Could someone please explain the connection between cyanosis being limited to a particular part of the body? I read that in tetralogy fallot the cyanosis is not limited to the lower body, as the shunt is intracardiac. what does this mean?
tetralogy of fallot
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Differential cyanosis (pink fingers and blue toes) occurs with PDAs (with pulmonary hypertension and right to left shunt). The brachiocephalic circulation gets oxygenated blood, but the PDA attaches to the aorta after the left subclavian and sends deoxygenated blood to the lower body.
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I'm not exactly sure how or why coarctation of the aorta got brought up, as tetralogy of Fallot is classically:
1. Right ventricular hypertrophy
2. Aortic override.
3. Ventricular septal defect.
4. Pulmonary stenosis.
The OP is asking why the cyanosis isn't limited to the lower limbs with tetralogy of Fallot (as in other right-to-left shunts, I'm assuming) and how this relates to intracardiac shunting.
The previous poster is correct in stating that PDAs result in lower limb cyanosis, as the PDA occurs distal to the aortic arch where the brachiocephalic/left common carotid/left subclavian arteries branch out. This limits the pumping of deoxygenated blood to the lower part of the body; hence, differential cyanosis of the lower limbs.
However, in tetralogy of Fallot, the shunting occurs through the ventricular septal defect (hence the "intracardiac shunting") as opposed to through a PDA. My understanding is that the combination of pulmonary stenosis/right ventricular hypertrophy leads to greater blood pressures in the right ventricle compared to the left ventricle; as a result, there is a net flow of deoxygenated blood from the right ventricle into the left ventricle with each pump of the heart (resulting in the shunt). Since the mixing of blood occurs before the arteries branch out, the entire body receives mixed blood as opposed to just the lower limbs, resulting in cyanosis.
This is just the way I understand your question; feel free to correct me or ask for clarification if I'm wrong (I'm taking Step I in about 2 weeks, so if I'm wrong or mistaken I would greatly appreciate the feedback).
the differential cyanosis in pda results from eisenmenger's as the pressures in the lungs build up (rt to left shunt); but what about initially when there is a predominant left to right shunt? shouldn't there be cyanosis all throughout as the lungs find themselves acutely overloaded?
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I could be wrong here, but when there is the L->R shunt, there isn't an issue with ventilation/Perfusion at all. I guess if pulmonary edema occured, you would have cyanosis due to the mismatch, however the pum. arteries are supposedly really good at constricting under higher pressure(to an extent) and that would keep the flow somewhat normal.
Also, I would think the left ventricle could possibly have a negligible amount of atrophy due to the perceived drop in afterload. I could be way off though. 😕
In the PDA you don't have a physiologic shunt(no increase in dead space), and the blood flow to the lungs is relatively normal so you still get perfusion. The reason you get the cyanosis in the R-L seems to be purely based on mixture, leading to hypoxemia by dilution(for lack of better word), opposed to physiologic shunt in V/Q issues.
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Whelp...There goes my misguided theory. I probably should've cracked a book.
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Left-to-right shunts don't typically result in cyanosis, though.
Is your question about tetralogy of Fallot or patent ductus arteriosus?
My initial question was actually about how differential cyanosis could occur, and less about the individual diseases. Now that you mention it, you are right, that's what I learned in my path class as well; it's the rt to left shunt instead of the left to right shunts that lead to blue babies. thanks for clearing that up.