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28 Cards in this Set

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wt loss after birth
FTT
5 and 10% of their birth weight, and will be back to birth weight by 10-14 days.

Failure to gain weight adequately in childhood is referred to as "failure to thrive."
below the 5th percentile for weight, below the 5th percentile in weight for length, or when the rate of growth results in the infant crossing more than 2 major lines on the standard infant growth curve.

two categories: organic and non-organic.
organic problemsless than 10%
ex. congenital heart defects, cystic fibrosis, gastroesophageal reflux, neurologic disorders and metabolic disease.

Psychosocial problems account for the majority of cases of non-organic failure to thrive. Poverty and neglect
many cases of failure to thrive, no specific etiology is found.
congestive heart failure (CHF)
respiratory distress, difficulty feeding and poor weight gain (also called failure to thrive).

diaphoresis b/c adrenergic activation
Bronchiolitis or pneumonia
respiratory distress, typically also with fever,
Anything causing respiratory difficulty in an infant can also cause difficulty with feedings.
Hyperbilirubinemia is
unlikely to cause poor feeding unless there is kernicterus, and there is no history of jaundice.
Sepsis
always an important consideration in a young infant. The early signs of sepsis can be subtle and non-specific
Poor feeding
may be sign of any GI disease including GE reflux, but the absence spitting up or emesis makes this less likely.
Hypotonia
may cause poor feeding, but is not expected to cause respiratory difficulty, and would more likely have been present from birth.
metabolic disorders
could potentially cause poor feeding. The negative newborn screen makes this less likely but it is still an important possibility.
murmurs
Grade I - faint and easily missed Grade II - obvious Grade III - loud Any murmur that is grade III, or is associated with a thrill (grade IV), is likely to be pathologic, and probably should be evaluated by a cardiologist. Diastolic murmurs are always pathologic. A continuous murmur is indicative of a patent ductus arteriosus, and is also pathologic. A gallop is an extra heart sound, quite different in character from a murmur, and very uncommonly heard in infants and children.

cyanosis assc with congenital heart defects most commonly tetrology of fallot (less cmmn- truncous arteriosus, transpotision of great vessels, tricuspid atresia, and total anomalous pulmonary venous return
holosystolic murmur
VSD, mitral insufficiency and tricuspid insufficiency all cause holosystolic murmurs
ejection murmur
ejection murmur is also systolic but does not start until after S1 because there is a delay from S1 to the onset of ejection - the isovolumic contraction time.

Ejection murmurs occur with aortic and pulmonic valve stenosis
normal liver edge
is palpated 1 to 2 cm below the right costal margin in a young infant

Hepatomegaly is a fairly consistent finding in children with congestive heart failure. Decreased renal blood flow, via activation of the renin-angiotensin system, leads to fluid retention, systemic venous congestion and hepatomegaly.

congenital infections, inborn errors of metabolism, anemias, and, less commonly, tumors

Liver size in children is often described by the distance below the right costal margin, rather than actual liver span. Thus, hyperexpansion of the lungs can create a false impression of hepatomegaly. In a child with apparent hepatomegaly and respiratory symptoms, it is important to try to assess the actual liver size
most common cause of a murmur in children.
Innocent murmurs are by far
Congenital heart defects, such as atrial or ventricular septal defects, aortic or pulmonic stenosis, and coarctation of the aorta are important too
3-7 years of age
most commonly heard innocent murmur is Still's murmur- musical or vibratory, and is heard best at LLSB in the supine position.
murmur heard in a young infant, or in a child who is not otherwise healthy, is less likely to be innocent- no other signs of significant heart disease? otherwise well? precordial activity normal? second heart sound normally split? Is the murmur more than grade II/VI? Is the oxygen saturation normal? If the answer to any of these questions is "no," the murmur should not be considered innocent.

Acute rheumatic fever, endocarditis, and cardiomyopathies are uncommon causes of heart murmurs in children, but must be considered, particularly in a child with a murmur and fever.
<3 defects detected in preschoolers
atrial septal defects @ 3-5 y/o.
widely split, fixed S2. distinguish an ASD from an innocent murmur.

Coarctation of the aorta can present in infancy or at any age beyond because it tends to be a progressive problem, gradually getting more severe
murmur, hypertension in the upper extremities, and a discrepancy between the upper and lower extremity blood pressures.



Bicuspid aortic valve is a common heart abnormality, but is often not detected until adolescence or adulthood.
<3 defects that present in infancy
Ventricular septal defects, aortic and pulmonic stenosis, patent ductus arteriosus, and tetralogy of Fallot
<3 defects not detected until adulthood
Bicuspid aortic valve is a common heart abnormality, but is often not detected until adolescence or adulthood.
Tetralogy of Fallot
(VSD, RV outflow tract obstruction, overriding aorta and RVH) causes cyanosis by obstructing pulmonary and causing right to left shunting through the VSD.

most common cyanotic heart defect
Isolated ventricular septal defects
15 to 20% of all congenital heart defects, and in most series are the most commonly encountered congenital cardiac defect.

VSDs vary in size from very small, clinically unapparent defects that close spontaneously to large, highly problematic defects that require surgical closure.
Transposition of the great arteries
most common heart defect presenting with cyanosis in the newborn period. This defect often requires urgent intervention to support mixing of oxygenated and de-oxygenated blood.
5Ts of cyanotic heart defects.
Truncus arteriosus, tricuspid atresia and total anomalous pulmonary venous return

transpositon and tetrology
murmur sounds
Aortic stenosis: systolic ejection murmur followed by an early diastolic murmur of AI.

Pulmonic stenosis: prominent systolic ejection click just after S1, and a harsh systolic ejection murmur.

Patent ductus arteriosus: The murmur is continuous, but a bit louder in systole.

Ventricular septal defect: This murmur is holosystolic, starting with S1. I would describe the sound as somewhat blowing.

The innocent murmur sounds vibratory and low pitched, and is heard best at the left lower sternal border. The vibratory quality is the most characteristic feature of an innocent murm
Other heart defects that present with a murmur and signs of congestive heart failure in infancy include
severe aortic stenosis or coarctation of the aorta, and a large patent ductus arteriosus (PDA). VSD

atrial septal defects, do not cause CHF. Most cyanotic heart defects, like tetralogy of Fallot, cause decreased pulmonary blood flow, and therefore do not cause CHF.
sx CHF in kids vs adults
infant with congestive heart failure presents primarily with feeding difficulties and respiratory symptoms. Rapid and labored respirations are common, and often lead to difficulty feeding. The history will often reveal that the infant is feeding for longer periods of time than normal, and that the feedings are terminated due to respiratory distress. Infants frequently become diaphoretic with feedings. Ultimately, due to poor feeding and increased caloric expenditure, poor weight gain ensues. Evidence of respiratory distress is prominent on physical examination with rapid, labored respirations. Tachycardia is common. A gallop rhythm is noted more often with primary cardiac contractile dysfunction than with volume overload lesions. Hepatomegaly is a reliable finding in infants with heart failure.

In contrast with adults who have congestive heart failure, rales, jugular venous distention, and peripheral edema are not commonly seen in infants.
ECG findings for VSD
prominent biventricular forces -- high voltage QRS complexes in leads V1 and V2, suggesting both LV volume overload and RV pressure overload.

RVH, due to RV pressure overload (pulmonary hypertension). This ECG also has an upright T wave in lead V1, which is an additional sign of RVH.

In a moderate size VSD, the classic ECG findings are LVH, due to LV volume overload.

In a small VSD, the ECG should be normal.


voltage is very age-dependent. Newborns and young infants normally have more right ventricular voltage, and have a more rightward axis, than older infants and adults

echo:
no pressure gradient from LV to RV.
left to right shunt (the LA and LV are dilated, indicating significant volume overload).
VSD
Anatomy: Defects of variable size located in either the membranous or muscular ventricular septum

Physiology: L to R shunt of blood during ventricular systole causing increased pulmonary blood flow, increased pulmonary venous return, and resultant left ventricular volume overload. Magnitude of shunt dependent upon size of defect and relationship between systemic and pulmonary vascular resistance.

Newborns have elevated pulmonary vascular resistance. Since the systemic and pulmonary vascular resistances (PVR) are nearly equal, there is no reason for blood to shunt through the VSD. Classic teaching is that VSD murmurs are not heard in the nursery

Clinical Picture:
1. Murmur and clinical signs usually are not present in the newborn nursery but are noted from several days to weeks of age.
2. Age of presentation and symptoms related to magnitude of L to R shunt which is determined by size of defect and pulmonary vascular resistance.
3. Large defects often present with CHF as pulmonary resistance falls in the first weeks of life.
4. Small defects usually cause no symptoms.
5. VSDs tend to diminish in size with time with spontaneous closure of approximately 75% of small defects and between 25-50% of all defects.
6. Hyperactive precordium, occasionally with a thrill at the lower left sternal border.
7.Intensity of murmur not reliably related to defect size.
8. CXR shows cardiomegaly with evidence for increased pulmonary blood flow.
drugs for CHF in kids
Diuretics are particularly effective at relieving the symptoms of CHF. Diuretics work to counteract the fluid retention that occurs as a result of activation of the renin-angiotensin system. Furosemide (Lasix) is the diuretic used most commonly for CHF in infants.

Digoxin has been shown in some studies to improve symptoms in infants with congestive heart failure due to a ventricular septal defect.
The mechanism responsible for the clinical improvement is not altogether clear, as infants with a ventricular septal defect do not have impaired contractility.

Although used in some patients, afterload reduction with an ACE inhibitor is not proven to be effective for CHF due to a VSD. There is convincing evidence that ACE inhibitors are effective at treating CHF due to cardiomyopathies.
Eisenmenger's disease
untreated for several years he will develop pulmonary Pulmonary vascular obstructive disease, or Eisenmenger's disease, is a truly horrible outcome for a patient with an unrepaired VSD.

The pulmonary vasculature constricts in response to exposure to high pressure and high flow. With chronic exposure to these conditions the pulmonary vasculature will develop permanent changes and loses the ability to relax, even if the VSD is closed. This causes the pulmonary vascular resistance to exceed the systemic resistance, and shunting through the VSD will shift to right to left. The patient will then develop cyanosis, progressing to polycythemia, heart failure and death. Most patients with Eisenmenger's disease will live into their twenties, but with a very impaired quality of life.

Patients with a large unrepaired VSD will universally develop Eisenmenger's disease. In general this will not occur before 6 months of age. In an infant with a large VSD and pulmonary hypertension, VSD closure is now recommended by 6 months of ages to completely prevent development of Eisenmenger's disease.
VSD repair surgery
on cardio-pulmonary bypass. The VSD is approached though an incision in the right atrium. The VSD is behind the septal leaflet of the tricuspid valve, which is retracted to reach the VSD. A patch of Dacron is then sewn over the defect on the right side of the septum, taking care not to damage the conduction system, which is very close to where the patch is placed.