ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

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ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM Powered By Docstoc
					ANATOMY AND PHYSIOLOGY
         OF THE
 CARDIOVASCULAR SYSTEM
          LOCATION OF THE HEART
 RESTS ON THE DIAPHRAGM
 NEAR THE MIDLINE OF THE THORACIC CAVITY
             PERICARDIUM
 CONFINES HEART TO THE
  MEDIASTINUM
 ALLOWS SUFFICIENT
  FREEDOM OF MOVEMENT.
 CONSISTS OF TWO
  PARTS:THE FIBROUS AND
  SEROUS.
 FIBROUS:THIN INELASTIC, DENSE IRREGULAR
 CONNECTIVE TISSUE
 ---HELPS IN PROTECTION, ANCHORS HEART TO
   MEDIASTINUM
 SEROUS: THINNER, MORE DELICATE DIVIDED INTO
 PARIETAL AND VISCERAL
LAYERS OF THE HEART WALL
 EPICARDIUM: COMPOSED OF MESOTHELIUM AND
 DELICATE CONNECTIVE TISSUE (IMPARTS A SLIPPERY
 TEXTURE TO THE OUTER SURFACE OF THE HEART).
 MYOCARDIUM:RESPONSIBLE FOR PUMPING
 ENDOCARDIUM: THIN LAYER OF ENDOTHELIUM
 WHICH IS CONTINOUS WITH THE LINING OF THE LARGE
 BLOOD VESSELS ATTACHED TO THE HEART.
CHAMBERS OF THE HEART
 FOUR CHAMBERS
 TWO AURICLES PRESENT
 SERIES OF GROOVES CALLED SULCI CONTAIN FAT AND
 CORONARY BLOOD VESSEL
SULCUS
       MYOCARDIAL THICKNESS AND
              FUNCTION

 ATRIA : THIN WALLED
 VENTRICLES :THICK
  WALLED
 LT VENTRICLE IS
  THICKER THAN THE RT
  VENTRICLE.
HEART VALVES AND CIRCULATION OF
            BLOOD
ATRIOVENTRICULAR & SEMILUNAR
           VALVES
        SYSTEMIC AND PULMONARY
              CIRCULATION
 LEFT SIDE IS A PUMP TO
  THE SYSTEMIC
  CIRCULATION.
 RIGHT SIDE IS A PUMP
  TO THE PULMONARY
  CIRCULATION.
     THE CONDUCTION SYSTEM
 INHERENT AND RHYTHMICAL BEAT
  IS DUE TO AUTORHYTHMIC FIBERS
  OF THE CARDIAC MUSCLE.
 THESE FIBERS HAVE 2 IMPORTANT
  FUNCTION
    - ACT AS PACE MAKER
    - FORM THE CONDUCTION
  SYSTEM
 SA NODE WOULD INITITATES ACTION POTENTIAL
  ABOUT EVERY 0.6 SEC OR 100 TIMES/MIN
 THE ANS ALTERS THE STRENGTH AND TIMING OF
  HEART BEATS.
   PHYSIOLOGIC CHARACTERISTICS OF
       THE CONDUCTION CELLS

 AUTOMATICITY
 EXCITABILITY
 CONDUCTIVITY
 RHYTHMICITY
 CONTRACTILITY
 TONICITY
CARDIAC CYCLE
                      ATRIAL SYSTOLE
 LASTS FOR 0.1 SEC
 ATRIAL DEPOLARIZATION CAUSES ATRIAL
  SYSTOLE
 IT CONTRIBUTES A FINAL 25mL OF BLOOD
  TO EACH VENTRICLE
 END OF ATRIAL SYSTOLE IS ALSO END OF
  VENTRICULAR DIASTOLE
 END-DIASTOLIC VOLUME IS 130 mL
              VENTRICULAR SYSTOLE
 LASTS FOR 0.3 SEC
 IT IS CAUSED BY VENTRICULAR
  DEPOLARIZATION
 ISOVOLUMETRIC CONTRACTION LASTS
  FOR 0.05 SECONDS WHEN BOTH THE
  SEMILUNAR AND ATRIOVENTRICULAR
  VLAVES ARE CLOSED.
 THE SL VALVES OPEN WHEN
-THE LEFT VENTRICULAR PRESSURES SURPASSES AORTIC
  PRESSURE(80 MM OF MERCURY)
-THE RIGHT VENTRICULAR PRESSURE RISES ABOVE
  PULMONARY PRESSURE (20 mmHg)
 SL VALVES OPEN FOR 0.25 SEC
 THE LEFT VENTRICLE EJECTS ABOUT 70 ML INTO
  THE AORTA
 THE RIGHT VENTRICLE EJECTS THE SAME VOLUME
  INTO THE PULMONARY TRUNK.
 END SYSTOLIC VOLUME IS 60mL IN EACH VENTRICLE
  .
              RELAXATION PERIOD
 BOTH ATRIA AND VENTRICLES ARE
  RELAXED .IT LASTS FOR 0.4 SEC.
 WHEN HEART BEATS FASTER THE
  RELAXATION TIME SHORTENS.
 VENTRICULAR REPOLARIZATION
  CAUSES VENTRICULAR DAISTOLE.
                 HEART SOUNDS
 PRODUCED FROM BLOOD
  TURBULENCE CAUSED BY
  CLOSING OF HEART VALVES
 S1 – ATRIOVENTRICULAR VALVE
  CLOSURE
 S2 – SEMILUNAR VALVE CLOSURE
 S3 – RAPID VENTRICULAR FILLING
 S4 – ATRIAL SYSTOLE
                    CARDIAC OUTPUT


 CO = SV X HR
mL/min   mL/beat   (Beats/min)

 FOR A RESTING ADULT
 CO = 70mL/beat x75beats/min
 = 5250 mL/min
 = 5.25 L/min
REGULATION OF STROKE VOLUME
 THREE FACTORS REGULATE STROKE VOLUME
-PRELOAD
-CONTRACTILITY
-AFTERLOAD
                      PRELOAD
 STRETCH OF CARDIAC MUSCLE PRIOR
  TO CONTRACTION.
 FRANK-STARLING LAW
 PRELOAD IS PROPOTIONAL TO END
  DIASTOLIC VLOUME
 IF HR IS MORE THAN 160 BEATS/MIN
  STROKE VOLUME DECLINES DUE TO
  SHORT FILLING TIME.
                  CONTRACTILITY
 IT IS THE STRENGTH OF CONTRACTION AT
  ANY GIVEN PRELOAD.
 POSITIVE AND NEGATIVE IONOTROPICS.
 STIMULATION OF SYMPATHETIC DIVISION
  OF ANS LEADS TO POSITVE IONOTROPIC
  EFFECT
 INHIBITION OF SYMPATHETIC DIVISION OF
  ANS LEADS TO NEGATIVE IONOTROPIC
  EFFECT
               AFTERLOAD
 THE PRESSURE THAT MUST BE OVERCOME BEFORE A
  SEMILUNAR VALVE CAN OPEN IS TERMED THE
  AFTERLOAD.
 INCREASE IN AFTERLOAD CAUSE DECREASE IN
  STROKE VOLUME
 HTN AND AHTEROSCLEROSIS INCREASES THE
  AFTERLOAD.
         REGUALTION OF HEART RATE
 SA NODE INITIATES 100
  BEATS/MIN IF LEFT TO ITSELF.
 TISSUE REQUIRE DIFFERENT
  VOLUME OF BLOOD FLOW
  UNDER DIFFERENT
  CONDITIONS(EX: EXERCISE)
 ANS AND HORMONES OF
  ADRENAL MEDULLA ARE
  IMPORTANT IN REGULATING THE
  HEART RATE.
   AUTONOMIC REGULATION OF HEART
               RATE
     INPUT TO                              HIGHER BRAIN CENTER:
  CARDIOVASCULAR                           CEREBRAL CORTEX, LYMBIC
       CENTRE                              SYSTEM, HYPOTHALAMUS
                                           SENSORY RECEPTORS:
SYMPATHETIC NEURONS                        PROPRIRECEPTORS,
    EXTEND FROM                            CHEMORECEPTORS,
                                           BARORECEPTORS.
 MEDULLA OBLANGATA

  THE SPINAL CORD
   (thoracic region)


   CARDIAC ACCELERATOR      TRIGERS NOR-
  NERVE EXTENDS TO SA, AV   EPINEPHRINE
          NODES
             NOR-EPINEPHRINE

                  HAS 2 EFFECTS
-IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS
                 DEPOLARIZATION
       -IN AV NODE,INCREASES CONTRACTILITY

         INCREASES STROKE VOLUME
      PARASYMPATHETIC EFFECT LEFT
PARASYMPATHETIC NERVE REACHES THE HEART VIA
                 VAGUS (x) NERVES

THEY RELAESE ACETYL CHOLINE, WHICH DECREASES THE
                    HEART RATE

AT REST PARASYMPATHETIC STIMULATION PREDOMINATES
CHEMICAL REGULATION OF HEART
            RATE
 HORMONES: EPINEPHRINE AND NOREPINEPHRINE,
  THROID HROMONE ALSO INCREASES HEART RATE
 CATIONS: ELEVATED K+ AND Na+ DECREASES
  HEART RATE, MODERATE INCREASE IN
  INTERSTITIAL Ca+ LEVELS SPEEDS HEART RATE.
    OTHER FACTORS IN HEART RATE
            REGULATION
 AGE
 GENDER PHYSICAL FITNESS
 BODY TEMPERATURE
        STRUCTURE
           AND
FUNCTIONS OF BLOOD VESSELS
    BODY CONTAINS THREE KINDS OF CAPILLARIES

 CONTINUOUS- LUNG, SMMOTH MUSCLE, CONNECTIVE
 TISSUES

 FENESTRATED- KIDNEY, SMALL INTESTINE,BRAIN


 SINUSOIDS- LIVER RED BONE MARROW, SPLEEN AND
 ENDOCRINE GLANDS
      BLOOD DISTRIBUTION IN THE
       CARDIOVASCULAR SYSTEM
 PULMONARY VESSELS - 9%
 HEART – 7%
 SYSTEMIC ARTERIES
AND ARTERIOLES
 SYSTEMIC CAPILLARIES – 7%
                           - 13%
 SYSTEMIC VEINS AND VENULES – 64%
  HEMODYNAMIC AFFECTING BLOOD
            FLOW
 BLOOD PRESSURE
 RESISTANCE
 VENOUS RETURN
                BLOOD PRESSURE

 DURING SYSTEMIC CIRCULATION, BLOOD PRESSURE FALLS AS
  THE DISTANCE FROM THE LEFT VENTRICLE INCREASES
 IN ARTERIOLES AND ARTERIES – 35 mm Hg
 IN VENOUS END OF CAPILLARIES– 16mm Hg
 WHEN BLOOD FLOW IN RT.VENTRICLE -0 mmHg
 MAP = DIASTOLIC PRESSURE +
     1/3 (SYS PRESSURE – DIASTOLIC PRESSURE)
     VASCULAR RESISTANCE

IT IS THE OPPOSTION TO BLOOD FLOW DUE TO
  FRICTION BETWEEN BLOOD AND THE WALLS OF
  BLOOD VESSELS.
VASCULAR RESISTANCE DEPENDS ON
 SIZE OF THE LUMEN-
  R IS INVERSELY PROPOTIONAL TO 1/d
 BLOOD VISCOSITY                     4

 TOTAL BLOOD VESSEL LENGTH
            VENOUS RETURN
DEPENDS ON
 HEART CONTRACTION
 PRESSURE IN THE RT ATRIUM


BESIDES THIS
 SKELETAL MUSCLE PUMP
 RESPIRATORY PUMP
     VELOCITY OF BLOOD FLOW
 VELOCITY IS INVERSELY PROPOTIONAL TO
  CROSS SECTIONAL AREA.
 VELOCITY DECREASES AS IT PROCEEDS FROM
  ARTERIES, ARTERIOLES,CAPILLAREIS
 VELOCITY INCREASES AS IT PROCEEDS FROM
  VENULES, VEINS.
 THIS ALLOWS EXCHANGE OF MATERIALS IN THE
  CAPILLARIES.
 CONTROL OF BLOOD
PRESSURE AND BLOOD
      FLOW
 ROLE OF CARDIOVASCULAR CENTRE
 PROPRIORECEOTORS
 BARORECEPTORS
 CHEMORECEPTORS
   NEURAL REGULATION 0F BLOOD
           PRESSURE
 BARORECEPTORS
 CHEMORECEPTORS
                   BARORECEPTORS
 PRESSURE SENSITIVE
  LOCATED IN THE AORTA,
  INTERNAL CAROTID AND
  OTHER LARGE ARTERIES.
 2 IMPORTANT
  BARORECEPTOR REFLEX
  ARE
    - CAROTID SINUS REFLEX
    - AORTIC REFLEX
     CHEMORECEPTOR REFLEX
PRESENT CLOSE TO THE
- BARORECEPTORS OF CAROTID SINUS AND ARCH OF
  AORTA
- THEY ARE CALLED CAROTID BODIES AND AORTIC
  BODIES.
    HORMONAL REGULATION OF
       BLOOD PRESSURE
 RENIN ANGIOTENSIN-ALDOSTERONE MECHANISM
 EPINEPHRINE AND NOR EPINEPHRINE
 ANTIDIURETIC HORMONE
 ATRIAL NATRIURETIC PEPTIDE
         AUTOREGULATION OF BLOOD
                PRESSURE
 ABILTY OF TISSUE TO AUTOMATICALLY
 ADJUST ITS BLOOD FLOW TO MATCH
 ITS METABLOIC DEMAND IS CALLED
 AUTOREGULATION. MAINLY DURING
 EXERCISE.
 TWO TYPE OF STIMULI CAUSES AUTOREGULATORY
 CHANGESHSICALY
  - PHYSICAL CHANGE
  - VASODILATING AND VASOCONSTRICTING CHEMICALS
             PHYSICAL CHANGES

 WARMING AND COOLING CAUSES VASODILATION AND
  VASOCONSTRICTION.
 SMOOTH MUSCLE IN ARTERIOLE EXHIBIT MYOGENIC
  RESPONSE
VASODILATING AND VASOCONSTRICTING
            CHEMICALS
   SEVERAL CELLS RELEASE A WIDE VARIETY OF
    CHEMICALS THAT ALTER THE BLOOD VESSEL
    DIAMETER
   VASODILATORS - K+, H+, LASCTIC ACID AND
    ADENOSINE AND MAINLY NO
   VASOCONSTRICTORS – THROMBAXANE A2 ,
    SEROTONIN AND ENDOTHELINS

				
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posted:11/13/2011
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