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 MEDIASTINUMALLOWS 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 FUNCTIONATRIA : THIN WALLEDVENTRICLES :THICK WALLEDLT VENTRICLE IS THICKER THAN THE RT VENTRICLE.

HEART VALVES AND CIRCULATION OF BLOOD

ATRIOVENTRICULAR & SEMILUNAR VALVES

SYSTEMIC AND PULMONARY CIRCULATIONLEFT 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/MINTHE ANS ALTERS THE STRENGTH AND TIMING OF HEART BEATS.

PHYSIOLOGIC CHARACTERISTICS OF THE CONDUCTION CELLSAUTOMATICITYEXCITABILITYCONDUCTIVITYRHYTHMICITYCONTRACTILITYTONICITY

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 VALVESS1 ATRIOVENTRICULAR VALVE CLOSURES2 SEMILUNAR VALVE CLOSURES3 RAPID VENTRICULAR FILLINGS4 ATRIAL SYSTOLE

CARDIAC OUTPUTCO = 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 EFFECTINHIBITION 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 VOLUMEHTN AND AHTEROSCLEROSIS INCREASES THE AFTERLOAD.

REGUALTION OF HEART RATESA 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 RATEINPUT TO CARDIOVASCULAR CENTRE

SYMPATHETIC NEURONS EXTEND FROM MEDULLA OBLANGATA

THE SPINAL CORD(thoracic region)HIGHER BRAIN CENTER:CEREBRAL CORTEX, LYMBIC SYSTEM, HYPOTHALAMUSSENSORY RECEPTORS:PROPRIRECEPTORS, CHEMORECEPTORS, BARORECEPTORS.CARDIAC ACCELERATOR NERVE EXTENDS TO SA, AV NODESTRIGERS 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 RATEHORMONES: EPINEPHRINE AND NOREPINEPHRINE, THROID HROMONE ALSO INCREASES HEART RATECATIONS: ELEVATED K+ AND Na+ DECREASES HEART RATE, MODERATE INCREASE IN INTERSTITIAL Ca+ LEVELS SPEEDS HEART RATE.

OTHER FACTORS IN HEART RATE REGULATIONAGEGENDER 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 SYSTEMPULMONARY VESSELS - 9%HEART 7%SYSTEMIC ARTERIES AND ARTERIOLESSYSTEMIC CAPILLARIES 7%SYSTEMIC VEINS AND VENULES 64%- 13%

HEMODYNAMIC AFFECTING BLOOD FLOWBLOOD PRESSURERESISTANCEVENOUS RETURN

BLOOD PRESSUREDURING SYSTEMIC CIRCULATION, BLOOD PRESSURE FALLS AS THE DISTANCE FROM THE LEFT VENTRICLE INCREASESIN 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 RESISTANCEIT 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 FLOWVELOCITY 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 CENTREPROPRIORECEOTORSBARORECEPTORSCHEMORECEPTORS

NEURAL REGULATION 0F BLOOD PRESSUREBARORECEPTORS 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 PRESSURERENIN ANGIOTENSIN-ALDOSTERONE MECHANISMEPINEPHRINE AND NOR EPINEPHRINEANTIDIURETIC HORMONEATRIAL NATRIURETIC PEPTIDE

AUTOREGULATION OF BLOOD PRESSUREABILTY 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 CHANGESWARMING 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 DIAMETERVASODILATORS - K+, H+, LASCTIC ACID AND ADENOSINE AND MAINLY NOVASOCONSTRICTORS THROMBAXANE A2 , SEROTONIN AND ENDOTHELINS