and we’re back! with BRAND SPANKIN' NEW tangents!
to snoo-finity ... and beyond!
NBME 21 Answers
A 2-week-old male newborn has a patent ductus ...
Higher than normal left ventricular cardiac output
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.
doesnt pre-load also decrease which would drop the C.O.?
@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
*another user noted that this wouldn't impact RV oxygen because the blood is added to the pulmonary artery, which has exited the RV.
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.
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).
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
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