Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
20%
28 19
8%
24
70%
45%
55%
65%
50%
65% 55%
35%
140
45 175
75
75 180
31
10 39
3
58 44 49 31 21 28 17 3
17
49
39 10
PULMONARY CIRCULATION
Fetal lung does not serve gas exchange function. PVR is high and PBF is low. This helps to reduce workload of fetal heart.
PULMONARY CIRCULATION
MPA continues as Ductus and RPA and LPA arise as branches. Medial layer is composed of smooth muscle predominantly in small pre acinar and large acinar level arteries. Further branches have no muscular component.
PULMONARY CIRCULATION
PA pressure rises gradually paralleling the rise in aortic pressure. TPR falls gradually but this fall when correlated with rise in lung weight, there is actually an increase in PVR towards term . PBF increases gradually.
PULMONARY CIRCULATION
MPA has forward flow throughout systole with a short period of backflow at end of systole. DA also has forward flow throughout systole. BPA has forward flow only through initial one third of systole followed by back flow through rest of systole and diastole. In humans forward flow is more prolonged.
PULMONARY CIRCULATION
Experiments show fetal PBF increases dramatically in response to increase in maternal PO2. This response is evident only in latter part of gestation. Doppler studies indicate similar changes in humans as well.
PULMONARY CIRCULATION
Fetal pulmonary endothelium behaves in a similar fashion as adult endothelium to vasodilators. Adrenomedullin has a potent and prolonged vasodilatory effect. Leukotriens may be responsible for maintaining high fetal PVR.
PULMONARY CIRCULATION
Breathing at birth is associated with a marked fall in PVR and rise in PBF. PA pressure does not fall as rapidly and remain elevated till the Ductus is widely patent. Once the ductus is closed, PA pressure can vary independent of systemic pressure.
ATRIUM
OLef t
ATRIUM
Left VENTRICLE
Pulmonary veins
LUNGS
Pulmonary arteries
Closure of Ductus arteriosus means that blood expelled from the right ventricle has to go to the lungs Aorta
PULMONARY CIRCULATION
Fetal lung does not serve gas exchange function. PVR is high and PBF is low. This helps to reduce workload of fetal heart.
PULMONARY CIRCULATION
MPA continues as Ductus and RPA and LPA arise as branches. Medial layer is composed of smooth muscle predominantly in small pre acinar and large acinar level arteries. Further branches have no muscular component.
PULMONARY CIRCULATION
PA pressure rises gradually paralleling the rise in aortic pressure. TPR falls gradually but this fall when correlated with rise in lung weight, there is actually an increase in PVR towards term . PBF increases gradually.
PULMONARY CIRCULATION
MPA has forward flow throughout systole with a short period of backflow at end of systole. DA also has forward flow throughout systole. BPA has forward flow only through initial one third of systole followed by back flow through rest of systole and diastole. In humans forward flow is more prolonged.
PULMONARY CIRCULATION
Experiments show fetal PBF increases dramatically in response to increase in maternal PO2. This response is evident only in latter part of gestation. Doppler studies indicate similar changes in humans as well.
PULMONARY CIRCULATION
Fetal pulmonary endothelium behaves in a similar fashion as adult endothelium to vasodilators. Adrenomedullin has a potent and prolonged vasodilatory effect. Leukotriens may be responsible for maintaining high fetal PVR.
PULMONARY CIRCULATION
Breathing at birth is associated with a marked fall in PVR and rise in PBF. PA pressure does not fall as rapidly and remain elevated till the Ductus is widely patent. Once the ductus is closed, PA pressure can vary independent of systemic pressure.
Septal defects
They in general do not modify the fetal circulation significantly. VSD may have a transient left to right shunt in systole. In OP ASD, due to close proximity of defect with TV, more than normal amount of SVC blood may enter the LA.
Septal defects
In atrioventricular septal defects, the obligatory flow from LV to RA will result in decrease in LV output and an increase in RV output. This will reduce the flow across the isthmus and can predispose to coarctation. It is the degree of severity of AV valve lesion and regurgitation which will determine the outcome.
LVOT Obstruction
Severe obstruction developing early result in a small LV with an increased mass.
LVOT Obstruction
SVC flow courses normally. Majority of IVC blood flow crosses TV to RV. Flow across the ductus increases.
LVOT obstruction
Decrease in saturation between DA and AA. LV systolic pressure increases slightly but not EDP. A retrograde flow in arch and ascending aorta indicates severe obstruction.
62 75/50
75/4
60
65
90/ 5 60
70/45
70
70/40 60 70/2 60 60
40
70
63 63 63 100/4 63 70/3 40
70
In pulmonary atresia, all systemic venous blood is carried to left side through foramen ovale and all blood supply to DA is provided through isthmus. Larger than normal foramen ovale, left sided chambers,AA and aortic isthmus.
RVOTO with intact IVS If severe RVOTO develops early in gestation,the flow through the ductus is reversed and carries only 8 to 10 % of cardiac output. The ductus will be narrower and will make an acute inferior angle with aorta. The ductus will remain patent for longer than normal duration.
TAPVC
Usually does not affect the development of fetus. If whole of PV return drains to SVC,LV will be totally free of PV blood and hence will be of higher saturation. Left atrium and left ventricle will be relatively small in TAPVC.
70/45 63
60 70/4 55 65 70/4
70
Aortopulmonary transposition
Compatible with fetal survival and normal intrauterine development. Does not affect the pattern of venous return. Blood with higher oxygen saturation will go to lungs. This will reduce the PVR and hence increase in PBF.
Aortopulmonary transposition
This will reduce the blood flow across the ductus and increases the flow across the isthmus. Blood with lower oxygen saturation perfuses coronary and cerebral circulation. Hence cerebral and coronary blood flow are increased considerably.
70/45
55
70/45 65
70/4 40
55
70
70/3
70
70/45 65
65 70/4
70/4
65 55
40
70
Truncus arteriosus
Various degree of mixing occurs just above the semilunar valve. Degree of mixing depends on morphology.In type 1,there is differential streaming of blood and in others there will be complete mixing. Ductus is usually small or absent and increased flow traverses through isthmus and it is large.
Ebsteins anomaly
Severe TR can manifest as in utero cardiac failure especially if foramen ovale is restrictive. Marked enlargement of RA and atrialised RV can cause septal displacement and compromise LV output. Functional pulmonary atresia can result and ductal flow may be reversed.
Ebsteins anomaly
Marked enlargement of right atrium can cause pulmonary hypoplasia Severe TR alters the preferential drainage of venacaval blood and causes complete mixing of blood in right atrium.
Tricuspid atresia
All of the venous return traverses foramen ovale and it is considerably larger than normal . Complete admixture of blood in the left atrium It is compatible with normal intrauterine development and survival.
Tricuspid atresia
If IVS is intact, whole PBF is from aorta through ductus and ductal flow is lesser than normal. 75% of combined VO traverses the isthmus and it tends to be larger. In the presence of VSD,the flow pattern is decided by the size of the defect and presence of pulmonary stenosis.