Download Cardiovascular system The heart

 The heart is a conical ,muscular organ that evolved into a four
chambered pump with four valves..
 The heart lies within a fibroelastic sac ,the pericardium, which
normally contains a small amount of clear ,serous fluid .
 The heart is interposed as a pump into the vascular system
,with the right side supplying the pulmonary circulation and
the left side the systemic circulation .
 The wall of the heart is composed of three layers :the
epicardium, the myocardium and the endocardium .
 The epicardium ,the outermost layer of the heart ,is the visceral
pericardium .
 The entire inner surface of the pericardium cavity is covered by
mesothelium .
 The subepicardial layer is attached to the myocardium and consist of
a thin layer of fibrous connective tissues, variable but generally
abundant amount of adipose tissue, and numerous blood vessels
,lymph vessel, and nerves.
 The myocardium is the muscular layer of the heart ,it consist of
cardiac muscle cells (myocytes) arranged in overlapping spiral
patterns .
 The myocardial thickness is related to the pressure present in each
camber ,thus the atria are thin walled and the ventricles are thicker .
 The thickness of the left ventricular free wall is approximately
threefold that of the right ventricle .
 The endocardium is the innermost layer of the heart and
lines the chambers and extents over projecting structures
,such as the valves ,chordae tendineae and papillary
muscles.
 The surface of the endocardium is endothelium that lies on
a thin layer of connective tissue.
 The subendocardial layer contains blood vessel ,nerves,
and connective tissue.
 The arterial supply to the heart is the left and right
coronary arteries which arise from the aorta .
 The arteries course over the heart in subepicardium and
give off perforating intramyocardial arteries that supply a
rich capillary bed throughout the myocardium.
 The ratio of the area of capillaries to that of muscle cells is
approximately 1:1 .
 Postmortem alterations in hearts must be recognized and
correctly interpreted.
 Rigor mortis occurs in myocardium as in skeletal muscle
and produces contracted ,rigid ventricular walls ,which
empties the more muscular left ventricular .after rigor
passes ,the ventricular wall relax.
Animals with prolonged heart disease may lack
adequate glycogen reserves in cardiac myocytes.
 As a result ,the ventricular chambers may fail to contract
during rigor mortis ,allowing a blood clot to form in the
left ventricle
 Cardiac muscle cells are surrounded by interstitial
components ,which include blood and lymph vessels,
nerves and connective tissue cells such as fibroblast
,histocyte ,mast cells, pericytes ,primitive mesenchymal
stem cells and extra cellular matrix elements of connective
tissue ,including collagen fibrile ,elastic fibers and acid
mucopolysaccharides .
 Cardiac muscle cells can be divided into two populations:
the working myocytes and the specialized fibers of the
conduction system .
 Adjacent myocyte are joined end to end by specialized
junctions known as intercalated disks and less frequently
by side to side connections termed lateral junctions..
 Multinucleated fibers with nuclei arranged in central rows
are frequently seen in hearts .
 The cytoplasm (sarcoplasm) of myocytes is largely
occupied by the contractile proteins that are highly
organized into sarcomers, the repeating contractile units of
the myofibril.
 Myofibrils are formed by end to end attachment of many
sarcomers .
 The cross striated or banded appearance of myocytes is
the result of sarcomeric organization into A bands
(myosin) and I bands (actin ) composed .
 Myocytes are enclosed by the sarcolemma ,which
consists of the plasma membrane and the covering
basal lamina .
 Other important components of cardiac muscle cells
appeared in Electron micrographs include abundant
mitochondria ,sarcoplasmic reticulum ( network of
intracellular tubules), ribosome ,cytoskeletal filaments
,glycogen particles ,lipid droplet and Golgi
complexes.
 Reaction to injury
 Cardiac muscle cells respond to injury by a limited spectrum
of reaction .
 Reversible morphologic alteration include cellular growth
disturbance that lead to atrophy or hyperatrophy .
 Sub lethal injuries or degeneration , such as fatty degeneration
,lipofuscinosis ,vascular degeneration ,and myocytolysis .
 Lethal injuries to myocytes result in necrosis or apoptosis .
 Necrosis of cardiac muscle cells is generally followed by
leukocytic invasion and phagocytosis of sarcoplasmic debris .
 The end result is persistence of collapsed sarcolemma (tubes)
of basal lamina surrounded by condense interstitial stroma and
vessels .
 In sever distruption of myocardium have residual changes of
fibroblast proliferation and collagen deposition to form scar
tissue.
 Regeneration of cardiac muscle cells generally dose not occur .
 Recent studies indicate that stem cells exist in adult animal and
human heart ,these cells in myocardial injury may differentiate
in to cardiac muscle cells.
 Hyperplasia of myocyte is a normal component of cardiac
growth in the first several month of life .then proliferation
causes normal growth then is the result of hypertrophy of
myocyte until cell size normal for the species are reached .
 Apoptosis is increasingly recognized for it is role in the development
of various myocardium lesion and cardiac disease .
 These condition include cardiac development ,ischemic injury ,
heart failure ,hypoxia ,pressure overload hypertrophy,
cardiotoxicity, oxygen free radicals .
 Cells dying by apoptosis shrink and form apoptotic bodies .
 In contract to cell death by necrosis , apoptosis is not accompanied
by an inflammatory reaction and fibrosis .
 Correlation between the severity of clinical cardiac disease and the
severity of myocardial injury can be poor, a small lesion at a critical
site such as ,apportion of the conduction system , can be fatal ,where
as a wide spread myocardial lesion, such as myocarditis, can be
asymptomatic.
 Cardiac pathophysiology
 The result of normal cardiac function include the
maintenance of adequate blood flow, called cardiac
output ,to peripheral tissue that provide delivery of
oxygen and nutrient ,the removal of carbon dioxide and
other metabolic waste product ,the distribution of
hormones and other cellular regulation ,and the
maintenance of a adequate thermo regulation and
glomerular filtration pressure (urine output ) the normal
heart has a three fold to five fold functional reserve
capacity . but this capacity can be lost in cardiac disease ,
 Compensatory mechanism operate in both normal and
disease heart. these mechanism include cardiac
dilation ,myocardial hypertrophy ,increase in heart
rate ,increase in peripheral resistance , increase in
blood volume and redistribution of blood flow these
compensatory mechanism can maintain cardiac
output for some time .

 Circulatory disturbance
 Hemorrhage is a frequent lesion of the pericardium ,
endocardium and myocardium .
 hemorrhage vary in size from petechial (1-2 mm) to
ecchymosis (2-10 mm) ,to suffusive (diffuse).
 Animal dying from septicemia ,endotoxemia ,anoxia , or
electrocution , often have prominent pericardial and
endocardial hemorrhage .
 In selenium ,Vit E deficiency ,in these case ,hydro
pericardium accompanies severe myocardial hemorrhage
that result in a red ,mottled appearance of the heart.
 Syndromes of cardiac failure or
decomposition
 Cardiac syncope ,an acute expression of cardiac
disease ,is characterized clinically by collapse ,loss of
consciousness and extreme changes in heart rate and
blood pressure and with or with out demonstrable
lesion ,the causes can be massive myocardial necrosis,
ventricular fibrillation ,heart block ,arrhythmias, and
reflex cardiac inhibition (e.g .,that associated with
high intestinal blockage).
 Congestive heart failure
 Usually develop slowly from gradual loss of cardiac
pumping efficiency associated with either pressure or
volume overload or myocardial damage.
 Pathogenically ,congestive heart failure is initiated by
development of cardiac disease (myocardial ,valvular
,congenital ,etc ) ,or increases work load associated with
pulmonary ,renal or vascular disease leading to losses of
cardiac reserve and development of decrease blood flow to
peripheral tissue(forward failure ) and accumulation of
blood behind the failing champers (back word failure ).
 Reduced renal blood flow creates hypoxia in the
kidneys and increases renin, released from
the
juxtaglomerular apparatus ,resulting in stimulation of
aldosterone released from the zona glomerulosa of
the adrenal cortex , sodium and water retention are the
result of the action of aldosterone on the renal tubules
,increased
plasma volume follows
, as dose
accumulation of edema fluid (mainly in body cavities ).
 Hypoxia also stimulate increased erythropoiesis in bone
marrow and extra medullary organs such as the spleen
causing polythemia and thus increase viscosity of the
blood .
 The hypervolemia from aldosterone
induced water
retention increased the workload on the all ready failing
heart .thus a vicious cycle of cardiac decomposition in
initiated that will lead to death from cardiac failure .
 Cardiac dilatation , hypertrophy and increased heart rate
can provide some compensation for the increased
workload .
 Acute left side heart failure is manifested by pulmonary
congestion and edema .
 Chronic heart failure is manifested by chronic passive
pulmonary congestion ,chronic edema
( heart failure cells)and fibrosis .
, hemosidrosis
 The most common causes
1. Myocardial contractility loss associated with myocarditis
,myocardial necrosis or cardiomyopathy
2. Dysfunction of the mitral or aortic valve .
3. Several congenital heart disease .
 Acute right site heart failure result in a cute passive
congestion leading to hepatomegaly and splenomegaly .
 Chronic right side heart failure result in hepatic
congestion (nutmeg liver) and severe sodium and water
retention than in left heart failure.
 The cause of right side failure include;
 1-Pulmonary hypertension .
 2-Cardiomyopathy.
 3-Disease of the tricuspid and pulmonary valve.