CVS

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
1. Endocardium, Myocardium (spiral muscles, individual capillaries to myocytes which rely on O2) and the Epiceardium- fibrous tissue attached to the visceral layer of peri
2. 1) STRUCTURE
Look for pallor in the Myocardium - this may be caused by; cell necrosis, fibrous tissue or Rigor mortis contraction. Need histo to differentiate
1. Also assess: Weight, shape, relative wall thickness, patency of the valves/ walls and signs of mineralisatio
2. POST MORTEM
2) REPAIR
1. 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
1. This may be PHYSIOLOGICAL (training) or PATHOLOGICAL (1* or 2*)
LAB DIAGNOSIS
1. Enzymes: Both CK and AST are released with necrosis but will or rise fast enough to detect early dz
2. 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.
  1. Pink tube, protease inhibitor, regrigeration, same day
  2. 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
3_ Congenital and Genetics...
1. These are common findings in BOTH large and small animals, ^ in pedigrees (often with inheridability) but poor association with teratogens (as opposed to people)
  1. 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
2. Failure of structures to CLOSE....
  1. 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.
  2. Atrial septal defect- either the FO or the septum itself. Blood shunts L-R, there is pulmonary hypertension and 1:1
  3. A ventricular septal defect- usually dorsal growth impaired (defect is hard to see) 1:1 and P. Hypertension
  4. 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
    1. Cyanosis
3. Abnormal valve developments
  1. Pulmonic stenosis- 2* hypertrophy and depending on severity- RSCHF may develop
  2. 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
  3. Valvular haemocyst- common finding in young that will regress
  4. Congenital valve malformations- reduced patency- less common
4. Large BV changes
  1. PRAA
    1. 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
  2. Transposition of the Aorta and P.Artery
    1. 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

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