NU 435 — Pediatric Nursing
Chapter 27: The Child with Cardiac Dysfunction
Final Exam Study Notes | NCLEX-Focused | Spring 2026
★ EXAM TIP: Tetralogy of Fallot is the most highly tested cardiac defect on NCLEX. Kawasaki
disease (especially aspirin use), SVT management, and digoxin pediatric considerations are also
top-yield topics.
1. Core Concept: Blood Flow Direction
Left ventricle systolic pressure ~120 mmHg vs. right ventricle ~25 mmHg. Blood always flows LEFT
→ RIGHT through any hole (high pressure to low pressure).
Fetal Structures (close at birth with O2 + pressure change)
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PDA (Patent Ductus Arteriosus) — connects aorta ↔ pulmonary artery; bypasses lungs in utero
PFO (Foramen Ovale) — connects RA ↔ LA; bypasses lungs in utero
Ductus Venosus — bypasses liver in utero
Premature infants: PDA may remain open → indomethacin (best), ibuprofen, or high-dose acetaminophen
to close it
NSAIDs close the ductus — reason pregnant women should NOT take NSAIDs (risk of closing fetal PDA)
Oxygen Saturation Reference
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Normal O2 saturation: ≥ 95%
Deoxygenated (venous) blood returning to right side: ~70–80%
Mixing lesion → SATs fall between those two values
CHD Classification — 4 Categories
Category
Color
Defects
Key Pattern
↑ Pulmonary Blood
Flow
PINK (acyanotic)
ASD, VSD, PDA, AVC
L→R shunt; CHF signs;
murmur
Obstructed Systemic
Flow
PINK/Shock
AS, CoA
Shock picture; 4extremity BP difference
↓ Pulmonary Blood
Flow
BLUE (cyanotic)
TOF, PS, PA, TA
Ductal-dependent; TET
spells; clubbing
Mixed Blood Flow
BLUE/Purple
TAPVR, TGA, Truncus,
HLHS
Near-complete mixing;
all need ASD
2. Congestive Heart Failure (CHF)
Clinical Manifestations
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Tachycardia — primary compensation for poor cardiac output
Sweating — especially with feeding in infants (HALLMARK: sweaty baby = something is wrong)
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Decreased urine output — kidneys need ~40% of cardiac output
Fatigue, weakness, restlessness, poor weight gain
Gallop rhythm, cardiomegaly — heart working overtime
Pulmonary congestion: grunting, flaring, retracting, tachypnea, crackles, cough, cyanosis
Systemic overload: hepatosplenomegaly, peripheral edema, JVD
Pale skin, delayed cap refill, poor pulses
Nursing Management
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Strict I&O — volume balance is critical in cardiac patients
Daily weights — same time, same clothing, same scale every day
Monitor ALL vitals including temperature — fever ↑ HR → ↑ cardiac demand → cardiac stress
HOB elevated — improves breathing; prevents atelectasis
Fluid restriction — minimize fluid overload on an already-stressed heart
Reduce strenuous activity; treat fever/infections promptly
Nutrition maintenance — high caloric demand even at rest (stress state burns calories)
Infection control — illness can rapidly decompensate these children
Developmentally appropriate stimulation — long hospital stays common
Skin assessment — edema → high risk for breakdown
Teaching family about all aspects of care
CHF Medications — Key Nursing Considerations
Drug
Purpose
Key Nursing Considerations
Digoxin
↑ contractility (squeeze);
slows HR
Check HR before giving — hold if below age-specific
threshold (NOT adult <60 rule). Check potassium. Watch
for bradycardia, arrhythmias. OTC/herbal interactions.
High toxicity risk.
Furosemide
(Lasix)
Diuretic — ↓
preload/volume
Monitor electrolytes (especially K+). Strict I&O.
Ototoxicity (high-yield NCLEX). First-line diuretic for
CHF.
ACE Inhibitors
(-pril: captopril,
enalapril)
↓ afterload and preload; ↓
SVR
Monitor BP. Watch for COUGH (very NCLEX testable).
Monitor edema and fluid balance.
Beta Blockers
(-lol:
metoprolol,
labetalol)
↓ HR and BP
Monitor HR and BP. Monitor GLUCOSE — especially in
infants and diabetics. Do NOT discontinue abruptly →
rebound tachycardia/hypertension.
DIGOXIN PEDIATRIC RULE: Hold threshold is AGE-BASED (e.g., hold if HR <110, <120, etc.
depending on age), NOT the adult rule of <60. Always verify the specific order and check the most
recent potassium before giving.
Digoxin toxicity- vomiting.
3. Increased Pulmonary Blood Flow (Acyanotic/Pink)
Pattern: Left → Right shunt. Lungs get excess blood → CHF signs. If untreated → pulmonary HTN
→ right ventricular hypertrophy → may become cyanotic over time.
Defect
What It Is
Symptoms
Management
VSD
(Ventricular
Septal Defect)
— Most common
CHD
Hole between
ventricles; L→R shunt
Murmur; CHF signs if
large; high risk respiratory
infection
Small: may close
spontaneously. Large: surgical
patch, suture, or device closure
via cath lab
ASD (Atrial
Septal Defect)
Hole between atria;
L→R shunt
Murmur; CHF signs; often
asymptomatic early
Device closure (cath lab) or
surgical patch; requires
cardiopulmonary bypass
PDA (Patent
Ductus
Arteriosus)
Ductus fails to close;
aorta ↔ PA
connection persists
Murmur; CHF; especially
in premature infants
Medical: indomethacin (best),
ibuprofen, or acetaminophen
(high-dose). Surgical: ligation
or Piccolo device closure
AV Canal (AVC)
Combined ASD + VSD
+ valve defects.
Associated with
Trisomy 21
CHF develops faster;
valve dysfunction; murmur
Surgical: patch holes and
repair/replace affected valves
(mitral, tricuspid)
MURMUR IN DELIVERY ROOM = most likely a VALVE problem (not ASD/VSD) — pressures have not
yet equilibrated at birth.
4. Decreased Pulmonary Blood Flow (Cyanotic/Blue)
Pattern: Not enough blood reaching lungs → chronic hypoxia → cyanosis, clubbing, polycythemia,
developmental delay. ALL are DUCTAL DEPENDENT — require Prostaglandin E1 (PGE1) to survive
until intervention.
Key Features (4
Components for TOF)
Symptoms
Management
Tetralogy of
Fallot (TOF) ★
MOST TESTED
4 defects: (1) Pulmonary
stenosis, (2) RV
hypertrophy, (3) VSD, (4)
Overriding aorta
Cyanosis; murmur;
TET spells; squatting
behavior in older
children
Surgical: fix pulmonary valve +
close VSD + reposition aorta.
TET spell management critical.
Pulmonary
Stenosis (PS)
Narrowed pulmonary
valve; stenosis =
narrowing
Murmur; mildmoderate cyanosis
depending on severity
Balloon dilation/valvuloplasty via
cath lab; valve replacement if
severe
Tricuspid Atresia
(TA)
Tricuspid valve absent;
RV underdeveloped;
must have ASD for
survival
Cyanosis; depends on
ASD size for mixing
PGE1; staged single-ventricle
palliation
Defect
TET Spells (Hypercyanotic Spells) — ★ PRIORITY NURSING INTERVENTION
TET spells can progress to cardiac arrest if not immediately recognized and treated. This is one of
the biggest nursing-driven interventions in pediatric cardiac care.
Triggers
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Crying, agitation, pain, fear, anxiety
Fever, infection, dehydration
Any elevated metabolic state (e.g., illness in hospital)
Pulmonary stenosis worsens acutely → less blood to lungs → acute onset cyanosis
Signs of a TET Spell
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Sudden severe cyanosis — blue lips, tongue, mucous membranes
O2 SATs can drop to 40%, even 12% in severe cases
Tachycardia, tachypnea
Pale, diaphoretic, poor pulses
Altered LOC, possible seizures if prolonged hypoxia
TET Spell Management — In Order
1. KNEE-TO-CHEST POSITION — increases venous return, ↑ SVR, fights elevated pulmonary pressures.
Older kids will spontaneously squat. FIRST and easiest intervention.
2. REMOVE irritating stimulus — minimize procedures, reduce crying/pain, quiet environment
3. OXYGEN — potent pulmonary vasodilator; helps relax reactive pulmonary vasculature
4. MORPHINE IV — peripheral vasodilation, relaxes pulmonary vasculature, sedation/analgesia (not fentanyl
— chosen specifically for pulmonary effects)
5. IV FLUID BOLUS — increases volume to counteract elevated pulmonary pressures (same mechanism as
knee-chest position)
6. CALL FOR HELP immediately — too many simultaneous interventions for one nurse; staff assist
PREVENTION: Use numbing cream, child life specialists, best blood drawers, warm environment —
minimize anything that makes the child cry or become agitated. Prevent fever, infection,
dehydration.
Long-Term Complications of Decreased Pulmonary Flow (Chronic Hypoxia)
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Clubbing of fingers/toes — chronic hypoxia to distal tissue
Polycythemia — body produces more RBCs to extract more oxygen (chronic low O2)
Developmental delay — chronic lower level oxygenation to brain
SATs can be chronically in 70s in some single-ventricle children
5. Obstructed Systemic Blood Flow (Acyanotic/Shock-Like)
Pattern: Blood cannot effectively exit left heart to body → SHOCK picture: hypotension, delayed
cap refill, poor pulses, decreased UO, altered mentation, end-organ dysfunction.
Defect
What It Is
Unique Finding
Management
Coarctation of
the Aorta (CoA)
Narrowing of aorta (near
ductus insertion); blood
can't reach lower body
4-EXTREMITY BP
DISCREPANCY: right arm
HIGH (pre-ductal), legs/left
arm LOW (post-ductal).
Bounding upper pulses,
weak lower pulses.
Pre/post-ductal SAT
difference on CHD screen.
PGE1 to keep PDA open;
surgical resection +
anastomosis; stent or
balloon dilation in older
children
CoA NCLEX KEY: Why do we take 4-extremity blood pressures on a newborn? → To screen for
Coarctation of the Aorta. Right arm (pre-ductal) will be hypertensive; lower extremities will be
hypotensive/weak pulses.
CoA in adolescents: Can present as unexplained persistent hypertension in one arm. Screen with 4extremity BPs.
6. Mixed Blood Flow (Cyanotic — Near-Complete Mixing)
Defect
Key Feature
Survival Requires
Management
TAPVR (Total
Anomalous
Pulmonary
Venous
Return)
All 4 pulmonary veins
connect to wrong
location (not left
atrium). Types:
supracardiac,
intracardiac, infradiaphragmatic
Must have ASD
(TA also needs ASD)
Reconnect all pulmonary veins to
left atrium; close ASD
TGA
(Transposition
of Great
Arteries)
Aorta from RV;
pulmonary artery from LV
→ two parallel circuits.
Baby born EXTREMELY
BLUE.
Must have ASD
(PFO) + PGE1. May
need balloon atrial
septostomy (BAS)
emergently.
Arterial switch procedure (reanastomose aorta + PA; reimplant
coronary arteries). Great outcomes
if caught early.
Truncus
Arteriosus
Single great vessel
(trunk) instead of
separate aorta + PA →
near-complete mixing
(~50% SATs)
Must have VSD
Assign trunk as aorta; create
conduit from RV to PA. Palliative —
conduit replacements needed as
child grows. May need transplant.
HLHS
(Hypoplastic
Left Heart
Syndrome) —
"Half a Heart"
Left side severely
underdeveloped (no flow
→ no growth in utero).
Right side normal.
Must have ASD;
PGE1 critical
3-staged palliation (Norwood →
Glenn → Fontan). NOT curative.
Stage 3 often fails in teenage years
→ transplant.
TGA RECOGNITION: Baby born blue that does NOT improve with oxygen → think TGA, not
respiratory. SATs may be in 70s even on high-flow O2.
Balloon Atrial Septostomy (BAS) for TGA: catheter fed across ASD, balloon inflated and
FORCEFULLY PULLED to tear septum open → emergent bedside procedure to increase mixing until
surgery.
7. Prostaglandin E1 (PGE1) — Must Know
Purpose & Use
Side Effects (3 Major)
Keeps ductus arteriosus OPEN by relaxing smooth
muscle in ductus wall. Used for ALL ductaldependent lesions: PS, TA, TOF (severe), CoA,
HLHS, TGA. IV ONLY — patient must be
hospitalized. Bridge to surgery/cath intervention —
NOT a long-term fix. Administered continuously until
definitive intervention.
1. APNEA — most dangerous; requires respiratory
support readiness. 2. HYPOTENSION. 3. FEVER.
Seizures rare but documented. These are ICU-level
patients due to these risks. Must have monitoring
equipment and airway support at bedside.
8. Cardiac Catheterization — Pre & Post
Pre-Procedure
Post-Procedure (Femoral Access)
• NPO (will receive sedation) • Document BASELINE
perfusion: all pulses, cap refill, BP all extremities (to
compare post-procedure) • Developmentally
appropriate preparation • Address family and child
anxiety • Baseline vital signs
• Direct pressure for ~15 minutes immediately postprocedure • BED REST WITH LEG EXTENDED — 4
to 6 hours (do NOT flex leg → disrupts clot) •
Limited activity for ~2 days after (clot formation not
complete) • Assess dressing for bleeding (increasing
drainage = remove and reassess) • Advance diet as
tolerated • Monitor for signs of infection at site •
Monitor neurovascular checks: pulse, warmth, cap
refill, sensation of affected extremity
9. Acquired Cardiac Conditions
9A. Infective Endocarditis
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Etiology: Bacterial colonization of heart valves. Risk ↑ with prior cardiac surgery, synthetic valves,
catheterizations, any heart intervention
Bacteria can also colonize on a healthy valve — not exclusive to surgical hearts
Manifestations: Flu-like, insidious onset — low-grade fever, fatigue, weight loss, malaise, weakness,
gallop rhythm, emboli risk
Diagnosis: Clinical + blood cultures + echocardiogram (look for vegetations on valves)
Management: Long-course IV antibiotics; monitoring
★ NCLEX KEY: Antibiotic prophylaxis BEFORE DENTAL PROCEDURES for any child with a valve
repair, replacement, or prior cardiac surgery. Dental procedures → bacteria enter bloodstream via
gingival tissue → risk of seeding heart valves.
9B. Rheumatic Fever
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Etiology: Untreated Group A Streptococcus (strep throat) → autoimmune sequela 2–4 weeks later. Not
everyone — combination of untreated infection + susceptibility.
Targets: MITRAL VALVE most commonly affected
Diagnosis: Jones Criteria — specific checklist of findings must be met (similar to JIA criteria)
Often self-limited but can cause permanent valve damage
Management: Treat original strep infection; symptom management; prevent recurrence
PREVENTION IS KEY: Treat strep throat early with antibiotics to prevent rheumatic fever. This is the
best nursing education point for families.
9C. Kawasaki Disease ★ HIGH YIELD
Only pediatric condition where HIGH-DOSE ASPIRIN is used therapeutically. Normally aspirin is
CONTRAINDICATED in children (Reye's syndrome risk). NCLEX TRAP: If you see aspirin + pediatric
patient → Kawasaki disease!
Acute systemic vasculitis of unknown cause. Affects all vessels, but coronary arteries are the critical concern.
Diagnostic Criteria — ≥5 Days Fever PLUS at Least 4 of 5 Findings
Criterion
Description
Fever ≥5 days
High fever (103°F+) for 5 or more days. Less than 5 days = not Kawasaki. Must be
persistent and non-responsive to antibiotics.
Conjunctival
injection
BILATERAL red eyes WITHOUT discharge/pus — not infected, blood vessels
are inflamed (vasculitis)
Oral changes
Strawberry tongue (red, bumpy); dry, cracked, bright red lips; erythema of oral
mucosa
Extremity changes
Swollen, red hands and feet → peeling of fingers and toes (desquamation); red
palms and soles
Polymorphous rash
Multiple shapes and appearances; looks different in different body areas; not a
specific type of rash
Cervical
lymphadenopathy
Neck lymph node swelling ≥1.5 cm; usually unilateral
Management
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IVIG (IV immunoglobulin) — calms the immune response; reduces inflammation
HIGH-DOSE ASPIRIN — stabilizes coronary artery dilation and aneurysms; then tapered to low-dose
Anticoagulation may be added — coronary artery aneurysm → clot risk → risk of MI in a child
Serial echocardiograms — monitor coronary artery dilation/aneurysm formation
REAL DANGER: The visible signs (fever, rash, red eyes, etc.) are uncomfortable but resolve. The
danger is CORONARY ARTERY ANEURYSM and risk of MI in a child. This is why aspirin and
monitoring are critical.
10. Dysrhythmias
Bradydysrhythmias
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Children's cardiac arrests are 99% RESPIRATORY in origin — not cardiac (opposite of adults)
Cause 1: Hypervagal tone — children are notoriously prone to vagal activation (crying, bearing down, rectal
temperature, anger) → HR drops
Cause 2: Hypoxia — treat the underlying hypoxia, HR normalizes
Hypotension can cause reflex bradycardia (usually transient)
AV Blocks: Consider LYME DISEASE — can cause 3rd degree heart block requiring pacing; resolves
with treatment
Supraventricular Tachycardia (SVT) — Most Common Pediatric Arrhythmia
Criteria for SVT
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Heart rate: >180 bpm in a child; >220 bpm in an infant (NOT SVT if below these thresholds)
NON-VARIABLE heart rate — 222…222…222 regardless of activity, crying, sleeping
No P waves on EKG — supraventricular = no atrial kick; P waves absent (QRST QRST QRST)
Caused by accessory pathway; Wolff-Parkinson-White syndrome associated
Can occur in structurally normal hearts
SVT Management
Status
First Line
Second Line
Compensated
(normal BP, mental
status, perfusion)
Vagal maneuvers: ice bag to face
(diving reflex), Valsalva, blow into
obstructed straw, rectal temperature
ADENOSINE IV — give in antecubital
(AC) closest to heart; stopcock method;
push adenosine immediately followed
by rapid flush (half-life = seconds). May
see brief flat line then conversion. Can
repeat doses.
Uncompensated
(hypotension,
altered mental
status)
Adenosine if immediately available
SYNCHRONIZED CARDIOVERSION
(electricity)
ADENOSINE KEY POINTS: Must be given in antecubital (AC) — NOT hand or foot. Use stopcock
method. Push adenosine then IMMEDIATELY push flush. Half-life is seconds. Patient may have a
brief flat line before converting — prepare family and team.
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Long-term management: Beta blockers until accessory pathway ablation (burn out the extra pathway)
Dilated cardiomyopathy = most common type in children; presents like CHF
11. Heart Transplant — Key Nursing Point
DO NOT give LIVE VACCINES to immunosuppressed transplant patients. This is a critical patient
safety/NCLEX point.
Quick Reference: Full Defect Summary
Category
Defects
Color
High-Yield Point
↑ Pulmonary Blood
Flow
ASD, VSD, PDA, AV
Canal
PINK
L→R shunt; CHF; murmur;
premature infants → PDA; Trisomy
21 → AV Canal; indomethacin
closes PDA
↓ Pulmonary Blood
Flow
TOF ★, PS, PA, TA
BLUE
Ductal-dependent; TET spells (kneechest, O2, morphine, fluid); clubbing,
polycythemia
Obstructed Systemic
Flow
AS, CoA
PINK/Shock
CoA: 4-extremity BP discrepancy
(right arm HIGH, legs LOW); PGE1;
screen with CHD screen
Mixed Blood Flow
TAPVR, TGA,
Truncus, HLHS
BLUE/Purple
TGA: blue at birth, doesn't improve
with O2; BAS; arterial switch. HLHS:
3-stage palliation. ALL need ASD.
Acquired Conditions
Endocarditis,
Rheumatic fever,
Kawasaki, SVT
N/A
Endocarditis: dental prophylaxis.
Rheumatic: treat strep early.
Kawasaki: high-dose aspirin (only
pediatric exception) + IVIG. SVT:
non-variable HR, adenosine via AC.
NU 435 | Chapter 27 | Final Exam Study Guide | Spring 2026