Exam 2 Flashcards
transposition of the great arteries (or vessels); TGA
Defect causing Mixed Blood Flow: switched aorta and pulmonary artery. no communication between lungs and body. Arterial Switch procedure performed as soon as possible after birth. give prostaglandin to keep PDA open until surgery
total anomalous pulmonary venous return (TAPVR)
defect that cases mixed blood flow: pulmonary veins empty into R atrium instead of L atrium. Mild cyanosis increases with feedings. Small LA and LV; put on prostaglandins immediately to keep PDA open. Balloon septostomay until baby is old enough to withstand the Surgery the reconnects pulmonary veins to LA.
Truncus Ateriorus
defect causing mixed blood flow. a single large vessel acts as both the aorta and pulmonary artery. VAD often present. Rastelli procedure closes VSD and creates passage to pulmonary arteries. repeated surgeries often needed. No contact sports.
hypoplastic left heart syndrome (HLHS)
defect causing mixed blood flow. Very small LV and aorta. One of the most severe defects. Give Prostin to keep PDA open. NO SUPPLEMENTAL O2 to prevent pulmonary vasoconstriction. Treated with Norwood surgical procedure (RV pumps to lungs and body), transplant, or palliative care. limited physical activity due to single ventricle. Neurodevelopmental probs.
ECMO
extra-corporeal membrane oxygenation: artificial heart and lung machine. outcomes decline if on this machine longer than two weeks.
Indomethacin
closes PDA
Prostin
keeps PDA open until surgery
Congestive Heart Failure (CHF)
inability of heart to meet metabolic demands of body. Caused by increased workload or decreased myocardial contractility. Failure of one side causes failure of the other.
when do you hold digoxin in an infant?
heart beats less than 80 beats/min (remember adults under 60) and 70 beats/min in toddlers
signs of digoxin toxicity
vomiting, pulse irregularities
tachycardia, sweating at rest, poor urine output, fatigue, poor feeding, poor pulses
CHF
hypoxemia vs hypoxia
hypoxemia: low oxygen in the blood
hypoxia is low oxygen in the tissues
cyanosis at 80-85% saturation
bacterial endocarditis
infection of valves/lining; result of abnormal/artificial valves, recent surgery, rheumatic fever. Nursing care focuses on Abx, repeat blood cultures, and observe for embolus. Educate on prophylaxis for invasive procedures.
rheumatic fever
autoimmune? commonly follows a strep infection. pain in joints, CHF symptoms, tachycardia, rash. give Abx and anti-inflammatories, rest. Educate on chorea (ticks of face and hands pill roll)-decreases once antiinflammatories do their thing. Abx for 6 months!!!
Kawasaki Disease
Phase 1 (1-10 days): fever > 5 days unresponsive to antipyretics, conjunctivitis, crusted/fissured lips, swollen hands and feet, erythema, lymphadenopathy Phase 2 (10-25 days): fever diminishes, irritability, anorexia, desquamation of hands and feet, arthritis, arthralgia, carditis Phase 3 (26-40+days): drop in ESR, diminishing signs of illness but inflammation still present
Kawasaki Disease Tx
treat with aspirin and IVIG
call physician if child refuses to walk-disease often affects spinal cord
hyperlipidemia
lower the content of sat fat and cholesterol; educate the entire family about proper nutrition
nursing care after cath
Direct pressure for 15 minutes without peeking
Pressure dressing for at least 6 hours
Vitals and neurovascular checks, including pulses, q 15 mins for 1 hour, then q 30 mins for 1 hour, then q hour for 4-8 hours
Bedrest for 6 hours, “quiet play” for first 24 hours
Monitor for: bleeding, arrhythmias, infection, excessive diuresis from dye
Promote fluid intake to flush out dye
shock
Perfusion no longer meets metabolic needs of body
Early: fear, irritability, narrowing pulse pressure, mild ↑HR, ↓UO, slower CRT
LATE: decreased LOC, weakening pulses, hypotension, tachypnea or apnea, anuria
shock Tx
Open airway, 100% oxygen
20 ml/kg boluses of LR or NS as ordered
IV epinephrine or other vasopressors as ordered
EKG and Pulse Ox, monitor temp
Consider cause: Sepsis? Allergy? Drugs? SCI?
pediatric cardiac assessment
Familial history of CHD Other genetic defects Maternal rubella in pregnancy Maternal age 40 Maternal weight under 100 or over 200 pounds Maternal IDDM Fetal Alcohol Syndrome Presence of other extracardiac birth defects
Unique aspects of childhood cardiac function until age 5
heart rate varies according to oxygen needs, accounting for higher resting heart rate in children
cardiac output dependent on heart rate until age 5
increased risk of heart failure due to inability to adapt to volume or pressure increases
muscle fibers of heart less developed
most frequent complaints from parents of kids with cardiac dysfunction
Trouble breathing
Trouble feeding
Colic and crying
Lack of bonding
hypopituitarism
Pituitary gland does not produce enough Growth Hormone (GH)
Child “falls off” growth chart, usually 3rd-5th percentile by age 2
Assessment: short stature, fontanels don’t close, poor muscle mass, teeth crowded/crooked
Treatment/Interventions: daily SQ GH ($$$), growth plotted every 6 months
Education/Teaching: social interaction, treat child based on age not size
SIADH
SIADH: problems stem from low sodium: tx strict I/O, daily weights, fluid overload, seizure precautions, long term ADH antagonists
precocious puberty
Early onset before 8 (girls) or 9 (boys)
Synthetic LRH to slow, or no treatment
Support with dress, peers
diabetes insipidus
Improper secretion of ADH–>uncontrolled diuresis
Polyuria, polydipsia, enuresis
Urine SG <1.005, weight loss 3-5%
Often temporary, NOT diabetes mellitus
excessive sweating and very high tachycardia, fever
thyroid storm-whenever you do a thyroidectomy-treat with beta blocker (propranolol), PTU, and MTZ
1 cause of ambiguous genetalia at birth
CAH: Congential adrenal hyperplasia
Tx: cortisone, salt
GENDER ASSIGNMENT: wait on gender assignment until you see how the child develops
acanthosis nigricans
darkening of skin in fold areas
cutaneous manifestation of hyperinsulinemia
precursor to DMII
BCP’s can also cause this. Never normal, bc elevated hormones cause this.
