Download heart valves

CIRCULATORY
SYSTEM
THE HEART
CIRCULATORY SYSTEM

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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
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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
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FUNCTIONS OF THE HEART

TWO MAJOR DIVISIONS

PULMONARY CIRCUIT
CARRIES BLOOD TO LUNGS (GILLS)
 GAS EXCHANGE: LOSE CO2, GAIN O2
 RIGHT SIDE OF MAMMALIAN HEART
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
SYSTEMIC CIRCUIT
CARRIES BLOOD TO BODY ORGANS
 GAS EXCHANGE: LOSE O2, GAIN CO2
 LEFT SIDE OF MAMMALIAN HEART
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HEART STRUCTURE
CHAMBERS
 ATRIA
RIGHT AND LEFT
 SEPARATED BY INTERATRIAL SEPTUM
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VENTRICLES
RIGHT AND LEFT
 SEPARATED BY INTERVENTRICULAR
SEPTUM
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BLOOD FLOW THROUGH THE
HEART
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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
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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
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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
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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
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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 mM x 10 - 20 mM)
 BRANCHED
 SINGLE NUCLEUS
 LESS DEVELOPED SR (SER)
 LARGER T-TUBULES (ADMIT Ca++)
 JOINED VIA INTERCALATED DISKS
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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
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CARDIAC METABOLISM
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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
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(AEROBIC, NO O2 DEBT, NO FATIGUE)
CARDIAC RHYTHM
HEARTBEAT
 INVERTEBRATES
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TRIGGERED BY NERVOUS SYTEM
VERTEBRATES
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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
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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
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SYSTOLE / DIASTOLE
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SYSTOLE
CONTRACTION OF A HEART CHAMBER
 REFERS TO VENTRICLE UNLESS
OTHERWISE NOTED
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DIASTOLE
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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)
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SOMETIMES HEARD IN CHILDREN AND
ADOLESCENTS
CARDIAC CYCLE
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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)


~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


PROPRIORECEPTORS
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INCREASED STROKE VOLUME
SIGNALS FROM MUSCLES/JOINTS
INCREASED VENOUS RETURN

INCREASED PRELOAD