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 SYMPATHETIC NEURONS EXTEND FROM MEDULLA OBLANGATA THE SPINAL CORD (thoracic region)
CARDIAC ACCELERATOR NERVE EXTENDS TO SA, AV NODES TRIGERS NOREPINEPHRINE HIGHER BRAIN CENTER: CEREBRAL CORTEX, LYMBIC SYSTEM, HYPOTHALAMUS SENSORY RECEPTORS: PROPRIRECEPTORS, CHEMORECEPTORS, BARORECEPTORS.
NOR-EPINEPHRINE HAS 2 EFFECTS -IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS DEPOLARIZATION -IN AV NODE,INCREASES CONTRACTILITY
INCREASES STROKE VOLUME
PARASYMPATHETIC NERVE REACHES THE HEART VIA LEFT VAGUS (x) NERVES
PARASYMPATHETIC EFFECT
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
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
PRESSURE SENSITIVE
BARORECEPTORS
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
