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Neonatal CCRN/CCRN‐K Certification Review Course:
Cardiovascular
Nancy McNeillRNC‐NIC, MSN, CNS, CPNP
12/2015
Cardiovascular 1
Testable Nursing Actions
Apply leads for cardiac monitoring
Identify, interpret, and monitor cardiac rhythms
Monitor hemodynamic status and recognize signs and symptoms of hemodynamic instability
Recognize normal fetal circulation and transition to extrauterine life
Recognize indications for and manage patients requiring
12‐lead ECG
Arterial catheter
Cardiac catheterization
Cardioversion
Central venous pressure monitoring
Invasive hemodynamic monitoring
Umbilical catheter
Fetal Circulation
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Cardiovascular 2
Transitional Circulation
Closing of fetal shunts
Once the baby is delivered: The placenta no longer oxygenates the blood
The lungs facilitate gas exchange in the infant
Newborn Circulation
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Cardiovascular 3
Cardiac Output
Volume of blood ejected by the heart in 1 minute
Normal 120–200 mL/kg/min
CO=SV x HR
Preload
Volume of blood in ventricles before the heart contracts
Delayed cord clamping
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Cardiovascular 4
Afterload
The resistance of blood leaving the ventricle
Afterload is dependent on systemic vascular resistance and pulmonary vascular resistance
Shock
Hypovolemic
Distributive
Cardiogenic
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Cardiovascular 5
Most Common Dysrhythmias
Sinus tachycardia
Sinus bradycardia
Supraventricular tachycardia
Complete heart block
Atrial flutter
Hyperkalemia
Placement of Cardiac Leads
Lead 1 is best lead for changes in P waves
Pilcher J. Pocket Guide to Neonatal EKG Interpretation.NICU INK Book Publishers; 2004.
12/2015
Cardiovascular 6
Sinus Tachycardia
HR=180–220
Brief episodes can be normal
Common causes: Hypovolemia
Hyperthermia
Pain
Infection
Shock
Hydrops
Pilcher J. Pocket Guide to Neonatal EKG Interpretation.NICU INK Book Publishers; 2004.
No treatment if the condition is transient
Treat the underlying cause of shock or respiratory failure
Sinus Tachycardia Treatment
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Cardiovascular 7
Sinus Bradycardia
HR <90
Responsible for 30% of arrhythmias in infants
Most common in premature infants
Common causes: Immaturity of central nervous system
Vagal stimulation
Apnea
Medication
Heart disease
Sinus node disease
Srinivasan S, et al. HHS Public Access. Accessed June 19, 2015.
Sinus Bradycardia
Pilcher J. Pocket Guide to Neonatal EKG Interpretation.NICU INK Book Publishers; 2004.
12/2015
Cardiovascular 8
Important to assess infant’s respiratory status
Stimulate or provide respiratory support
If bradycardia continues, begin resuscitation based on NRPguidelines
Bradycardia is most often the result of hypoxia causing a depression of the myocardium or slowing of the heart rate
Sinus Bradycardia Treatment
HR >220
Most common dysrhythmia in newborns Occurs in 1.5–4/1,000 neonates
Causes Cardiac defects
Wolff‐Parkinson‐White Syndrome
Myocarditis
Supraventricular Tachycardia
Cloherty JP, et al. Manual of Neonatal Care.Moak JP. Prog Pediatr Cardiol. 2000;11(1):25–38.
Pilcher J. Pocket Guide to Neonatal EKG Interpretation. NICU INK Book Publishers; 2004.
12/2015
Cardiovascular 9
Supraventricular Tachycardia Treatment
Determine stable vs unstable supraventricular tachycardia (SVT)
If stable, consider vagal maneuver and/or adenosine
If unstable or vagal maneuver unsuccessful, treat with adenosine, propranolol, procainamide, or amiodarone
Infants who are in shock or congestive heart failure need rapid treatment of SVT IV adenosine if IV access
Synchronized cardioversion
Complete Heart Block
1 in 22,000 births
Mothers with lupus
Complete blockage of impulse between atria and ventricles
Friedman D, et al. Images Paediatr Cardiol. 2003;5(3):36–48.Pilcher J. Pocket Guide to Neonatal EKG Interpretation.
NICU INK Book Publishers; 2004.
12/2015
Cardiovascular 10
Complete Heart Block
Causes
Infections
Congenital heart defects
Myocarditis
Trauma
Lupus
Genetic
Complete Heart Block
Treatment Temporary or permanent pacing
Isoproterenol
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Cardiovascular 11
Atrial Flutter
Sawtooth appearance on EKG
Causes Damage to sinus node
Congenital heart disease
Cardiac catheterization
Digoxin toxicity
Occurs most often in structurally normal heart
Pilcher J. Pocket Guide to Neonatal EKG Interpretation.NICU INK Book Publishers; 2004.
Atrial Flutter
Treatment Digoxin
Propranolol
If unstable, then cardioversion
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Cardiovascular 12
Hyperkalemia
Serum potassium >6.5 meq/L
Causes Hemorrhage
Bruising
Prematurity
Acidosis
Renal failure
Verklan MT, et al. Core Curriculum for Neonatal IntensiveCare Nursing. Elsevier Saunders; 2015.
Hyperkalemia
Causes tall tented T wave and disappearance of P wave and widening of the QRS This is abnormal conduction through the ventricle
Appears like v tach but is NOT
Treatment Diuretic depletes potassium; secretion of potassium from urine
IV calcium
Glucose/insulin infusion to push potassium into cell
Sodium bicarbonate to correct acidosis
Albuterol pushes potassium into cell
Sodium polystyrene sulfonate (Kayexalate) removes potassium
CARDIOVERSION DOES NOT WORK
Merenstein GB, et al. Handbook of Neonatal Intensive Care.Mosby; 2011.
12/2015
Cardiovascular 13
Cardiac Defects
Cyanotic Tetralogy of Fallot (TOF)
Transposition of the greater arteries (TGA) or vessels (TGV)
Truncus arteriosus
Tricuspid Atresia
Hypoplastic Left Heart Syndrome (HLHS)
Acyanotic Patent ductus arteriosus (PDA)
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Atrioventricular canal (AVC)
Pulmonic stenosis (PS)
Aortic stenosis (AS)
Coarctation of the aorta
Cardiac Defects
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Cardiovascular 14
Tetralogy of Fallot
1 in 5,000 live births
Accounts for 10% of all
defects
Combination of four defects: Pulmonary stenosis
VSD
Overriding aorta
Right ventricular hypertrophy
Centers for Disease Control and Prevention. Accessed June 19, 2015.
Tetralogy of Fallot
Presentation depends on the degree of pulmonary stenosis (pink TOF vs blue TOF)
Cyanosis, hypoxia, and dyspnea present with severe obstruction
Tachypneic
Murmur detected
CXR will show a “boot‐shaped heart”
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Cardiovascular 15
Tetralogy of Fallot
Treatment Propranolol
PGE1 infusion to maintain duct patency
Careful use of oxygen therapy
Blalock‐Taussig procedure—palliative surgery
Corrective surgery Prognosis is poor without surgery
Verklan MT, et al. Core Curriculum for Neonatal IntensiveCare Nursing. Elsevier Saunders; 2015.
Occurs in 1 per 5,000 births
(predominantly male)
Most common cause of cyanosis
Position of the main arteries is reversed
Ductal dependent defect
Diagnosis usually made within the first week of life
Centers for Disease Control and Prevention. Accessed June 19, 2015.
Transposition of the Greater Arteries or Vessels
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Cardiovascular 16
Transposition of the Greater Arteries or Vessels
Cyanosis is present and becomes more prevalent
No murmur unless VSD is present
CXR may show “egg on a string” appearance
Echocardiogram is the standard diagnostic tool
This is a cardiac emergency
Transposition of the Greater Arteries or Vessels
Treatment/management
Correction on metabolic acidosis
Prostaglandin (PGE1) to maintain duct patency (mixing)
Balloon septostomy
Blade septostomy
Pulmonary artery banding
Corrective surgery Arterial switch operation (Dr. Jatene and Dr. Yacoub)
Mustard and Senning procedure
Rastelli procedure
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Cardiovascular 17
Truncus Arteriosus
1 per 33,000 births
Artery arises from both ventricles and overrides VSD
Three types Type I: Most common; short pulmonary artery from base of the trunk which divides to the right and left arteries
Type II: The left and right pulmonary arteries arise from the posterior side of the trunk
Type III: The right and left pulmonary arteries arise from different origins of the lateral side of the trunk
Centers for Disease Control and Prevention. Accessed June 19, 2015.
Truncus Arteriosus
Clinical manifestations Bounding pulses
Widened pulse pressure
Signs and symptoms of CHF
Harsh murmur
CXR will show cardiomegaly and pulmonary markings
Echocardiogram and Doppler are the standard diagnostic tools
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Cardiovascular 18
Truncus Arteriosus
Treatment
Manage CHF Diuretics
Digoxin
ACE inhibitors
Surgical repair Homograft
Patch to close VSD
Separation of the arteries from the trunk
Tricuspid Atresia
1 per 18,000 live births
Failure of the development of the tricuspid valve
Associated with a PFO or VSD
Pulmonary stenosis or atresia may also be present
Centers for Disease Control and Prevention. Accessed June 19, 2015.
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Cardiovascular 19
Tricuspid Atresia
Clinical manifestations
Cyanosis
Dyspnea
CHF
Murmur if associated with VSD, PDA, or stenosis
Tricuspid Atresia
Management Balloon septostomy to improve mixing of blood
Oxygen
Bicarbonate
PGE1
Blalock‐Taussig procedure
Pulmonary artery banding
Fontan or modified Fontan procedure
Bidirectional Glenn procedure on or off bypass
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Cardiovascular 20
Hypoplastic Left Heart Syndrome
2–2.6 per 10,000 births
Obstruction of blood to left side of the heart
Hypoplastic left ventricle
Absent or small mitral valve
Absent or small aortic valve
Ascending aorta is small
May have ASD
Pulmonary congestion and edema
Centers for Disease Control and Prevention. Accessed June 19, 2015.
Hypoplastic Left Heart Syndrome
Clinical manifestations Tachypnea
Dyspnea
CHF
Become rapidly ill as the PDA begins to close Mottling
Gray pallor
Diminishing pulses
Shock
CXR will show cardiomegaly
Echocardiogram done to diagnose; detected prenatally
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Cardiovascular 21
Hypoplastic Left Heart Syndrome
Management/treatment
Initial Management includes:
PGE1
Managing acidosis
Sedation
Balloon septostomy
Ventilation management
Staged surgical repair (Norwood 3–5 years to complete)
Cardiac transplant
Acyanotic
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Cardiovascular 22
Patent Ductus Arteriosus
Fourth most common cardiac lesion
8 of 1,000 premature births, 2 of 1,000 full term births
Persistent patency of the duct or failure of it to close
Prostaglandins inhibit the closure of this duct
Maintains fetal circulation in utero and meant to close after birth
National Heart, Blood, and Lung Institute. Accessed June 19, 2015.
Patent Ductus Arteriosus
Clinical manifestations Cardiomegaly
Bounding peripheral pulses
Widening pulse pressure
Low diastolic blood pressure
Metabolic acidosis
Continuous murmur may be auscultated in upper left sternal border
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Cardiovascular 23
Patent Ductus Arteriosus
Echocardiograph is the gold standard for diagnosis
B‐type natriuretic peptide levels of 70–100 pg/mL can be used to identify a PDA
Patent Ductus Arteriosus
Treatment/management Fluid restriction
Diuretics
Ventilation therapy
NSAIDs (indomethacin and ibuprofen)
Surgical management (ligation)
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Cardiovascular 24
Patent Ductus Arteriosus
Lipooxygenasepathway
Leukotrienes
Cyclooxygenasepathway
Prostaglandins
Cyclooxygenase inhibitors
Indomethacin (NeoProfen)
Prostaglandin synthase inhibitors
Arachidonic Acid Pathways
Atrial Septal Defect
1 per 5,000 births
More common in females
Defect in the formation of the
septum or patent foramen ovale
Usually asymptomatic
Systolic murmur may be detectable
Failure to thrive
Recurrent respiratory infections may occur
Centers for Disease Control and Prevention. Accessed June 19, 2015.
12/2015
Cardiovascular 25
Atrial Septal Defect
Defect may close on its own
Manage CHF if present
Surgical repair
Transcatheter closure
Ventricular Septal Defect
2 per 1,000 births
Most common of all defects (about 50%)
Abnormal opening of the septum between the right and left ventricle
Centers for Disease Control and Prevention. Accessed June 19, 2015.Reller MD, et al. J Pediatr. 2008;153(6):807–813.
12/2015
Cardiovascular 26
Ventricular Septal Defect
Clinical manifestations
Small VSD Asymptomatic with a murmur
Moderate VSD Asymptomatic with a murmur, fatigue, and respiratory infections
Large VSD Signs and symptoms of CHF
Loud murmur
Cardiomegaly on CXR
Echocardiograph done to diagnose
Ventricular Septal Defect
Treatment 50%–75% of small VSD will close spontaneously (muscular)
Surgical banding of pulmonary artery
Surgical suturing of defect
Surgical patching of defect
Transcatheter device
Prognosis is excellent
Topol EJ, ed. Textbook of Cardiovascular Medicine. Lippincott Williams & Wilkins; 2007.
12/2015
Cardiovascular 27
Atrioventricular Canal
Also known as endocardial cushion defect
1 per 9,000 births
Common in Down syndrome
Craig B. Heart. 2006;92(12):1879 – 1885.
National Institutes of Health. Accessed June 19, 2015.
Clinical manifestations Respiratory distress
Active precordium
Murmur
Respiratory infections
CXR will show cardiomegaly
Atrioventricular Canal
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Cardiovascular 28
Treatment
Treat CHF with digoxin and diuretics
Pulmonary artery banding
Primary repair closure
Atrioventricular Canal
1 in every 14,000 live births
Narrowing in or below the pulmonary valve
Depending on the degree of stenosis, may be ductal‐dependent or ductal‐independent
Murmur
Hepatomegaly
CXR will show cardiomegaly
Echocardiography is used to diagnose
Pulmonic Stenosis
American Heart Association. Accessed June 19, 2015.
12/2015
Cardiovascular 29
Pulmonic Stenosis
Treatment:
Oxygen, bicarbonate, PGE1
Balloon valvuloplasty
Surgical valvotomy if valvuloplasty is not effective
Aortic Stenosis
1 in 24,000 births
More likely in males
Anatomy includes: Valvular (most common)
Subvalvular
Supravalvular (least common)
Increased left ventricular pressure
Excess blood to the lungs
Sadowski SL. Crit Care Nurs Clin North Am. 2009;21(1):37–48.
American Heart Association. Accessed June 19, 2015.
12/2015
Cardiovascular 30
Aortic Stenosis
Clinical findings
Asymptomatic at birth
Murmur detected
Congestive heart failure symptoms
CXR will show cardiomegaly
Aortic Stenosis
Treatment Acidosis management and fluid restriction
If critical, use PGE1
Balloon valvuloplasty
Valvotomy or valve replacement
Ross‐Konno procedure
12/2015
Cardiovascular 31
Coarctation of the Aorta
Accounts for 7% of cardiac lesions
More common in males
Most common form is juxtaductal
Common in Turner syndrome
Constriction of the aorta
Kenny D, et al. Cardiol J. 2011:18(5):487–495.
American Heart Association. Accessed June 19, 2015.
Coarctation of the Aorta
Congestive heart failure due to high afterload
Pulses decreased or absent in the lower extremities
Blood pressure higher in upper extremities
CXR will show enlarged heart and pulmonary vascular markings
Echocardiogram is the standard tool to detect, but cannot rule out coarctation in patients with PDA
MRI can determine location of coarctation
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Cardiovascular 32
Coarctation of the Aorta
Treatment
CHF management
PGE1
Palliative balloon angioplasty to open narrowing
Stent placement
Surgical correction (resection, reanastomosis, or patch)
Vascular Rings and Slings
Occur secondary to abnormal development of aortic arch
Can cause compression to the trachea and esophagus
Symptoms include respiratory distress and stridor
The Children’s Hospital of Philadelphia. Accessed June 19, 2015.
12/2015
Cardiovascular 33
Management After Cardiac Surgery
Noninvasive monitoring
ECG
Blood pressure
Continuous pulse oximetry
Urine output
Cerebral near‐infrared spectroscopy
Management After Cardiac Surgery
Invasive monitoring Arterial pressures
Right‐sided cardiac pressures
Pulmonary artery pressure
Left‐sided cardiac pressure
Epicardial pacing
Hemodynamic monitoring
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Cardiovascular 34
Review Questions
A. SVT
B. Complete heart block
C. Junctional ectopic tachycardia
D. Hyperkalemia
Question 1
What is the most common neonatal dysrhythmia?
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Cardiovascular 35
Question 1—Rationale
A. SVT—This is the most common neonatal dysrhythmia
Complete heart block—Typically associated with lupus, which isn’t very common
Junctional ectopic tachycardia—Typically occurs in neonates after cardiac repair, not the most common
Hyperkalemia—Usually found in premature babies who are critically ill and acidotic. This is a unique situation
What is the most common neonatal dysrhythmia?
A. Hypoxia
B. Pain
C. Fever
D. NICU admission
Question 2
The most common cause of bradycardia in the newborn population is:
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Cardiovascular 36
Question 2—Rationale
A. Hypoxia—The most common cause of bradycardia in a newborn. Most infants have bradycardia for the same reasons they have apnea; often, bradycardia results from the baby having apnea. Apnea is defined as a pause >15–20 seconds in a baby’s regular breathing
Pain—A sympathetic response which causes heart rate acceleration
Fever—A sympathetic response which causes heart rate acceleration
Hypercapnia—May be responsible for tachypnea but not bradycardia
The most common cause of bradycardia in the newborn population is:
A. Placenta
B. Heart
C. Lung
D. Kidney
Question 3
The organ responsible for gas exchange in utero is the:
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Cardiovascular 37
Question 3—Rationale
A. Placenta—The placenta is responsible for all gas exchange in utero
Heart—Not responsible for gas exchange; responsible for pumping blood around in utero
Lung—Once baby is born, the lung is responsible; only function in utero is to practice breathing and to grow
Kidney—Function of the kidney in utero is to produce amniotic fluid
The organ responsible for gas exchange in utero is the:
A. Ductus arteriosus
B. Foramen ovale
C. Ductus venosus
D. VSD
Question 4
The fetal vessel connecting the pulmonary artery to the descending aorta is:
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Cardiovascular 38
Question 4—Rationale
A. Ductus arteriosus—A short vessel that shunts blood from the pulmonary artery directly to the ascending aorta, bypassing the lungs, before birth
Foramen ovale—The connection at the atrial septum opening; it connects the left atria to the right atria
Ductus venosus—The fetal vein that passes through the liver to the inferior vena cava
VSD—Early opening in the embryologic heart. The VSD is a hole in the wall separating the two lower chambers of the heart
The fetal vessel connecting the pulmonary artery to the descending aorta is:
A. Resuscitation equipment
B. Cooling mattress
C. Inotropes
D. Chest tube
Question 5
Your patient in the NICU has cyanotic heart disease and was started on PGE. The most important thing for the nurse to have available at the bedside is:
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Cardiovascular 39
Question 5—Rationale
A. Resuscitation equipment—bag valve mask. The nurse should be prepared to treat the apnea that may occur as a side effect of administering PGE
Cooling mattress—An infant may become flush and have a fever from administration of PGE, but placing a cooling mattress is not the treatment of choice for this symptom and is not the most important intervention
Inotropes—PGE administration does not cause hypotension
Chest tube—PGE is not known to cause air leaks
Your patient in the NICU has cyanotic heart disease and was started on PGE. The most important thing for the nurse to have available at the bedside is:
References
American Heart Association. Aortic valve stenosis (AVS). Available at: American Heart Association. Available at: http://www.heart.org/HEARTORG/Conditions/CongenitalHeartDefects/AboutCongenital
HeartDefects/Aortic‐Valve‐Stenosis‐AVS_UCM_307020_Article.jsp. Accessed June 19, 2015.
American Heart Association. Pulmonary valve stenosis. Available at: http://www.heart.org/HEARTORG/Conditions/CongenitalHeartDefects/AboutCongenitalHeartDefects/Pulmonary‐Valve‐Stenosis_UCM_307034_Article.jsp. Accessed June 17, 2015.
Centers for Disease Control and Prevention. Available at: http://www.cdc.gov. Accessed June 17, 2015.
Centers for Disease Control and Prevention. Facts about atrial septal defects. Available at: http://www.cdc.gov/ncbddd/heartdefects/atrialseptaldefect.html. Accessed June 19, 2015.
Centers for Disease Control and Prevention. Facts about coarctation of the aorta. Available at: http://www.cdc.gov/ncbddd/heartdefects/coarctationofaorta.html. Accessed June 19, 2015.
Centers for Disease Control and Prevention. Facts about hypoplastic left heart syndrome. Available at: http://www.cdc.gov/ncbddd/heartdefects/hlhs.html. Accessed June 19, 2015.
Centers for Disease Control and Prevention. Facts about dextro‐transposition of the great arteries (d‐TGA). Available at: http://www.cdc.gov/ncbddd/heartdefects/d‐tga.html. Accessed June 19, 2015.
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Cardiovascular 40
References
Centers for Disease Control and Prevention. Facts about triscupid atresia. Available at: http://www.cdc.gov/ncbddd/heartdefects/tricuspid‐atresia.html. Accessed June 19, 2015.
Centers for Disease Control and Prevention. Facts about truncus arteriosus. Available at: http://www.cdc.gov/ncbddd/heartdefects/truncusarteriosus.html. Accessed June 19, 2015.
Cloherty JP, Eichenwald EC, Hansen AR, Stark AR, eds. Manual of Neonatal Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
Craig B. Atrioventricular septal defect: from fetus to adult. Heart. 2006;92(12):1879–1885.
Friedman D, Duncanson L, Glickstein J, Buyon J. A review of congenital heart block. Images Paediatr Cardiol. 2003;5(3):36–48.
Kenny D, Hijazi ZM. Coarctation of the aorta: from fetal life to adulthood. Cardiol J. 2011;18(5):487–495.
Klabunde RE. Cardiovascular Physiology Concepts. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2011.
Martin RJ, Fanaroff AA, Walch MC. Fanaroff and Martin’s Neonatal‐Perinatal Medicine. 10th ed. Philadelphia, PA: Elsevier Inc.; 2015.
Merenstein GB, Gardner SL, eds. Handbook of Neonatal Intensive Care. 7th ed. St. Louis, MO: Mosby; 2011.
References
Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol. 2000;11(1):25–38.
National Heart, Blood, and Lung Institute. What is patent ductus arteriosus? Available at: http://www.nhlbi.nih.gov/health/health‐topics/topics/pda/. Accessed June 19, 2015.
National Institutes of Health. Atrioventricular canal (endocardial cushion defect). Available at: http://www.nlm.nih.gov/medlineplus/ency/imagepages/19877.htm. Accessed June 19, 2015.
Pilcher J. Pocket Guide to Neonatal EKG Interpretation. 2nd ed. Petaluma, CA: NICU INK Book Publishers; 2004.
Reller MD, Strickland MJ, Riehle‐Colarusso, Mahle WT, Correa A. Prevalence of congenital heart defects in metropolitan Atlanta, 1998–2005. J Pediatr. 2008;153(6):807–813.
Sadowski SL. Congenital cardiac disease in the newborn infant: past, present, and future. Crit Care Nurs Clin North Am. 2009;21(1):37–48.
Srinivasan S, Strasburger J. Overview of fetal arrhythmias. HHS Public Access. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326657/. Accessed June 19, 2015.
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Cardiovascular 41
References
The Children’s Hospital of Philadelphia. About vascular ring. Available at: http://www.chop.edu/conditions‐diseases/vascular‐ring/about#.VYSSFZDJBIJ. Accessed June 19, 2015.
Topol EJ, ed. Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.
Verklan MT, Walden M. Core Curriculum for Neonatal Intensive Care Nursing. 5th ed. Philadelphia, PA: Elsevier Saunders; 2015.
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