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Anatomy and-physiology-of-the-cardiovascular-system-medical-surgical-nursing-ppt

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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 mL/min mL/beat (Beats/min) FOR A RESTING ADULT CO = 70mL/beat x75beats/min = 5250 mL/min = 5.25 L/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 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
  • 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 EFFECTLEFT PARASYMPATHETIC NERVE REACHES THE HEART VIA 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% - 13% SYSTEMIC VEINS AND VENULES – 64%
  • 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.
  • 51. HORMONAL REGULATION OF BLOOD PRESSURE RENIN ANGIOTENSIN-ALDOSTERONE MECHANISM EPINEPHRINE AND NOR EPINEPHRINE ANTIDIURETIC HORMONE ATRIAL NATRIURETIC PEPTIDE
  • 52. AUTOREGULATION OF BLOOD PRESSURE ABILTY OF TISSUE TO AUTOMATICALLY ADJUST ITS BLOOD FLOW TO MATCH ITS METABLOIC DEMAND IS CALLED AUTOREGULATION. MAINLY DURING EXERCISE.
  • 53. TWO TYPE OF STIMULI CAUSES AUTOREGULATORY CHANGESHSICALY - PHYSICAL CHANGE - VASODILATING AND VASOCONSTRICTING CHEMICALS
  • 54. PHYSICAL CHANGES WARMING AND COOLING CAUSES VASODILATION AND VASOCONSTRICTION. SMOOTH MUSCLE IN ARTERIOLE EXHIBIT MYOGENIC RESPONSE
  • 55. 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