Transcript DOWNLOAD ANATOMY AND PHYSIOLOGY OF THE

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
CARDIOVASCULAR
CENTRE
HIGHER BRAIN CENTER:
CEREBRAL CORTEX, LYMBIC
SYSTEM, HYPOTHALAMUS
SENSORY RECEPTORS:
SYMPATHETIC NEURONS
EXTEND FROM
MEDULLA OBLANGATA
PROPRIRECEPTORS,
CHEMORECEPTORS,
BARORECEPTORS.
THE SPINAL CORD
(thoracic region)
CARDIAC ACCELERATOR
NERVE EXTENDS TO SA, AV
NODES
TRIGERS NOREPINEPHRINE
NOR-EPINEPHRINE
HAS 2 EFFECTS
-IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS
DEPOLARIZATION
-IN AV NODE,INCREASES CONTRACTILITY
INCREASES STROKE VOLUME
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
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
 TOTAL BLOOD VESSEL LENGTH
4
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