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| the scientific study of the heart and the treatment of its disorders |
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| heart, blood vessels, and the blood |
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| major divisions of circulatory system |
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–pulmonary circuit –systemic circuit |
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-right side of heart -carries blood to lungs for gas exchange and back to heart |
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-left side of heart -supplies oxygenated blood to all tissues of the body and returns it to the heart |
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–fully oxygenated blood arrives from lungs via pulmonary veins –blood sent to all organs of the body via aorta |
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–lesser oxygenated blood arrives from inferior and superior vena cava –blood sent to lungs via pulmonary trunk |
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| where the heart is located which is between the lungs |
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| wide, superior portion of heart, blood vessels attach here |
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| inferior end, tilts to the left, tapers to point |
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-double-walled sac (pericardial sac) that encloses the heart –allows heart to beat without friction, provides room to expand, yet resists excessive expansion –anchored to diaphragm inferiorly and sternum anteriorly |
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| visceral pericardium (epicardium) |
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–heart covering –serous membrane covering heart –adipose in thick layer in some places –coronary blood vessels travel through this layer |
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| -space inside the pericardial sac filled with 5-30 mL of pericardial fluid |
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| –inflammation of the membranes |
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–smooth inner lining of heart and blood vessels –covers the valve surfaces and continuous with endothelium of blood vessels |
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–layer of cardiac muscle proportional to work load -muscle spirals around heart which produces wringing motion –fibrous skeleton of the heart |
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| fibrous skeleton of the heart |
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-framework of collagenous and elastic fibers -provides structural support and attachment for cardiac muscle and anchor for valve tissue -electrical insulation between atria and ventricles important in timing and coordination of contractile activity |
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| atrioventricular (AV) valves |
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| controls blood flow between atria and ventricles |
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| right AV valve that has 3 cusps |
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| left AV valve that has 2 cusps |
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-cords connect AV valves to papillary muscles on floor of ventricles -prevent AV valves from flipping inside out or bulging into the atria when the ventricles contract |
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-control flow into great arteries –open and close because of blood flow and pressure |
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| pulmonary semilunar valve |
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| -in opening between right ventricle and pulmonary trunk |
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| -in opening between left ventricle and aorta |
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| myocardial infarction (MI) (heart attack) |
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–interruption of blood supply to the heart from a blood clot or fatty deposit (atheroma) can cause death of cardiac cells within minutes –some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium –sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation –atheroma (blood clot or fatty deposit) often obstruct coronary arteries –cardiac muscle downstream of the blockage dies –heavy pressure or squeezing pain radiating into the left arm –some painless heart attacks may disrupt electrical conduction pathways, lead to fibrillation and cardiac arrest -silent heart attacks occur in diabetics & elderly –MI responsible for about half of all deaths in the United States |
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–chest pain from partial obstruction of coronary blood flow –pain caused by ischemia of cardiac muscle –obstruction partially blocks blood flow –myocardium shifts to anaerobic fermentation producing lactic acid stimulating pain |
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| striated, short, thick, branched cells, one central nucleus surrounded by light staining mass of glycogen |
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| join cardiocytes end to end |
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-gap junctions allow ions to flow between cells –can stimulate neighbors |
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| -repair of damage of cardiac muscle is almost entirely done by scarring |
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-depends almost exclusively on aerobic respiration used to make ATP –rich in myoglobin and glycogen –huge mitochondria –fill 25% of cell |
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| adaptable to organic fuels used |
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| –fatty acids (60%), glucose (35%), ketones, lactic acid and amino acids (5%) |
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| Cardiac Conduction System |
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•coordinates the heartbeat •sinoatrial (SA) node •atrioventricular (AV) node •atrioventricular (AV) bundle (bundle of His) •Purkinje fibers •signal pass from cell to cell through gap junctions |
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-modified cardiocytes –initiates each heartbeat and determines heart rate –signals spread throughout atria –pacemaker in right atrium near base of superior vena cava |
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| atrioventricular (AV) node |
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–located near the right AV valve at lower end of interatrial septum –electrical gateway to the ventricles –fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles from any other route |
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| atrioventricular (AV) bundle (bundle of His) |
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–bundle forks into right and left bundle branches –these branches pass through interventricular septum toward apex |
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| –nervelike processes spread throughout ventricular myocardium |
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| sympathetic nerves (raise heart rate) |
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–fibers terminate in SA and AV nodes, in atrial and ventricular myocardium, as well as the aorta, pulmonary trunk, and coronary arteries -increase heart rate and contraction strength -dilates coronary arteries to increase myocardial blood flow |
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| parasympathetic nerves (slows heart rate) |
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–pathway begins with nuclei of the vagus nerves in the medulla oblongata -parasympathetic stimulation reduces the heart rate |
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| atrial or ventricular contraction |
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| atrial or ventricular relaxation |
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| normal heartbeat triggered by the SA node |
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| another parts of heart fires before SA node |
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| region of spontaneous firing |
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| if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm |
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| intrinsic ventricular rhythm |
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| if both SA and AV nodes are not functioning, rate set at 20 to 40 bpm |
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–any abnormal cardiac rhythm –failure of conduction system to transmit signals (heart block) -bundle branch block -total heart block (damage to AV node) |
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–serious arrhythmia caused by electrical signals reaching different regions at widely different times -heart can't pump blood and no coronary perfusion –kills quickly if not stopped |
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| strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm |
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•abnormalities in conduction pathways •myocardial infarction •nodal damage •heart enlargement •electrolyte and hormone imbalances |
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| one complete contraction and relaxation of all four chambers of the heart |
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| occurs while ventricles are in diastole |
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| occurs while ventricles in systole |
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| all four chambers relaxed at same time |
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-causes a fluid to flow (fluid dynamics) –pressure gradient -pressure difference between two points –measured in mm Hg with a manometer or sphygmomanometer |
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-opposes fluid flow –great vessels have positive blood pressure –ventricular pressure must rise above this resistance for blood to flow into great vessels |
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| •auscultation •first heart sound (S1) •second heart sound (S2) •S3 •exact cause of each sound is not known with certainty |
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| listening to sounds made by body |
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| louder and longer “lubb”, occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall |
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| softer and sharper “dupp” occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall |
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| rarely heard in people over 30 |
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| congestive heart failure (CHF) |
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-results from the failure of either ventricle to eject blood effectively –usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure -eventually leads to total heart failure |
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–blood backs up into the lungs causing pulmonary edema –shortness of breath or sense of suffocation |
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| right ventricular failure |
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–blood backs up in the vena cava causing systemic or generalized edema –enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet |
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–the difference between a person's maximum and resting CO –increases with fitness, decreases with disease |
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| surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips |
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| resting adult heart rate above 100 bpm |
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| resting adult heart rate of less than 60 bpm |
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| cardiac centers in the medulla |
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| receive input from many sources and integrate it into the 'decision' to speed or slow the heart |
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| higher brain centers affect heart rate |
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–cerebral cortex, limbic system, hypothalamus -sensory or emotional stimuli |
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| also receives input from muscles, joints, arteries, and brainstem |
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| in the muscles and joints |
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-signal cardiac center -pressure sensors in aortaand internal carotid arteries -blood pressure decreases, signal rate drops, cardiac center increases heart rate -if blood pressure increases, signal rate rises, cardiac center decreases heart rate |
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| •in aortic arch, carotid arteries and medulla oblongata •sensitive to blood pH, CO2 and O2 levels |
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| chemoreflexes and baroreflexes |
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| responses to fluctuation in blood chemistry, are both negative feedback loops |
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| stimulates catecholamine secretion |
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| increases number adrenergic receptors on heart so more responsive to sympathetic stimulation |
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| inhibits cAMP breakdown prolonging adrenergic effect |
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| –excess K+ in cardiocytes –myocardium less excitable, heart rate slows and becomes irregular |
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| –deficiency K+ in cardiocytes –cells hyperpolarized, require increased stimulation |
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| –excess of Ca2+ –decreases heart rate and contraction strength |
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| –deficiency of Ca2+ –increases heart rate and contraction strength |
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| Exercise and Cardiac Output |
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•proprioceptors signal cardiac center –at beginning of exercise, signals from joints and muscles reach the cardiac center of brain –sympathetic output from cardiac center increases cardiac output •increased muscular activity increases venous return –increases preload and ultimately cardiac output •increase in heart rate and stroke volume cause an increase in cardiac output –increased stroke volume allows heart to beat more slowly at rest –athletes with increased cardiac reserve can tolerate more exertion than a sedentary person |
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| coronary artery disease (CAD) |
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–a constriction of the coronary arteries –usually the result of atherosclerosis –endothelium damaged by hypertension, virus, diabetes or other causes –monocytes penetrate walls of damaged vessels and transform into macrophages •absorb cholesterol and fats to be called foam cells –look like fatty streak on vessel wall –can grow into atherosclerotic plaques (atheromas) –platelets adhere to damaged areas and secrete platelet-derived growth factor •attracting immune cells and promoting mitosis of muscle and fibroblasts, and the deposition of collagen •bulging mass grows to obstruct arterial lumen |
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| accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen |
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•causes angina pectoris, intermittent chest pain, by obstructing 75% or more of the blood flow •immune cells of atheroma stimulate inflammation –may rupture –traveling clots or fatty emboli may result •cause coronary artery spasms due to lack of secretion of nitric oxide (vasodilator) •arteriosclerosis |
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| inflammation transforms atheroma into a hardened complicated plaque |
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•unavoidable risk factors -heredity, aging, being male •avoidable risk factors –obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet |
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