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TLL CH18 HEART

HEART

QuestionAnswer
ISOVOLUMETRIC CONTRACTION IS PHASE ALL VALES ARE CLOSED PHASE 2
EJECTION PHASE VENT PRESSURE EXCEEDS PRESSURE IN THE LG ARTIES, FORCING THE SL VALVES OPEN
END SYSTOLIC VOLUME VOLUME OF BLOOD REMAINING IN EACH VENTRICLE
ISOVOLUMETRIC REAXATION OCCURS IN EARLY DIASTOLE
CO= HR X SV=
CARDIAC OUTPUT VOLUME OF BLOOD PUMPED BY EACH VENT IN ONE MINUTE
THREE MAIN FACTORS FOR SV PRELOAD...CONTRACTILITY.....AFTERLOAD
PRELOAD DEGREE OF STRENCH OF CARDIAC MUSCLE CELLS BEFORE THEY CONTRACT
FRANK STARLING LAW THE AMOUNT OF STRECTCHING OF CARDIAC MUSCLE FIBERS HELPS REGULATE STOKE VOLUME AND MAINTAIN EQUAL OUTPUT FROM BOTH VENTRICLES
CONTRACTILITY CONTRACTILE STRENGTH AT A GIVEN MUSCLE LENTH, INDEPENDENT OF MUSCLE STRETCH AND EVD
POS INOTROPIC AGENTS INCREASE CONTRACTILILY, INCREASE CA, HORMONES THYROXINE, GLUCAGON, EPI
NEG INOTROPIC AGENTS DECREASE CONTRACTILITY, ACIDOSIS, INCREASE EXTRACELLUR "K", CA CHANNEL BLOCKERS
AFTERLOAD PRESSURE THAT MUST BE OVERCOME FOR VENTRICLES TO EJECT BLOOD
POS CHRONOTROPIC FACTORS INCREASE HR
NEG CHONOTROPIC FACTERS DECREASE HR
SYMPATHETIC NERVOUS SYSTEM IS ACTIVATED BY EMOTIONAL OR PHY STRESSORS
NOREPINEPHRINE CAUSE THE PACEMAKER TO FIRE MORE RAPILY(AND AT THE SAME TIME INCREASES CONTRACTILITY)
AT REST THE CARDIAC MUSCLES ARE SHORTER THAN OPTIMAL LENGTH
WHAT INCREASES VENOUS RETURN SLOW HEARTBEAT AND EXERCISE
INCREASED VENOUS RETURN...... DISTENDS THE VENTRICLES AND INCREASES CONTRACTION FORCE
VENOUS RETURN THE FLOW OF BLOOD BACK TO THE HEART
ATRIAL (BAINBRIDGE) REFLEX A SYPATHETIC REFLEX INTIATED BY INCREASED VENOUS RETURN
EPINEPHRINE FROM ADRENAL MEDULLA ENHANCES HEARTRATE AND CONTRACTILILY
THYROXINE INCREASE HR ION CONCENTRATIONS(CA,K)MUST BE MAINTAINED FOR NORMAL HEART FUNCTION
SUPERFICIAL FIBROUS PERICARDIUM...FUNCTIONS PROTECS, ANCHORS AND PREVENTS OVER FILLING
DEEP TWO LAYED PERICARDIUM SEROUS PERICARDIUM
PARIETAL LAYER LINES THE INTERNAL SURFACE OF THE FIBROUS PERICARDIUM
VISCERAL LAYER (EPICARDIUM) ON EXTERNAL SURFACE OF THE HR
PERICARDIAL CAVITY SEPARATED BY FLUID FILLED (HELPS DECREASE FRICTION)
MYOCARDIUM SPIRAL BUNDLES OF CARDIAC MUSCLE CELLS
FIBROUS SKELETON OF THE HEART CRISSCROSSING, INTERLACING LAYER OF CONNECTIVE TISSUE
MYOCARDIUM (FUNCTION) ANCHORS CARDIAC MUSCLE FIBERS SUPPORTS GREART VESS AND VALVES LIMITS SPREAD OF ACTION POTENTIALS TO SPECIFIC PATHS
ENDOCARDIUM CONTINUOUS WITH ENDOTHELIAL LINING OF BLOOD VESS
PULMONARY CIRCUIT IS A SHORT LOW PRESSURE CIRCULATION
SYSTEMIC CIRCUIT BLOOD ENCOUNTER MUCH RESTANCE IN THE LONG PATHWAYS
ARTERIA SUPPLY VARIES CONSIDERABLY AND CONTAINS MANY ANASTOMOSES (JUNCTIONS) AMONG BRANCHES
ARTERIES ON THE HEART RT & LT CORONARY, MARGINAL, CIRCUMFLEX, AND ANTERIOR INTERVENTRICLAR ARTERIES
VEINS SMALL CARDIAC, ANTERIOR CARDIAC AND GREAT CARDIAC VEINS
CARDIAC MUSCLE CELLS SHORT, FAT, BRANCHED, STRIATED, AND INTERCONNECTED
CONNECTIVE TISSUE MATRIX (ENDOMYSIUM) CONNECTS TO THE FIBROUS SKELETON
INTERCALATED DISC JUNCTIONS BETWEEN CELLS ANCHOR CARDIAC CELLS
DESMOSOMES (BOND) PREVENT CELLS FROM SEPARTING DURING CONTRCTION
GAP JUNCTIONS ALLOW IONS TO PASS; ELECTRICALLY COUPLE ADJACENT CELLS AND ENSURES THE HEART CONTRACTS AS A UNIT
HEART MUSCLE BEHAVES AS A....... FUNCTIONAL SYNCYTIUM
DEPOLARIZATION OF THE HEART IS..... RYTHMIC AND SPONTANEOUS ABOUT 1% OF CARDIAC CELLS HAVE AUTOMATICITY
DEPOLARIZATION OPENS..... VILTAGE-GATED FAST NA CHANNELS IN THE SARCOLEMMA
DEPOLARIZATION WAVE IN T TUBLES CAUSES.... THE SR TO RELEASE CA
DEPOLARIZATION WAVE ALSO...... OPENS SLOW CA CHANNELS IN THE SARCOLEMMA
WHAT PROLONGS THE DEPOLARIZATION PHASE (PLATEAU) CA SURGE
Created by: TERRI LUCKETT
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