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ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

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.

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ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

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  1. ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM

  2. LOCATION OF THE HEART • RESTS ON THE DIAPHRAGM • NEAR THE MIDLINE OF THE THORACIC CAVITY

  3. PERICARDIUM • CONFINES HEART TO THE MEDIASTINUM • ALLOWS SUFFICIENT FREEDOM OF MOVEMENT. • CONSISTS OF TWO PARTS:THE FIBROUS AND SEROUS.

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

  5. LAYERS OF THE HEART WALL

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

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

  8. CHAMBERS OF THE HEART

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

  10. SULCUS

  11. MYOCARDIAL THICKNESS AND FUNCTION • ATRIA : THIN WALLED • VENTRICLES :THICK WALLED • LT VENTRICLE IS THICKER THAN THE RT VENTRICLE.

  12. HEART VALVES AND CIRCULATION OF BLOOD

  13. ATRIOVENTRICULAR & SEMILUNAR VALVES

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

  15. 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

  16. 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.

  17. PHYSIOLOGIC CHARACTERISTICS OF THE CONDUCTION CELLS • AUTOMATICITY • EXCITABILITY • CONDUCTIVITY • RHYTHMICITY • CONTRACTILITY • TONICITY

  18. CARDIAC CYCLE

  19. 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

  20. 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.

  21. 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

  22. 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 .

  23. 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.

  24. 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

  25. 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)

  26. REGULATION OF STROKE VOLUME • THREE FACTORS REGULATE STROKE VOLUME -PRELOAD -CONTRACTILITY -AFTERLOAD

  27. 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.

  28. 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

  29. 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.

  30. 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.

  31. AUTONOMIC REGULATION OF HEART RATE HIGHER BRAIN CENTER: CEREBRAL CORTEX, LYMBIC SYSTEM, HYPOTHALAMUS SENSORY RECEPTORS: PROPRIRECEPTORS, CHEMORECEPTORS, BARORECEPTORS. INPUT TO CARDIOVASCULAR CENTRE SYMPATHETIC NEURONS EXTEND FROM MEDULLA OBLANGATA THE SPINAL CORD (thoracic region) CARDIAC ACCELERATOR NERVE EXTENDS TO SA, AV NODES TRIGERS NOR-EPINEPHRINE

  32. NOR-EPINEPHRINE HAS 2 EFFECTS -IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS DEPOLARIZATION -IN AV NODE,INCREASES CONTRACTILITY INCREASES STROKE VOLUME

  33. 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

  34. 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.

  35. OTHER FACTORS IN HEART RATE REGULATION • AGE • GENDER PHYSICAL FITNESS • BODY TEMPERATURE

  36. STRUCTURE AND FUNCTIONS OF BLOOD VESSELS

  37. 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

  38. BLOOD DISTRIBUTION IN THE CARDIOVASCULAR SYSTEM • PULMONARY VESSELS - 9% • HEART – 7% • SYSTEMIC ARTERIES AND ARTERIOLES • SYSTEMIC CAPILLARIES – 7% • SYSTEMIC VEINS AND VENULES – 64% - 13%

  39. HEMODYNAMIC AFFECTING BLOOD FLOW • BLOOD PRESSURE • RESISTANCE • VENOUS RETURN

  40. 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

  41. MAP = DIASTOLIC PRESSURE + 1/3 (SYS PRESSURE – DIASTOLIC PRESSURE)

  42. VASCULAR RESISTANCE IT IS THE OPPOSTION TO BLOOD FLOW DUE TO FRICTION BETWEEN BLOOD AND THE WALLS OF BLOOD VESSELS.

  43. VASCULAR RESISTANCE DEPENDS ON • SIZE OF THE LUMEN- R IS INVERSELY PROPOTIONAL TO 1/d • BLOOD VISCOSITY • TOTAL BLOOD VESSEL LENGTH 4

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

  45. 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.

  46. CONTROL OF BLOOD PRESSURE AND BLOOD FLOW

  47. ROLE OF CARDIOVASCULAR CENTRE • PROPRIORECEOTORS • BARORECEPTORS • CHEMORECEPTORS

  48. NEURAL REGULATION 0F BLOOD PRESSURE • BARORECEPTORS • CHEMORECEPTORS

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

  50. 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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