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Cardiovascular system (pathology II) - Coggle Diagram
Cardiovascular system (pathology II)
Structure of heart and blood flow
Post Mortem changes
Rigor mortis
contracted heart, rigid walls
left ventricle may be empty of blood bcs of contractraction
Post mortem clot (chicken fat clot)
may be present within atrium and right ventricle
seen in horse because of the ability of equine erythrocyte to undergo Rouleaux formation
also can be seen in septic animals
Gross:
the clot are shiny and gelatinous
chicken fat clots: yellow appearance at one end and red at the other
Hemoglobin imbibition
Sectioning
sectioned in echoplane sectioning-so that can compare the gross pathological changes to the ultrasound taken in live animal
DISEASE OF MYOCARDIUM
Composed of cardiac muscle (myocytes)
Respond to injury much like the skeletal muscle
Cardiac muscle has greater liability because of its continual activity and dependance on aerobic glycolysis
Papilllary muscles of left ventricle
seem to be more sensitive believed to be due to the vascular supply of the heart
Thickness of left ventricular free wall is approximately 3 times compared to right ventricle when measured in transverse section across the middle of the ventricles
this result from the greater pressure in systemic circulation than in pulmonary circuit
newborn animal: right and left ventricle are equal in thickness
Myocardial reaction to injury
Reversible
Reversible morphologic alteration of myocardium
changes are due to workload requirement
Atrophy
Hypertrophy
Sublethal injuries
Myofibres are still viable- but may be injured and not functioning well
Fatty degeneration
Lipofuscin
Vacuolar degeneration
Myocytolysis
Lethal injuries
Myocardial cell death
Necrosis
Inflammation present
Often followed by leukocytic invasion + phygocytosis of debris
can be look myocarditis
macrophage invasion and phagocytosis of necrotic material
fibroblast proliferation result in fibrosis with collagen deposition
the end result is
Fibrosis
Apoptosis
Myofibres shrink and form apoptotic bodies
No inflammation
Minimal fibrosis
Compensatory mechanisms
occur with an increase of demand in workload
Cardiac dilatation
Causes: same with hypertrophy but cannot undergo hypertorphy because of the following reasons:
insufficient time
inadequate nutrition
Diseases myocardium
Detection at necropsy: can be difficult
Terminal lesion in many cardiac disease process
Myocardial Hypertrophy
Definition
: reversible increase in the mass but not number of myocardial cells
Cellular stages Of cardiac hyperthrophy
Initiation
: increase in cell size by increasing the number of sarcomeres and mitochondria
Compensation
: stable hyperfunction of the heart. absence or minimal clinical signs of the heart failure
Deterioration
: degeneration of hyperthrophied cardiomyocytes, loss of myocardial contractility and frank evidence of heart failure
Pathophysiology:
^ number of myofibril
^ size of myocardial fibre (muscle fibre contain many myofibrils)
^ size of mitochondria
^ number of ribosome
synthesis of abnormal proteins
^ collagen
^ in cell volume compared to vascular supply
^ metabolic requirements and oxygen consumption
*3 & 7 are the reason why hypertropic myocardium can cause failure
Type of hypertropy
Concentric Cardiac Hypertrophy (Pressure Overload Hypertrophy)
Definition:
an increase in mass of the ventricle w/o accompanying increase in end diastolic volume
Necropsy findings:
increased thickness of ventricular wall and size of papillary muscle of affected chamber
ventricular chamber size may decrease
in general:
Right sided heart hypertrophy (RVH) : cause the heart base broader
Left sided heart hypertrophy (LVH) : produce more rounded shape of heart
Pathophysiology:
sarcomere increase in number parallel to long axis of cells (wider)
Cause: Pressure overload
Examples: Aortic stenosis(LVH), pulmonic stenosis (RVH), Pulmonary hypertension(RVH), systemic hypertension (LVH), Hyperthyroidism- enhanced production of myocardial contractile protein
Eccentric Cardiac Hypertrophy (Volume Overload Hypertrophy)
Defintion:
an increase in myocardial mass accompanied by an increased end diastolic volume and ventricular volume
Pathophysiology:
Sarcomeres increase in number in length and width
Causes: Volume overloads
Local pathological changes: Valvular insufficiency or Congenital defect with shunt
^ blood volume
develop in later stages of disease that cause concentric hypertrophy
Necropsy findings:
Enlarged cardiac chamber
Heart tends to be globose in shape, ventricular walls are usually thin
Papillary muscle may be attenuated
Endocardium may be white due to fibrosis
Detection:
Wall thickness measurement is not reliable bcs in eccentric hypertophy, the wall may be thin.
Good detection using % heart weight relative to body weight.
% increased in hypertrophied heart
increasing % also can be due to normal physiological hypertrophied
Decompensation
(Cardiac failure)
Congestive Heart Failure (CHF)
Definition
: Heart is not able to pump blood at normal rate that can support requirement of metabolizing tisssue
or - cardiac output is lower that venous return
Lesion
Left Heart Failure
: cause pulmonary edema
Right heart failure
: cause centribular hepatic congestion and generalized edema resulting from increased hydrostatic pressure
Disease of
Myocardium
Pericardium
Endocardium
