Pathophysiology of early and late cyanosis

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R->L shunt puts deoxygenated blood directly into systemic circulation. L->R shunt increases the volume of blood going through pulmonary vasculature, which causes proliferation of vascular smooth muscle over a long period of time, eventually becoming significant enough to reverse the normal L>R pressure gradient to R>L (becomes a R->L shunt and causes cyanosis for the same reason as in early cyanosis). The reversal of pressure gradients is called Eisenmenger syndrome
 
You can have transient episodes of cyanosis (e.g. in ToF), but those are still due to reversal of the shunt (the cause of the reversal is different though - physiologic increases in right sided pressure/resistance rather than pathologic)
 
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