You are on page 1of 62

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

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

CAPILLARIES

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
 

RIGHT SIDE OF MAMMALIAN HEART

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

LEFT SIDE OF MAMMALIAN HEART

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

VENTRICLES
RIGHT AND LEFT  SEPARATED BY INTERVENTRICULAR SEPTUM

BLOOD FLOW THROUGH THE HEART

RIGHT ATRIUM

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

RIGHT VENTRICLE
 

LEFT ATRIUM

LEFT VENTRICLE
 

HEART VALVES
  

 

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

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

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

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

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)

A.K.A. VISCERAL PERICARDIUM

MYOCARDIUM
THICKEST LAYER  CARDIAC MUSCLE

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

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

INCREASED SURFACE AREA CONTACT

MECHANICAL JUNCTIONS
FASCIA ADHERENS (ACTIN)  DESMOSOMES

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

TRIGGERED BY NERVOUS SYTEM TRIGGERED BY HEART ITSELF

VERTEBRATES

CARDIAC RHYTHM
CARDIAC MYOCYTES  AUTORHYTHMIC

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

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

 

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

DIASTOLE

PERIOD DURING WHICH A HEART CHAMBER RELAXES AND FILLS WITH BLOOD

ELECTROCARDIOGRAM

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

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)

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

STROKE VOLUME (SV)

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

~5 LITERS/MIN RESTING (TOTAL VOLUME)

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

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

PHYSICAL ACTIVITY BLOOD PRESSURE pH, [O2], [CO2]

BARORECEPTORS

CHEMORECEPTORS

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

INCREASED STROKE VOLUME SIGNALS FROM MUSCLES/JOINTS INCREASED PRELOAD

PROPRIORECEPTORS

INCREASED VENOUS RETURN