Cardiac Dysfunction in Children Flashcards
abnormalities present at birth are called
congenital
abnormalities/disease processes that occur after birth are called
aquired
what dx procedure is done first for suspected cardiac disease
electrocardiogram
what nursing care should be done post cardiac cath
V/S Q15min pulses for equality assess pain extremity temp and color check insertion site I and O extremity straight for 4-8hrs oral intake to flush dye out get child to void
where should you apply pressure if catheter entry site is bleeding
1 in above entry site
*position child flat and call doc
what home care instructions are important for post cardiac cath
keep site clean avoid tub baths after limit activity for 24hrs avoid strenuous exercise regular diet tylenol or ibuprofen for pain follow up
blood flows from area of higher pressure to lower pressure
left to right shunt
change in pressure so that blood is shunted from the right side of the heart to the left
right to left shunt
what 3 defects have left to right shunting of blood and cause increased pulmonary blood flow
atrial septal defect (ASD)
ventricular septal defect (VSD)
patent ductus arteriosus (PDA)
abnormal opening between the atria
atrial septal defect
abnormal opening between right and left ventricles
ventricular septal defect
what is VSD’s percentage of spontaneous closure
20-60%
failure of the fetal ductus arterioles to close within first few weeks of life
patent ductus arteriosus
*blood flows form aorta to pulmonary artery
why is indomethacin (indocin) given to PDA pt’s
prostaglandin keeps PDA open so a prostaglandin inhibitor will help it close
what defect has a decreased pulmonary blood flow, shunts desaturated blood right to left, and sends desaturated blood to system circulation
tetralogy of fallot
what are the 4 cardiac defects that cause tetralogy of fallot
VSD
Pulmonary stenosis
Overriding Aorta
Right Ventricular Hypertrophy
what is the “clinical picture” for Tetralogy of fallot
cyanosis tachypnea acute episodes of cyanosis and hypoxia(hyper cyanotic spells) clubbing growth retardation
how are hyper cyanotic spells started in TOF
by feedings, crying, defecation, or stressful procedures
what are nursing interventions for hyper cyanotic spells of TOF
“squatting” position
calm the infant
blow by 100% oxygen
get help
what 3 defects are obstructive
coarctation of the aorta
aortic stenosis
pulmonic stenosis
blood exiting heart meets area of anatomic narrowing (stenosis)
obstructive defects
narrowing of the aorta at or near the insertion of the ductus arteriosus
coarctation of the aorta (COA)
- increase pressure proximal to the defect
- decreased pressure distal to the defect
what is the “clinical picture” of a pt who has coarctation of the aorta
elevated BP in arms/bounding pulses in arms
decreased BP in legs/weak or absent pulses in lower extremities
cool lower extremities
what defect will we take 4 different sites of BP in newborns
coarctation of the aorta
narrowing of the aortic valve causing left vent enlargement, decreased cardiac output, increased left atrial pressure
aortic stenosis
what is the “clinical picture” for a NEWBORN with aortic stenosis
decreased cardiac output faint pulses hypotension tachycardia poor feeding
what is the “clinical picture” for a CHILD with aortic stenosis
exercise intolerance
chest pain
SOB
syncope
what cardiac defect is the only one that has activity restrictions
aortic stenosis
narrowing of pulmonary artery that decreases pulmonary blood flow, and causes right vent hypertrophy
pulmonic stenosis
what cardiac defect is “mixed”
hypoplastic Left Heart Syndrome (HLHS)
underdevelopment of the left side of the heart
“single ventricle”
HLHS
why will a HLHS pt be on a prostaglandin drip
to keep PDA open because this is the only way they are getting blood flow systemically
what is the “clinical picture” for HLHS
mild cyanosis HF lethargy cold hands and feet once PDA closes it leads to cardiac collapse
is it normal to see HLHS pt with O2 sats of 70-80%
yes
*theres not an actual correction of this defect and they don’t have a long term life expectancy
heart can’t pump enough blood out to the rest of the body to meet the body’s demand for energy
congestive heart failure
what are S/S of CHF
difficulty feeding (ftt) tachypnea at rest dyspnea retractions activity intolerance weight gain r/t fluid retention hepatomegaly
what classes of meds improve cardiac function
digitalis glycoside (digoxin) ACE inhibitors (capto, enla, and lisinopril) Beta Blockers (caredilol)
improve contraction of the heart (take a good strong beat)
digoxin
reduce after load and easier for heart to pump
ace inhibitors (prils)
decrease HR and BP causing vasodilation
carvedilol
before giving digoxin what should be done
apical pulse for 1 min
*infant= don’t give below 90-110bpm
older child= don’t give below 70bpm
what are S/S of digoxin toxicity to watch for at home
nausea, vomiting, anorexia, bradycardia, dysrhythmias
what is important to teach parents about digoxin
do NOT mix with fluids or food if dose is missed don't double up if child vomits don't give extra dose keep locked in safe place call poison control in accidental overdose
what are side effects of ACE inhibitors
hypotension
dry cough
renal dysfunction
what are used to decrease accumulated fluid volume treatment
Diuretics: furosemide, chlorothiazide, spironolactone
what are clinical manifestations of chronic hypoxemia
polycythemia and clubbing
infection of the valves and inner lining of the heart caused by bacteria that enter the blood stream and settle in the heart lining, heart valve, or blood vessel
infective endocarditis
what are the most common organisms that cause infective endocarditis
strep viridans and staph aureus
who are at higher risk for IE
children who have undergone surgical repair or palliative surgery
what is the “clinical picture” of IE
hx of dental procedure, urinary or intestinal tract procedure unexplained fever weight loss lethargy malaise anorexia new murmur or change in existing
what is the tx for IE
blood cultures (to see what type it is) abx (IV 2-8wks) EKG monitoring *could cause stoke because it could break off and lodge somewhere it is fatal if left untreated
how can IE be prevented
maintaining good oral hygiene
inflammatory disease that occurs from GABHS
rheumatic fever
what are risk factors for RH
hx of group A strep infection
fam hx
environmental factors
when is the onset of RF
2-4wks after a strep throat infection
*ASO titer to find out if it was strep or not
what is the “clinical picture” of RF
MAJOR: carditis polyarthritis erythema marginatum chorea subQ nodules MINOR: arthralgia fever elevated ESR and CRP
what is the dx criteria for RF
modified jones criteria= 2 MAJOR manifestations or 1 MAJOR and 2 MINOR manifestations *plus + for strep
what is the tx for RF
abx 10day course then prophylactic (PO daily or IM monthly)
asprin to reduce fever, control inflammation
bedrest during acute illness
acute systemic vasculitis
kawasaki disease
*principal are of involvement is coronary artery aneurysms
what are risk factors for KD
younger than 5
males
asians or asian decent
what is the dx criteria for KD
no specific test but will have elevated CRP, ESR and CBC (platelet count)
what lab is different between KD and RF
KD has high platelet count
what is the acute phase of KD (first 10 days)
fever 5+days VERY IRRITABLE red on hands and feet strawberry tongue Bilateral conjunct inflammation polymorphous rash
what is the subacute phase of KD (greatest risk for developing coronary artery problems) 11-25 days
desquamation of fing and toe
cont irritability
thrombocytosis (>600,000-800,000
what is the convalescent phase of KD
all clinical signs resolved
blood val normal
beau’s lines on finger and toe nails
what is the tx for KD
high doses of IV gamma globulin (reduces incidence of coronary artery abnorms)
ASA
what nursing interventions can we do for KD pts
cool cloths, unscented lotions, loose clothing, mouth care including lubricant for lips
clear liquids and soft foods during acute phase
quiet environment so they can rest
