NRSG 446 - Exam 3 | STUDY GUIDE | 2025/2026
Terms in this set (81)
- pulse oximeter on upper and lower extremities
NRSG cardiac screening - >24 hrs old before discharge
- thrill is not normal!
heart cannot pump as well as it should (fluid backs up in lung and
body does not get enough O2 rich blood) -> increase HR, thickened
walls, filling capacity decreases so less blood ejected
- causes: CHD
- sx: tachycardia, poor circulation, weight gain (fluid overload),
congestive HF tachypnea, SOB, cyanosis, grunting, wheezing, pulmonary
congestion/edema, difficulty feeding, hepatomegaly,
diaphoresis, edema
- goal: reduce workload of heart and increase CO
- NRSG: monitor vitals, daily weights, RR for 1 min, strict I&O
digoxin and diuretics, Gavage feeding, energy saving
interventions
digoxin the ox: slows down the heart to contract strongly
- for CHF and arrhythmias
- assess apical HR for 1 min before admin (hold if too low)
- 1 hr before meals or 2 hr after
HF digoxin
- rinse out mouth or brush teeth
- Dig Toxicity: blurred vision, anorexia, poor feeding, n/v,
bradycardia, dysrhythmias (DO NOT REPEAT IF VOMITED)
0.8-2 ng/mL
foramen ovale hole b/t right and left atria
ductus arteriosus blood vessel that connects aorta to pulmonary artery (close within 72 hrs of
life)
acyanotic CHD (left->right = increase pulmonary blood flow)
- hole b/t atria
atrial septal defect (ASD) - systolic murmur
- surgical closure recommended before school age
- can lead to CHF and atrial dysrhythmias if not corrected
, acyanotic CHD (left->right = increase pulmonary blood flow)
- hole b/t ventricles
- loud, hard systolic murmur
ventricular septal defect (VSD)
- small holes may close spontaneously
- large defects -> Eisenmenger syndrome or CHF
- surgical closure
acyanotic CHD (left->right = increase pulmonary blood flow)
- blood vessel opening b/t aorta and pulmonary artery
- continuous machine-like murmur
patent ductus arteriosus (PDA)
- causes pulmonary HTN
- may require med indomethacin (NSAID) or surgical intervention to close
- can lead to CHF; increased risk of stroke, infection, aneurism
NSAID that inhibits prostaglandin E
indomethacin (PDA)
- helps to constrict PDA, closing patent ductus arteriosus
left to right shunt unrepaired -> pulmonary arteries are
overworked and stiffen -> permanent irreversible damage to
Eisenmenger syndrome
blood vessels in lungs that causes blood to reverse flow
*LIFE THREATENING
obstructive defect
- aorta gets pinched off and can't get enough blood to lower extremities
- obstructive narrowing of aorta (common in aortic valve or near DA)
coarctation of the aorta - systolic murmur with thrill
- uppers strong/bounding pulses and lowers weak/absent
- surgical correction with dilation
- increased risk of ischemic or hemorrhagic stroke and aneurysm
cyanotic defect with right->left blood flow
- pulmonary artery and aorta are swapped
transposition of the great
- incompatible with life (unless ASD, VSD, or PDA present)
vessels/arteries
- emergent infusion of prostaglandin E to keep DA open
- acts as smooth muscle relaxant
prostaglandin E1 (transposition of
GA/GV) - makes PDA
cyanotic defect with mixed blood flow
- pulmonary artery and aorta share trunk creating one vessel within the heart
truncus arteriosus - mixed blood to lungs and body
- increased pulmonary resistance
- surgical correction
cyanotic defect with mixed blood flow "RAPS"
1. Right ventricular hypertrophy
2. aorta displacement
3. pulmonary (valve) stenosis
Tetralogy of Fallot (TOF) 4. septal defect (VSD)
- 'tet' spells (decrease oxygenation saturation and
development of cyanotic appearance after crying, feeding,
activity, or when agitiated) relieved by squatting or knee-chest
position
- multiple surgeries required
Terms in this set (81)
- pulse oximeter on upper and lower extremities
NRSG cardiac screening - >24 hrs old before discharge
- thrill is not normal!
heart cannot pump as well as it should (fluid backs up in lung and
body does not get enough O2 rich blood) -> increase HR, thickened
walls, filling capacity decreases so less blood ejected
- causes: CHD
- sx: tachycardia, poor circulation, weight gain (fluid overload),
congestive HF tachypnea, SOB, cyanosis, grunting, wheezing, pulmonary
congestion/edema, difficulty feeding, hepatomegaly,
diaphoresis, edema
- goal: reduce workload of heart and increase CO
- NRSG: monitor vitals, daily weights, RR for 1 min, strict I&O
digoxin and diuretics, Gavage feeding, energy saving
interventions
digoxin the ox: slows down the heart to contract strongly
- for CHF and arrhythmias
- assess apical HR for 1 min before admin (hold if too low)
- 1 hr before meals or 2 hr after
HF digoxin
- rinse out mouth or brush teeth
- Dig Toxicity: blurred vision, anorexia, poor feeding, n/v,
bradycardia, dysrhythmias (DO NOT REPEAT IF VOMITED)
0.8-2 ng/mL
foramen ovale hole b/t right and left atria
ductus arteriosus blood vessel that connects aorta to pulmonary artery (close within 72 hrs of
life)
acyanotic CHD (left->right = increase pulmonary blood flow)
- hole b/t atria
atrial septal defect (ASD) - systolic murmur
- surgical closure recommended before school age
- can lead to CHF and atrial dysrhythmias if not corrected
, acyanotic CHD (left->right = increase pulmonary blood flow)
- hole b/t ventricles
- loud, hard systolic murmur
ventricular septal defect (VSD)
- small holes may close spontaneously
- large defects -> Eisenmenger syndrome or CHF
- surgical closure
acyanotic CHD (left->right = increase pulmonary blood flow)
- blood vessel opening b/t aorta and pulmonary artery
- continuous machine-like murmur
patent ductus arteriosus (PDA)
- causes pulmonary HTN
- may require med indomethacin (NSAID) or surgical intervention to close
- can lead to CHF; increased risk of stroke, infection, aneurism
NSAID that inhibits prostaglandin E
indomethacin (PDA)
- helps to constrict PDA, closing patent ductus arteriosus
left to right shunt unrepaired -> pulmonary arteries are
overworked and stiffen -> permanent irreversible damage to
Eisenmenger syndrome
blood vessels in lungs that causes blood to reverse flow
*LIFE THREATENING
obstructive defect
- aorta gets pinched off and can't get enough blood to lower extremities
- obstructive narrowing of aorta (common in aortic valve or near DA)
coarctation of the aorta - systolic murmur with thrill
- uppers strong/bounding pulses and lowers weak/absent
- surgical correction with dilation
- increased risk of ischemic or hemorrhagic stroke and aneurysm
cyanotic defect with right->left blood flow
- pulmonary artery and aorta are swapped
transposition of the great
- incompatible with life (unless ASD, VSD, or PDA present)
vessels/arteries
- emergent infusion of prostaglandin E to keep DA open
- acts as smooth muscle relaxant
prostaglandin E1 (transposition of
GA/GV) - makes PDA
cyanotic defect with mixed blood flow
- pulmonary artery and aorta share trunk creating one vessel within the heart
truncus arteriosus - mixed blood to lungs and body
- increased pulmonary resistance
- surgical correction
cyanotic defect with mixed blood flow "RAPS"
1. Right ventricular hypertrophy
2. aorta displacement
3. pulmonary (valve) stenosis
Tetralogy of Fallot (TOF) 4. septal defect (VSD)
- 'tet' spells (decrease oxygenation saturation and
development of cyanotic appearance after crying, feeding,
activity, or when agitiated) relieved by squatting or knee-chest
position
- multiple surgeries required
