‫ﻣﺪﻝ‪ Simulink‬ﺍﺛﺮ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺭﻭﻱ ﺑﺪﻥ ﺍﻧﺴﺎﻥ‬

‫ﺣﻤﻴﺪ ﺭﺿﺎ ﺍﺣﻤﺪﻱ ﺭﺍﺩ*‪ ،‬ﻣﺤﻤﺪ ﺭﺿﺎ ﺟﺎﻫﺪ ﻣﻄﻠﻖ*‪ ،‬ﻭﺣﻴﺪ ﺭﺿﺎ ﻧﻔﻴﺴﻲ**‪ ،‬ﻣﻨﻮﭼﻬﺮ ﺍﻗﺒﺎﻝ**‬
‫)*( ﺩﺍﻧﺸﮕﺎﻩ ﻋﻠﻢ ﻭ ﺻﻨﻌﺖ ﺍﻳﺮﺍﻥ ﺩﺍﻧﺸﻜﺪﻩ ﻣﻬﻨﺪﺳﻲ ﺑﺮﻕ‪-‬ﻛﻨﺘﺮﻝ ﻭ )**( ﺳﺎﺯﻣﺎﻥ ﭘﮋﻭﻫﺸﻬﺎﻱ ﻋﻠﻤﻲ ﺻﻨﻌﺘﻲ ﺍﻳﺮﺍﻥ‬
‫‪ahmadyrad@yahoo.com‬‬

‫‪ -۱‬ﻣﻘﺪﻣﻪ‪:‬‬ ‫ﭼﻜﻴﺪﻩ‪ :‬ﺩﺭ ﺍﻳﻦ ﻣﻘﺎﻟﻪ ﻣﺪﻝ ﺷﺒﻴﻪﺳﺎﺯﻱ ﺑﺪﻥ ﺍﻧﺴﺎﻥ ﺷﺎﻣﻞ‬
‫ﻋﻠﻲ ﺭﻏﻢ ﭘﻴﺸﺮﻓﺖ ﺳﺮﻳﻊ ﺗﻜﻨﻮﻟﻮﮊﻱ‪ ،‬ﺍﻓﺖ ﻓﺸﺎﺭ ﺧﻮﻥ ﻭ‬ ‫ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ‪ ،‬ﺳﻴﺴﺘﻢ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﻭ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ ﺩﺭ‬
‫ﻧﺎﭘﺎﻳﺪﺍﺭﻱ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ ﺑﻪ ﻋﻨﻮﺍﻥ ﻳﻚ ﻋﺎﺭﺿﻪ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ‬ ‫ﺑﺪﻥ ﻭ ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻥ ‪ ANS‬ﻭ ﺍﺛﺮ‬
‫ﻫﻨﻮﺯ ﺑﺎﻗﻲ ﻣﺎﻧﺪﻩ ﺍﺳﺖ‪ ،‬ﺑﻌﻼﻭﻩ ﺑﻪ ﻋﻠﺖ ﺍﻳﻨﻜﻪ ﻓﺎﻛﺘﻮﺭﻫﺎﻱ ﺯﻳﺎﺩﻱ‬ ‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﺑﺪﻥ ﺍﻧﺴﺎﻥ )ﺷﺎﻣﻞ ﺁﺑﮕﻴﺮﻱ ‪ Ultrafiltration‬ﻭ‬
‫ﺑﺮ ﺭﻭﻱ ﺍﻓﺖ ﻓﺸﺎﺭ ﺧﻮﻥ ﺗﺎﺛﻴﺮ ﺩﺍﺭﻧﺪ‪ ،‬ﻟﺬﺍ ﻃﺮﺍﺣﻲ ﺑﻬﺘﺮﻳﻦ ﺭﻭﺵ‬ ‫ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ ﺩﺭ ﻣﺎﻳﻊ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻭ ﻓﻠﻮﻱ ﺧﻮﻥ ﺩﺭ ﻏﺸﺎ‬
‫ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻣﺸﻜﻞ ﻣﻲﺑﺎﺷﺪ]‪.[١‬‬ ‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ(؛ ﺑﺎ ﻫﺪﻑ ﺗﻮﺍﻧﺎﻳﻲ ﺑﺮﺭﺳﻲ ﻭ ﺁﻧﺎﻟﻴﺰ ﺭﻭﺷﻬﺎﻱ ﻛﻨﺘﺮﻟﻲ‬
‫ﻋﻮﺍﺭﺽ ﻧﺎﺷﻲ ﺍﺯ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺩﺭ ﺑﺪﻥ ﺑﻴﻤﺎﺭﺍﻥ ﻋﻤﻮﻣﹰﺎ ﺑﻪ ﻋﻠﺖ‬ ‫ﻣﺨﺘﻠﻒ ﻭ ﺗﺎﺛﻴﺮ ﺗﻐﻴﻴﺮ ﭘﺎﺭﺍﻣﺘﺮﻫﺎ ﻭ ﻋﻮﺍﻣﻞ ﻣﺨﺘﻠﻒ ﻧﺎﺷﻲ ﺍﺯ‬
‫ﻛﺎﻫﺶ ﺑﻴﺶ ﺍﺯ ﺣﺪ ﭘﻼﺳﻤﺎﻱ ﺧﻮﻥ ﺩﺭ ﺍﺛﺮ ﻋﻤﻠﻴﺎﺕ ﺁﺑﮕﻴﺮﻱ ﻭ‬ ‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﻭﺿﻌﻴﺖ ﻫﻤﻮﺩﻳﻨﺎﻣﻴﻜﻲ ﺑﻴﻤﺎﺭ‪ ،‬ﺍﺭﺍﺋﻪ ﺷﺪﻩ‬
‫ﻛﺎﻫﺶ ﺍﺳﻤﻮﻻﺭﻳﺘﻲ )‪ (osmolarity‬ﺩﺭ ﻣﻨﺎﻃﻖ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ ﺑﺪﻥ‬ ‫ﺍﺳﺖ‪ ،‬ﻛﻪ ﺑﺮ ﺍﺳﺎﺱ ﺟﻌﺒﻪ ﺍﺑﺰﺍﺭ ‪ Simulink‬ﻧﺮﻡﺍﻓﺰﺍﺭ‬
‫ﺭﺥ ﻣﻲﺩﻫﺪ]‪ ،[۲‬ﻟﺬﺍ ﺑﺮﺍﻱ ﺟﻠﻮﮔﻴﺮﻱ ﺍﺯ ﺍﻳﻦ ﻋﻮﺍﺭﺽ ﻭ ﻫﻤﭽﻨﻴﻦ‬ ‫®‪ MATLAB‬ﻃﺮﺍﺣﻲ ﺷﺪﻩ ﺍﺳﺖ‪.‬‬
‫ﻛﺎﻫﺶ ﻣﺪﺕ ﺯﻣﺎﻥ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻳﻚ ﻣﺤﺪﻭﺩﻩ ﺑﺎﺭﻳﻚ ﺑﺮﺍﻱ‬ ‫ﻣﺪﻝ ﺑﺪﻥ ﺑﻴﻤﺎﺭ ﺩﺭ ﺑﻴﺶ ﺍﺯ ‪ ۴۰‬ﺑﻠﻮﻙ ﻛﻪ ﻫﺮﻛﺪﺍﻡ ﺑﻴﺎﻧﮕﺮ ﻋﻤﻠﻜﺮﺩ‬
‫ﺗﻐﻴﻴﺮﺍﺕ ﻧﺮﺥ ﺁﺑﮕﻴﺮﻱ ﻭ ﻏﻠﻈﺖ ﺳﺪﻳﻢ ﺩﺭ ﻣﺎﻳﻊ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻭﺟﻮﺩ‬ ‫ﻳﻚ ﺑﺨﺶ ﺍﺯ ﺑﺪﻥ ﻣﻲﺑﺎﺷﺪ‪ ،‬ﺍﺭﺍﺋﻪ ﺷﺪﻩ ﺍﺳﺖ ﻭ ﺩﺍﺭﺍﻱ ﺑﻴﺶ ﺍﺯ‪۹۰‬‬
‫ﺩﺍﺭﺩ ﻛﻪ ﺍﺯ ﻋﻮﺍﺭﺽ ﻛﻮﺗﺎﻩ ﻣﺪﺕ ﻭ ﺑﻠﻨﺪ ﻣﺪﺕ ﻧﺎﺷﻲ ﺍﺯ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ‬ ‫ﻣﺘﻐﻴﻴﺮ ﻓﻴﺰﻳﻮﻟﻮﮊﻳﻜﻲ ﻭ ﻫﻤﻮﺩﻳﻨﺎﻣﻴﻜﻲ ﺑﻴﻤﺎﺭ ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﻫﻤﮕﻲ‬
‫ﺟﻠﻮﮔﻴﺮﻱ ﻣﻲﻛﻨﺪ]‪.[٣‬‬ ‫ﺩﺭ ﺣﻴﻦ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻗﺎﺑﻞ ﻣﺎﻧﻴﺘﻮﺭ ﻛﺮﺩﻥ ﻣﻲﺑﺎﺷﻨﺪ‪.‬‬
‫ﭘﺎﺭﺍﻣﺘﺮﻫﺎﻱ ﻣﺨﺘﻠﻔﻲ ﺑﺮ ﺍﺳﺎﺱ ﺭﻭﺍﺑﻂ ﻏﻴﺮﺧﻄﻲ ﺑﺮﺍﻱ ﺛﺎﺑﺖ‬ ‫ﺍﺯ ﺍﻳﻦ ﻣﺪﻝ ﻣﻲﺗﻮﺍﻥ ﺑﻪ ﻋﻨﻮﺍﻥ ﻳﻚ ﻣﺒﻨﺎ ﺑﺮﺍﻱ ﺗﺤﻘﻴﻘﺎﺕ ﻣﺪﻝ‪-‬‬
‫ﻧﮕﻪﺩﺍﺷﺘﻦ ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺩﺭ ﺣﻴﻦ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺗﺎﺛﻴﺮﮔﺬﺍﺭ‬ ‫ﻣﺒﻨﺎﻱ ﺍﺛﺮ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﺑﺪﻥ ﺍﻧﺴﺎﻥ ﻭ ﻃﺮﺍﺣﻲ ﻛﻨﺘﺮﻝ‬
‫ﻫﺴﺘﻨﺪ ﻭ ﺩﺭ ﺍﻳﻦ ﻣﻴﺎﻥ ﺳﻴﺴﺘﻢ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﻋﺼﺒﻲ‬ ‫ﻛﻨﻨﺪﻩﻫﺎﻱ ﻣﺨﺘﻠﻒ ﺑﺮﺍﻱ ﺑﻬﺒﻮﺩ ﺭﺍﻧﺪﻣﺎﻥ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻛﻪ ﻧﻴﺎﺯ ﺑﻪ‬
‫)‪ (ANS‬ﻧﻘﺶ ﺍﺻﻠﻲ ﺭﺍ ﺩﺭ ﺗﻨﻈﻴﻢ ﻓﺸﺎﺭ ﺧﻮﻥ ﻭ ﺣﻔﻆ ﺑﻴﻤﺎﺭ ﺩﺭ‬ ‫ﻣﺪﻟﻲ ﺑﺮﺍﻱ ﺗﺴﺖ ﻋﻤﻠﻜﺮﺩ ﻛﻨﺘﺮﻟﺮ ﺩﺍﺭﻧﺪ‪ ،‬ﺍﺳﺘﻔﺎﺩﻩ ﻛﺮﺩ‪.‬‬
‫ﺷﺮﺍﻳﻂ ﭘﺎﻳﺪﺍﺭ ﺑﺎ ﺍﺳﺘﻔﺎﺩﻩ ﺍﺯ ﺗﻨﻈﻴﻢ ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﻭ ﺣﺠﻢ‬
‫‪ unstressed‬ﻭﺭﻳﺪﻱ ﻭ ﻧﺮﺥ ﺿﺮﺑﺎﻥ ﻗﻠﺐ‪ ،‬ﺑﺎﺯﻱ ﻣﻲﻛﻨﺪ]‪.[٣‬‬ ‫ﻭﺍﮊﻩﻫﺎﯼ ﮐﻠﻴﺪﻱ‪ :‬ﻣﺪﻝﺳﺎﺯﻱ‪ ،‬ﻫﻤﻮﺩﻳﺎﻟﻴﺰ‪ ،‬ﺷﺒﻴﻪﺳﺎﺯﻱ‬
‫ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻣﻮﺍﺭﺩ ﺫﻛﺮ ﺷﺪﻩ ﻟﺰﻭﻡ ﻭﺟﻮﺩ ﻳﻚ ﻣﺪﻝ ﺭﻳﺎﺿﻲ ﻛﻪ‬ ‫‪ ،Simulink‬ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ‪ ،‬ﺳﻴﺴﺘﻢ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﻭ ﻳﻮﻧﻬﺎ‬
‫ﺍﻣﻜﺎﻥ ﺑﺮﺭﺳﻲ ﻭ ﺁﻧﺎﻟﻴﺰ ﺭﻭﺷﻬﺎﻱ ﻛﻨﺘﺮﻟﻲ ﻣﺨﺘﻠﻒ ﻭ ﺗﺎﺛﻴﺮ ﺗﻐﻴﻴﺮ‬ ‫ﻭ ﺍﻭﺭﻩ‪ ،‬ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻥ‬
‫ﺍﻓﺖ ﺍﻧﺮﮊﻱ )ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ( ﺩﺭ ﻗﺴﻤﺖ ﺳﺮﺧﺮﮔﻲ ﺗﺎ ﻣﻮﻳﺮﮔﻲ‬ ‫ﭘﺎﺭﺍﻣﺘﺮﻫﺎ ﻭ ﻋﻮﺍﻣﻞ ﻣﺨﺘﻠﻒ ﻧﺎﺷﻲ ﺍﺯ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﺑﻴﻤﺎﺭ ﺭﺍ‬
‫ﺑﺎ )‪ ،(Rs1‬ﺩﺭ ﻗﺴﻤﺖ ﻣﻮﻳﺮﮔﻲ ﺑﺎ )‪ (Rs2‬ﻭ ﺩﺭ ﻗﺴﻤﺖ ﻣﻮﻳﺮﮔﻲ‬ ‫ﻧﺸﺎﻥ ﺩﻫﺪ‪ ،‬ﺍﺣﺴﺎﺱ ﻣﻲﺷﻮﺩ‪.‬‬
‫ﺗﺎ ﻭﺭﻳﺪﻱ ﺑﺎ )‪ (Rs3‬ﺷﺒﻴﻪﺳﺎﺯﻱ ﺷﺪﻩ ﺍﺳﺖ‪.‬‬ ‫ﺩﺭ ﺭﻭﺵ ﺁﻧﺎﻟﻴﺰ ﻣﺪﻝ‪-‬ﻣﺒﻨﺎﻱ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺍﺯ ﻣﺪﻝ ﺭﻳﺎﺿﻲ ﻭ‬
‫ﺷﺒﻴﻪﺳﺎﺯﻱ ﻛﺎﻣﭙﻴﻮﺗﺮﻱ ﺍﺳﺘﻔﺎﺩﻩ ﻣﻲﺷﻮﺩ‪ .‬ﺍﻳﻦ ﺭﻭﺵ ﺑﺎﻋﺚ ﻣﻲﺷﻮﺩ‬
‫ﻛﻪ ﻳﻚ ﺍﻧﺘﺨﺎﺏ ﺑﻬﻴﻨﻪ ﺍﺯ ﺷﺮﺍﻳﻂ ﻋﻤﻠﻜﺮﺩﻱ ﺩﺭ ﺣﻴﻦ ﻋﻤﻠﻴﺎﺕ‬
‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻧﻈﻴﺮ ﭘﺮﻭﻓﺎﻳﻞ ﺁﺑﮕﻴﺮﻱ‪ ،‬ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎ ﺩﺭ ﻣﺤﻠﻮﻝ‬
‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮﺍﻱ ﻛﺎﻫﺶ ﻋﻮﺍﺭﺽ ﻧﺎﺷﻲ ﺍﺯ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﭼﻪ ﺩﺭ ﺣﻴﻦ‬
‫ﻋﻤﻠﻴﺎﺕ ﻭ ﭼﻪ ﺩﺭ ﺯﻣﺎﻥ ﺑﻴﻦ ﺩﻭ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﻪ ﺩﺳﺖ ﺁﻳﺪ‪.‬‬
‫ﺑﻌﻼﻭﻩ ﺍﻣﻜﺎﻥ ﺁﻧﺎﻟﻴﺰ ﺍﺛﺮ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﺣﺠﻢ ﺧﻮﻥ‪ ،‬ﻓﺸﺎﺭ‬
‫ﻼ ﺷﺮﺍﻳﻂ ﻫﻤﻮﺩﻳﻨﺎﻣﻴﻜﻲ ﻭ ﻓﻴﺰﻳﻮﻟﻮﮊﻳﻜﻲ ﺑﻴﻤﺎﺭ ﺩﺭ ﺣﻴﻦ‬
‫ﺧﻮﻥ ﻭ ﻛ ﹰ‬
‫ﺷﺒﻴﻪﺳﺎﺯﻱ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻭﺟﻮﺩ ﺩﺍﺭﺩ‪.‬‬
‫ﺷﻜﻞ ‪ :۱‬ﻣﺪﺍﺭ ﺍﻟﻜﺘﺮﻳﻜﻲ ﺷﺒﻴﻪﺳﺎﺯﻱ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ‬ ‫ﻣﺪﻝ ﺍﺭﺍﺋﻪ ﺷﺪﻩ ﺩﺭ ﺍﻳﻨﺠﺎ ﺷﺎﻣﻞ ﺩﻳﻨﺎﻣﻴﻚ ﻗﻠﺐ ﻭ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ‬
‫ﻋﺮﻭﻗﻲ )ﺷﺎﻣﻞ ﻫﺮ ﺩﻭ ﻗﺴﻤﺖ ﺷﺸﻲ ﻭ ﺷﺮﻳﺎﻧﻲ( ﻭ ﺩﻳﻨﺎﻣﻴﻚ ﺩﻭ‬
‫ﺩﻳﻨﺎﻣﻴﻚ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ ﺷﺒﻴﻪ ﻣﺪﺍﺭ ﺍﻟﻜﺘﺮﻳﻜﻲ ﺍﺭﺍﺋﻪ ﺷﺪﻩ ﺩﺭ‬
‫ﮔﺮﻭﻩ ﻣﺨﺘﻠﻒ ﺍﺯ ﮔﻴﺮﻧﺪﻩﻫﺎﻱ ﻓﺸﺎﺭ ﻭ ﺩﻳﻨﺎﻣﻴﻚ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﻭ‬
‫ﺷﻜﻞ ‪ ۱‬ﻣﻲﺑﺎﺷﺪ‪ .‬ﺩﺭ ﻣﻌﺎﺩﻻﺕ ﺭﻳﺎﺿﻲ ﺍﺭﺍﺋﻪ ﺷﺪﻩ ‪ R‬ﺣﺠﻢ ﻭ ‪C‬‬ ‫ﻳﻮﻧﻬﺎﻱ ﺳﺪﻳﻢ ﻭ ﭘﺘﺎﺳﻴﻢ ﻭ ﺍﻭﺭﻩ ﺩﺭ ﺑﺪﻥ ﻭ ﺩﺍﺧﻞ ﻓﻴﻠﺘﺮ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ‬
‫ﻭ ﺩﻳﻨﺎﻣﻴﻚ ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻥ ﻣﻲﺑﺎﺷﺪ]‪[٤‬‬
‫ﻣﻘﺎﻭﻣﺖ ﻫﻴﺪﻭﻟﻴﻜﻲ ﺭﺍ ﻣﺸﺨﺺ ﻣﻲﻛﻨﺪ]‪.[٤‬‬

‫‪dp sa‬‬ ‫‪1 ‬‬ ‫‪P − Pac‬‬ ‫‪‬‬ ‫‪ -۲‬ﺗﺸﺮﻳﺢ ﺑﺨﺶﻫﺎﻱ ﻣﺪﻝ ﻭ ﭼﮕﻮﻧﮕﻲ ﻛﺎﺭ ﺁﻧﻬﺎ‪:‬‬
‫=‬ ‫‪×  ql − sa‬‬ ‫‪‬‬
‫‪dt‬‬ ‫‪C sa ‬‬ ‫‪Rs1‬‬ ‫‪‬‬
‫ﺍﻳﻦ ﻣﺪﻝ ﺷﺎﻣﻞ ﺳﻪ ﻗﺴﻤﺖ ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﻋﺒﺎﺭﺗﻨﺪ ﺍﺯ‪ :‬ﺩﻳﻨﺎﻣﻴﻚ‬
‫‪dp ra‬‬ ‫‪1‬‬ ‫‪ P − Pra‬‬ ‫‪‬‬
‫=‬ ‫‪⋅  sv‬‬ ‫‪− q r ‬‬
‫‪dt‬‬ ‫‪C ra‬‬ ‫‪ Rsv‬‬ ‫‪‬‬ ‫ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ‪ ،‬ﺩﻳﻨﺎﻣﻴﻚ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﻭ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ ﻭ‬
‫‪dp pa‬‬ ‫‪1‬‬ ‫‪‬‬ ‫‪Ppa − Ppv‬‬ ‫‪‬‬ ‫ﺩﻳﻨﺎﻣﻴﻚ ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻥ‪.‬‬
‫=‬ ‫‪⋅  qr −‬‬ ‫‪‬‬
‫‪dt‬‬ ‫‪C pa‬‬ ‫‪‬‬ ‫‪R pa‬‬ ‫‪‬‬
‫‪‬‬ ‫‪‬‬
‫‪dp pv‬‬ ‫‪1‬‬ ‫‪ Ppa − Ppv Ppv − Pla‬‬ ‫‪‬‬ ‫‪ -۱-۲‬ﺩﻳﻨﺎﻣﻴﻚ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ‪:‬‬
‫=‬ ‫‪⋅‬‬ ‫‪−‬‬ ‫‪‬‬
‫‪dt‬‬ ‫‪C pv‬‬ ‫‪ R‬‬ ‫‪R pv‬‬ ‫‪‬‬
‫‪‬‬ ‫‪pa‬‬ ‫‪‬‬
‫ﺩﻳﻨﺎﻣﻴﻚ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ ﻗﺴﻤﺘﻬﺎﻱ ﺯﻳﺮ ﺭﺍ ﻣﺪﻝ ﻣﻲﻛﻨﺪ‪.۱ :‬‬
‫‪dpla‬‬ ‫‪1‬‬ ‫‪ Ppv − Pla‬‬ ‫‪‬‬
‫=‬ ‫‪⋅‬‬ ‫‪− ql ‬‬
‫‪dt‬‬ ‫‪Cla‬‬ ‫‪ R‬‬ ‫‪‬‬ ‫ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ )‪ .۲ (systemic arterial‬ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ ‪(systemic‬‬
‫‪‬‬ ‫‪pv‬‬ ‫‪‬‬
‫‪dv‬‬ ‫)‪ .۳ vein‬ﻓﺸﺎﺭ ﺩﻫﻠﻴﺰ ﺭﺍﺳﺖ )‪ .۴ (right atrium‬ﻓﺸﺎﺭ ﺩﻫﻠﻴﺰ‬
‫‪= − Fa + Rv − Q f + Qin f‬‬
‫‪dt‬‬
‫‪(arterial‬‬ ‫ﭼﭗ )‪ .۵ (left atrium‬ﻓﺸﺎﺭ ﺳﺮﺧﺮﮔﻲ ﻣﻮﻳﺮﮔﻲ‬
‫= ‪Psv‬‬
‫‪1‬‬
‫) ‪(V − Vu − Csa Psa − C pa Ppa − C pv Ppv − Cra Pra − Cla Pla‬‬
‫‪C sv‬‬ ‫)‪ .۶ capillary‬ﻓﺸﺎﺭ ﺳﻴﺎﻫﺮﮔﻲ ﻣﻮﻳﺮﮔﻲ )‪.۷ (venous capillary‬‬
‫‪q‬‬
‫‪Gv ⋅ qa + v‬‬ ‫ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺗﻨﻔﺴﻲ )‪ .۸ (pulmonary arteries‬ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ‬
‫‪Rs 2‬‬
‫= ‪Pac‬‬
‫‪1‬‬ ‫ﺗﻨﻔﺴﻲ )‪(pulmonary vein‬؛ ﻛﻪ ﻫﺮ ﻗﺴﻤﺖ ﺷﺎﻣﻞ ﻳﻚ ﻣﻘﺎﻭﻣﺖ‬
‫‪Ga .Gv − 2‬‬
‫‪Rs 2‬‬
‫ﻫﻴﺪﺭﻭﻟﻴﻜﻲ ﻛﻪ ﻧﺸﺎﻥ ﺩﻫﻨﺪﻩ ﺗﻠﻔﺎﺕ ﺍﻧﺮﮊﻱ ﺑﻪ ﺳﺒﺐ ﻭﻳﺴﻜﻮﺯﻳﺘﻪ‬
‫‪q‬‬
‫‪Ga ⋅ qv + a‬‬
‫‪Rs 2‬‬ ‫ﺧﻮﻥ ﻭ ﻇﺮﻓﻴﺘﻲ ﻛﻪ ﻧﺸﺎﻥ ﺩﻫﻨﺪﻩ ﻣﻘﺪﺍﺭ ﺣﺠﻢ ﺧﻮﻥ ﺫﺧﻴﺮﻩ ﺷﺪﻩ‬
‫= ‪Pvc‬‬
‫‪1‬‬
‫‪Ga ⋅ Gv − 2‬‬ ‫ﺩﺭ ﺁﻥ ﻗﺴﻤﺖ ﻣﻲﺑﺎﺷﺪ‪.‬‬
‫‪Rs 2‬‬
‫‪V pl = V − Vrc‬‬
 ‫‪ -۲-۲-۲‬ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ‪:‬‬ ‫‪Vrc‬‬ ‫‪V pl‬‬
‫= ‪HCT‬‬ ‫‪= 1−‬‬
‫‪V‬‬ ‫‪V‬‬
‫ﺩﺭ ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ )ﺳﻪ ﻗﺴﻤﺘﻲ(‪ ،‬ﻋﻠﺖ ﺍﺻﻠﻲ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ‬
‫ﺑﻴﻦ ﻣﻨﺎﻃﻖ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﻭ ﺩﺍﺧﻞﺳﻠﻮﻟﻲ ﻭﺟﻮﺩ ﺍﺧﺘﻼﻑ ﻓﺸﺎﺭ‬ ‫‪ -۲-۲‬ﺩﻳﻨﺎﻣﻴﻚ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﻭ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ‪:‬‬
‫ﺍﺳﻤﺰﻱ ﺑﻴﻦ ﺩﻭ ﻃﺮﻑ ﻏﺸﺎ ﺳﻠﻮﻝﻫﺎ ﻣﻲﺑﺎﺷﺪ؛ ﻛﻪ ﺍﻳﻦ ﺍﺧﺘﻼﻑ‬ ‫ﺩﺭ ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﺩﺭ ﺑﺪﻥ‪ ،‬ﺑﺪﻥ ﺭﺍ ﺑﻪ ﺳﻪ ﻗﺴﻤﺖ ﻛﻪ ﺷﺎﻣﻞ‬
‫ﻓﺸﺎﺭ ﺑﻪ ﻭﺳﻴﻠﻪ ﺍﺧﺘﻼﻑ ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎﻳﻲ ﺍﺯ ﻗﺒﻴﻞ ﺳﺪﻳﻢ‪ ،‬ﭘﺘﺎﺳﻴﻢ ﻭ‬ ‫ﻣﻨﺎﻃﻖ ﺩﺍﺧﻞ ﺳﻠﻮﻟﻲ‪ ،‬ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﻭ ﭘﻼﺳﻤﺎ ﻣﻲﺑﺎﺷﺪ‪ ،‬ﺗﻘﺴﻴﻢ‬
‫ﺩﻳﮕﺮ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ ﺗﻌﻴﻴﻦ ﻣﻲﺷﻮﺩ‪ .‬ﻭﻟﻲ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﺑﻴﻦ ﻣﻨﺎﻃﻖ‬ ‫ﻣﻲﻛﻨﻴﻢ ﻭﻟﻲ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺍﻳﻨﻜﻪ ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎﻱ ﺍﺻﻠﻲ ﺩﺭ ﭘﻼﺳﻤﺎ‬
‫ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﻭ ﭘﻼﺳﻤﺎ ﺑﻪ ﺍﺧﺘﻼﻑ ﻓﺸﺎﺭ ﻫﻴﺪﺭﻭﻟﻴﻜﻲ ﻭ ‪ oncotic‬ﺩﺭ‬ ‫ﻭ ﺑﺨﺶ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﺗﻘﺮﻳﺒﹰﺎ ﻳﻜﺴﺎﻥ ﺍﺳﺖ‪ ،‬ﻟﺬﺍ ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﻳﻮﻧﻬﺎ‬
‫ﻣﻮﻳﺮﮔﻬﺎ ﺑﺴﺘﮕﻲ ﺩﺍﺭﺩ‪ .‬ﻓﺸﺎﺭ ‪ oncotic‬ﺩﺭ ﭘﻼﺳﻤﺎ ﻭ ﻣﺎﻳﻊ‬ ‫ﻭ ﺍﻭﺭﻩ ﺩﺭ ﺑﺪﻥ ﺭﺍ ﺑﻪ ﺩﻭ ﺑﺨﺶ ﺩﺍﺧﻞﺳﻠﻮﻟﻲ ﻭ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ‬
‫ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﺑﻪ ﻭﺳﻴﻠﻪ ﻣﻌﺎﺩﻻﺕ ‪ [٥] Landis-Pappenheimer‬ﺑﺎ‬ ‫ﺗﻘﺴﻴﻢ ﻣﻲﻛﻨﻴﻢ ﻛﻪ ﺑﺨﺶ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ ﻣﺠﻤﻮﻉ ﺑﺨﺶ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ‬
‫ﻓﺮﺽ ﺍﻳﻨﻜﻪ ﭘﺮﻭﺗﺌﻴﻦﻫﺎ ﺗﻮﺍﻧﺎﻳﻲ ﻋﺒﻮﺭ ﺍﺯ ﻏﺸﺎ ﻣﻮﻳﺮﮔﻬﺎ ﻭ ﻏﺸﺎ‬ ‫ﻭ ﭘﻼﺳﻤﺎ ﻣﻲﺑﺎﺷﺪ]‪.[٢‬‬
‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺭﺍ ﻧﺪﺍﺭﻧﺪ‪ ،‬ﻣﺤﺎﺳﺒﻪ ﻣﻲﺷﻮﺩ‪ .‬ﻭ ﻓﺸﺎﺭ ﻫﻴﺪﺭﻭﻟﻴﻜﻲ ﺩﺭ‬
‫ﻣﻨﺎﻃﻖ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﺑﻪ ﺻﻮﺭﺕ ﺗﺎﺑﻌﻲ ﺍﺯ ﺣﺠﻢ ﻣﺎﻳﻊ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ‬ ‫‪ -۱-۲-۲‬ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ‪:‬‬
‫ﻣﺤﺎﺳﺒﻪ ﻣﻲﺷﻮﺩ‪.‬‬ ‫ﺩﺭ ﻣﺪﻝ ﺟﺎﺑﺠﺎﻳﻲ ﻳﻮﻧﻬﺎ ﻭ ﺍﻭﺭﻩ ﺩﺭ ﺑﺪﻥ ﺩﻭ ﻳﻮﻥ ﺍﺻﻠﻲ )ﺳﺪﻳﻢ ﻭ‬
‫ﺩﺭ ﻧﻬﺎﻳﺖ ﺗﻮﺍﺯﻥ ﺑﻴﻦ ﻧﺮﺥ ﺁﺑﮕﻴﺮﻱ ﺍﺯ ﺧﻮﻥ ﻭ ﻧﺮﺥ ﺗﺰﺭﻳﻖ ﺁﺏ‬ ‫ﭘﺘﺎﺳﻴﻢ( ﻭ ﺍﻭﺭﻩ ﻣﺪﻝ ﻣﻲﺷﻮﺩ‪ .‬ﻧﺮﺥ ﺟﺎﺑﺠﺎﻳﻲ ﻳﻮﻧﻬﺎ ﺍﺯ ﻗﺴﻤﺖ‬
‫ﻭﺭﻭﺩﻱ ﺑﻪ ﭘﻼﺳﻤﺎ ﺍﺯ ﻏﺸﺎ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻭ ﺁﺏ ﻭﺭﻭﺩﻱ ﺑﻪ ﭘﻼﺳﻤﺎ ﺍﺯ‬ ‫ﺩﺍﺧﻞﺳﻠﻮﻟﻲ ﺑﻪ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ ﺑﻪ ﻏﻠﻈﺖ ﺁﻥ ﻳﻮﻧﻬﺎ ﺩﺭ ﺁﻥ ﻗﺴﻤﺖ‬
‫ﻃﺮﻳﻖ ﻏﺸﺎ ﻣﻮﻳﺮﮔﻬﺎ‪ ،‬ﻧﺮﺥ ﻛﺎﻫﺶ ﻳﺎ ﺍﻓﺰﺍﻳﺶ ﺣﺠﻢ ﭘﻼﺳﻤﺎﻱ‬ ‫ﺑﺴﺘﮕﻲ ﺩﺍﺭﺩ‪ .‬ﺩﺭ ﻣﺪﻝ ﺳﺪﻳﻢ ﻭ ﭘﺘﺎﺳﻴﻢ ﺿﺮﻳﺐ ﺟﺎﺑﺠﺎﻳﻲ ﺟﺮﻡ‬
‫ﺧﻮﻥ ﺭﺍ ﺗﻌﻴﻴﻦ ﻣﻲﻛﻨﺪ‪.‬‬ ‫ﺷﺎﻣﻞ ﺟﺎﺑﺠﺎﻳﻲ ﻓﻌﺎﻝ ﻭ ﻏﻴﺮﻓﻌﺎﻝ ﻣﻲﺑﺎﺷﺪ ﺩﺭ ﺣﺎﻟﻲ ﻛﻪ ﺑﺮﺍﻱ‬
‫ﻛﺎﻫﺶ ﺣﺠﻢ ﭘﻼﺳﻤﺎﻱ ﺧﻮﻥ ﺑﺎﻋﺚ ﺍﻓﺰﺍﻳﺶ ﻓﺸﺎﺭ ‪ oncotic‬ﺩﺭ‬ ‫ﺟﺎﺑﺠﺎﻳﻲ ﺍﻭﺭﻩ ﻓﻘﻂ ﺍﻧﺘﻘﺎﻝ ﻏﻴﺮﻓﻌﺎﻝ ﺩﺭ ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﻣﻲﺷﻮﺩ‪.‬‬
‫ﭘﻼﺳﻤﺎ ﻣﻲﺷﻮﺩ ﻭ ﺩﺭ ﻧﺘﻴﺠﻪ ﻧﺮﺥ ﺑﺎﺯﻳﺎﺑﻲ ﭘﻼﺳﻤﺎ ﺍﻓﺰﺍﻳﺶ ﻣﻲﻳﺎﺑﺪ‬ ‫ﺩﺭ ﻣﻌﺎﺩﻻﺕ ﺯﻳﺮ ‪ ،Vj‬ﺣﺠﻢ ﻗﺴﻤﺖ ‪ j‬ﺭﺍ ﻣﺸﺨﺺ ﻣﻲﻛﻨﺪ‪ .‬ﺩﺭ‬
‫ﻭﻟﻲ ﺩﺭ ﺍﺛﺮ ﻛﺎﻫﺶ ﺣﺠﻢ ﻣﺎﻳﻊ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ‪ ،‬ﻓﺸﺎﺭ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﺍﻓﺖ‬ ‫ﺣﺎﻟﻴﻜﻪ ‪ Csj‬ﻏﻠﻈﺖ ﻳﻮﻥ ‪ s‬ﺭﺍ ﺩﺭ ﻗﺴﻤﺖ ‪ j‬ﻣﺸﺨﺺ ﻣﻲﻛﻨﺪ]‬
‫ﻣﻲﻛﻨﺪ ﻭ ﺍﻳﻦ ﭘﺪﻳﺪﻩ ﺩﺭ ﺣﻴﻦ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻧﺮﺥ‬ ‫‪[٢،٦،٧‬‬

‫ﺑﺎﺯﻳﺎﺑﻲ ﭘﻼﺳﻤﺎ ﺩﺭ ﺧﻮﻥ ﻣﻲﺷﻮﺩ ﻛﻪ ﻫﺮﭼﻪ ﺑﻪ ﺍﻧﺘﻬﺎﻱ ﺯﻣﺎﻥ‬ ‫‪Vex = V pl + Vis‬‬

‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻧﺰﺩﻳﻚﺗﺮ ﺷﻮﻳﻢ‪ ،‬ﺍﺛﺮ ﺁﻥ ﺑﻴﺸﺘﺮ ﻣﻲﺷﻮﺩ‪.‬‬ ‫‪C s ,ex = C s ,is ≅ C s , pl‬‬
‫ﻣﻌﺎﺩﻻﺕ ﺭﻳﺎﺿﻲ ﺫﻳﻞ ﺩﻳﻨﺎﻣﻴﻚ ﺟﺎﺑﺠﺎﻳﻲ ﺁﺏ ﺩﺭ ﺑﺪﻥ ﻣﻲﺑﺎﺷﺪ]‬ ‫‪dM s ,ic‬‬
‫) ‪= − K s ⋅ (C s ,ic − Bs C s ,ex‬‬
‫‪:[٢،٦،٨‬‬ ‫‪dt‬‬
‫‪dM s ,ex‬‬
‫‪dVic‬‬
‫) ‪= − K f (C is − C ic‬‬
‫‪= K s ⋅ (C s ,ic − Bs C s ,ex ) − J s + Qinf ⋅ C s ,inf‬‬
‫‪dt‬‬ ‫‪dt‬‬
‫‪M K ,ic + M Na ,ic + M u ,ic + M eq ,ic‬‬ ‫[‬ ‫]‬
‫‪J s = Ds ⋅ (1 − Q f / Qes ) + Q f ⋅ C s ,ex − Ds ⋅ (1 − Q f / Qes ) ⋅ C s ,d‬‬
‫= ‪C ic‬‬
‫‪Vic‬‬ ‫[‬
‫‪Qe,s = QB ⋅ Fp ⋅ (1 − HCT ) + Fr ⋅ γ s ⋅ RDs‬‬ ‫]‬
‫‪M K ,ex + M Na ,ex + M u ,ex + M eq ,eu‬‬ ‫‪M s ,ic‬‬
‫= ‪Cis = C ex‬‬ ‫= ‪C s ,ic‬‬
‫‪V pl + Vis‬‬
‫‪Vic‬‬
‫‪dVis‬‬
‫‪= K f ⋅ (C is − C ic ) + Fa − Rv‬‬ ‫‪M s ,ex‬‬
‫‪dt‬‬ ‫= ‪C s ,ex‬‬
‫‪Vis + V pl‬‬
‫‪C p ,cs = C p ,isn ⋅ Visn / Vis‬‬
‫‪C p , pl = C p , p ln ⋅ V p ln / V pl‬‬
‫‪Pis = Eis (Vis − Visn ) + Pisn‬‬
 ‫ﻭ ﺍﮔﺮ ‪: pla < plat‬‬
‫‪ -۳-۲‬ﺩﻳﻨﺎﻣﻴﻚ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻥ ‪:ANS‬‬
‫) ‪dδ (t‬‬
‫‪= [Gδ ⋅ (Plat − Pla ) − δ (t )] / τ δ‬‬
‫‪dt‬‬ ‫ﺩﺭ ﺍﻳﻦ ﺳﻴﺴﺘﻢ ﻓﺮﺽ ﺑﺮ ﺍﻳﻦ ﺍﺳﺖ ﻛﻪ ﺳﻴﺴﺘﻢ ﺗﻨﻈﻴﻢ ﻛﻨﻨﺪﻩ ﻛﻮﺗﺎﻩ‬
‫ﻣﺪﺕ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ ﺑﺮ ﺍﺳﺎﺱ ﻓﻌﺎﻟﻴﺖ ﺩﻭ ﮔﺮﻭﻩ ﺍﺯ ﮔﻴﺮﻧﺪﻩﻫﺎﻱ‬
‫ﻛﻨﺘﺮﻝ ﺿﺮﺑﺎﻥ ﻗﻠﺐ ﻧﻴﺰ ﺷﺎﻣﻞ ﻣﻌﺎﺩﻻﺗﻲ ﺷﺒﻴﻪ ﻣﻌﺎﺩﻻﺕ ﻣﻘﺎﻭﻣﺖ‬
‫ﻓﺸﺎﺭ ﻳﻜﻲ ﺑﺮﺍﻱ ﮔﺮﺩﺵ ﺧﻮﻥ ﺷﺮﻳﺎﻧﻲ )‪ (high pressure‬ﻭ‬
‫ﺷﺮﻳﺎﻧﻲ ‪ systemic‬ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﺑﻪ ﺻﻮﺭﺕ ﺯﻳﺮ ﺍﺳﺖ]‪:[٤‬‬
‫ﺩﻳﮕﺮﻱ ﺑﺮﺍﻱ ﮔﺮﺩﺵ ﺧﻮﻥ ﺗﻨﻔﺴﻲ )‪ (low pressure‬ﻓﻌﺎﻟﻴﺖ‬
‫‪dT 1‬‬
‫) ‪= (σ T − T‬‬
‫‪dt τ T‬‬ ‫ﻣﻲﻛﻨﺪ ﻭ ﺍﻃﻼﻋﺎﺕ ﺣﺎﺻﻞ ﺍﺯ ﺍﻳﻦ ﮔﻴﺮﻧﺪﻩﻫﺎ ﺩﺭ ﺳﻴﺴﺘﻢ ﻋﺼﺒﻲ‬
‫) ‪Tmin + Tmax ⋅ exp( X T / K T‬‬ ‫ﻣﺮﻛﺰﻱ ﺟﻤﻊﺁﻭﺭﻱ ﻣﻲﺷﻮﻧﺪ ﻭ ﺳﭙﺲ ﺳﻴﮕﻨﺎﻟﻬﺎﻱ ﺗﻨﻈﻴﻤﻲ ﻻﺯﻡ‬
‫= ‪σT‬‬
‫) ‪1 + exp( X T / K T‬‬ ‫ﺑﺮﺍﻱ ﺍﺻﻼﺡ ﭘﺎﺭﺍﻣﺘﺮﻫﺎﻱ ﺳﻴﺴﺘﻢ ﻗﻠﺒﻲ ﻋﺮﻭﻗﻲ )ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ‪،‬‬
‫‪∆σ T‬‬
‫= ‪KT‬‬ ‫ﻧﺮﺥ ﺿﺮﺑﺎﻥ ﻗﻠﺐ ﻭ ﺣﺠﻢ ‪ unstressed‬ﻭﺭﻳﺪﻱ( ﺗﻮﻟﻴﺪ ﻣﻲﺷﻮﻧﺪ‪.‬‬
‫‪4‬‬
‫) ‪X T = GaT ⋅ (Psa − Psan ) + GcT ⋅ (Pra − Pran‬‬ ‫ﺑﺨﺸﻲ ﺍﺯ ﻣﻜﺎﻧﻴﺰﻡ ﺧﻮﺩ ﺗﻨﻈﻴﻤﻲ ﺩﺭ ﺍﺛﺮ ﺗﻐﻴﻴﺮﺍﺕ ﻓﺸﺎﺭﻱ ﻛﻪ ﺩﺭ‬

‫‪Tmax = σ Tn + ∆σ T‬‬
‫ﻓﺸﺎﺭ ﺑﺎﻻ ﺩﺭ ﻗﺴﻤﺖ ﺷﺮﻳﺎﻧﻲ ﻭ ﻓﺸﺎﺭ ﭘﺎﻳﻴﻦ ﺩﺭ ﻗﺴﻤﺖ ﮔﺮﺩﺵ‬
‫‪2‬‬
‫ﺧﻮﻥ ﺗﻨﻔﺴﻲ ﺍﺗﻔﺎﻕ ﻣﻲﺍﻓﺘﺪ‪ ،‬ﺍﻧﺠﺎﻡ ﻣﻲﺷﻮﺩ‪.‬‬
‫)) ‪Tmin = Tmax − ∆σ T (1 − δ (t‬‬
‫ﺑﻌﻼﻭﻩ ﺯﻣﺎﻧﻲ ﻛﻪ ﺣﺠﻢ ﺧﻮﻥ ﻛﻤﺘﺮ ﺍﺯ ﻳﻚ ﺣﺠﻢ ﺑﺤﺮﺍﻧﻲ ﻣﻲﺷﻮﺩ‬
‫ﻣﻌﺎﺩﻻﺕ ﺯﻳﺮ ﻣﻜﺎﻧﻴﺰﻡ ﻛﻨﺘﺮﻝ ﺣﺠﻢ ﻭﺭﻳﺪﻱ ﺭﺍ ﺗﺸﺮﻳﺢ ﻣﻲﻛﻨﺪ ]‬ ‫ﻣﺮﺣﻠﻪ ﺩﻭﻡ ﻋﻤﻠﻴﺎﺕ ﺧﻮﺩ ﺗﻨﻈﻴﻤﻲ ﺁﻏﺎﺯ ﻣﻲﺷﻮﺩ‪ .‬ﺍﻳﻦ ﻣﺮﺣﻠﻪ ﺑﻪ‬
‫‪:[٤،٩‬‬ ‫ﻭﺳﻴﻠﻪ ﻳﻚ ﺍﻓﺰﺍﻳﺶ ﻧﺎﮔﻬﺎﻧﻲ ﺩﺭ ﺣﺠﻢ ‪ unstressed‬ﻭﺭﻳﺪﻱ ﻭ‬
‫‪dVusv‬‬ ‫‪1‬‬ ‫ﻛﺎﻫﺶ ﺩﺭ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ ﻭ ﻧﺮﺥ ﺿﺮﺑﺎﻥ ﻗﻠﺐ ﺍﻧﺠﺎﻡ ﻣﻲﺷﻮﺩ‪.‬‬
‫) ‪= (σ v − Vusv‬‬
‫‪dt‬‬ ‫‪τv‬‬ ‫ﺩﺭ ﺍﻳﻨﺠﺎ ﺗﺎﺛﻴﺮﺍﺕ ﺑﺎﻓﺮ ﻣﺎﻳﻊ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﭼﻪ ﺑﺮﺍﻱ ﺑﻲﻛﺮﺑﻨﺎﺕ ﻭ ﭼﻪ‬
‫) ‪σ v = Vusv min + Vusv max ⋅ exp( X v / K v‬‬
‫ﺑﺮﺍﻱ ﺍﺳﺘﺎﺕ ﻗﺎﺑﻞ ﺷﺒﻴﻪﺳﺎﺯﻱ ﺍﺳﺖ‪.‬‬
‫‪∆σ v‬‬
‫= ‪Kv‬‬ ‫ﺍﺳﺘﺎﺕ ﺩﺭ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﻪ ﻋﻨﻮﺍﻥ ﺑﺎﻓﺮ ﺑﺎﻋﺚ ﺗﻨﮓ ﺷﺪﻥ ﺭﮔﻬﺎ ﻭ‬
‫‪4‬‬
‫) ‪X v = Gav ⋅ (Psa − Psan ) + Gcv (Pra − Pran‬‬ ‫ﺗﺎﺛﻴﺮﺍﺕ ﻧﺎﻣﻄﻠﻮﺏ ﺭﻭﻱ ﻓﺸﺎﺭ ﺧﻮﻥ ﺑﻴﻤﺎﺭ ﻣﻲﺷﻮﺩ؛ ﻛﻪ ﺍﻳﻦ‬

‫‪Vusv max = σ vn + ∆σ v‬‬

‫ﺗﺎﺛﻴﺮﺍﺕ ﺑﺮ ﺭﻭﻱ ﻛﺎﻫﺶ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ ﺩﺭ ﻣﺪﻝ ﺁﻭﺭﺩﻩ ﺷﺪﻩ‬
‫‪2‬‬
‫ﺍﺳﺖ‪.‬‬
‫)) ‪Vusv min = Vusv max − ∆σ v (1 − δ (t‬‬
‫ﻛﻨﺘﺮﻝ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ ‪ systemic‬ﺑﺪﻥ ﺑﺎ ﻣﻌﺎﺩﻻﺕ ﺯﻳﺮ‬
‫ﺗﻮﺻﻴﻒ ﻣﻲﺷﻮﺩ]‪:[٤‬‬
‫‪-٣‬ﻧﺘﺎﻳﺞ ﺷﺒﻴﻪﺳﺎﺯﻱ ﻣﺪﻝ ﺑﺪﻭﻥ ﻛﻨﺘﺮﻟﺮ‪:‬‬
‫‪dRs1‬‬ ‫‪1‬‬
‫ﺩﺭ ﺍﻳﻦ ﺑﺨﺶ ﻧﺘﺎﻳﺞ ﺩﻭ ﺷﺒﻴﻪﺳﺎﺯﻱ ﻣﺨﺘﻠﻒ ﻛﻪ ﺩﺭ ﻫﺮ ﻣﺮﺗﺒﻪ ﺑﺮﺍﻱ‬ ‫=‬ ‫) ‪(σ R − Rs1‬‬
‫‪dt‬‬ ‫‪τR‬‬
‫) ‪Rs1 max + Rs1min ⋅ exp( X R / K R‬‬
‫ﺷﺒﻴﻪﺳﺎﺯﻱ ﺑﻴﻤﺎﺭﻱ ﺑﺎ ﺷﺮﺍﻳﻂ ﺧﺎﺹ ﻓﻴﺰﻳﻮﻟﻮﮊﻳﻜﻲ ﻭ‬
‫= ‪σR‬‬
‫ﻫﻤﻮﺩﻳﻨﺎﻣﻴﻜﻲ‪ ،‬ﺗﻌﺪﺍﺩ ﻣﻌﺪﻭﺩﻱ ﺍﺯ ﭘﺎﺭﺍﻣﺘﺮﻫﺎ ﻧﺴﺒﺖ ﺑﻪ ﻣﻘﺎﺩﻳﺮ‬ ‫) ‪1 + exp( X R / K R‬‬
‫ﻧﺮﻣﺎﻟﺸﺎﻥ ﺗﻐﻴﻴﺮ ﻛﺮﺩﻩﺍﻧﺪ‪ ،‬ﺍﺭﺍﺋﻪ ﻣﻲﺷﻮﺩ‪.‬‬ ‫) ‪X R = GaR ⋅ (Psa − Psan ) + GcR ⋅ (Pra − Pran‬‬

‫‪Rs1min = δ Rn − σ R‬‬
‫‪mmHg‬‬
‫ﺑﻴﻤﺎﺭ ﻫﻤﻮﺩﻳﺎﻟﻴﺰﻱ ﺩﺭ ﺷﺮﻭﻉ ﻋﻤﻠﻴﺎﺕ ﺩﺍﺭﺍﻱ ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ‬ ‫∆‬
‫‪2‬‬
‫‪Kg‬‬ ‫‪bit/min‬‬
‫‪ ۳‬ﻣﻲﺑﺎﺷﺪ‪ ،‬ﻛﻪ‬ ‫‪ ۷۲‬ﻭ ﺁﺏ ﺍﺿﺎﻓﻲ‬ ‫‪ ۱۰۰‬ﻭ ﺿﺮﺑﺎﻥ ﻗﻠﺐ‬ ‫) ‪Rs1max = Rs1min + ∆σ R ⋅ (1 − δ (t )) ⋅ ε (t‬‬
‫‪Kg‬‬
‫‪ ۳‬ﺁﺏ ﺍﺿﺎﻓﻲ ﺍﺯ ﺑﻴﻤﺎﺭ ﺭﺍ ﺩﺭ ﻃﻮﻝ ﻣﺪﺕ ‪۴‬‬ ‫ﻗﺼﺪ ﮔﺮﻓﺘﻦ‬
‫ﺑﺮﺍﻱ )‪ δ(t‬ﺩﺍﺭﻳﻢ‪ ،‬ﺍﮔﺮ ‪: Pla ≥ Plat‬‬
‫‪ml‬‬
‫‪ ۷۵۰‬ﺩﺭ ﺳﺎﻋﺖ ﺭﺍ ﺩﺍﺭﻳﻢ‪.‬‬ ‫ﺳﺎﻋﺖ ﺑﺎ ﻧﺮﺥ ﺛﺎﺑﺖ‬
‫) ‪dδ (t‬‬
‫‪=0‬‬
‫‪dt‬‬
‫ﻣﻜﺎﻧﻴﺰﻡﻫﺎﻱ ﻛﻨﺘﺮﻝ ﻛﻨﻨﺪﻩ ﻧﻈﻴﺮ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ ﻭ ﺣﺠﻢ‬ ‫ﺩﺭ ﺷﻜﻞ ‪ ٢‬ﺑﻴﻤﺎﺭﺍﻧﻲ ﻛﻪ ﺳﻴﺴﺘﻢ ﻛﻨﺘﺮﻝ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ ﺩﺭ‬
‫‪ unstressed‬ﻭﺭﻳﺪﻱ ﺑﻪ ﻧﻘﻄﻪ ﺍﺷﺒﺎﻉ ﺧﻮﺩ ﻣﻲﺭﺳﻨﺪ ﻭ ﻓﺸﺎﺭ‬ ‫ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺧﻮﺩ ﺗﻨﻈﻴﻢ ﺑﺪﻧﺸﺎﻥ ﺑﻪ ﺳﺮﻋﺖ ﻛﺎﺭﺍﻳﻲ ﺧﻮﺩ ﺭﺍ ﺍﺯ‬
‫ﺷﺮﻳﺎﻧﻲ ﺷﺮﻭﻉ ﺑﻪ ﻛﺎﻫﺶ ﻣﻲﻛﻨﺪ‬ ‫ﺩﺳﺖ ﻣﻲﺩﻫﺪ ﺭﺍ ﻣﺪﻝ ﻣﻲﻛﻨﻴﻢ ﻭ ﺍﻳﻦ ﻭﺿﻌﻴﺖ ﺭﺍ ﺑﺎ ﺗﻐﻴﻴﺮ‬
‫ﭘﺎﺭﺍﻣﺘﺮﻫﺎﻱ )‪ (∆σR=0.3, Gav=42, Gcv=1250‬ﺷﺒﻴﻪﺳﺎﺯﻱ‬
‫ﻣﻲﻛﻨﻴﻢ‪ .‬ﻫﻤﺎﻥ ﻃﻮﺭ ﻛﻪ ﺩﺭ ﺷﻜﻞ‪ ٥‬ﻣﺸﺎﻫﺪﻩ ﻣﻲﺷﻮﺩ‪ ،‬ﻓﺸﺎﺭ‬
‫ﺷﺮﻳﺎﻧﻲ ﺑﻪ ﻋﻠﺖ ﻋﺪﻡ ﺗﻮﺍﻧﺎﻳﻲ ﺳﻴﺴﺘﻢ ﻓﻴﺪﺑﻚ ﺍﺗﻮﻣﺎﺗﻴﻚ ﺑﺪﻥ ﺩﺭ‬
‫ﺗﻨﻈﻴﻢ ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ‪ ،‬ﻛﺎﻫﺶ ﺩﺍﺷﺘﻪ ﺍﺳﺖ‪.‬‬

‫ﺷﻜﻞ ‪ :٣‬ﺷﺒﻴﻪ ﺳﺎﺯﻱ ﺑﺪﻭﻥ ﻛﻨﺘﺮﻟﺮ‪٢‬‬

‫‪ -٥‬ﻧﺘﻴﺠﻪﮔﻴﺮﻱ‪:‬‬
‫ﺩﺭ ﺍﻳﻦ ﻣﻘﺎﻟﻪ ﻣﺪﻝ ﺑﺪﻥ ﻳﻚ ﺑﻴﻤﺎﺭ ﻫﻤﻮﺩﻳﺎﻟﻴﺰﻱ ﻭ ﻭﺍﻛﻨﺸﻬﺎﻱ ﺑﺪﻧﻲ‬
‫ﺷﻜﻞ ‪ :٢‬ﺷﺒﻴﻪ ﺳﺎﺯﻱ ﺑﺪﻭﻥ ﻛﻨﺘﺮﻟﺮ‪١‬‬
‫ﺑﻴﻤﺎﺭ ﺑﻪ ﻋﻤﻠﻴﺎﺕ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺭﺍ ﺑﺎ ﺍﺳﺘﻔﺎﺩﻩ ﺍﺯ ﺟﻌﺒﻪ ﺍﺑﺰﺍﺭ‬
‫‪ Simulink‬ﻧﺮﻡﺍﻓﺰﺍﺭ ®‪ MATLAB‬ﻧﻤﺎﻳﺶ ﺩﺍﺩﻩ ﺷﺪﻩ ﺍﺳﺖ‪ ،‬ﺍﺯ‬ ‫ﺩﺭ ﺷﻜﻞ ‪ ٣‬ﻓﺮﺽ ﺷﺪﻩ ﺍﺳﺖ ﻛﻪ ﺑﻴﻤﺎﺭﺍﻥ ﻣﻮﺭﺩ ﻣﻄﺎﻟﻌﻪ ﺩﺭ ﺷﺮﺍﻳﻂ‬
‫ﺍﻳﻦ ﻣﺪﻝ ﻣﻲﺗﻮﺍﻥ ﺑﻪ ﻋﻨﻮﺍﻥ ﻳﻚ ﻣﺒﻨﺎ ﺑﺮﺍﻱ ﺗﺤﻘﻴﻘﺎﺕ ﻣﺪﻝ‪-‬ﻣﺒﻨﺎ ﺍﺛﺮ‬ ‫‪ baroreflex‬ﺷﺮﻳﺎﻧﻲ ﻭ ﺗﻨﻔﺴﻲ ﻧﺮﻣﺎﻟﻲ ﻗﺮﺍﺭ ﺩﺍﺭﺩ‪ .‬ﺍﻣﺎ ﺩﺍﺭﺍﻱ ﻧﺮﺥ‬
‫ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﺑﺮ ﺭﻭﻱ ﺑﺪﻥ ﺍﻧﺴﺎﻥ ﻭ ﻃﺮﺍﺣﻲ ﻛﻨﺘﺮﻝ ﻛﻨﻨﺪﻩﻫﺎﻱ‬ ‫ﺑﺎﺯﻳﺎﺑﻲ ﭘﻼﺳﻤﺎﻱ ﻛﻤﻲ ﻣﻲﺑﺎﺷﺪ‪ ،‬ﺑﺮﺍﻱ ﻣﺪﻝ ﻛﺮﺩﻥ ﺍﻳﻦ ﻋﺎﺭﺿﻪ ﺩﺭ‬
‫ﻣﺨﺘﻠﻒ ﻛﻪ ﻧﻴﺎﺯ ﺑﻪ ﻣﺪﻟﻲ ﺑﺮﺍﻱ ﺗﺴﺖ ﻋﻤﻠﻜﺮﺩ ﻛﻨﺘﺮﻟﺮ ﺩﺍﺭﻧﺪ‪،‬‬ ‫ﻣﺪﻝ ﺿﺮﻳﺐ ﻧﻔﻮﺫﭘﺬﻳﺮﻱ ﻣﻮﻳﺮﮔﻬﺎﻱ ﺳﺮﺧﺮﮔﻲ ﻭ ﺳﻴﺎﻫﺮﮔﻲ ) ‪La ،‬‬

‫ﺍﺳﺘﻔﺎﺩﻩ ﻛﺮﺩ‪.‬‬ ‫‪ (Lv‬ﺭﺍ ﻛﺎﻫﺶ ﺩﺍﺩﻩ ﻭ ﻓﺸﺎﺭ ﺍﻻﺳﺘﺎﻧﺲ ﺑﺨﺶ ﻣﻴﺎﻥﺑﺎﻓﺘﻲ ﺭﺍ ﺍﻓﺰﺍﻳﺶ‬
‫ﻣﻲﺩﻫﻴﻢ‪ .‬ﺑﺮﺍﻱ ﺗﻮﺻﻴﻒ ﺭﻓﺘﺎﺭ ﻣﺪﻝ ﺩﺭ ﺍﻳﻦ ﻗﺴﻤﺖ‪ ،‬ﺑﻪ ﻋﻠﺖ‬
‫‪ -۶‬ﻣﺮﺍﺟﻊ‪:‬‬ ‫ﺍﻳﻨﻜﻪ ﺑﻴﻤﺎﺭﺍﻥ ﺩﺍﺭﺍﻱ ﻧﺮﺥ ﺑﺎﺯﻳﺎﺑﻲ ﭘﻼﺳﻤﺎﻱ ﻛﻤﻲ ﻣﻲﺑﺎﺷﻨﺪ‪ ،‬ﻟﺬﺍ‬
‫‪[1] Mauro Ursino and Marina innocenti “Mathematical‬‬ ‫ﺑﻴﻤﺎﺭ ﺩﭼﺎﺭ ﻛﺎﻫﺶ ﺳﺮﻳﻊﺗﺮﺣﺠﻢ ﭘﻼﺳﻤﺎﻱ ﺧﻮﻥ ﻭ ﺩﺭ ﻧﺘﻴﺠﻪ‬
‫‪investigation of some physiological factors involved‬‬
‫‪in hemodialysis hypotension” Artificial organs Vol.‬‬ ‫ﺍﻓﺖ ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ ﻣﻲﺷﻮﻧﺪ‪ .‬ﻛﺎﻫﺶ ﺩﺭ ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ ﻳﻚ ﭘﺎﺳﺦ‬
‫‪21(8)، pp. 891-902١٩٩٧ ،‬‬
‫‪[2] M. Ursino، L. Coli، C. Brighenti “prediction of‬‬ ‫ﻗﻮﻱ ﺍﺯ ‪ cardiopulmonary‬ﺭﺍ ﺩﺭ ﭘﻲ ﺧﻮﺍﻫﺪ ﺩﺍﺷﺖ ﻛﻪ ﺑﺎﻋﺚ‬
‫‪solute kinetics acid-base status and blood volume‬‬
‫‪changes during profiled Hemodialysis” Annals of‬‬
‫ﺣﻔﻆ ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺩﺭ ‪ ۲‬ﺳﺎﻋﺖ ﺍﻭﻝ ﻫﻤﻮﺩﻳﺎﻟﻴﺰ ﻣﻲﺷﻮﺩ‪ .‬ﺑﻌﺪ ﺍﺯ‬
‫‪biomedical engineering Vol.28، pp. 204-216٢٠٠٠ ،‬‬ ‫ﺣﺪﻭﺩ ‪ ۲‬ﺍﻟﻲ ‪ ۳‬ﺳﺎﻋﺖ‪ ،‬ﻣﻜﺎﻧﻴﺰﻡ ‪cardiopulmonary receptor‬‬
‫‪[3] P. Wabel، U. Moissl، R. Isermann “Model based‬‬
‫‪identification and control of patient parameters‬‬ ‫ﺗﻮﺍﻧﺎﻳﻲ ﺣﻔﻆ ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺭﺍ ﺑﻪ ﺍﻧﺪﺍﺯﻩ ﻛﺎﻓﻲ ﻧﺨﻮﺍﻫﺪ ﺩﺍﺷﺖ ﻭ‬
‫‪during the hemodialysis treatment” Darmstadt‬‬
‫‪University of technology‬‬ ‫ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺷﺮﻭﻉ ﺑﻪ ﺍﻓﺖ ﻣﻲﻛﻨﺪ ﻭ ‪arterial baroreflex‬‬
‫‪[4] M. Ursino، M. Innocenti “modeling arterial‬‬
‫‪hypotension during Hemodialysis” Artificial organs‬‬
‫ﺷﺮﻭﻉ ﺑﻪ ﻓﻌﺎﻟﻴﺖ ﻣﻲﻛﻨﺪ ﻭ ﺩﺭ ﻧﻬﺎﻳﺖ ﭘﺲ ﺍﺯ ‪ ۳‬ﺳﺎﻋﺖ‬
‫‪Vol. 21(8)، pp. 873-890١٩٩٧ ،‬‬
Pvc:‫ﻓﺸﺎﺭ ﺳﻴﺎﻫﺮﮔﻲ ﻣﻮﻳﺮﮔﻲ‬ [5] Landis EM، Pappenheimer JR، “Exchange of
substances through the capillary walls” In:
Vpl:‫ﺣﺠﻢ ﭘﻼﺳﻤﺎﻱ ﺧﻮﻥ‬ Hamilton WF، Dow P، eds. Handbook of
physiology، Vol. 2 Sec.2، Circulation، pp. 961-
HCT:‫ﻫﻤﺎﺗﻮﻛﺮﻳﺖ‬ 1034،
[6] Baldamus CA, Ernst W, Frei U, Koch KM,
Vex:‫ﺣﺠﻢ ﺁﺏ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ‬ “sympathetic and hemodynamic response to
Vis:‫ﺣﺠﻢ ﺁﺏ ﻣﻴﺎﻥ ﺑﺎﻓﺘﻲ‬ volume removal during deferent forms of renal
replacement therapy” Nephron 31:324-32, 1982
Vic:‫ﺣﺠﻢ ﺁﺏ ﺩﺍﺧﻞ ﺳﻠﻮﻟﻲ‬ [7] Grandi F, Avanzolini G, Cappello A, Chiari L,
“computer simulation of urea and electrolytes
Cs,is:‫ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎﻱ ﻣﻴﺎﻥ ﺑﺎﻓﺘﻲ‬ kinetics during hemodialysis” Computational
mechanics Publication, 625-32, 1995
Cs,ex:‫ﻏﻠﻈﺖ ﻳﻮﻧﻬﺎﻱ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ‬ [8] Landis EM, Pappenheimer JR, “Iexchange of
Ms,ic:‫ﺣﺠﻢ ﻳﻮﻧﻬﺎﻱ ﺩﺍﺧﻞ ﺳﻠﻮﻟﻲ‬ substances through the capillary walls. In: Hamilton
WF, Dow P, eds. Handbook Of physiology, Vol 2,
Ms,ex:‫ﺣﺠﻢ ﻳﻮﻧﻬﺎﻱ ﺧﺎﺭﺝ ﺳﻠﻮﻟﻲ‬ Sec 2, Circulation Washington DC, American
physiological society, 961-1034, 1963
Qf:‫ﻧﺮﺥ ﺁﺑﮕﻴﺮﻱ‬ [9] Ursino M, Antonucci M, Belardinelli E, “Role of
active changes of in venous capacity by the carotid
Qe,s:‫ﻓﻠﻮﻱ ﻣﻮﺛﺮ ﻳﻮﻧﻬﺎﻱ ﻣﻮﺟﻮﺩ ﺩﺭ ﺧﻮﻥ ﻋﺒﻮﺭﻱ ﺍﺯ ﻏﺸﺎ‬
baroreflex; analysis with mathematical model” Am
Cic:‫ﻏﻠﻈﺖ ﻣﺠﻤﻮﻉ ﻳﻮﻧﻬﺎ ﺩﺭ ﺩﺍﺧﻞ ﺳﻠﻮﻟﻲ‬ J Physiol 267(heart Circ Physiol, 36):H2531-46,
1994
Cis:‫ﻏﻠﻈﺖ ﻣﺠﻤﻮﻉ ﻳﻮﻧﻬﺎ ﺩﺭﻣﻴﺎﻥ ﺑﺎﻓﺘﻲ‬
Cp,cs:‫ﻏﻠﻈﺖ ﭘﺮﻭﺗﺌﻴﻦ ﻫﺎ ﺩﺭ ﻣﻴﺎﻥ ﺑﺎﻓﺘﻲ‬ :‫ ﺿﻤﻴﻤﻪ‬-۷
Cp,pl:‫ﻏﻠﻈﺖ ﭘﺮﻭﺗﺌﻴﻦ ﻫﺎ ﺩﺭﭘﻼﺳﻤﺎ‬ Psa: ‫ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ‬
Pis:‫ﻓﺸﺎﺭ ﻣﻴﺎﻥ ﺑﺎﻓﺘﻲ‬ Pra: ‫ﻓﺸﺎﺭ ﺩﻫﻠﻴﺰ ﺭﺍﺳﺖ‬
Rs1:‫ﻣﻘﺎﻭﻣﺖ ﺷﺮﻳﺎﻧﻲ‬ Ppa:‫ﻓﺸﺎﺭ ﺷﺮﻳﺎﻧﻲ ﺗﻨﻔﺴﻲ‬
T:‫ﺿﺮﺑﺎﻥ ﻗﻠﺐ‬ Ppv:‫ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ ﺗﻨﻔﺴﻲ‬
Vusv:‫ﺣﺠﻢ ﺗﺤﺮﻳﻚ ﻧﺸﺪﻩ ﻭﺭﻳﺪﻱ‬ Pla:‫ﻓﺸﺎﺭ ﺩﻫﻠﻴﺰ ﺟﭗ‬
V:‫ﺣﺠﻢ ﺧﻮﻥ‬
Psv:‫ﻓﺸﺎﺭ ﻭﺭﻳﺪﻱ‬
Pac:‫ﻓﺸﺎﺭ ﺳﺮﺧﺮﮔﻲ ﻣﻮﻳﺮﮔﻲ‬