2822451
CVS
- 1) The heart is one of the most active systems in
the body, with dysfuction quickly causing
death- 60% in the Western world (maily caused
by lipid abnormalities). Animals less effected-
die early (PA) + lipids ~ normal
- Structure; Four chambers, two pumps,
3:1 thickness and pressure between L
and R side. there are four valves... Av's-
right and left, Pulmonic and Aortic
- Endocardium, Myocardium (spiral
muscles, individual capillaries to
myocytes which rely on O2) and the
Epiceardium- fibrous tissue attached to
the visceral layer of peri
- 1) STRUCTURE
- Endocardium, Myocardium (spiral
muscles, individual capillaries to
myocytes which rely on O2) and the
Epiceardium- fibrous tissue attached to
the visceral layer of peri
- Look for pallor in the Myocardium - this may be
caused by; cell necrosis, fibrous tissue or Rigor
mortis contraction. Need histo to differentiate
- Also assess: Weight, shape, relative wall
thickness, patency of the valves/ walls and
signs of mineralisatio
- POST MORTEM
- Also assess: Weight, shape, relative wall
thickness, patency of the valves/ walls and
signs of mineralisatio
- 2) REPAIR
- Cardiac myocytes cannot regenerate so necrosis can
only be replaced by fibrosis reducing strength and
contraction. The heart has a 3-5 fold reserve function
but the compensation will occur- CHF develops. Then
there is "decompensation"- thinning and death
- Cardiac myocytes cannot regenerate so necrosis can
only be replaced by fibrosis reducing strength and
contraction. The heart has a 3-5 fold reserve function
but the compensation will occur- CHF develops. Then
there is "decompensation"- thinning and death
- 3) Changes in heart SIZE
- This may be
PHYSIOLOGICAL (training) or
PATHOLOGICAL (1* or 2*)
- This may be
PHYSIOLOGICAL (training) or
PATHOLOGICAL (1* or 2*)
- LAB DIAGNOSIS
- Enzymes: Both CK and AST are released with
necrosis but will or rise fast enough to detect
early dz
- Cardiopet proBNP. BNP is a peptide involved
in fluid haemostasis ad BP regulation. Its
secreted in response to volume overload,
cardiac hypertrophy and hypoxia... the worse,
the more released.
- Pink tube,
protease inhibitor,
regrigeration,
same day
- In dogs- used to differentiate
chronic bronchitis or LSCHF, high
levels have been suggetsive to
idicate. Less evidence to support
whether tmt is workig. In cats-
brochitis Vs CHF yes but not for
HCM
- Pink tube,
protease inhibitor,
regrigeration,
same day
- Enzymes: Both CK and AST are released with
necrosis but will or rise fast enough to detect
early dz
- 3_ Congenital and Genetics...
- These are common findings in BOTH large and small
animals, ^ in pedigrees (often with inheridability) but
poor association with teratogens (as opposed to people)
- Many cause a turbulent blood flow (murmurs),
seen best in fresh specimes as formalin causes
contraction. This makes defects (such as PDA) difficult to
see
- Many cause a turbulent blood flow (murmurs),
seen best in fresh specimes as formalin causes
contraction. This makes defects (such as PDA) difficult to
see
- Failure of structures to CLOSE....
- PDA: Female poodles (but all dogs) -
occurs when the ductus arteriousus
(vessel from aorta to P.artery) does not
become the ligametum structure.
There is no BP differentaition- 3;1
becomes 1:1.
- Atrial septal defect- either the FO
or the septum itself. Blood shunts
L-R, there is pulmonary
hypertension and 1:1
- A ventricular septal defect-
usually dorsal growth impaired
(defect is hard to see) 1:1 and P.
Hypertension
- TETROLOGY OF FALLOT- there are four
conditions: Ventricular septal defect,
pulmonary stenosis, transposition of the
aorta and 2* (compensation) RV
hypertrophy. Blood pumps abnormally
from right to left into circulation
- Cyanosis
- Cyanosis
- PDA: Female poodles (but all dogs) -
occurs when the ductus arteriousus
(vessel from aorta to P.artery) does not
become the ligametum structure.
There is no BP differentaition- 3;1
becomes 1:1.
- Abnormal valve developments
- Pulmonic stenosis- 2* hypertrophy
and depending on severity- RSCHF
may develop
- Subaortic stenosis- pigs/ dogs is a thick band of
fibrous tissue below the aortic valve. 2* proximal
aorta dilation, ventricular hypertrophy. The turbulent
blood flow predisposes myocardial infarct. Dogs have
either LSCHF or sudden death
- Valvular haemocyst-
common finding in young
that will regress
- Congenital valve
malformations- reduced
patency- less common
- Pulmonic stenosis- 2* hypertrophy
and depending on severity- RSCHF
may develop
- Large BV changes
- PRAA
- There is no change to blood flow if the right aortic
arch persists but the ligament
contracts over the esophagus. Clinical onset:
Regurgitation and mega- oseophagus. Snip it
- There is no change to blood flow if the right aortic
arch persists but the ligament
contracts over the esophagus. Clinical onset:
Regurgitation and mega- oseophagus. Snip it
- Transposition of the Aorta and P.Artery
- These cause severe clinical signs- born dead or die
rapidly post natally and are rare. Typically; both
the aorta and P.Artery arise from the RV OR aorta
attaches half to the left ventricle, half to the right
- These cause severe clinical signs- born dead or die
rapidly post natally and are rare. Typically; both
the aorta and P.Artery arise from the RV OR aorta
attaches half to the left ventricle, half to the right
- PRAA
- These are common findings in BOTH large and small
animals, ^ in pedigrees (often with inheridability) but
poor association with teratogens (as opposed to people)
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