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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
B11
Cardiology Review
Lyn Vargo, PhD, NNP-BC
Clinical Assistant Professor
Stony Brook University
NNP Program
University of Missouri, Kansas City
The speaker has signed a disclosure form and indicated she has no significant financial interest or relationship with the
companies or the manufacturer(s) of any commercial product and/or service that will be discussed as part of this presentation.
Session Summary
This presentation will provide an overview of cyanotic, acyanotic, obstructive, and other congenital heart
defects. There will also be a brief discussion regarding tacharrhythmias, brady arrhythmias, and pulseless
arrests, as well as compensated, decompensated, and irreversible shock.
Session Objectives
Upon completion of this presentation, the participant will:

understand principles related to cardiac physiology, neonatal cardiac physiology, fetal circulation,
transitional circulation and their relationship to congenital heart disease;

recognize characteristics of different acyanotic, cyanotic and obstructive cardiac lesions and their
typical presentation;

be able to describe specific management strategies for different categories of cardiovascular
problems;

be able to discuss different rhythm disturbances seen in the neonate;

recognize different types of shock and treatment strategies.
Test Questions
1. In fetal circulation:
a. Left ventricular output is higher than right ventricular output
b. About 30% of the combined ventricular output goes to the fetal lungs
c. Right ventricular output is higher than left ventricular output
2. In the neonatal autonomic nervous system:
a. The parasympathetic nervous system is more well developed than the sympathetic
nervous system
b. The sympathetic nervous system is more well developed than the parasympathetic
nervous system
c. Autonomic control of the heart rate is better controlled by catecholamine stimulation than
by vagal stimulation
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
3. Infants with acyanotic lesions (left-to-right shunt lesions) typically present:
a. At 2-3 days of age when the PDA closes
b. When the pulmonary vascular resistance falls
c. At birth
4. Which of the following drugs should be used to treat Wolff-Parkinson-White (WPW) Syndrome in
the neonate?
a. Digoxin
b. Verapamil
c. Propanolol
5. In tricuspid atresia treatment with PGE 1 to maintain ductal patency would:
a. Increase pulmonary blood flow
b. Increase systemic blood flow
c. Should not be used
6. A Blalock-Taussig shunt is:
a. An intra-atrial shunt that allows shunting of blood from the left atrium to right atrium
b. A shunt between a subclavian artery & a pulmonary artery that increases pulmonary blood
flow
c. An anastomosis between the aorta & pulmonary artery that provides systemic blood flow
References
Blackburn (2007). Maternal, fetal & neonatal physiology: A clinical perspective. Philadelphia: WB Saunders.
Brodsky & Martin (2003). Neonatology review. Philadelphia: Hanley Belfus, Inc.
Cloherty, et al. (2007). Manual of neonatal care. Philiadelphia: Lippincott-Raven Publishers.
Gomella, et al. (2009). Neonatology: Management, procedures, on-call problems, diseases & drugs. New York: McGrawHill.
Kenner, et al. (2007). Comprehensive neonatal nursing. St. Louis: Elsevier Saunders.
Martin, et al. (2006). Neonatal-perinatal medicine: Diseases of the fetus & infant. St. Louis: Mosby Elsevier.
Merenstein & Gardner (2006). Handbook of neonatal intensive care. St. Louis: Mosby Elsevier.
Park M.K. (2008). Pediatric cardiology for practitioners. St. Louis: Mosby Elsevier.
Polin, et al. (2008). Hemodynamics and cardiology: Neonatology questions & controversies. Philadelphia: WB Saunders.
Session Outline
See presentation handout on the following pages.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Basic Cardiovascular
Principles
Neonatal Cardiac
Review
Lyn Vargo,
PhD, RN, NNP-BC
Fetal Circulation
Key Points of Fetal Circulation
 The placenta not the lung is the organ of gas
exchange.
• Umbilical vein paO2 is 30-35 mmHg or 80-90%
saturated (Importance of fetal hemoglobin).
 Fetuses do not have a series circulation they have a
parallel
ll l circulation.
i l ti
Th
The right
i ht & lleft
ft ventricles
t i l each
h
eject different amounts of blood & both oxygenate
different parts of the body.
 The left ventricle provides the most oxygenated blood
to the heart, brain & upper extremities (preductal)
(1/3 of CVO) (paO2 26-28 or saturation of 65%).
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Key Points of Fetal Circulation
Transitional Circulation
 The right ventricle is primarily responsible for
supplying less oxygenated blood to the
descending aorta, lower body & placenta
(post ductal) (2/3 of CVO)(paO2 15-25—55%
saturated.))
 A very small amount of the blood coming from
the RV goes to the fetal lungs for growth &
development of the fetal lungs (^PVR in lungs)
(paO2 15-25—55% saturated).
 In the fetal heart right sided pressures are
higher than left sided pressures (by10-12%).
• Parallel circulation must change to
series circulation
• Immediate closure of ductus venosus &
foramen ovale.
• Closure of PDA at 48-96 hours of age
• Decrease in pulmonary vascular
resistance which occurs suddenly at
birth & then continues to decrease over
first 4-6 weeks of life.
Cardiac Output
4 Physiologic Components of
SV in the Neonate
 CO=HEART RATE (HR) X STROKE
VOLUME (SV)
 3 COMPONENTS OF STROKE
VOLUME:
1. preload
2. afterload
3. contractility
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 Heart rate—most important in determining
cardiac output in the neonate & fetus.
 Neonates have a decreased ability to increase
stroke volume because the fetal myocardium
has relatively few contractile elements & is
poorly innervated by the sympathetic nervous
system.
 Parasympathetic System predominates in the
neonate.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Most common signs of Cardiac
Disease
What about Murmurs?
 **Cyanosis—5mg/dl reduced hemoglobin in
the peripheral capillary blood.
 **Congestive Heart failure
 Respiratory Distress—occurs due to
increased pulmonary congestion.
congestion
 Most infant’s with cyanosis from cardiac
disease don’t have respiratory distress.
 If cyanosis is caused by fixed right-to left
shunt (cardiac lesion), increasing inspired O2
will have little effect.
 Remember, the absence of a murmur does
not rule out CHD. Up to 20% of infants who
die from CHD during the first month of life
don’t have a murmur.
 Innocent murmurs—Occur
murmurs Occur during first 48
hours, usually Grade I-II, are usually systolic,
and aren’t associated with other symptoms.
 Pathologic murmurs—Persist beyond 48
hours, may occur at birth, day 3, one week or
when PVR falls, may be louder than a Grade
II. May be diastolic.
Definition of Congestive Heart
Failure
Cause of Congestive Heart
Failure
 The blood supply to the body is
insufficient to meet the metabolic
demands of the organs
organs.
 CHF is a manifestation of an underlying
disease or defect, rather than a disease
itself.
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1. Volume Overload
2. Pressure Overload
3. Cardiomyopathy
4. Dysrhythmias
5. Anemia
6. Asphyxia
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Sympathetic Stimulation &
CHF
Signs & Symptoms of CHF











Tachycardia*
Hepatomegaly*
Tachypnea*
Cardiac Enlargement
Gallop Rhythm
Decreased peripheral pulses & skin mottling
Decreased Urine output
Diaphoresis
Decreased activity
Failure to thrive/feeding problems
Diminished cardiac output
Neonatal Shock
Types of shock
 Definition: Blood flow to tissues is inadequate
to meet metabolic requirements leading to
tissue hypoxia, metabolic acidosis, irreversible
cellular changes & subsequent cellular death.
 3 types:
 1. Compensated—usually vasoconstricted &
BP maintained.
 2. Decompensated– infant becomes
hypotensive.
 3. Irreversible—end organ failure/death
 Hypovolemic shock: perinatal events
(tight nuchal cord, cord avulsion, cord
prolapse, placental abruption, fetomaternal transfusion, birth trauma).
 Distributive shock: sepsis
 Cardiogenic shock: Asphyxia, metabolic
problems, CHD, arrhythmias, bacterial
or viral infection, obstruction to venous
return (pneumos).
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Acyanotic Heart Defects
 Typically present with Left-to-right shunting of
blood
 Lesions include PDA, VSD, ASD, AV canal
(Endocardial cushion defect)
g & symptoms
y p
include signs
g of p
pulmonary
y
 Signs
overcirculation & CHF
 Most typically won’t present until pulmonary
vascular resistance has fallen at 4-6 weeks of
age (exceptions are PDA in preterm infant &
AV canal)
 May present with some signs of respiratory
distress due to pulmonary over circulation
Patent Ductus Arteriosus
c

l





Presents with pulmonary
overcirculation
Bounding pulses
Widened pulse pressure
G d II-IV/VI
Grade
IV/VI continuous
ti
or “machinery” murmur
Preemies may present
with systolic murmur.
Cardiomegaly &
increased pulmonary
congestion on x-ray
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Left-to-right Shunt Lesion CXR
Typical Findings:
Cardiomegaly
Increased pulmonary
vascular markings
Ventricular Septal Defect
 Most common cause of
CHF.
 Harsh, Pansystolic
murmur best heard at
3rd-4
3rd
4th left ICS at sternal
border
 CXR shows cardiomegaly
& ^ PV markings.
 Size of defect will
determine presentation &
management.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Atrial Septal Defect
 3 types.
 Rarely develop failure.
 May have a Grade II/III/VI
systolic ejection murmur
best heard at upper left
sternal border.
 S2 may be widely split &
fixed (older infants).
Cyanotic Lesions
 Cyanotic Lesions with decreased pulmonary blood
flow (usually not in respiratory distress):
Tricuspid atresia
Tetralogy of Fallot
Tricuspid Insufficiency (perinatal asphyxia).
Ebstein’s
Ebstein
s Anomaly
Typically blood is shunted from right side of heart to left
side of heart
Cyanosis may initially only occur with crying
Level of cyanosis dependent on amount of blood flow to
the lungs.
CXR generally have decreased pulmonary markings.
Oligemic

AV Canal
 30% occur in infants with
Downs.
 May be complete or
partial.
yp
yp
present with
 Typically
failure early due to
shunting at both atrial &
ventricular level.
 Grade III-IV/VI
holosystolic regurgitant
murmur at lower left
sternal border.
Right-to-Left Shunt Lesion CXR
 Prostaglandin
generally life saving
with these cyanotic
lesions by providing
pulmonary blood flow
from systemic
circulation.
.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Cyanotic Lesions
 Cyanotic Lesions with increased pulmonary
blood flow (generally mixing lesions):
Transposition
Truncus Arteriosus
TAPVR
Mixing or separation of pulmonary venous return
& systemic venous return.
Many of these infants will have CHF as well &
some respiratory distress.
CXR will have normal or increased PV markings
& ? Big heart.
Tetralogy of Fallot
 1. Large VSD.
 2. Pulmonary stenosis or
right ventricular outflow
obstruction.
g aorta
 3. Overriding
 4. Hypertrophied Right
ventricle.
 Cyanotic. Pulmonary
blood flow may be duct
dependent.
 Grade III-V/VI systolic
ejection murmur at middle
& upper left sternal
border.
Management of Cyanotic
Lesions with Decreased Flow
Tricuspid Atresia
 Right ventricle may be
hypoplastic.
 More than 90% of
patients have a VSD
y be ductal dependent
p
 May
(especially if no VSD).
 Management is geared to
providing pulmonary
blood flow.
 A single S2 is often heard
in infants with tricuspid
atresia.
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 Prostaglandin—provides pulmonary blood
flow. From aorta to pulmonary artery to lungs.
 Palliative shunt—Blalock Taussig operation
(systemic to pulmonary shunt using Gor-Tex ).
 Definitive repair through a Fontan procedure
(communication between right atrium &
pulmonary artery) or a Glenn Procedure (SVC
to RPA) followed by a Fontan.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
TAPVR—Mixing Lesion
Cyanotic Lesions
with Increased
Flow Mixing
Flow---Mixing
Lesions
Transposition
 3 types.
 Pulmonary veins connect
to right atrium in one of
three ways.
 Complete cardiac mixing
of arterial & venous
blood.
 Blood flow to body is
totally dependent on flow
through right-to-left shunt
through patent foramen
or ASD.
 Murmurs are rare.
Ebstein’s Anomaly
 Parallel circuitry—
separate circuits for
pulmonary & systemic
blood.
 Only mixing of blood
g ASD,,
occurs through
VSD or PDA.
 Cyanosis apparent in
varying degrees.
 CXR variable vascularity.
 Murmurs if present are
those of associated
lesions.
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





Low insertion of tricuspid valve
which incorporates right
ventricle making it very small.
Tricuspid insufficiency present
in varying degrees.
Right-to-left shunting at
foramen.
Pulmonary blood flow
significantly decreased.
Huge heart on x-ray.
Nonspecific systolic murmur,
diastolic murmurs, clicks &
triple & quadruple rhythm
heard.
Dysrhythmias frequent—WPW
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Ebstein’s Anomaly CXR
Truncus Arteriosus—3 Types.
 One great vessel arises from
both ventricles with overriding
VSD.
 This artery has one valve &
gives rise to pulmonary,
coronary & systemic arteries.
 Mixing of blood occurs in the
common chamber.
 Varying degrees of cyanosis.
 S2 is single. Loud pansystolic
murmur often heard at LLSB.
Left Sided Obstructive Lesions
Left Sided Obstructive Lesion
CXR
 Will present with s/s of hypoperfusion & respiratory
 Occurs suddenly when the PDA closes. distress.
 Hypoperfusion (shock) is due to inadequate ejection
of blood by left ventricle into systemic
circulation=hypotension
circulation
hypotension & metabolic acidosis.
acidosis
 May have some degree of arterial desaturation, but
mostly lethargy, mottling, pallor, poor pulses, &
respiratory distress.
 CXR will show pulmonary congestion & cardiomegaly.
 Examples: HLHS, Coarctation of the aorta, & critical
aortic stenosis.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Coarctation of the Aorta
 Constriction or discrete
narrowing of aorta.
 Most commonly occurs at
junction of aorta & PDA
(juxtaductal).
 Blood flow to body occurs
through
g PDA. Once PDA
closes. Left ventricle must
pump very hard to get through
narrow area.
 Bicuspid aortic valve is
common (80%).
 VSDs are common (40%)
 Prostaglandin life saving for
providing blood flow to body
when PDA closes.
 BP differences.
Hypoplastic Left Heart Syndrome

1.
Clinical spectrum of:
Severe mitral stenosis or
atresia
2. Severe aortic stenosis or
atresia
3. Left ventricular hypoplasia
4
4.
Severe coarctation
Coronary artery flow is retrograde.
Systemic circulation depends on
PDA & prostaglandin!
Aren’t really cyanotic— shocky!
Cardiomegaly with increased
Pulmonary congestion.
Nonspecific systolic murmur in 2/3
of infants.
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Prostaglandin E1
 Must be given by continuous infusion
 Side effects include: Apnea, peripheral
vasodilation (flush), hypotension, fever,
seizures, bradycardia, irritability, muscle
twitching or jitteriness
jitteriness, lethargy
lethargy,
hypoglycemia, hypocalcemia,
hyperbilirubinemia, diarrhea, and
thrombocytopenia.
 Dose: Initial 0.05-0.1micrograms/kg/minute.
Use smallest dose possible
 Maintenance 0.01-0.05micrograms/kg/min
Hypoplastic Left Heart
Syndrome Treatment
 Surgery—Norwood initially. Glenn shunt
& then Fontan.
 Transplantation
 Palliative Care
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Critical Aortic Stenosis
Aortic Stenosis
 Obstruction of the valve can occur above the
valve (supravalvular), at the aortic valve
(valvular) or below the valve (subvalvular).
 Valvular is most common.
y
murmur in upper
pp
 Grade II-IV/VI harsh systolic
right sternal border. The intensity of the
murmur is unrelated to the severity of the
obstruction.
 Infants have CHF due to pressure load of left
ventricle.
 Can appear shocky when PDA closes.
Prostaglandin helpful.
Rhythm Disturbances
 Tachyarrhythmias
1. sinus tachycardia
2 **supraventricular
2.
supraventricular
tachycardia
 Bradyarrhythmias
 Pulseless arrest
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Dysrhythmias
 Benign : sinus bradycardia, sinus tachycardia, sinus
dysrhythmias. Generally require no treatment.
 Pathologic: SVT (most common), Atrial flutter &
fibrillation, V-tach & complete AV block.
1. SVT is a result of dual AV nodal pathways , rapid
g an accessory
y bundle ((Ex: WPW),
),
conduction through
or the existence of an ectopic atrial pacemaker. HR
over 200. No change in HR with activity. Regular RR.
 12-24 hours after occurs, infant will develop CHF.
 Treatment includes, vagal maneuvers, adenosine,
cardioversion (Use Synchronous mode always only!!).
 Medications used after conversion include Digoxin
(not with WPW though), propranolol IV (no CHF),
esmolol, amiodarone, flecainide or procainamide.
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FANNP 24TH NATIONAL NNP SYMPOSIUM: CLINICAL UPDATE AND REVIEW
Dysrhythmias
2. Atrial
Bradyarrhythmias
flutter is diagnosed when the atrial rate is greater
than 220 minute. P waves are regular, characteristic
saw-tooth pattern.
 Often suggests serious organic heart disease.
 Ventricular rate will depend on degree of AV block.
 Atrial fibrillation very rare & is also almost always
associated with serious heart disease.
 Difficult to treat.
3. Ventricular Tachycardia is also associated
with severe disease. Use DC cardioversion. Lidocaine
also helpful.Maintenance treatment includes, inderal
lidocaine, phenytoin, lidocaine, procainamide or
amiodarone.
4. In complete AV block the ventricular rate is
slower than atrial rate & there is no
association b/w these rates. Bradycardia.
 There is a strong association b/w this &
maternal collagen disorders (Lupus).
 Treatment isn’t necessary unless HR slow &
failure occurs. Will need pacemaker. Can try
Isoproterenol may be tried to ^ rate until pacer
in.
Electrolytes & Drugs Effects
on Cardiac Rhythm Strips
Hypertrophic
Cardiomyopathy
 Digoxin toxicity—May cause decreased Heart
rate, prolonged PR interval, AV block.
 Hypokalemia (<2.5)—depressed ST segment,
biphasic T wave, Prominent U wave. May
develop prolonged PR & block
 Hyperkalemia—Tall T wave (K >6.0)
 >7.5, long PR interval, wide QRS duration,
Tall T wave
 >9.0 absent P wave, sinusoidal QRS wave,
asystole and ventricular fibrillation can occur.
 Hypocalcemia—Prolonged QT interval
 Hypercalcemia—Shorter QT interval
 Increased myocardial fiber size and # causes
hypertrophy of the ventricle with smaller than normal
ventricular cavity.
 The heart contracts better, but filling is impaired by
relaxation abnormalities. Subaortic obstruction may
occur.
 Often seen in IDMs is thought to be due to
hyperinsulinemia.
 Ventricular septum wall is usually more hypertrophied.
 CHF can develop as well as gallops & systolic
murmur along LSB. Cardiomegaly evident.
 Generally resolves spontaneously, but treatment
includes general supportive care, B-adrenergic
blockers (propranolol). Do NOT use digoxin.
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