First of all, I am very sorry if this is in the wrong thread sectiion.
I need sum help in biology. I cannot seem to find the relationship between the effect of emphysema and Fick's law in realtion to the effect of the diffusion capacity.
Its such a load of rubbish.....I know the answer but I need a few points to back up my point. :confused: (evidence in other words from any type of resource).
I study sciences, and I know it sounds like im being cheeky, but im not...
Oh well.....I've got my answer and I'm typing it up.
This is the whole load of info I got to back up my point:
Emphysema is a disease marked by destruction in the alveoli.
The basic job of the alveoli are:
· The walls of the alveoli become inflamed and damaged. Over time they lose elasticity and pockets of dead air (called bullae) form in the injured areas.
· These pockets impair the ability to exhale and normal working of the lungs.
· Inhalation, however, is not impaired and until the late stages of the disease, oxygen and carbon dioxide levels are normal.
Ayyy ayy..Thats simple but good one.
Wud u mind if I asked you to help me with other coursework in the future. U seem to know wat ur talking about (Well, u better do )
AS level....its fun but I hate having to quote from sum Einstiens work (Fick and the rest of them).
I've cut up the lungs which was fantastic....I went back home and noticed a little strand of lung (meat) hanging on my sleeve. (sum wud think its sick.....but for me it was funny).
I was going to giv it to the cat next door, then I thought....naaa, I wont kill it YET!
here hope this will help: don't know much about Biology but found this artce
"Effects of Emphysema on Diaphragm Microvascular Oxygen Pressure
DAVID C. POOLE, CASEY A. KINDIG, and BRAD J. BEHNKE
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, Kansas
Pulmonary emphysema impairs lung and respiratory muscle function leading to restricted physical capacity and accelerated morbidity and mortality consequent to respiratory muscle failure. In the absence of direct evidence, an O2 supply-demand imbalance within the diaphragm and other respiratory muscles in emphysema has been considered the most likely explanation for this failure. To test this hypothesis, we utilized phosphorescence quenching techniques to measure mean microvascular PO2 (PO2m) within the medial costal diaphragm of control (C, n = 10) and emphysematous (E, elastase instilled, n = 7) hamsters. PO2m and mean arterial pressure (MAP) were measured in the spontaneously breathing anesthetized hamster at inspired O2 percentages of 10, 21, and 100, and across a range of mean MAPs from 40 to 115 mm Hg. At each inspired O2, diaphragm PO2m was significantly (p < 0.05) lower in E animals (10%: C, 19 ± 3; E, 9 ± 2; 21%: C, 32 ± 2; E, 21 ± 2; 100%: C, 60 ± 8; E, 36 ± 9 mm Hg). At 21% inspired O2, the PO2m decrease was correlated with reduced MAP in both C (r = 0.968) and E (r = 0.976) animals. We conclude that diaphragmatic PO2m (and therefore microvascular O2 content) is decreased in emphysematous hamsters reflecting a greater diaphragmatic O2 utilization at rest and a lower O2 extraction reserve. According to Fick's law, this lower PO2m will mandate an exaggerated fall in intramyocyte PO2, which is expected to accelerate muscle glycogen depletion and consequently fatigue. This provides empirical evidence in support of one possible mechanism for respiratory muscle failure in emphysema. "
“If you punish, then punish with the like of that wherewith you were afflicted. But if you endure patiently, indeed it is better for the patient. Endure you patiently. Your patience is not except through the help of Allah." (al-Nahl 16:126-127)
here hope this will help: don't know much about Biology but found this artce
"Effects of Emphysema on Diaphragm Microvascular Oxygen Pressure
DAVID C. POOLE, CASEY A. KINDIG, and BRAD J. BEHNKE
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, Kansas
Pulmonary emphysema impairs lung and respiratory muscle function leading to restricted physical capacity and accelerated morbidity and mortality consequent to respiratory muscle failure. In the absence of direct evidence, an O2 supply-demand imbalance within the diaphragm and other respiratory muscles in emphysema has been considered the most likely explanation for this failure. To test this hypothesis, we utilized phosphorescence quenching techniques to measure mean microvascular PO2 (PO2m) within the medial costal diaphragm of control (C, n = 10) and emphysematous (E, elastase instilled, n = 7) hamsters. PO2m and mean arterial pressure (MAP) were measured in the spontaneously breathing anesthetized hamster at inspired O2 percentages of 10, 21, and 100, and across a range of mean MAPs from 40 to 115 mm Hg. At each inspired O2, diaphragm PO2m was significantly (p < 0.05) lower in E animals (10%: C, 19 ± 3; E, 9 ± 2; 21%: C, 32 ± 2; E, 21 ± 2; 100%: C, 60 ± 8; E, 36 ± 9 mm Hg). At 21% inspired O2, the PO2m decrease was correlated with reduced MAP in both C (r = 0.968) and E (r = 0.976) animals. We conclude that diaphragmatic PO2m (and therefore microvascular O2 content) is decreased in emphysematous hamsters reflecting a greater diaphragmatic O2 utilization at rest and a lower O2 extraction reserve. According to Fick's law, this lower PO2m will mandate an exaggerated fall in intramyocyte PO2, which is expected to accelerate muscle glycogen depletion and consequently fatigue. This provides empirical evidence in support of one possible mechanism for respiratory muscle failure in emphysema. "
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