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NBME 21 Answers

nbme21/Block 2/Question#5

A 2-week-old male newborn has a patent ductus ...

Higher than normal left ventricular cardiac output

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 +2  upvote downvote
submitted by heavy_neighborhood(2),

PDA flows from the Aorta ==> Pulmonary arteries, by passing the RV so there is no change in O2 in the RV.

felxordigitorum  The "steal" from the aorta during diastole requires increased cardiac output to compensate. Extremely premature infants have limited ability to increase stroke volume and thus use increased heart rate to increase cardiac output. https://www.ncbi.nlm.nih.gov/books/NBK430758/ +  




 +2  upvote downvote
submitted by jotajota94(10),

PDA flows from aorta to pulmonary artery decreasing afterload. Therefore cardiac output increases

seagull  doesnt pre-load also decrease which would drop the C.O.? +  
hungrybox  @seagull I think it would increase preload b/c more blood is going into the pulmonary arteries -> lungs -> pulmonary veins -> eventually more blood in left atrium/ventricle -> inc preload +3  




 +0  upvote downvote
submitted by didelphus(17),

A PDA essentially creates a high-flow heart failure situation in the baby. Since a fraction of the LV output is returned without reaching the body, in order to maintain a normal CO to the body the left ventricle must pump a higher volume. This would also cause higher than normal pulmonary capillary flow.

I think some of the other question are getting at the idea that we don't know the direction of flow for sure. If the flow was aorta-->lungs, the systemic PO2 would be normal and RV PO2 high. But if it's opposite, the opposite would be true.

Since PDAs are maintained by PGE2, that would contribute to a low peripheral vascular resistance.

didelphus  *another user noted that this wouldn't impact RV oxygen because the blood is added to the pulmonary artery, which has exited the RV. +3  




 +0  upvote downvote
submitted by d_holles(32),

Here's an excellent image from AMBOSS if people are having difficulty visualizing this: https://imgur.com/a/VmhQRWm





 +0  upvote downvote
submitted by hello(58),

This is the actual correct explanation:

PDA causes blood to flow from descending aorta to patent ductus arteriosus into pulmonary circulation ("right-to-left")

The "steal" from the aorta during diastole requires increased cardiac output to compensate to deliver adequate amount of blood to rest of body

Source: https://www.ncbi.nlm.nih.gov/books/NBK430758/





 +0  upvote downvote
submitted by masonkingcobra(60),

Link

necrotizingfasciitis  Going off of the comments people have posted above & kinda bringing things together: PDA flows from aorta to pulmonary arteries, which reverses after birth. This means de-oxygenated blood flow from the pulmonary arteries to the aorta & less volume being sent to the LF side of the heart. This results in a decreased afterload because there is less blood flowing from the lungs to re-fill the LF ventricle, & the heart is still pumping with the same force as before, so the same volume of blood is leaving, but less in entering the LF side of the heart. From here, you use CO = SV x HR SV = preload - afterload (which is decreased due to the PDA) This results in SV being larger than normal, so when you plug that into CO = SV x HR you get a higher number for cardiac output. +  
didelphus  The ductus arteriosus flows from PA --> aorta in utero to bypass the lungs, which have extremely high resistance to flow. This reverses after birth due to a drop in PGE2 (which was supplied by the placenta) and increase in left-sided systemic resistance. So a PDA typically flows aorta --> PA (assuming there are no other defects). +  




 +0  upvote downvote
submitted by moneysacs(0),

Why is does a PDA after birth result in "higher than normal left ventricular cardiac output" over increased "right ventricular PO2"? Does the pulm artery --> aorta shunt become reversed after birth, so higher oxygen aorta blood would flow back into the right ventricle? I get that more blood would be pumped to the left ventricle, resulting in RVH/LVH, but don't understand the O2 bit.

usmleuser007  1) higher than normal CO b/c blood is shunted from aorta to pulmonary arteries. This blood is added to the volume that was pumped into the pulmonary arteries by the RV. Now when the oxygenated blood returns to the LA & LV, the O2 content would be greater d/t higher blood volume. Also for that same reason more blood is returning to the LV (d/t LV volume plus fraction of RV volume). This increased the CO. Right--> Left shunts have late cyanosis b/c the RV is pushing against the excess pressure generated by the LV. This leads to Eisenmenger Syndrome as RV enlarges and pushes against the pressure from the LV in the PDA. Thus shifting Left to right to right to Left and thus the late cyanosis +1  
temmy  The anatomy is aorta-pulmonary artery-pulmonary veins-left atrium-left ventricle Notice that the blood did not come across the right heart at all and because of the LEFT TO RIGHT shunt of the PDA, we add more volume to the LEFT side. Hence the increased left ventricular output +2