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

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

  1. 1. ANATOMY AND PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM
  2. 2. LOCATION OF THE HEART RESTS ON THE DIAPHRAGM NEAR THE MIDLINE OF THE THORACIC CAVITY
  3. 3. PERICARDIUM CONFINES HEART TO THE MEDIASTINUM ALLOWS SUFFICIENT FREEDOM OF MOVEMENT. CONSISTS OF TWO PARTS:THE FIBROUS AND SEROUS.
  4. 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. 5. LAYERS OF THE HEART WALL
  6. 6. EPICARDIUM: COMPOSED OF MESOTHELIUM AND DELICATE CONNECTIVE TISSUE (IMPARTS A SLIPPERY TEXTURE TO THE OUTER SURFACE OF THE HEART).
  7. 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. 8. CHAMBERS OF THE HEART
  9. 9. FOUR CHAMBERS TWO AURICLES PRESENT SERIES OF GROOVES CALLED SULCI CONTAIN FAT AND CORONARY BLOOD VESSEL
  10. 10. SULCUS
  11. 11. MYOCARDIAL THICKNESS AND FUNCTION ATRIA : THIN WALLED VENTRICLES :THICK WALLED LT VENTRICLE IS THICKER THAN THE RT VENTRICLE.
  12. 12. HEART VALVES AND CIRCULATION OF BLOOD
  13. 13. ATRIOVENTRICULAR & SEMILUNAR VALVES
  14. 14. SYSTEMIC AND PULMONARY CIRCULATION LEFT SIDE IS A PUMP TO THE SYSTEMIC CIRCULATION. RIGHT SIDE IS A PUMP TO THE PULMONARY CIRCULATION.
  15. 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. 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. 17. PHYSIOLOGIC CHARACTERISTICS OF THE CONDUCTION CELLS AUTOMATICITY EXCITABILITY CONDUCTIVITY RHYTHMICITY CONTRACTILITY TONICITY
  18. 18. CARDIAC CYCLE
  19. 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. 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. 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. 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. 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. 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. 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. 26. REGULATION OF STROKE VOLUME THREE FACTORS REGULATE STROKE VOLUME -PRELOAD -CONTRACTILITY -AFTERLOAD
  27. 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. 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. 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. 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. 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. 32. NOR-EPINEPHRINE HAS 2 EFFECTS -IN SA NODE, SPEEDS THE RATE OF SPONTANEOUS DEPOLARIZATION -IN AV NODE,INCREASES CONTRACTILITY INCREASES STROKE VOLUME
  33. 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. 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. 35. OTHER FACTORS IN HEART RATE REGULATION AGE GENDER PHYSICAL FITNESS BODY TEMPERATURE
  36. 36. STRUCTURE AND FUNCTIONS OF BLOOD VESSELS
  37. 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. 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. 39. HEMODYNAMIC AFFECTING BLOOD FLOW BLOOD PRESSURE RESISTANCE VENOUS RETURN
  40. 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. 41. MAP = DIASTOLIC PRESSURE + 1/3 (SYS PRESSURE – DIASTOLIC PRESSURE)
  42. 42. VASCULAR RESISTANCE IT IS THE OPPOSTION TO BLOOD FLOW DUE TO FRICTION BETWEEN BLOOD AND THE WALLS OF BLOOD VESSELS.
  43. 43. VASCULAR RESISTANCE DEPENDS ON SIZE OF THE LUMEN- R IS INVERSELY PROPOTIONAL TO 1/d BLOOD VISCOSITY TOTAL BLOOD VESSEL LENGTH 4
  44. 44. VENOUS RETURN DEPENDS ON HEART CONTRACTION PRESSURE IN THE RT ATRIUM BESIDES THIS SKELETAL MUSCLE PUMP RESPIRATORY PUMP
  45. 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. 46. CONTROL OF BLOOD PRESSURE AND BLOOD FLOW
  47. 47. ROLE OF CARDIOVASCULAR CENTRE PROPRIORECEOTORS BARORECEPTORS CHEMORECEPTORS
  48. 48. NEURAL REGULATION 0F BLOOD PRESSURE BARORECEPTORS CHEMORECEPTORS
  49. 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. 50. CHEMORECEPTOR REFLEX PRESENT CLOSE TO THE - BARORECEPTORS OF CAROTID SINUS AND ARCH OF AORTA - THEY ARE CALLED CAROTID BODIES AND AORTIC BODIES.
  51. 51. HORMONAL REGULATION OF BLOOD PRESSURE RENIN ANGIOTENSIN-ALDOSTERONE MECHANISM EPINEPHRINE AND NOR EPINEPHRINE ANTIDIURETIC HORMONE ATRIAL NATRIURETIC PEPTIDE
  52. 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. 53. TWO TYPE OF STIMULI CAUSES AUTOREGULATORY CHANGESHSICALY - PHYSICAL CHANGE - VASODILATING AND VASOCONSTRICTING CHEMICALS
  54. 54. PHYSICAL CHANGES WARMING AND COOLING CAUSES VASODILATION AND VASOCONSTRICTION. SMOOTH MUSCLE IN ARTERIOLE EXHIBIT MYOGENIC RESPONSE
  55. 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

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