs and cats, pigs and calves. (2-3 mo with no clinical signs). The left ventricular endocardium is diffusely thickened with fibro-elastic tissue.