VSD and CHF

Question 1

Failure to thrive

Answer 1

failure to gain weight appropriately (

Question 2

Feeding patterns in young infants

Answer 2

Breastfed - 10-30 minutes a time every 2 hours

Bottle fed - every 3-4 hours

Question 3

DDx for respiratory distress and feeding difficulty

Answer 3

CHF - congenital defects
Respiratory infection - anything causing resp distress can cause poor feeding
Sepsis - signs can be nonspecific
Metabolic Disorder - almost all of them can cause poor feeding

Question 4

Cardiac Exam

Answer 4

Complete exam includes looking at patient color, palpate precordial, assess pulses, auscultate
Precordial - if overactive, heart has increased workload

Question 5

Grading murmur intensity

Answer 5

I - faint
II - obvious
III - loud
IV - associated with thrill

Question 6

Holosystolic murmur

Answer 6

The murmur starts with S1 and encompasses all of systole

- VSDs, mitral insufficiency, tricuspid insufficiency

Question 7

Ejection murmur

Answer 7

occurs during systole but not until after S1

- aortic and pulmonic valve stenosis

Question 8

Hepatomegaly in infants

Answer 8

normal liver edge = 1-2 cm below ribs

• hepatomegaly consistent with CHF
• decreased renal blood flow –> activates renin-angiotensin system –> fluid retention –> venous congestion –> hepatomegaly

Question 9

Signs of CHF in infant

Answer 9

Poor feeding, diaphoresis, poor growth, active precordium, hepatomegaly
- inefficient circulation leads to adrenergic activation –> increased metabolic demands –> poor weight gain

Question 10

Innocent murmurs

Answer 10

common (70-80% at one time have murmur) –> cause no distress or symptoms
- make sure no other alarming signs before brushing off

Question 11

Murmurs discovered around 3-5 years old

Answer 11

ASD - wide, fixed split of S2

Coarctation of Aorta - progressive, HTN in upper extremities

Question 12

VSD murmur

Answer 12

Ventricular septal defect - very common

• vary in clinical importance, size
• holosystolic mumur starting with S1

Question 13

Tetralogy of Fallot

Answer 13

VSD, Overriding aorta, pulmonary stenosis, RVH

• cyanosis through obstruction of pulmonary artery
• R –> L shunt

Question 14

Transposition of great vessels

Answer 14

vessels switched, severe cyanosis and urgent, early intervention is required

Question 15

Aortic Stenosis

Answer 15

systolic ejection murmur followed by early diastole murmur

Question 16

Pulmonic stenosis

Answer 16

prominent systolic click just after S1, harsh systolic ejection murmur

Question 17

PDA

Answer 17

continuous machine like murmur

Question 18

Heart defects that cause CHF

Answer 18

VSD
Aortic Stenosis
Coarctation of Aorta
Large PDA

Question 19

Evaluating a congenital heart defect

Answer 19

EKG
Chest Xray
Echo

Question 20

Hallmark of CXR in L–>R shunts

Answer 20

cardiomegaly, increased pulmonary vascular markings, pulmonary edema

Question 21

EKG findings in VSD

Answer 21

prominent biventricular forces (high QRS in V1 and V2) –> LV volume overload and RV pressure overload

• large VSD –> RVH
• moderate VSD –> LVH

Question 22

Admission criteria for congenital heart disease

Answer 22

not everyone needs admission for management

• present with cyanosis or CHF = admit
• shock = admits

Question 23

VSD

Answer 23

persistent communication between ventricles
- either membranous or muscular septum
Phys: L–>R shunt –> increased pulmonary blood flow –> increased pulmonary return –> LVH –>

Question 24

Clinical picture of VSD

Answer 24

murmur and signs not present in nursery (high pulmonary vascular resistance –> no shunting)
- large defecst = CHF as pulmonary resistance falls

Question 25

Treatment of CHF

Answer 25

Furosemide - lasix to get extra fluid off accumulated by renal system
Digoxin - not clear but has shown to improve symptoms of CHF from VSD
Enalapril - afterload reduction promotes forward flow rather than thru VSD

Question 26

Eisenmenger’s Syndrome

Answer 26

HORRIBLE OUTCOME FOR VSD
- pulmonary vasculature constricts in response to high flow and high pressure –> permanent changes and pulmonary vasculature unable to relax –> shifts to R->L shunt -> death