• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/57

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

57 Cards in this Set

  • Front
  • Back
What is the most common CHD with symptoms initially presenting in adulthood?
ASD, Secundum type
How many types of ASDs are there?
What % are Secundum?
4 types:
Secundum 90%, Primum,
Sinovus venosus Upper and Lower
What is a secundum ASD NOT? How do we know?
Not a patent foramen ovale; that would allow only right to left flow; this is left to right.
What % of patients with secundum type ASD develop pulmonary hypertension?
<10% - it is well tolerated usually
What are patients with secundum type ASD at risk for?
Paradoxical embolism
Where are primum defects causing ASD located?
Just above the tricuspid annulus
Where are the secundum type ASDs located?
Right in the interatrial septum
What are the primum type ASDs often associated with?
AVSD
Where are upper sinus venosus defects causing ASDs located?
What about lower ones?
Upper: by the SVC

Lower: by the coronary sinus
What are sinus venosus defects usually associated with/
Anomalous right pulmonary vein
What are the 4 physiologic effects of an ASD?
-Right volume overload 4X
-Dilated tricuspid and pulmonic valves - regurgitation
-Dilated pulmonary vascular bed
-Obstructive pneumonia
Where in the lungs will obstructive pneumonia develop in an ASD?
-Left upper lobe
-Right middle lobe
What will auscultation show in an ASD?
Wide S2 splitting
What can develop in a wide ASD?
-Increased pulmonary vascular resistance
-R-L shunt (reversal)
-Ultimately cyanosis
What % of all CHDs are VSDs?
21%
What happens in 75-80% of small VSDs?
Spontaneous closure
What % of VSDs are
-isolated
-associated w/ other intracardiac lesions
Isolated = 30%

Associated = 70%
What % of VSDs are
-Perimembranous
-Subpulmonic or intramuscular
-AVSD
Perimemb = 90%
Subpulmon/intramusc = 8%
AVSD = 2%
What determines the significance of a VSD?
Size
What are the 3 features of a small VSD?
(Symptom/Pressure)
-High pressure gradient across the small opening
-Loud murmur
-Normal RV pressure
What is considered a medium sized VSD?
1/3 - 2/3 the diameter of the aorta
What happens to most med sized VSDs?
The pressure gradient tends to close them spontaneously
Why can medium VSDs close?
The defect is restrictive to flow
Can Large VSDs close? What is considered large? Why can't they close?
No; the size of the aorta; the defect is not restrictive to flow.
What is the pressure gradient in a large VSD?
Non-existent - the pressure in the ventricles is equalized
What determines whether pulmonary hypertension will develop in a large VSD?
The degree of pulmonary stenosis
What normally needs to be done for large VSDs?
Surgical closure - to prevent pulmonary hypertension
So most VSDs are what?
Perimembranous
What area is considered perimembranous?
The outflow tract of the LV, just under the aortic valve.
What tissue can be used to close a perimembranous VSD?
Reduncant tricuspid leaflet tissue
What will result if there is deficient septal commissural tissue?
Right atrial -> left ventricular septal defect
Where is an "outlet defect" VSD?
In the outlet tract beneath the pulmonic valve
Why is an outlet defect called "doubly committed"?
Because the VSD is beneath both the pulmonic and the aortic valves; the right aortic cusp can herniate thru the VSD and cause aortic regurgitation
What is an inlet defect VSD?
An AVSD
Where are AVSDs seen?
Below the papillary muscle of the conus.
What do left-right shunts do as pulmonary hypertension develops?
Reverse into right-left shunts
How are med-large defects treated?
By repairing them in the 1st year before pulmonary hypertension onset
What are most PDAs?
Isolated defects - 90%
What are three important histologic features of the ductus?
-LH/RH spiral smooth muscle
-Thick intima
-Increased mucoid substance
What maintains the patency and relaxation of the ductus in utero?
Prostaglandins E2 and I2
What happens at delivery?
-Prostaglandins are lost
-Increased oxygen causes ductal contraction
How soon after birth does the ductus close?
12 hours
What is the 2nd stage in ductus closing, and when does it occur?
-Fibrous replacement of muscle
-Fibrous obliteration of lumen
Occurs by weeks 2-3
What happens to preemies in regards to their ductus?
They don't lose responsiveness to prostaglandins, so their ductus remains patent; this is not considered a CHD though.
What is a HALLMARK symptom of PDA?
Machine gun like harsh murmur

-Holosystolic
What is the ultimate result of a PDA?
R-L reversal and obstructive pulmonary vascular disease
Why is PDA so bad for the heart, when it's the systemic aortic blood that is flowing back into pulmonary circulation?
It steals the coronary blood, causing LV hypoperfusion and mural ischemia
What are 2 treatments for PSD?
-Surgery (w/in first year)
-Indomethacin/NSAIDs
What is another name for an AVSD?
Endocardial cushion defect
What are the 2 components that make up an AVSD?
-Deformed anterior leaflet of the mitral valve
-Primum atrial septal defect
What are 2 variations of an AVSD?
-Partial form
-Complete form
What is a Partial AVSD?
Incomplete fusion of the endocardial cushions
What is a Complete AVSD?
Complete failure of the endocardial cushions to fuse
What is the result of Partial AVSD?
Mitral valve insufficiency
What is the result of Complete AVSD?
a hole in the heart
What is the major cardiac alteration in AVSD?
Volume hypertrophy of all four chambers of the heart.
What are 30% of AVSDs due to?
Trisomy 21