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ANATOMY AND PHYSIOLOGY OF THE
CARDIOVASCULAR SYSTEM
LOCATION OF THE HEARTRESTS ON THE DIAPHRAGM NEAR THE MIDLINE OF THE THORACIC CAVITY
PERICARDIUMCONFINES 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
MEDIASTINUMSEROUS: 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 PUMPINGENDOCARDIUM: THIN LAYER OF
ENDOTHELIUM WHICH IS CONTINOUS WITH THE LINING OF THE LARGE BLOOD VESSELS ATTACHED TO THE HEART.
CHAMBERS OF THE HEART
FOUR CHAMBERSTWO AURICLES PRESENTSERIES 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 SYSTEMINHERENT 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
AUTOMATICITYEXCITABILITYCONDUCTIVITYRHYTHMICITYCONTRACTILITYTONICITY
CARDIAC CYCLE
ATRIAL SYSTOLELASTS FOR 0.1 SEC ATRIAL DEPOLARIZATION CAUSES
ATRIAL SYSTOLEIT CONTRIBUTES A FINAL 25mL OF
BLOOD TO EACH VENTRICLEEND OF ATRIAL SYSTOLE IS ALSO
END OF VENTRICULAR DIASTOLEEND-DIASTOLIC VOLUME IS 130 mL
VENTRICULAR SYSTOLELASTS FOR 0.3 SECIT 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 PERIODBOTH 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 SOUNDSPRODUCED 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
FOR A RESTING ADULT CO = 70mL/beat x75beats/min = 5250 mL/min = 5.25 L/min
mL/min mL/beat (Beats/min)
REGULATION OF STROKE VOLUMETHREE FACTORS REGULATE STROKE
VOLUME-PRELOAD-CONTRACTILITY-AFTERLOAD
PRELOADSTRETCH OF CARDIAC MUSCLE
PRIOR TO CONTRACTION.FRANK-STARLING LAWPRELOAD IS PROPOTIONAL TO
END DIASTOLIC VLOUMEIF HR IS MORE THAN 160
BEATS/MIN STROKE VOLUME DECLINES DUE TO SHORT FILLING TIME.
CONTRACTILITYIT 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
AFTERLOADTHE 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
SYMPATHETIC NEURONS EXTEND
FROM MEDULLA OBLANGATA
THE SPINAL CORD(thoracic region)
HIGHER BRAIN CENTER:
CEREBRAL CORTEX, LYMBIC SYSTEM, HYPOTHALAMUS
SENSORY RECEPTORS:
PROPRIRECEPTORS, CHEMORECEPTORS, BARORECEPTORS.
CARDIAC ACCELERATOR NERVE EXTENDS TO SA,
AV NODES
TRIGERS NOR-EPINEPHRINE
NOR-EPINEPHRINE
HAS 2 EFFECTS-IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS
DEPOLARIZATION -IN AV NODE,INCREASES CONTRACTILITY
INCREASES STROKE VOLUME
PARASYMPATHETIC EFFECTPARASYMPATHETIC 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
AGEGENDER PHYSICAL FITNESSBODY 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 ARTERIOLESSYSTEMIC CAPILLARIES – 7%SYSTEMIC VEINS AND VENULES – 64%
- 13%
HEMODYNAMIC AFFECTING BLOOD FLOW
BLOOD PRESSURERESISTANCEVENOUS RETURN
BLOOD PRESSURE
DURING SYSTEMIC CIRCULATION, BLOOD PRESSURE FALLS AS THE DISTANCE FROM THE LEFT VENTRICLE INCREASES
IN ARTERIOLES AND ARTERIES – 35 mm HgIN VENOUS END OF CAPILLARIES– 16mm HgWHEN 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 ONSIZE OF THE LUMEN- R IS INVERSELY PROPOTIONAL TO 1/dBLOOD VISCOSITYTOTAL BLOOD VESSEL LENGTH
4
VENOUS RETURNDEPENDS ONHEART CONTRACTIONPRESSURE IN THE RT ATRIUM
BESIDES THISSKELETAL MUSCLE PUMPRESPIRATORY 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
PROPRIORECEOTORSBARORECEPTORSCHEMORECEPTORS
NEURAL REGULATION 0F BLOOD PRESSURE
BARORECEPTORS CHEMORECEPTORS
BARORECEPTORSPRESSURE SENSITIVE
LOCATED IN THE AORTA, INTERNAL CAROTID AND OTHER LARGE ARTERIES.
2 IMPORTANT BARORECEPTOR REFLEX ARE
- CAROTID SINUS REFLEX
- AORTIC REFLEX
CHEMORECEPTOR REFLEXPRESENT 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 EPINEPHRINEANTIDIURETIC HORMONEATRIAL 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
CHEMICALSSEVERAL 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