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- outer layer of pericardium, inner layer of pericardial sac |
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inner layer of pericardium |
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between parietal and visceral layers contains pericardial fluid (lubricant) |
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divides atria and ventricles |
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Anterior & posterior interventricular sulcus |
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separate ventricles, contain blood vessels |
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Characteristics of cardiac muscle cells |
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-Small size -Single, central nucleus -branching interconnections between cells -Intercalated discs |
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Atrioventricular (AV) valves |
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Connect right atrium to right ventricle and left atrium to left ventricle The fibrous flaps that form bicuspid (2) and tricuspid (3) valves Permit blood flow in one direction: atria to ventricles |
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Receives blood from head, neck, upper limbs, and chest |
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Receives blood from trunk, viscera, and lower limbs |
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Cardiac veins return blood to coronary sinus Coronary sinus opens into right atrium |
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Before birth- opening through interatrial septum Connects the two atria Seals off at birth, forming fossa ovalis |
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Contain prominent muscular ridges On anterior atrial wall and inner surfaces of right auricle |
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Muscular ridges on internal surface of right (and left) ventricle Includes moderator band: – Ridge contains part of conducting system – Coordinates contractions of cardiac muscle cells |
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Conus arteriosus (superior end of right ventricle) leads to pulmonary trunk Pulmonary trunk divides into left and right pulmonary arteries Blood flows from right ventricle to pulmonary trunk through pulmonary valve Pulmonary valve has three semilunar cusps Pulmonary semilunar valve |
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Blood gathers into left and right pulmonary veins Pulmonary veins deliver to left atrium Blood from left atrium passes to left ventricle through left atrioventricular (AV) valve Two-cusped bicuspid valve or mitral valve Prevents backflow during ventricular contraction |
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Holds same volume as right ventricle Much larger; muscle is thicker and more powerful Similar internally to right ventricle but does not have moderator band |
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Blood leaves left ventricle through aortic valve into ascending aorta Ascending aorta turns (aortic arch) and becomes descending aorta |
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Atrioventricular (AV) valves |
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Blood pressure closes valve cusps during ventricular contraction Papillary muscles tense chordae tendineae: prevent valves from swinging into atria |
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pulmonary & aortic tricuspid valves Prevent backflow from pulmonary trunk and aorta into ventricles, have no muscular support |
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Cardiac (fibrous) skeleton |
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4 bands around heart valves & bases of pulmonary trunk & aorta- stabilize valves Electrically insulate ventricular cells from atrial cells |
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Originate at aortic sinuses at base of aorta Highest blood pressure in systemic circuit Elastic rebound forces blood through coronary arteries between contractions |
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Supplies blood to left ventricle, left atrium, interventricular septum 2 main branches of left coronary artery Circumflex artery Anterior interventricular artery |
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- Supplies blood to right atrium, portions of both ventricles, and cells of sinoatrial (SA) and atrioventricular nodes |
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Empties into right atrium |
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Empties into right atrium |
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Empties into right atrium |
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Empties into right atrium |
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Empties into right atrium |
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2 types of cardiac muscle cells |
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Conducting system Controls and coordinates heartbeat Contractile cells Produce contractions that propel blood |
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Step 1:SA node activity and atrial activation begin Step 2: Stimulus spreads across the atrial surfaces and reaches the AV node. Step 3:There is a 100 msec delay at the AV node. Atrial contraction begins.After traveling through AV node, impulse conducted through the AV bundle and bundle branches in the interventricular septum to Purkinje fibers. Step 4: The impulse travels along the interventricular septum within the AV bundle and the bundle branches to the purkinje fibers and, via the moderator band, to the papillary muscles of the right ventricle. Step 5: Purkinje fibers distribute impulse through ventricles. Atrial contraction completed, ventricular contraction begins. |
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Abnormal cells generate high rate of action potentials Bypass conducting system, disrupt ventricular contractions Results in pumping efficiency reduction |
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P wave: atria depolarization QRS complex: ventricles depolarize, ventricles contracting shortly after R wave T wave: ventricles repolarize |
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Contraction of a cardiac muscle cell is produced by an increase in Ca2+ concentration around myofibrils 1. calcium ions crossing plasma membrane during plateau phase provide about 20% of Ca required for a contraction 2. Arrival of extracellular Ca2+ triggers release of calcium ion reserves from sarcoplasmic reticulum. |
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4 phases of the cardiac cycle |
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atrial systole, atrial diastole, ventricular systole, ventricular diastole |
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8 steps in the cardiac cycle |
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1. atrial systole 2. atria eject blood into ventricles 3. Atria systole ends 4. Ventricular systole 5. Ventricular ejection 6. ventricular pressure falls 7. Ventricular diastole 8. Atrial pressure is higher than ventricular pressure |
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End-diastolic volume (EDV) |
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Amount of blood in each ventricle at end of ventricular diastole |
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Produced by AV valves closing, start of ventricular contraction |
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produced by semilunar valves closing, beginning of ventricular filling |
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End-systolic volume (ESV) |
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Amount of blood remaining in each ventricle at end of ventricular systole |
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Amount of blood pumped out of each ventricle during a single beat SV=EDV-ESV |
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Absolute refractory period |
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membrane cannot respond at all Na+ channels already open, closed or inactivated Usually lasts the duration of plateau and initial period of rapid repolarization |
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Relative refractory period |
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Na+ channels closed but can open if stronger than normal stimulus Action potential lasts 30 X’s longer than skeletal muscle |
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Cardioacceleratory center |
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controls sympathetic neurons (increases heart rate) |
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controls parasympathetic neurons (slows heart rate) |
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Effects on the SA Node (heart rate) |
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Any factor that changes rate of spontaneous depolarization or duration of repolarization will alter heart rate by changing time required to reach threshold Resting membrane potential Rate of depolarization |
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Ach- parasympathetic stimulation |
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Open chemically gated K+ channels- slowing depolarization, extending repolarization- Slows the heart |
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NE- sympathetic stimulation |
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Binds beta-1 receptors, open Na+ -Ca2+ channels, increases rate of depolarizaton, shortens repolarization- speeds the heart |
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adjusts heart rate in response to increase in venous return -Stretch receptors in right atrium trigger increase in heart rate through increased sympathetic activity Rate of venous return to heart increases, heart rate & cardiac output increase as well |
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Factors affecting the stroke volume |
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The greater the EDV, the larger the stroke volume At rest EDV is low, myocardium stretches less Stroke volume is low With exercise, EDV increases, myocardium stretches more Stroke volume increases |
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As EDV increases, stroke volume increases |
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Ventricular expansion is limited by: |
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Myocardial connective tissue The cardiac (fibrous) skeleton The pericardial sac |
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Preload- Ventricular stretching during diastole Contractility- Force produced during contraction, at a given preload Afterload- Tension the ventricle produces to open the semilunar valve and eject blood |
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Contractility is affected by: |
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Autonomic activity Hormones Increase contractility- positive inotropic action Stimulate Ca2+ entry into cardiac muscles, increasing force & duration of ventricular contraction Decrease contractility- negative inotropic action Block Ca2+ entry into cardiac muscles Factors include: ANS activity, hormones, changes in extracellular ion concentration |
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Effects of Autonomic Activity on Contractility |
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Sympathetic stimulation- POSITIVE effect NE released by cardiac nerves E and NE released by suprarenal medullae Causes ventricles to contract with more force Increases ejection fraction and decreases ESV |
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Effects of Autonomic Activity on Contractility |
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Parasympathetic stimulation- NEGATIVE effect Acetylcholine released by vagus nerves Produces hyperpolarization & inhibition Reduces force of cardiac contractions |
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Pharmaceutical drugs mimic hormone actions |
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Stimulate beta receptors- mimic E, NE Stimulate Ca2+ channels alpha-1 receptor Treat hypertension- beta or alpha blockers (negative effect) Calcium channel blockers- negative effect |
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Effects of Autonomic Activity on Contractility Afterload |
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tension ventricle produces to open semilunar valve and eject blood Afterload increased by any factor that restricts arterial blood flow As afterload increases, stroke volume decreases Indirect relationship |
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difference between resting and maximal cardiac output |
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