Presentation on theme: "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,"— Presentation transcript:
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, hemosidrosis ( heart failure cells)and fibrosis. 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.