PDA Flashcards
Incidence
- more in females
- congenital rubella syndrome
- preterm infants
Anatomical defect
1- persistence of ductus arteruosis
2- distal to the origin of pt subclavian artery
Hemodynamics
During iu life
• there is no lung functioning ~> + pulmonary pressure ~> blood shunting from pulmonary to aorta
After fetal life
• ductus is closed , lung is opened ~> aorta gains pressure , pulmonary loses its high pressure gradually ( thus in the first week there is low pg between rt , lt ~> onset in vsd, pda is in second week of life ) ~> shunting of blood from aorta to pulmonary during both systole , diastole
• lung plethora
• lt artial , ventricular enlargement ( volume overload)
Why patent during iu life ? Vice versa
1-hypoxia
They both help in relaxing
2- + pg
3- the only way ( high flow )
Vice versa
1- no hypoxia ( lung is functioning )
2- pg is destroyed by the lungs
3- will not be the only way as lung is opened
Closure of ductus
1- functionally with 24 h due what is mentioned before
2- anatomically within weeks by fibrosis
Talk about small PDA ( his- exam- inv- ttt)
1- his : asymptomatic
2- exam
General : normal
Cardiac : murmur
- continous ( but higher in systole)
- machinery
- max intensity at lt infraclavicular area
3- inv
Xray, ecg : normal
Eco : 3
4- ttt
Surgical Catheter
Prophylactic against infective endocarditis
Talk about large pda ( his , exam)
1- history :
Onset : second week of life
- (6)
Dysnea , difficult suckling , recurrent chest inf , ftt, excersise intolerance , excessive sweating
2- exam
General :
1- ftt
2- recurrent chest inf
3- hf
4- HYPERDYNAMIC CIRC : big pulse volume ( water hammer sign )
Cardiac :
Insp, palp
1- lt v enlargement
2- systolic thrills in lt infraclavicular area ( very deep )
Ausc
1- auccentuted s2 ( pulmonary htn)
2- murmur :
- continous ( especially in systole due big pg )
- machinery
- max intensity on lt infraclavicular area or inside scapula ( بيسمع لورا
3- soft ejection ( mid ) systolic murmur ( pulmonary htn )
Why big pulse volume
V= SBP - DBP
Systolic p is not affected as mich as diastolic as the lt ventricle will compensate the blood shunted by + its own p preserving the systolic p while diastolic p is decreased due to continous running off blood from aorta to pulmonary thus the gap will increase
120 - 40
Complications - inv of large pda
Comp
1- hf
2- recurrent chest inf
3- infective endocarditis
4- ftt
5- pulmonary obst ~> eisenmenger syndrome but it causes differntial cyanosis as it is in the low half of body ( as pda is below the subclavian)
Inv
1- xray :
- lt v enlargement
- pulmonary dilation
- lung plethora
2- ecg : lt v enlargement
3- echo :
- size , position, blood flow
- pulmonary p ( prognosis)
- cardiac dilation, efficacy of contractility in lt ventricle
Ttt
Medical
•Ttt of
- hf
- infective endocarditis
- recurrent chest inf
• Medical closure by
* indomethicin , ibuprofen, paracetamol
* in the fist two weeks only
* be aware of se of indomethcin ( nephritis ) thus
Following with kidney function test , bleeding profile
Surgical
Indications : failed medical ttt + over 6 kg infant
(Either small or large as it wont close as it is fibrotic , cant spasm )
Surgical or catheter
Banding of pa can occur in postponed cases
Why is aorta named as second heart
As it dilates ( stretches ) in systole to work as shock absorber
And recoils in diastole pushinf blood forward