Nursing 54A - Peds Cardiac: Cardiac Pathophysiology in Pediatrics. Complete Study Guide.

Document Content and Description Below

Cardiac Pathophysiology in Pediatrics Fetal Circulation Placental Oxygenation  We get O2 from the placenta, it comes up through the umbilical vein, thru the inferior vena cava and into the righ... t atrium then thru the foramen ovale into the left atrium, left ventricle, and out to the body  Thru the superior vena cava, where there’s deoxygenated blood returning from the upper part of the body it travels into the right atrium and gets mixed with oxygenated blood that came from the placenta via the inferior vena cava.  After entering the right atria some of the blood will leave the right atria through the tricuspid valve into the RV and some of it can go to the pulmonary artery (but blood will try to avoid the lungs because in infants the pressure is very high in the lungs). It avoids the lungs thru use of the ductus arteriosis shunt, which shunts blood away from high pressured lungs and instead to the aorta (this blood is oxygenated bc it mixes with the oxygenated blood that comes from the umbilical vein thru the inferior vena cava into the right atrium) and to the rest of the body.  (SN: the blood that travels thru the inferior cava can mix with the blood in the right atria…there is no vessel? It goes thru the foramen ovale (shunts that diverts blood away from the lung)  Everyone post neonatally- the lungs have low pressure, huge amount of space, easy to go to.  In fetuses the lung vasculature is very high pressure bc there is no O2 in the lungs, filled with amniotic fluid. This causes that hypoxic vasoconstriction response in the lungs- the blood doesn’t want to go to the lungs. It gets diverted from the lungs ex.  Some blood goes to the lungs. Enough to main perfusion, delivery of O2  Placental oxygenation o Inferior vena cava, RA, FO, LA, LV, AO  Low arterial oxygenation o There is mixing of oxygenated and deoxygenated blood which is why fetal O2 stats are low o Fetal pO2 30-35 mmHg o Fetal O2 saturation 60-70% o Thats why when babies are born, they don’t have a brightly colored look.  Tissue oxygenation maintained with high cardiac output (the hrtbeat is really fast. They increase delivery) o Tachynea and tachycardia are their main methods of compensations o High cardiac output= tachycardia o That’s why in infants- slow HR is a very bad things bc it decreases tissue oxygenation bc they are totally relying on that fast HR for tissue oxygenation o There is a left shift of the O2 curve (as well)  One of the biggest factors of O2 transport and delivery is cardiac output . Ex. HR is the biggest determinant of cardiac output (refer to figure13- 13 p. 266) As an adult we don’t have: Ductus venosus – connection of the umbilical vein with the inferior vena cava Shunts:  Foramen ovale  Dustus arteriosis They all close at a certain point The ductus arteriosus closes at: A. 12-15 weeks gestation B. 28-32 weeks gestation C. Within 12 hours of delivery D. 24 -72 hours of life E. Is dependent on the type of delivery Transitional circulation Involves the closing of some of these shunts and duct. SN: Resistance- opposition to passage  Pulmonary vascular resistance (drops dramatically [Show More]

Last updated: 1 year ago

Preview 1 out of 24 pages