ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

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ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR
SYSTEM
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LOCATION OF THE HEART

• RESTS ON THE DIAPHRAGM
• NEAR THE MIDLINE OF THE THORACIC CAVITY

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PERICARDIUM

• CONFINES HEART TO THE MEDIASTINUM
• ALLOWS SUFFICIENT FREEDOM OF MOVEMENT.
• CONSISTS OF TWO PARTSTHE FIBROUS AND SEROUS.

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• FIBROUSTHIN INELASTIC, DENSE IRREGULAR
  CONNECTIVE TISSUE
• ---HELPS IN PROTECTION, ANCHORS HEART TO
  MEDIASTINUM
• SEROUS THINNER, MORE DELICATE DIVIDED INTO
  PARIETAL AND VISCERAL

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LAYERS OF THE HEART WALL
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• EPICARDIUM COMPOSED OF MESOTHELIUM AND DELICATE
  CONNECTIVE TISSUE (IMPARTS A SLIPPERY TEXTURE TO
  THE OUTER SURFACE OF THE HEART).

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• MYOCARDIUMRESPONSIBLE FOR PUMPING
• ENDOCARDIUM THIN LAYER OF ENDOTHELIUM WHICH IS
  CONTINOUS WITH THE LINING OF THE LARGE BLOOD
  VESSELS ATTACHED TO THE HEART.

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CHAMBERS OF THE HEART
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• FOUR CHAMBERS
• TWO AURICLES PRESENT
• SERIES OF GROOVES CALLED SULCI CONTAIN FAT AND
  CORONARY BLOOD VESSEL

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SULCUS
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MYOCARDIAL THICKNESS AND FUNCTION

• ATRIA THIN WALLED
• VENTRICLES THICK WALLED
• LT VENTRICLE IS THICKER THAN THE RT VENTRICLE.

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HEART VALVES AND CIRCULATION OF BLOOD
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ATRIOVENTRICULAR SEMILUNAR VALVES
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SYSTEMIC AND PULMONARY CIRCULATION

• LEFT SIDE IS A PUMP TO THE SYSTEMIC CIRCULATION.
• RIGHT SIDE IS A PUMP TO THE PULMONARY CIRCULATION.

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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

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• 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.

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PHYSIOLOGIC CHARACTERISTICS OF THE CONDUCTION
CELLS

• AUTOMATICITY
• EXCITABILITY
• CONDUCTIVITY
• RHYTHMICITY
• CONTRACTILITY
• TONICITY

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CARDIAC CYCLE
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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

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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.

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• 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

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• 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 .

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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.

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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

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CARDIAC OUTPUT

• CO SV X HR
• FOR A RESTING ADULT
• CO 70mL/beat x75beats/min
• 5250 mL/min
• 5.25 L/min

mL/min mL/beat (Beats/min)
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REGULATION OF STROKE VOLUME

• THREE FACTORS REGULATE STROKE VOLUME
• -PRELOAD
• -CONTRACTILITY
• -AFTERLOAD

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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.

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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

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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.

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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.

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AUTONOMIC REGULATION OF HEART RATE

• INPUT TO CARDIOVASCULAR CENTRE
• SYMPATHETIC NEURONS EXTEND FROM MEDULLA OBLANGATA
  
• THE SPINAL CORD
• (thoracic region)

HIGHER BRAIN CENTER CEREBRAL CORTEX, LYMBIC
SYSTEM, HYPOTHALAMUS SENSORY RECEPTORS PROPRIRECE
PTORS, CHEMORECEPTORS, BARORECEPTORS.
CARDIAC ACCELERATOR NERVE EXTENDS TO SA, AV NODES
TRIGERS NOR-EPINEPHRINE
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• NOR-EPINEPHRINE
• HAS 2 EFFECTS
• -IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS
  DEPOLARIZATION
• -IN AV NODE,INCREASES CONTRACTILITY
• INCREASES STROKE VOLUME

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PARASYMPATHETIC EFFECT

• PARASYMPATHETIC NERVE REACHES THE HEART VIA LEFT
  VAGUS (x) NERVES
• THEY RELAESE ACETYL CHOLINE, WHICH DECREASES THE
  HEART RATE
• AT REST PARASYMPATHETIC STIMULATION PREDOMINATES

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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.

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OTHER FACTORS IN HEART RATE REGULATION

• AGE
• GENDER PHYSICAL FITNESS
• BODY TEMPERATURE

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STRUCTURE AND FUNCTIONS OF BLOOD VESSELS
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• 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

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BLOOD DISTRIBUTION IN THE CARDIOVASCULAR SYSTEM

• PULMONARY VESSELS - 9
• HEART 7
• SYSTEMIC ARTERIES
• AND ARTERIOLES
• SYSTEMIC CAPILLARIES 7
• SYSTEMIC VEINS AND VENULES 64

- 13
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HEMODYNAMIC AFFECTING BLOOD FLOW

• BLOOD PRESSURE
• RESISTANCE
• VENOUS RETURN

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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

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• MAP DIASTOLIC PRESSURE
• 1/3 (SYS PRESSURE DIASTOLIC PRESSURE)

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VASCULAR RESISTANCE

• IT IS THE OPPOSTION TO BLOOD FLOW DUE TO FRICTION
  BETWEEN BLOOD AND THE WALLS OF BLOOD VESSELS.

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VASCULAR RESISTANCE DEPENDS ON

• SIZE OF THE LUMEN-
• R IS INVERSELY PROPOTIONAL TO 1/d
• BLOOD VISCOSITY
• TOTAL BLOOD VESSEL LENGTH

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VENOUS RETURN

• DEPENDS ON
• HEART CONTRACTION
• PRESSURE IN THE RT ATRIUM
• BESIDES THIS
• SKELETAL MUSCLE PUMP
• RESPIRATORY PUMP

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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.

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CONTROL OF BLOOD PRESSURE AND BLOOD FLOW
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ROLE OF CARDIOVASCULAR CENTRE

• PROPRIORECEOTORS
• BARORECEPTORS
• CHEMORECEPTORS

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NEURAL REGULATION 0F BLOOD PRESSURE

• BARORECEPTORS
• CHEMORECEPTORS

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BARORECEPTORS

• PRESSURE SENSITIVE LOCATED IN THE AORTA, INTERNAL
  CAROTID AND OTHER LARGE ARTERIES.
• 2 IMPORTANT BARORECEPTOR REFLEX ARE
• - CAROTID SINUS REFLEX
• - AORTIC REFLEX

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CHEMORECEPTOR REFLEX

• PRESENT CLOSE TO THE
• BARORECEPTORS OF CAROTID SINUS AND ARCH OF AORTA
• THEY ARE CALLED CAROTID BODIES AND AORTIC BODIES.

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HORMONAL REGULATION OF BLOOD PRESSURE

• RENIN ANGIOTENSIN-ALDOSTERONE MECHANISM
• EPINEPHRINE AND NOR EPINEPHRINE
• ANTIDIURETIC HORMONE
• ATRIAL NATRIURETIC PEPTIDE

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AUTOREGULATION OF BLOOD PRESSURE

• ABILTY OF TISSUE TO AUTOMATICALLY ADJUST ITS
  BLOOD FLOW TO MATCH ITS METABLOIC DEMAND IS
  CALLED AUTOREGULATION. MAINLY DURING EXERCISE.

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• TWO TYPE OF STIMULI CAUSES AUTOREGULATORY
  CHANGESHSICALY
• - PHYSICAL CHANGE
• - VASODILATING AND VASOCONSTRICTING
  CHEMICALS

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PHYSICAL CHANGES

• WARMING AND COOLING CAUSES VASODILATION AND
  VASOCONSTRICTION.
• SMOOTH MUSCLE IN ARTERIOLE EXHIBIT MYOGENIC
  RESPONSE

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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