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27 Cards in this Set
- Front
- Back
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HEART - GENERAL ANATOMY
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pump for the circulatory system: 5L blood/min, located in
thoracic cavity in the lower MEDIASTINUM, off center to the left. |
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PERICARDIUM
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multi-layered membrane enclosing heart in the pericardial cavity
1. FIBROUS PERICARDIUM: superficial portion of pericardium made of dense fibrous CNT. Anchors heart to mediastinum, protects heart, prevents overfilling (does not stretch) 2. SEROUS PERICARDIUM: serous membrane deep to fibrous pericardium. a. PARIETAL PERICARDIUM –serous layer deep to fibrous pericardium b. VISCERAL PERICARDIUM – serous layer on surface of heart c. PERICARDIAL CAVITY – filled with serous fluid. Small space between visceral and parietal pericardial layers |
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B. HEART WALL
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1. EPICARDIUM: outer layer = visceral pericardium
2. MYOCARDIUM: middle layer = cardiac m. (bulk of heart) 3. ENDOCARDIUM: inner layer = endothelium -simple squamous epithelium lining chambers and valves -continuous with endothelium lining blood vessels |
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APEX
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inferior point of heart
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BASE
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posterior portion where vena cavae, aorta and pulmonary aa and vv. attach to heart
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FOUR CHAMBERS OF HEART
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1. TWO ATRIA: superior, small, thin-walled: receive blood from body, pump/drain to
ventricle on same side. a. AURICLES: wrinkled flaps "ears" on ant. portions b. INTERATRIAL SEPTUM: between R and L atria *FOSSA OVALIS: closed up hole (Foramen Ovale) from fetal circulation c. PECTINATE M.: bundles found in atrial walls d. ATRIOVENTRICULAR GROOVE: indent between atria and ventricles 2. TWO VENTRICLES: inferior, large, thick-walled: receive blood from atria, pump blood out of heart a. TRABECULAE CARNEAE M.: bundles found in ventricular walls b. PAPILLARY M.: attach trabeculae carnea to valve flaps c. INTERVENTRICULAR SEPTUM: between R and L ventricles d. R ventricle is anterior and thinner-walled than L e. L ventricle is posterior and thicker-walled forms apex |
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VALVES OF HEART
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allow for one-way blood flow thru heart
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ATRIOVENTRICULAR VALVES (AV VALVES)
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a. CUSPS = valve flaps: close off passageways between atria and ventricles
b. CHORDAE TENDINEAE: "strings" attaching cusps to PAPILLARY M. c. R. AV VALVE = TRICUSPID VALVE -three cusps *regulates blood from RA to RV d. L. AV VALVE = BICUSPID = MITRAL VALVE -two cusps *regulates blood from LA to LV |
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SEMILUNAR VALVES
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three half balloons "cusps" of cnt
a. prevent back flow of blood from arteries into vent. b. PULMONARY SLV: at base of PULMONARY TRUNK A. -prevents backflow into RV d. AORTIC SLV: at base of AORTA A. -prevents backflow into LV |
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VESSEL RULE
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1. VEINS: bring blood to atria (TO HEART)
2. ARTERIES: take blood away from ventricles (FROM HEART) |
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COLOR RULE FOR BLOOD (BLOOD VESSELS)
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1. RED: oxygenated - usually aa, except: pulmonary and umbilical aa, which carry
deoxygenated blood 2. BLUE: deoxygenated - usually vv, except: pulmonary and umbilical vv. which carry oxygenated blood |
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RIGHT SIDE OF HEART: PULMONARY CIRCULATION PUMP
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*GOAL: O2-poor blood from body; pump to lungs to get O2 & lose CO2 (why
RV is smaller, short distance) a. BLOOD INTO RA from -SUPERIOR VENA CAVA: from head, neck, arms -INFERIOR VENA CAVA: from lower half of body -CORONARY SINUS: from cardiac m. (heart wall) b. BLOOD THRU TRICUSPID VALVE TO RV c. RV PUMPS BLOOD THRU PULMONARY SEMILUNAR VALVE THRU PULMONARY TRUNK A. TO LUNGS d. at lungs, blood drops off CO2 and picks up O2 |
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2. LEFT SIDE OF HEART: SYSTEMIC CIRCULATION PUMP
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*GOAL: receive O2-rich blood from lungs and pump out to whole body (why
LV is large - blood goes far) a. BLOOD INTO LA -via 4 (may be more or fewer) pulmonary vv b. BLOOD THRU BICUSPID VALVE INTO LV c. LV PUMPS BLOOD THRU AORTIC SEMILUNAR VALVE THRU ASCENDING AORTA OUT TO WHOLE BODY |
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PART OF SYSTEMIC CIRCULATION: CORONARY CIRCULATION
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*GOAL: O2-rich blood from ASCENDING AORTA to cardiac m.; drain O2-
poor blood from cardiac m. to CORONARY SINUS a. ASCENDING AORTA: first part of aorta b. CORONARY AA.: first branches off aorta carry O2-rich blood to cardiac m., located in the atrioventricular sulcus 1) R. CORONARY A.: branches into a) MARGINAL A.: down rt. side of heart b) POSTERIOR INTERVENTRICULAR A. 2) L. CORONARY A.: branches into a) ANTERIOR INTERVENTRICULAR A. b) CIRCUMFLEX A. c. CARDIAC VV.: many small veins lead to CORONARY SINUS carry O2- poor blood back to R atrium |
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BLOCKED CORONARY A.
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1) ANGINA PECTORIS: pain: low blood and oxygen to myocardium
2) MYOCARDIAL INFARCTION (HEART ATTACK): due to prolonged blockage, causes death of cardiac m. 3) BYPASS SURGERY: add vessel to go around blockage (commonly use Great Saphenous V. and Internal Mammary A.) |
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HEART PHYSIOLOGY
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both atria contract at same time, both ventricles contract at the same time
A. CARDIAC MUSCLE CELLS: striated, short & branched, binucleate/uninucleate 1. INTERCALLATED DISCS: between cells a. GAP JUNCTIONS: allow open communications, fast travelling impulses -FUNCTIONAL SYNCYTIUM: cells contract as a unit -atria together followed by the -ventricles together b. DESMOSOMES: prevent separation during contraction 2. Ca++ for muscle contraction flows into the sarcoplasm from sarcoplasmic reticulum (not highly developed) and thru T-tublules (wide) from extracellular fluid 3. rely on AEROBIC RESPIRATION of glucose, fatty acids, or any other fuel: LG MITOCHONDRIA 4. Two types of cardiac m. cells a. contractile muscle cells: primary cell type in heart wall - contract b. autorhythmic muscle cells: minority of heart wall cells – set contraction rhythm |
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MECHANISM OF CONTRACTION (MECHANICAL) CONTRACTILE CELLS
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ACTION POTENTIAL: Na+ into cell during depolarization
2. Ca+ into sarcoplasm causes sliding filaments *more Ca+ from extracellular fluid causes PLATEAU in AP *long absolute refractory period due to PLATEAU, lasts almost as long as contraction: NO TETANUS POSSIBLE 3. K+ efflux causes repolarization 5. GAP JUNCTIONS: transmit info from cell to cell so myocardium contracts as a unit 6. NO NERVOUS STIMULATION IS NEEDED TO CAUSE CARDIAC M. CONTRACTION: has AUTORHYTHMIC CELLS to do this |
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AUTORHYTHMIC CELLS AND ELECTRICAL CONDUCTION THRU HEART
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AUTORHYTHMIC CELLS:noncontractile cells - form ELECTRICAL
CONDUCTION SYSTEM (synchronizes contractions of atria & ventricles) a. like neural tissue: initiate/distribute ACTION POTENTIALS thru myocardium b. no stable RMP due to Na+ leaking into cells c. continuously depolarize toward threshold set pace of contraction = PACEMAKER POTENTIALS d. at threshold, Ca+ rushes in to create AP e. K+ rushes out for repolarization |
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INTERNAL ELECTRICAL CONDUCTION SYSTEM
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all made of autorhythmic
cells each could start cardiac cycle. The fastest depolarizing cells set the pace) a. SA NODE = SINOATRIAL NODE = PACEMAKER OF HEART 1) cell cluster near post. wall of RA near SVC, creates “sinus rhythm” 2) depolarizes to threshold 75 x/min (if NOT under PSNS neural suppression, rate = 120x/min) 3) Impulses travel thru ATRIAL MYOCARDIUM -simultaneous atrial contraction -stimulates next part of conduction system b. AV NODE = ATRIOVENTRICULAR NODE (50 bpm) 1) cell cluster in RA floor near interatrial septum 2) atrial muscle cells cut off from ventricular muscle cells by av groove, only get stimulus to contract via conduction system 3) AV node cells conduct more slowly than rest of conduction system, delays impulses to ventricles by 0.1sec due to fewer gap junctions. *ATRIA FINISH CONTRACTING BEFORE VENT. BEGIN c. AV BUNDLE = BUNDLE OF HIS: in interventricular septum picks up signal from AV node (30 bpm) d. R. AND L. BUNDLE BRANCHES: branch off AV bundle travel thru interventricular septum to apex (30 bpm) e. PURKINJE FIBERS = CONDUCTION MYOFIBRILS (30 bpm) 1) branch off r and l bundle branches 2) carry AP to myocardium of ventricles 3) ventricles contract simultaneously and relax as SA node begins again 4) vent contraction is from apex up, squeezing blood out of vent towards great arteries |
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ECG = ELECTROCARDIOGRAM
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GRAPHIC recording of the ELECTRICAL events of the heart
detected on the body surface A. DEFLECTION WAVES: upward/downward deflections of ECG-represent depolarization and repolarization events in the cardiac cycle (ELECTRICAL!!!!) 1. P wave: depolarization of the atrial myocardium -occurs before contraction of atria 2. QRS COMPLEX: depolarization of the ventr. myocardium -occurs before contraction of ventricles 3. T WAVE: repolarization of vent. myocardium -occurs before relaxation of ventricles *** there is no wave for atrial repolarization, it occurs during ventricular depolarization and is obscurred by the QRS complex B. PQRST wave is consistant for a normal heart, variations in ECG represent problems: 1. large P: enlarged atria 2. absent P: SA node not working, AV node has taken over 3. lg. Q: heart attack |
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CARDIAC CYCLE: all MECHANICAL EVENTS
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(contraction and relaxation) related to flow of
blood thru the heart in one beat A. atria contract and relax then ventricles contract and relax B. DIASTOLE: relaxation SYSTOLE: contraction C. HEART RATE: measured in beats per minute (bpm) -normal = 72 bpm - 75 bpm -TACHYCARDIA = fast -BRADYCARDIA = slow |
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SERIES OF EVENTS IN CARDIAC CYCLE (approx. 0.8 sec)
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1. both atria and ventricles in DIASTOLE (.4 sec)
-SL valves closed -AV valves open 2. ATRIAL SYSTOLE = .1 sec -atria contract -blood forced into ventricles thru open AV valves 3. ATRIAL DIASTOLE: atria relax for next .7 sec. 4. VENTRICULAR SYSTOLE: during atrial diastole = .3 sec -ventricles contract -AV valves close, SL valves open -blood forced out of vent. into pulmonary A and aorta 5. VENTRICULAR DIASTOLE: .5 sec -SL valves close, AV valves open |
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HEART SOUNDS
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due to tissues/blood vibrations as valves open/close
A. FIRST HEART SOUND "LUB": due to closure of av valves B. SECOND HEART SOUND "DUPP": due to closure of SL valves C. MURMURS: abnormal heart sounds: faulty valves |
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CARDIAC OUTPUT (CO), STROKE VOLUME (SV), AND HEART RATE (HR)
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A. CO: blood vol. pumped by 1 vent./1 min.= effectiveness of heart
B. SV: blood pumped by one ventricle in 1 beat: normal = 70ml/beat C. HEART RATE: beats per minute normal = 75 bpm D. CO = SV x HR : CO = 70ml/beat x 75beats/min CO = 5250ml/min -> normal CO = 5L = total blood in body E. CO will change if body needs change or if change HR or SV |
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THINGS THAT AFFECT SV (& thus CO)
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. EDV (END DIASTOLIC VOL.): how much blood in vent. before it contracts
* STARLING'S LAW OF THE HEART: stretch ventricle, heart contracts more forcibly, increasing SV 2. VRR (VENOUS RETURN RATE): return of blood to heart * increase VRR, increase EDV, increase SV 3. SYNS STIMULATION: increases contraction force, increases SV 4. Long term exercise increases strength of heart and increases SV |
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THINGS THAT AFFECT HEART RATE (& thus CO)
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1. SA node regulation
2. BLOOD PRESSURE (BP) feed back loops a. aortic & internal carotid barroreceptors sense BP changes b. if BP low, signals sent to medulla, to SYNS to inc. stimulation CAUSING: inc. HR -> inc. CO -> inc. BP c. if BP high, signals to medulla, to PSNS to inc. stimulation CAUSING: dec. HR -> dec. CO -> dec. BP 3. EMOTIONS 4. EPINEPHRINE: from adrenals increase HR 5. CHEMORECEPTORS: sensing chemical changes in blood hi CO2 -> low blood pH -> signal to medulla ->increase HR to get more blood to lungs, tissues 6. TEMPERATURE: hi temp, increase HR 7. EXERCISE immediate effect: increase heart rate and cardiac output long term effect: increases strength of heart and increases SV, so if CO remains the same (body needs do not change), then HR would drop (at rest) |
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Continued:
CONDUCTION SYSTEM THINGS THAT AFFECT HEART RATE |
d. R. AND L. BUNDLE BRANCHES: branch off AV bundle travel thru interventricular septum to apex (30 bpm)
e. PURKINJE FIBERS= CONDUCTION MYOFIBRILS (30 BPM) 1) branch off r and l bundle branches 2)carry AP to mycardium of ventricles 3) ventricles contract simultaneously and relax as SA node begins again 4) vent contraction is from apex up, squeezing blood out of vent towards great arteries 7. EXERCISE - immediate effect: increase heart rate and cardiac output long term effect: increases strength of heart and increases SV, so if CO remains the same (body needs do not change), then HR would drop (at rest) 8. [ELECTROLYTES] in blood lower [Ca++], lower HR (CA ++ stimulates contraction hi [NA+], hi [K+], lower HR |
