The “NORMAL” Heart. Cardiac Anatomy (cross section). Cardiac anatomy (external). Cardiac Auscultation. Cardiac Circulation. CYANOTIC Tetrology of Fallot (TOF) Transposition of the greater arteries (TGA). ACYANOTIC Atrial Septal Defect (ASD) Ventricular Septal Defect (VSD)
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
An opening (hole) between the atria allowing blood from the higher pressure left atria to enter the lower pressure right atria.
Degree of symptoms depends on the size of the hole. A child with a small ASD will have virtually no clinical symptoms but will have a significant murmur (the smallerthe hole, the louder the murmur).The smaller ASD can close spontaneously.
The child with a large ASD will exhibit s/s of CHF.
Repair can be performed in two ways
A child with an unrepaired ASD does not require SBE prophylaxis.
A opening (hole) between the right and left ventricle. VSD’s are the most common birth defect in children. Can range from a pin point sized hole to a large opening (virtually no septal wall present).
Causes increased pulmonary blood flow and left to right shunting of blood flow, this increased flow cause increased work load on the RV predisposing the child to CHF.
A VSD is normally an acyanoticdefecthoweverIn very LARGE VSD’s ( there is virtually no septal wall) accompanied by significant congestive heart failure , cyanosis can be present.
Child will exhibit s/s of CHF:
The vast majority of small VSD’s close spontaneously. The moderate-large will require open heart surgery to repair.
The child with a VSD will require SBE prophylaxis for life.
A localized narrowing (coarctation) of the aorta
Will cause increased pressure proximal to the defect (head and upper extremities) and decreased pressure to distal (body and lower extremities)
Clinical Manifestations of COA (dependant on the degree of coarctation):
In infants with a significant COA, there can be s/s of CHF with rapid progression to the infant being critically ill with acidosis and hypotension. At this stage they will require intubation and Inotropic support until repair can be completed.
With a milder degree of coarctation, the defect might not be diagnosed until it begins to produce symptoms (dizziness, headache, numbness in lower extremities, epitasis, syncope) Some children are not diagnosed until adolescence.
Can be achieved in 2 ways:
A child with a COA will require SBE prophylaxis for life.
The failure of the fetal ductus arterious (the artery connecting the pulmonary artery and the aorta) to close within the first few weeks of life. In utero the PDA allows the blood to pass between the aorta and pulmonary artery by passing the lungs, it normally closes within the first 72 hrs -1 week after birth.
Depending on how large the PDA is, when a large ductus stays open (patent), systemic BP becomes greater than pulmonary BP and the additional blood begins to shunt from the aorta across the ductus to the pulmonary artery, this is a left to right shunt.
This shunt through the pulmonary artery through the lungs increases the workload of the left side of the heart and RV, which increases pulmonary vascular congestion and pulmonary vascular resistance which may cause increased right ventricular pressure and RV hypertrophy.
There are 3 treatments available to close the ductus:
The child with a PDA will need SBE prophylaxis for oneyear after the duct is successfully closed.
These four defects combine to allow blood flow to bypass the lungs and enter the left side of the heart (and sending unoxygentated blood to the systemic circulation), this is called a Right to Left shunt.
They are hypercyanotic spells when there is an increase in the right to left shunting of blood (less oxygenated blood is getting to systemic circulation).
TET spells can be precipitated by:
Degree of clinical manifestations and symptoms
will depend on the degree of pulmonic stenosis.
In CHD, CHF is usually caused by:
One sided heart failure (as seen in adults) is rare in children, failure of one ventricle will almost always lead to failure of the other.
decreased myocardial contraction,
increased after load =
impaired myocardial function CHF
When starting Digoxin in a pediatric patient, children must be digitalized which means
to give their loading dose in 3 doses, 8 hours apart
1st dose = ½ of TDD
2nd dose = ¼ of TDD, 8 hours after the first dose. EKG must be done before the 3rd dose.
3rd dose = ¼ of TDD, 8 hours after the 2nd dose.
Infant (2 month old) with a large VSD has congestive heart failure.
Order: Digoxin maintenance dose : 0.05mg, po,q12h
Childs weight: 8 lbs
Pediatric dosing parameters:
child: 1 mth-2 years: 0.01mg- 0.02 mg/kg in 2 divided dose
Drug available: Pediatric elixir: 0.05 mg/1ml
What is the dose parameter according to the child's weight?
How many milligrams would the child receive per day?
How many milliliters would the child receive per dose?
Is the dose within safe dosing parameters?
1) Convert child's weight in lbs to kg - 8lbs divided by 2.2 = 3.6kg
Calculate safe drug parameters: 0.01mg/kg/day x 3.6 kg = 0.36 mg/day
0.02mg/day x 3.6kg= 0.72mg/day
2) How many milligrams would the child receive per day? 0.1mg
3) How many milliters would the child receive with each dose?
order is for 0.05mg q12 hours
Drug available is 0.05mg/ml
Child would receive 1 ml per dose
4) Is dose within safe parameters ? NO
The order is for 0.05 mg/q12 hours = 0.1 mg/day
Safe dose range for this pt is 0.36mg/day – 0.72mg/day
Order is MORE THAN safe dose
Do not give - notify MD ASAP