Perfusion Limited and Diffusion Limited - drmek

[ArchivalUser]

Plz.. I need an easy explanation for the Perfusion limited and diffusion limited...
Appreciate it
Thnx

[ArchivalUser]

Plzzzzzzzzzzz anyone to expalin it

[ArchivalUser]

Ventilation defects – best example is resp distress syndrome (aka hyaline membrane dz in children). In adults, this is called Adult RDS, and has a ventilation defect. Lost ventilation to the alveoli, but still have perfusion; therefore have created an intrapulmonary shunt. Exam question: pt with hypoxemia, given 100% of O2 for 20 minutes, and pO2 did not increase, therefore indicates a SHUNT, massive ventilation defect.

Perfusion defects – knock off blood flow
MCC perfusion defect = pulmonary embolus, especially in prolonged flights, with sitting down and not getting up. Stasis in veins of the deep veins, leads to propagation of a clot and 3-5 days later an embolus develops and embolizes. In this case, you have ventilation, but no perfusion; therefore there is an increase in dead space. If you give 100% O2 for a perfusion defect, pO2 will go UP (way to distinguish vent from perfusion defect), b/c not every single vessel in the lung is not perfused.

Therefore, perfusion defects because an increase in dead space, while ventilation defects cause intrapulmonary shunts. To tell the difference, give 100% O2 and see whether the pO2 stays the same, it does not go up (shunt) or increases (increase in dead space).

Diffusion defect – something in the interphase that O2 cannot get through…ie fibrosis. Best example–Sarcoidosis (a restrictive lung disease); O2 already have trouble getting through the membrane; with fibrosis it is worse. Another example–Pulmonary edema; O2 cannot cross; therefore there is a diffusion defect. Another example is plain old fluid from heart failure leads to dyspnea, b/c activated the J reflex is initiated (innervated by CN10); activation of CN10, leads to dyspnea (can’t take a full breath) b/c fluid in interstium of the lung, and the J receptor is irritated.
These are the four things that cause hypoxemia (resp acidosis, ventilation defects, perfusion defects, and diffusion defects)-(Goljan)

[ArchivalUser]

this is a general rule for any any part of body but makes more sense when you apply into respiratory vascular system. let's picture o2 in alveoli which is trying to pass through the membrane along the length of capillary and alveolar membrane. the main force to let o2 pass through is concentration differance and here is presure difference. in ideal situation it is around 100mmhg in alveoli and 40 at the begining of pul cap. but in the length of cap. membrane do you have this difference inorder o push o2 pass through the membrane?in ideal situation in 2/3 of the length presure difference become equal and this raises he cap. o2 from 40 to 100 a the end of cap or begining of pul. vein. this mechanism has been called diffusion limited. in some pahological situation this lenght could drop to 1/3 and the rest of 2/3 you couldn't see presure difference. so if you want to tranfer more o2 in that part you should change the flow. then we call perfusion limited. some gas at the beging of pul cap make the presure diff. equal very quickly therefore the passing force through the membrane should be limited to perfusion. hope i works and goodluck in your exam.

[ArchivalUser]

so basically a shunt refers to perfusion without ventilation. But in kaplan video they are listing shunts as a perfusion limited condition....finding it very difficult to relate the two?? somebody please explain!! thank u...