Circulation And The Heart

CIRCULATORY SYSTEM THE HEART

CIRCULATORY SYSTEM   

BLOOD BLOOD VESSELS HEART

BASIC HEART STRUCTURE ANIMAL HEART  ATRIUM/ATRIA (1 OR 2) RECEIVE BLOOD RETURNING TO HEART  MAMMALIAN HEART POSSESSES 2 ATRIA 

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VENTRICLES (1 OR 2) PUMP BLOOD FROM THE HEART  MAMMALIAN HEART POSSESSES 2 VENTRICLES 

BASIC HEART STRUCTURE ANIMAL HEART  ARTERIES CARRY BLOOD FROM THE HEART  ARTERY  ARTERIOLE  CAPILLARIES 

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CAPILLARIES 

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SITE OF GAS AND NUTRIENT EXCHANGE

VEINS RETURN BLOOD TO THE HEART  CAPILLARIES  VENULES  VEINS 

FUNCTIONS OF THE HEART 

TWO MAJOR DIVISIONS 

PULMONARY CIRCUIT CARRIES BLOOD TO LUNGS (GILLS)  GAS EXCHANGE: LOSE CO , GAIN O 2 2 

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RIGHT SIDE OF MAMMALIAN HEART

SYSTEMIC CIRCUIT CARRIES BLOOD TO BODY ORGANS  GAS EXCHANGE: LOSE O , GAIN CO 2 2 

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LEFT SIDE OF MAMMALIAN HEART

HEART STRUCTURE CHAMBERS  ATRIA RIGHT AND LEFT  SEPARATED BY INTERATRIAL SEPTUM 

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VENTRICLES RIGHT AND LEFT  SEPARATED BY INTERVENTRICULAR SEPTUM 

BLOOD FLOW THROUGH THE HEART 

RIGHT ATRIUM 

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RIGHT VENTRICLE  

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RECEIVES O2-POOR BLOOD FROM RIGHT ATRIUM PUMPS O2-POOR BLOOD TO LUNGS

LEFT ATRIUM 

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RECEIVES O2-POOR BLOOD FROM BODY

RECEIVES O2-RICH BLOOD FROM LUNGS

LEFT VENTRICLE  

RECEIVES O2-RICH BLOOD FROM LEFT ATRIUM PUMPS O2-RICH BLOOD TO BODY ORGANS

HEART VALVES   

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CONSIST OF FIBEROUS FLAPS ENSURE UNIDIRECTIONAL FLOW OPEN AND CLOSE IN RESPONSE TO PRESSURE DIFFERENCES BETWEEN SIDES ATRIOVENTRICULAR (AV) VALVES SEMILUNAR VALVES

HEART VALVES ATRIOVENTRICULAR (AV) VALVES  RIGHT AV VALVE 

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A.K.A. TRICUSPID VALVE

LEFT AV VALVE A.K.A. BICUSPID VALVE  A.K.A. MITRAL VALVE 

HEART VALVES ATRIOVENTRICULAR (AV) VALVES  ATRIUM  VENTRICLE  VENTRICLE RELAXED VALVE OPEN  ATRIUM  VENTRICLE BLOOD FLOW 

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VENTRICLE CONTRACTS VENTRICLE PRESSURE INCREASES  VALVE CLOSES  PREVENTS BACK FLOW 

HEART VALVES ATRIOVENTRICULAR (AV) VALVES  PAPILLARY MUSCLES CONTRACT WITH REST OF VENTRICLE  PULL ON CHORDAE TENDINEAE 

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CHORDAE TENDINEAE CONNECT AV VALVE CUSPS TO PAPILLARY MUSCLES OF  REINFORCE AV VALVES  PREVENT PROLAPSE 

HEART VALVES SEMILUNAR VALVES  VENTRICLE  ARTERY  VENTRICLE RELAXED PRESSURE HIGHER IN ARTERIES  VALVE CLOSED 

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VENTRICLE CONTRACTS PRESSURE HIGHER IN VENTRICLE  VALVES FORCED OPEN  BLOOD FLOWS FROM HEART 

HEART STRUCTURE PERICARDIUM  DOUBLE-WALLED SAC  ENCLOSES HEART  CONTAINS PERICARDIAL FLUID (5-30 ML)  GREATLY REDUCES FRICTION

HEART STRUCTURE HEART WALL  EPICARDIUM (OUTER) 

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A.K.A. VISCERAL PERICARDIUM

MYOCARDIUM THICKEST LAYER  CARDIAC MUSCLE 

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ENDOCARDIUM SMOOTH INNER LINING  CONTINUOUS WITH BLOOD VESSELS 

HEART STRUCTURE MYOCARDIUM  THICKEST; CARDIAC MUSCLE  MUSCLE FIBERS CONNECTED BY FIBROUS (PROTEIN) SKELETON STRUCTURAL SUPPORT  SOMETHING TO PULL AGAINST  ELECTRICAL NONCONDUCTOR 

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ALLOWS ATRIA AND VENTRICLES TO CONTRACT SEPARATELY

CARDIAC MUSCLE STRUCTURE CARDIAC MUSCLE CELLS  “MYOCYTES” / “CARDIOCYTES” STRIATED  SHORT, THICK (50 – 100 µ M x 10 - 20 µ M)  BRANCHED  SINGLE NUCLEUS  LESS DEVELOPED SR (SER)  LARGER T-TUBULES (ADMIT Ca++)  JOINED VIA INTERCALATED DISKS 

CARDIAC MUSCLE STRUCTURE INTERCALATED DISK FEATURES  INTERDIGITATING FOLDS 

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INCREASED SURFACE AREA CONTACT

MECHANICAL JUNCTIONS FASCIA ADHERENS (ACTIN)  DESMOSOMES 

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ELECTRICAL JUNCTIONS GAP JUNCTIONS  ELECTRICALLY STIMULATE NEIGHBORS 

CARDIAC METABOLISM       

EXCLUSIVELY AEROBIC MYOGLOBIN-RICH (STORED O2) GLYCOGEN-RICH (STORED SUGAR) LARGE MITOCHONDRIA (25% VS 2%) MULTIPLE FUELS USABLE VULNERABLE TO O2 DEFICIENCY NOT PRONE TO FATIGUE 

(AEROBIC, NO O2 DEBT, NO FATIGUE)

CARDIAC RHYTHM HEARTBEAT  INVERTEBRATES 

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TRIGGERED BY NERVOUS SYTEM

VERTEBRATES 

TRIGGERED BY HEART ITSELF

CARDIAC RHYTHM CARDIAC MYOCYTES  AUTORHYTHMIC 

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SPONTANEOUS DEPOLARIZATION AT REGULAR INTERVALS

SOME SPECIALIZED TO GENERATE ACTION POTENTIALS “CARDIAC CONDUCTION SYSTEM”  SINOATRIAL (SA) NODE  ATRIOVENTRICULAR (AV) NODE 

CARDIAC RHYTHYM SINOATRIAL (SA) NODE  MYOCYTES IN RIGHT ATRIUM  “PACEMAKER”  INITIATES HEARTBEAT  DETERMINES HEART RATE  FIRING RATE REDUCED BY NERVES  70 – 80 BEATS PER MINUTE (BPM)

CARDIAC RHYTHYM SINOATRIAL (SA) NODE  CELLS LACK STABLE RESTING MEMBRANE POTENTIAL  SPONTANEOUSLY DEPOLARIZE AND REPOLARIZE AT REGULAR INTERVALS (~0.8 SEC)  EACH DEPOLARIZATION INITIATES ONE HEARTBEAT  GENERATE ACTION POTENTIAL

CARDIAC RHYTHYM SA ACTION POTENTIAL  SPREADS THROUGHOUT ATRIAL MYOCARDIUM  ATRIA CONTRACT ~SIMULTANEOUSLY  SIGNAL REACHES AV NODE (50MSEC)  DELAYED AT AV NODE (100 MSEC)  VENTRICLES FILL DURING DELAY

CARDIAC RHYTHYM ATRIOVENTRICULAR (AV) NODE  NEAR RIGHT AV VALVE  ELECTRICAL GATEWAY TO VENTRICLES  DISTRIBUTES SIGNAL TO VENTRICULAR MYOCARDIUM AV BUNDLE  PURKINJE FIBERS 

CARDIAC RHYTHYM 

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SIGNAL TRAVELS FROM AV THROUGH VENTRICULAR MYOCARDIUM VENTRICULES CONTRACT ~SIMULTANEOUSLY (PAPILLARY MUSCLES CONTRACT FIRST)

CARDIAC RHYTHYM CARDIAC ACTION POTENTIALS  PROLONGED DEPOLARIZATION 200 - 250 MSEC VS. 2 MSEC  RESULT OF SLOW Ca++ CHANNELS 

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SUSTAINED CONTRACTION LONGER REFRACTORY PERIOD 200 MSEC VS. 1 – 2 MSEC  PREVENTS WAVE SUMMATION, TETANUS 

SYSTOLE / DIASTOLE 

SYSTOLE CONTRACTION OF A HEART CHAMBER  REFERS TO VENTRICLE UNLESS OTHERWISE NOTED 

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DIASTOLE 

PERIOD DURING WHICH A HEART CHAMBER RELAXES AND FILLS WITH BLOOD

ELECTROCARDIOGRAM 

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ELECTRICAL CURRENTS GENERATED IN THE HEART TRAVEL WEAKLY THROUGH ALL BODY TISSUES THESE CURRENTS CAN BE MEASURED USING ELECTRODES APPLIED TO THE SKIN

P WAVE  SIGNAL FROM SA NODE DEPOLARIZES ATRIA  ATRIAL SYSTOLE ~100 MSEC AFTER P WAVE BEGINS

QRS COMPLEX  FIRING OF THE AV NODE  ONSET OF VENTRICULAR DEPOLARIZATION  ATRIAL REPOLARIZATION / DIASTOLE OBSCURED  VENTRICULAR SYSTOLE IMMEDIATELY AFTER

S – T SEGMENT  MYOCARDIAL ACTION POTENTIAL PLATEAU  VENTRICLES ARE CONTRACTING  BLOOD EJECTED FROM VENTRICLES

T WAVE  VENTRICULAR REPOLARIZATION BEFORE DIASTOLE  (REPOLARIZATION TAKES LONGER THAN DEPOLARIZATION)

HEART SOUNDS 

FIRST AND SECOND HEART SOUNDS S1 AND S2  “LUBB-DUPP”  OCCUR IN CONJUNCTION WITH HEART VALVES CLOSING  BLOODSTREAM TURBULENCE 

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THIRD HEART SOUND (S3) 

SOMETIMES HEARD IN CHILDREN AND ADOLESCENTS

CARDIAC CYCLE     

ATRIAL SYSTOLE ATRIAL DYASTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE QUIESCENT PERIOD

CARDIAC CYCLE QUIESCENT PERIOD  NO CONTRACTION OF ANY HEART CHAMBERS  ATRIA ARE FILLING

CARDIAC CYCLE ATRIAL SYSTOLE  SA NODE FIRES  ATRIA DEPOLARIZE  P WAVE OF ECG PRODUCED  ATRIA CONTRACT  BLOOD PRESSURE IN ATRIA INCREASES  BLOOD FORCED INTO VENTRICLES

CARDIAC CYCLE ISOVOLUMETRIC CONTRACTION  ATRIA REPOLARIZE, RELAX  ATRIA IN DIASTOLE FOR REMAINDER  VENTRICLES DEPOLARIZE, CONTRACT  VENTRICULAR PRESSURE INCREASES  AV VALVES CLOSE  HEART SOUND S1  NO BLOOD EJECTED YET

CARDIAC CYCLE VENTRICULAR EJECTION  VENTRICULAR PRESSURE EXCEEDS ARTERIAL PRESSURE  SEMILUNAR VALVES OPEN  BLOOD EJECTED INTO ARTERIES  NOT ALL BLOOD EXPELLED  AMOUNT EJECTED = STROKE VOLUME  % = EJECTION FRACTION

CARDIAC CYCLE ISOVOLUMETRIC RELAXATION  EARLY IN VENTRICULAR DIASTOLE  BLOOD BRIEFLY FLOWS BACKWARDS  SEMILUNAR VALVES CLOSE  HEART SOUND S2  AV VALVES NOT YET OPEN  NO BLOOD TAKEN IN YET

CARDIAC CYCLE VENTRICULAR FILLING  VENTRICULAR PRESSURE DROPS  AV VALVES OPEN  VENTRICLES BEGIN TO FILL  HEART SOUND S3  (COMPLETELY FILLED BY ATRIAL SYSTOLE)  P WAVE PRODUCED

CARDIAC OUTPUT 

HEART RATE (HR) (BEATS/MIN) 

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STROKE VOLUME (SV) 

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~75 BPM AT REST ~70 ML/BEAT AT REST

CARDIAC OUTPUT (CO) CO = HR * SV  75 * 70 = 5,000 ML/MIN AT REST  CARDIAC OUTPUT IS NOT CONSTANT 

CARDIAC OUTPUT CARDIAC OUTPUT IS NOT CONSTANT  RESTING 

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~5 LITERS/MIN RESTING (TOTAL VOLUME)

VIGOROUS EXERCISE ~21 LITERS/MIN IN GOOD CONDITION  ~35 LITERS/MIN OLYMPIC ATHLETE 

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CO = HR * SV, 

CO INCREASED BY HR OR SV INCREASE

CARDIAC OUTPUT HEART RATE  EASILY MEASURED (PULSE)  70 – 80 AVERAGE RESTING RATE  TACHYCARDIA: RESTING >100 BPM  BRACHYCARDIA: RESTING <60 BPM  REGULATED BY NERVOUS SYSTEM

CARDIAC OUTPUT HEART RATE  REGULATED BY CARDIAC CENTER OF MEDULLA OBLONGATA CARDIOACCELATORY CENTER  CARDIOINHIBITORY CENTER 

CARDIAC OUTPUT HEART RATE  CARDIOACCELATORY CENTER  THORACIC SPINAL CORD  CARDIAC ACCELERATOR NERVES  SECRETE NOREPINEPHRINE  BINDS TO RECEPTORS IN HEART  INCREASES HEART RATE

CARDIAC OUTPUT HEART RATE  CARDIOINHIBITORY CENTER  VAGUS NERVES  SECRETE ACETYLCHOLINE  SEND SIGNALS TO AV AND SA NODES  FIRE LESS FREQUENTLY  INTRINSIC HEART RATE IS 100 BPM

CARDIAC OUTPUT HEART RATE  CARDIAC CENTER RECEIVES INPUT FROM MULTIPLE SOURCES 

PROPRIORECEPTORS 

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BARORECEPTORS 

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PHYSICAL ACTIVITY BLOOD PRESSURE

CHEMORECEPTORS 

pH, [O2], [CO2]

CARDIAC OUTPUT STROKE VOLUME  GOVERNED BY THREE FACTORS PRELOAD  CONTRACTILITY  AFTERLOAD 

CARDIAC OUTPUT STROKE VOLUME  PRELOAD  VENTRICULAR MYOCARDIUM TENSION PRIOR TO CONTRACTION  SKELETAL MUSCLES MASSAGE VEINS AND INCREASE VENOUS RETURN  MORE TENSION WHEN MYOCARDIUM CONTRACTS  MORE FORCEFUL CONTRACTION  MORE BLOOD EXPELLED

CARDIAC OUTPUT CONTRACTILITY  CONTRACTION FORCE FOR A GIVEN PRELOAD  MYOCYTES MORE RESPONSIVE TO STIMULATION  AFFECT Ca++ CONCENTRATIONS  (Ca++ REQUIRED FOR MUSCLE EXCITATION / CONTRACTION)

CARDIAC OUTPUT CONTRACTILITY  Ca++ CONCENTRATIONS INCREASED BY EPINEPHRINE, NOREPINEPHRINE  GLUCAGON, cAMP  DIGITALIS 

CARDIAC OUTPUT AFTERLOAD  BLOOD PRESSURE IN ARTERIES JUST OUTSIDE OF SEMILUNAR VALVES  INCREASED AFTERLOAD REDUCES STROKE VOLUME  CAUSED BY ANYTHING IMPEDING ARTERIAL CIRCULATION

CARDIAC OUTPUT EFFECTS OF EXERCISE  INCREASED CARDIAC OUTPUT  VENTRICULAR HYPERTROPHY 

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PROPRIORECEPTORS 

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INCREASED STROKE VOLUME SIGNALS FROM MUSCLES/JOINTS

INCREASED VENOUS RETURN 

INCREASED PRELOAD