One cause is endotoxic shock – peripheral resistance arterioles are dilated, therefore an increase in C3a, C5a, NO, leading to increased venous return to the heart and the heart eventually gives up. There are also many other causes, and they relate to Pouseau’s law – viscosity/radius to the fourth power. So, if you vasodilate the peripheral resistance arterioles, and you decrease TPR, more blood returns to the right heart, the left heart has to deal with it, too, and pt runs the risk of high output failure. So, one cause of the vasodilatation is septic shock, while the other is thiamine deUiciency. Problem in thiamine def: ATP depletion: smooth muscle cells and peripheral resistance arterioles need ATP, therefore they do not work as well, and there is vasodilatation of the peripheral arterioles, leading to high output failure.
So, thiamine def can produce high out put failure b/c vasodilatation of those vessels.
Graves’s dz – hyperthyroidism – thyroid hormone increases the synthesis of beta receptors in the heart. Get an increase in force of contraction, and more blood.
Systolic pressures are higher, and go into high output failure.
AV Uistulas – ie get stabled in the leg; and develop an AV malformation, where there is arteriole blood bypassing the microcirculation going directly to the venous circulation and the blood comes back faster to the heart than normal; a bruit can be heard over the mass and it will be pulsatile; if you press the proximal portion of it, heart rate would slow (Brenham’s sign) – these are all signs of AV 5istula, leading to high output failure.
So, 3 examples of high output failure are endotoxic shock, graves, and AV Uistulas
V. Congenital heart dz
A. Know fetal circulation (which vessels have the least/most O2); remember that the baby is NOT exchanging blood with O2 in the lungs. Pulmonary vessels in the fetus look like they have pulmonary HTN – they are so thick that it is extremely hard to get blood through the pulmonary artery into the LV b/c very little blood can go there – this is why baby needs a patent ductus to get blood out. Where is O2 coming from? Coming from chorionic villus dipping into lake of blood, which derives from mom’s spiral arterioles. Have chorionic villi dipping into blood and extracting O2 from it. Obviously, this is not as good an O2 source as the lungs; therefore, you want a high af5inity Hb to be able to get what little O2 is down in the area – this is why babies have HbF, b/c of its high af5inity to grab O2 from the blood. Bad news is that it gets the O2, but doesn’t want to give it up (says mine) – it left shifts the curve. What is compensatory response? This left shift causes tissue hypoxia, which will cause EPO to be released and the kid will have an 18 gram Hb – b/c of this, all newborns (in a sense) have polycythemia. This is the way around HbF’s high af5inity for O2 – more RBC’s made, more Hb, and baby gets more O2.
Order of O2 passing: O2 goes through syncytiotrophoblast of chorionic villus, into the cytotrophoblast, then through the myxomatous stroma of the chorionic villus, then into the blood vessel. The blood vessels of the chorionic villis all coalesce to form the umbilical vein. This has the highest O2 content. It goes to the liver and it can go two ways: 1) into the hepatic sinusoids and recollects into the hepatic vein and gets dumped into the IVC; and 2) ductus venosis and straight into the IVC. Then it goes up the right side of the heart; the foramen ovale is open in all fetuses (its not closed) – so all this blood is coming up the IVC – will it go straight across, through the foramen ovale and into the left atrium, or will it go into the IVC into the right atrium, down to through the tricuspid valve, and into the right ventricle? It will go through the foramen ovale. So, all this oxygenated blood will go directly from the right atrium of the foramen ovale into the left atrium, then the left ventricle and out the aorta. What about SVC blood valve? It is coming from the superior part of the right atrium (its not gonna make a left turn and go through the foramen ovale). It will go straight down, through the tricuspid valve into the right ventricle. Now, it will go out the pulmonary artery. This is a PROBLEM b/c the pulmonary vessels are too thick
and it’s encountering this tremendous amount of pressure. To counter this problem, kept the patent ductus open (which is kept open by the PGE2, a vasodilator, made by the placenta) – so, there is a right to left shunt and blood can get out of the pulmonary artery and dumped back into the aorta. Then, when the baby is born and takes its 5irst breath, the pulmonary vessels (that were all shut), all open within a millisecond, and blood is going through those pulmonary arteries and gas exchange is occurring through the lungs in literally seconds. Also, the patent ductus closes and forms the ligamentum arteriosum. This is normal fetal circulation. Vessels with the least O2 are the 2 umbilical arteries, and the one with the most amount of O2 is the umbilical vein.
B. Shunts:
Look at O2 saturations (this is how they dx them – they catheterize, measure O2 saturations in different chambers, and know which direction the shunts are going.
Need to get used to two terms – step up and step down.
If you have a left to right shunt, and have oxygenated blood going into unO2’d blood, what is happening to O2 saturation on the right side? Step up b/c mixing O2’d with unO2’d blood.
If you have a right to left shunt with unO2’d blood going into the O2’d blood?
Step down.
The O2 saturation on the right side of the heart in blood returning from the body is 75%. The O2 saturation on the left side is 95%.
C. VSD (MC)
Who’s stronger -‐ left or right ventricle? Left, therefore the direction of the shunt is left to right. So, oxygenated blood will be dumped into the right ventricle, leading to step up. Also, it will pump it out of the pulmonary artery, leading to step up. So, you have a step up of O2 in right vent and pul artery. What if this is not corrected? With this mech, you are volume overloading the right side of the heart b/c of all that blood coming over. The outcome of this will be pulmonary HTN (the pulmonary artery has to deal with more blood and must contract more – leading to pul HTN) – Once pul HTN occurs, right ventricle will have a problem contracting and it will get hypertrophied. Suddenly, you run the risk of reversing a shunt b/c then right ventricle could eventually be stronger than the left. So, it will be a right to left shunt – this is called Eisenmenger’s syndrome. So, an uncorrected left to right shunt has the potential for producing Eisenmenger’s syndrome. After reversal of the shunt occurs, pt will have cyanosis (aka cyanosis tardive). Most VSD’s close spontaneously and some need to be patched.
D. ASD
Normal for a fetus to have a patent foramen ovale; it is not normal once they are born. Which direction will blood go through the foramen ovale? Left to right (b/c the left side is always stronger than the right). Therefore, what will happen to the right atrium? Step up – so it will go from 75 to 80%. What will happen to the right ventricle and pulmonary artery? Step up. So, what is the main diff in O2 saturations in VSD vs ASD? ASD is step up of O2 also in the right atrium. Are you volume overloading the right heart? Yes. So do you run a risk for Eisenmenger’s? Yes. What else are at increased risk for? Paradoxical embolization.
What if you weren’t lucky enough to have a DVT in the leg, and it embolize up and the pressures of the right side of the heart are increasing, and you have a patent foramen ovale – will there be an embolus that can go from the right atrium to the left atrium and will have a venous clot in arterial circulation? Yes – this occurs in pts with ASD.
MC teratogen that has ASD associated with it? Fetal alcohol syndrome (1/5000) E. PDA
It’s normal in a fetus but not when they are born. Connection between the aorta and pulmonary artery – which is stronger? Aorta. So, oxygenated blood goes from left and get dumped in the pulmonary artery before going into the lungs. So, what happens in the pulmonary artery? Step up. So, now its 80% O2 saturation – the pulmonary artery is the only thing that has a step up of O2. Then will go under the lungs and the pulmonary vein will have the normal 95% O2 sat. B/c there is an opening between these, there is blood going back and forth during systole and diastole – machinery murmur – where is it heard best? Between shoulder blades.
Can you vol. overload the right heart? Yes. Pulmonary HTN? Yes. Now which way will the shunt go? Will go the same way when it was a fetus; you will have unO2’d blood dumping into the aorta. Where does the ductus empty? Distal to the subclavian artery – so, the baby will have pink on top and blue on bottom b/c dumping unO2’d blood below the subclavian artery, therefore will have differential cyanosis – pink on top, cyanotic on bottom. What is the teratogen assoc with PDA? Congenital Rubella. If you had a PDA, can you close it off without surgery? Yes.
How? Indomethacin -‐ this is a potent NSAID, which would inhibit PGE2, and therefore would start constricting and close on its own.