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Neonatal Objectives
Cardiovascular
1. Review prenatal and postnatal formation of the
Physiology cardiovascular system

2. Review the fetal, transitional, and persistent fetal

circulations

3. Review the relevant impact of oxygen on

newborn resuscitation

Embryologic formation of QUESTION: WHEN DOES

the cardiovascular system THE FORMATION OF THE
NEONATAL HEART BEGIN?

ANSWER

QUESTION: WHEN DOES

THE HEART STARTS TO
BEAT?

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ANSWER

Day 21
The heart tube

Day 23
Looping begins
Day 27
Almost ready for circulation

RA LA Endocardial cushion

RV LV

Neonatal myocardium
 Neonatal myocardial contraction is weaker than in
childhood or adulthood:
Postnatal cardiovascular  Less contractile elements

development  More connective tissue

 Myofibrils are less organized
 Inefficient calcium utilization
 Minor reasons
Copyright free via Creative Commons,
 Contractile protein immaturity PLoS One. 2013; 8(11): e80709.

 Inefficient energy storage and utilization

 Immature cellular regulation of the action potential

• Teitel DF, Cassidy SC, Fineman JR. Circulation Physiology. In: Moss AJ, Allen HD, eds.Moss and Adams' Heart Disease in Infants,
Children, and Adolescents: Including the Fetus and Young Adult: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.
• Baum VC, Palmisano BW. The immature heart and anesthesia. Anesthesiology 1997; 87: 1529-1548.

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Neonatal myocardium
 Traditionally, it was thought that neonatal cardiac output
is almost entirely heart rate dependent
 However, neonatal hearts do respond to alterations in
preload and afterload, but less so than in adults.
 But the neonatal Starling curve is narrow, meaning less
ability to alter stroke volume based on loading conditions
 Overall, high metabolic demands of neonates require
heart to operate at near-maximal capacity at most times

• Baum VC, Palmisano BW. The immature heart and anesthesia. Anesthesiology 1997; 87: 1529-1548.

Neonatal myocardium Neonatal myocardium

 Neonatal heart operates at near-maximal capacity at
most times
 Thus stressors (e.g. hypoxia, anesthesia) risk rapid
decompensation in neonates:
 Many anesthetics reduce O2 consumption, but…
 Overall myocardial suppression and lower heart rates under
anesthesia risk
 Likely worse in the setting of acute or chronic hypoxia
 The neonatal and fetal heart does respond to sympathetic
stimulation
 Sympathetic nervous system is immature at birth
 Parasympathetic innervation dominates
 Exaggerated vagal responses to various stimuli
 Sympathetic nervous system is mature by late infancy

• Baum VC, Palmisano BW. The immature heart and anesthesia. Anesthesiology 1997; 87: 1529-1548. • Baum VC, Palmisano BW. The immature heart and anesthesia. Anesthesiology 1997; 87: 1529-1548.
• Schure AY, Dinardo JA. Cardiac physiology and pharmacology. In: Coté CJ, Lerman J, Anderson BJ, eds. Coté and Lerman's a practice
of anesthesia for infants and children, 5th edn. Philadelphia, PA: Elsevier, 2013.

The hypoxic environment

 Fetal circulation is relatively hypoxic compared to the
mother and after birth

Fetal circulation  PO2 of umbilical vein blood entering fetus is 30 mmHg

 PO2 of blood returning to placenta is 16 mmHg
 Presence of fetal shunts allows best utilization of limited
O2 to fetal tissues
 3 fetal shunts:
 Ductus venosus
 Foramen ovale
 Ductus arteriosus

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Ductus venosus Fetal Circulation

 Umbilical venous blood from the placenta has high • Course of the oxygenated umbilical vein blood:
velocity and PO2 •  bypasses liver via ductus venosus
 Ductus venosus is crucial to allow this fast, oxygenated •  mixes with IVC
blood to bypass liver •  eustachian valve shunts towards PFO  LA
•  LA  LV  aortic valve
 ~50% of umbilical venous blood passes through ductus
•  aorta  coronary and carotid arteries
venosus, the remainder is distributed to both lobes of the
liver
• Therefore, oxygenated blood from the umbilical vein
perfuses the brain and coronary arteries by shunting
 This blood preferentially streams to the coronary arteries across the liver (via the ductus venosus) and shunting
and brain (shown in next several slides) across the right heart (via the foramen ovale)

• Rudolph AM. Hepatic and ductus venosus blood flows during fetal life. Hepatology. 1983 Mar;3(2):254–8.
• See diagram on next slide

Fetal Circulation
SVC
Aorta PA
• Desaturated SVC blood from the fetal brain takes a
different course:
• SVC RA  tricuspid valve (not to PFO)
PFO
RA •  pulmonary valve
EuV •  ductus arteriosus
•  descending aorta
LV
•  back to placenta for oxygenation
RV
Ductus
venosus
• See diagram on next slide
Liver

Umbilical vein
IVC
Greg Latham, MD

SVC Ductus
arteriosus
25% 65%
55%
Pulmonary
50% artery
PDA Oxygen Saturation Pulmonary
SVC
Aorta PA of Fetal Blood 40% vein

65%
RA
TV Hepatic
50%
vein

65%
Liver

RV LV IVC
55%
Ductus 25% Aorta
venosus 80%
Umbilical
vein
Liver

Umbilical vein
IVC Umbilical arteries
Greg Latham, MD
Placenta

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21%
SVC Ductus SVC
10% arteriosus
10%
59%
Pulmonary 31% Pulmonary
7%
artery artery

Pulmonary Pulmonary
vein vein
Combined Cardiac Combined Cardiac
Output of Fetal Output of Fetal
Blood – Right Blood – Left 34%

Ventricle Hepatic
66%
Ventricle Hepatic
vein vein

Liver Liver

IVC IVC
69%
Aorta Aorta

Umbilical Umbilical
vein 45% vein

24%

Umbilical arteries Umbilical arteries

Placenta Placenta

The hypoxic environment

• Fetal oxygen delivery (DO2) is maintained in the
relative hypoxic environment because:
1. High cardiac output
2. High hemoglobin
3. Greater O2 affinity of hemoglobin F for enhanced O2
uptake at the placenta
4. Lower pH in fetal organs for enhanced O2 release at the
tissue level

• Schure AY, Dinardo JA. Cardiac physiology and pharmacology. In: Coté CJ, Lerman J, Anderson BJ, eds. Coté and Lerman's a practice
of anesthesia for infants and children, 5th edn. Philadelphia, PA: Elsevier, 2013.
• Giardina B, et al. Physiological Relevance of the Overall ΔH of Oxygen Binding to Fetal Human Hemoglobin. J MolBiol 1993, 229,
512-516

Transitional circulation
• Transitional circulation = transition from fetal to
Transitional circulation normal (adult) circulation
• Transitional circulation begins when umbilical cord is
clamped and lungs are inflated
• Clamping umbilical cord:
• Removal of low-resistance placenta  increase in SVR
• Increase in SVR  increased left heart pressures
• Breathing after birth:
• Lung expansion and increased PaO2
•  8- to 10-fold drop in PVR
•  Significant increase in pulmonary blood flow

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Transitional Circulation - PFO Transitional Circulation - PDA

• Cord clamping and lung inflation cause increased SVR and decreased • The ductus arteriosus remains patent in utero due to
PVR, respectively hypoxia, mild acidosis and placental prostaglandins.
Removal of these factors after delivery causes functional
• This causes increased pulmonary blood flow and increased blood
return to the left atrium closure with anatomic closure occurring weeks later
Copyright free via Creative Commons,
• LA pressure > RA pressure  closes Eur Heart J. 2012 Mar; 33(6): 705–713. • Persistent PDA often occurs in premature infants with lung
the flap-like foramen ovale. disease. Indomethacin, via its anti-prostaglandin action can
• Functional closure of PFO occurs be used to try and close a PDA
quickly but anatomic closure usually • Before anatomic closure of the PDA and PFO, pRA > pLA can
requires weeks. cause reversion to fetal circulation (R  L shunt and
• A PFO that is probe patent persists cyanosis)
in approximately 25% of adults • Hypothermia, hypercarbia, acidosis, hypoxia and sepsis can
all cause a reversion to fetal circulation

Transitional Circulation - DV
• Flow through ductus venosus stops immediately
when umbilical cord clamped Persistent fetal circulation and
• Full, irreversible closure occurs in 1-2 weeks Persistent pulmonary
• Fibrotic remnant is called ligamentum venosum
hypertension of the newborn
(PPHN)

Copyright free via Creative Commons,

Ann Pediatr Cardiol. 2013 Jul-Dec; 6(2): 173–175.

Persistent pulmonary hypertension of

Persistent fetal circulation the newborn (PPHN)
• Persistent fetal circulation = right-to-left flow across • PPHN = persistently high PVR after birth
the foramen ovale and/or ductus arteriosus, as in • Most common cause is parenchymal lung disease
utero (e.g. meconium aspiration and respiratory distress
• Two primary causes: syndrome)
• Congenital heart disease
• Persistent pulmonary hypertension of the newborn (PPHN)
• Other causes:
• Sepsis
Copyright free via Creative Commons, • Alveolar-capillary dysplasia
Pol J Radiol. 2014; 79: 164–168.

Sagittal reconstructed (A) and volume

• Surfactant dysfunction
*
• Severe lung hypoplasia
rendering (B) dual source CT images of
a 15-day girl with a large PDA and
* pulmonary arterial hypertension

• Konduri GG, Kim UO. Advances in the diagnosis and management of persistent pulmonary hypertension of the newborn.Pediatr
Clin North Am 2009; 56: 579-600.
• Cabral JEB, Belik J. Persistent pulmonary hypertension of the newborn: recent advances in pathophysiology and treatment.J
Pediatr (Rio J) 2013; 89: 226-242.

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PPHN PPHN and anesthesia care

• High PVR limits pulmonary blood flow and left atrial • Goal: maintain adequate oxygenation, myocardial
filling  high RA pressure keeps PFO open function, and systemic perfusion
• High PVR, hypoxia, and hypercarbia (acidosis) keep • Avoid worsening PVR, so avoid:
PDA open • Hypoxia
• Thus combination of right-to-left shunts at PFO and • Acidosis (hypercarbia)
PDA as well as poor alveolar ventilation cause • Excessive PEEP
hypoxemia • Atelectasis
• Catecholamine release (light anesthesia)
• Treatment ranges from simple supplemental O2 to
extracorporeal membrane oxygenation (ECMO)
• Konduri GG, Kim UO. Advances in the diagnosis and management of persistent pulmonary hypertension of the newborn.Pediatr
Clin North Am 2009; 56: 579-600.

PPHN and anesthesia care

• Increased FiO2 causes pulmonary vasodilation, but
• Hyperoxia can be harmful to newborn Newborn resuscitation
• Maximal pulmonary vasodilation occurs at relatively low
O2 levels and the use of oxygen
• Thus, titrate O2 to lowest acceptable amount, with goal
PaO2 of 60-90 mmHg
• Maintain normocapnia
• Use inhaled nitric oxide if required
• Ensure adequate systemic BP; use inotropes as
needed
• Konduri GG, Kim UO. Advances in the diagnosis and management of persistent pulmonary hypertension of the newborn.Pediatr
Clin North Am 2009; 56: 579-600.
• Schure AY, Dinardo JA. Cardiac physiology and pharmacology. In: Coté CJ, Lerman J, Anderson BJ, eds. Coté and Lerman's a practice
of anesthesia for infants and children, 5th edn. Philadelphia, PA: Elsevier, 2013.

Newborn resuscitation &

Newborn O2 saturations
potential effects of O2
• Transition to extrauterine life = marked increase in • Newborn hyperoxia can be toxic and lead to irreversible injury:
oxygen saturations in term newborns • 1 breath of 100% oxygen decreases minute ventilation; longer duration can
lead to chronic lung injury
• Normal saturations in term infants: • Resuscitation with 80% O2 in delivery room decreases cerebral blood flow for 2
Time after birth Median SpO2 (interquartile range) hours
• Exposure to high FiO2 for 3 minutes or longer may be associated with increased
1 minute 68% (60–77) risk of childhood cancer
2 minutes 76% (65–84) • Can lead to oxidative stress and production of oxygen free radicals, lasting at
3 minutes 81% (71–90) least 28 days
• Animal studies provide evidence of apoptotic cell death in the brain after
4 minutes 88% (78–94) various exposure to increased FiO2
5 minutes 92% (83–96)
• Effects are likely greater in premature compared to full term newborns, due
7 minutes 95% (90–97) to lack of adequate protective antioxidant levels
10 minutes 97% (94–98)
• Goldsmith JP, Kattwinkel J. The role of oxygen in the delivery room. Clin Perinatol 2012; 39: 803-815.
Dawson JA, et al. Defining the reference range for oxygen saturation for infants after birth. • Deuber C, Abbasi S, Schwoebel A, Terhaar M. The toxigen initiative: targeting oxygen saturation to avoid sequelae in very preterm
PEDIATRICS. 2010 Jun;125(6):e1340–7. infants. Adv Neonatal Care. 2013 Apr;13(2):139–45.

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Newborn resuscitation & O2 Newborn resuscitation & O2

• Because insufficient or excessive oxygenation can be harmful • Although resuscitation of a term newborn should be initiated with room air,
to the newborn infant, recommendations exist for newborn relative hypoxia is detrimental and must be avoided!
resuscitation: • Pre-ductal SpO2 (right upper extremity) must be used to guide targeted
• Use oximetry; assessment of color is unreliable SpO2 levels during delivery room resuscitation:
• 1 minute after delivery - 60-65%
• For babies born at term, it is best to begin resuscitation with air rather
than 100% oxygen. • 2 minutes after delivery - 65-70%
• Administration of supplementary oxygen should be regulated by • 3 minutes after delivery - 70-75%
blending oxygen and air, and the concentration delivered should be • 4 minutes after delivery - 75-80%
guided by oximetry. • 5 minutes after delivery - 80-85%
• If the heart rate is below 60 bpm after 90 seconds of resuscitation, the • 10 minutes after delivery - 85-95%
oxygen concentration should be increased to 100% until recovery of a • Note: these goals are in delivery room, NOT operating room!
normal heart rate.
• Perlman JM, Wyllie J, Kattwinkel J, et al. Part 11: Neonatal resuscitation: 2010 International Consensus on Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.Circulation 2010; 122: S516-538. • Kattwinkel J, et al. Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
• Kattwinkel J, et al. Neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. PEDIATRICS. 2010 Nov;126(5):e1400–13.
Emergency Cardiovascular Care. PEDIATRICS. 2010 Nov;126(5):e1400–13.

Newborn Resuscitation Algorithm.

Newborn care in OR
• Normoxia is goal (>94%)
• Avoid both hypoxemia (increased risk of mortality)
and hyperoxemia (risk of ROP), especially in
preterm
• Beware of over-ventilation; a PaCO2 of 40-50 is
beneficial:
• Decreased lung injury
• Increase cerebral blood flow
• Increased O2 unloading at the tissue level
Kattwinkel J et al. Pediatrics 2010;126:e1400-e1413
Thome UH, Ambalavanan N. Permissive hypercapnia to decrease lung injury in ventilated preterm neonates.Semin Fetal Neonatal
Med. 2009 Feb;14(1):21–7.
©2010 by American Academy of Pediatrics

Cardiovascular presentations
Pediatric • Collapse
Cardiology
• The blue baby

• Syncope

• Palpitations

• Chest pain

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ECG in a 2 year old

THE ECG

Terminologies The Conduction System

• Cardiac Action Potential
- The action potential of a ventricular muscle cell • Sinoatrial Node - 60 to 100 bpm
• Polarization • Atrioventricular Junction - 40 to 60 bpm
- the resting state during which no electrical activity occurs in • Bundle of His
the heart.
• Purkinje fibers - 20 to 40 bpm
• Depolarization = Stimulation
- Depolarization is not the same as contraction.
Depolarization is an electrical event that is expected to result
in contraction, which is a mechanical event.

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ECGs in children
• Heart rate >100 beats/min
• Rightward QRS axis > +90°
• T wave inversions in V1-3 (“juvenile T-wave
pattern”)
• Dominant R wave in V1
• RSR’ pattern in V1
• Marked sinus arrhythmia
• Short PR interval (< 120ms) and QRS duration
(<80ms)
• Slightly peaked P waves
• Q waves in the inferior and left precordial leads.

Electrodes

Lead Placement

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The normal ECG

• QRS variable with age - Newborn 50-80ms, at 16
years 75-115ms

• cQTC under 6/12: 490ms, 440ms otherwise

• Notched t waves; may be normal in V2&3

• Transient Wenckebach during sleep

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The normal ECG

• Parameters vary through age
CHEST PAIN
• Right ventricular dominance owing to high
pulmonary pressures, normalise at ~6/12

• T waves; usually upright in most leads for first 7/7,

then downwards in most leads until adolescence.

•Upright t waves in childhood may reflect RVH.

Chest pain
Non cardiac chest pain
Common but usually benign presentation
4436 presentations age < 19 yrs over 3 1/2 year period • 56% musculoskeletal
in a tertiary PED (Pediatric Emergency Department) in
USA • 12% asthma/ wheeze
•0.6% deemed cardiac
•37% arrhythmia • 8% infection
•29% pericardial
•17% myocarditis • 6% GI – gastritis and GERD
•13% AMI (Acute Myocardial Infarction)
•4% PE (Pulmonary Embolism) • 4% sickle cell disease
American Journal of Emergency Medicine Volume 29, Issue 6 , Pages 632-638, July 2011)

Texidor’s twinge
• also known as: Precordial catch syndrome SYNCOPE
• acute, non-radiating left sided chest pain in an
adolescent
• occurs suddenly, exacerbated during inspiration
and resolves in a few minutes.

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Syncope
Syncope Red Flags
• 15-20% all children will have an episode
• History of cardiac disease
Vasovagal • Family history of SCD
Reflex anoxic seizures
Neurally mediated Orthostatic • Recurrent episodes
• Exertional
Structural
Cardiomyopathy • Prolonged LoC
Cardiac Arrythmias • Associated chest pain / palpitations
• Medications that can alter cardiac conduction
Psychogenic
Non CVS Factitious
Neurological non syncope e.g. Seizure

Sudden Cardiac Death

• Myocarditis
• HOCM (Hypertrophic Obstructive Cardiomyopathy) PALPITATIONS
• Cyanotic / Acyanotic congenital heart disease
• Valvular heart disease
• Complete heart block
• WPW (Wolff-Parkinson-White syndrome)
• Long QT syndrome
• Marfan’s syndrome
• CAD
• Anomalous coronary arteries

Heart rate
Cardiac arrhythmias in children
• Likely to be the result rather than the cause
Age Bradycardia Tachycardia
of acute illness
<1y < 80 min-1 > 180 min-1
>1y < 60 min-1 > 160 min-1
• Often preceded by hypoxia, acidosis and / or
hypotension

• Primary cardiac arrhythmias are uncommon

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Bradycardia Bradycardia - causes

• Bradyarrythmias rare in structurally normal hearts
• Usually pre-terminal following hypoxia and
ischaemia
• Vagal stimulation
• Raised ICP
• Poisoning with digoxin/ beta-blockers
• Congenital CHB seen in infants of mothers with anti
ro and la antibodies

Tachycardia
Bradycardia Treatment rdia
• Oxygenation Narrow QRS complex Broad QRS complex

• Adrenaline – 10mcg/kg
ST VT or SVT
SVT Treat as VT
• Atropine - Consider when vagal stimulation e.g. airway
instrumentation – 20mcg/kg

• Pacing (rarely required)

Sinus Tachycardia ST – Treat the cause

• Physiological response: • Compensatory
mechanism for:

Crying Respiratory failure

Exercise Hypovolemia
Anxiety/fear Sepsis
Pain Anemia

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Supraventricular tachycardia Supraventricular Tachycardia

• Most common primary cardiac arrhythmia in
children

• Paroxysmal, regular, narrow QRS complexes

• Caused by re-entry mechanism through an

accessory pathway or AV conduction system

• HR > 220 bpm in infants or > 180 bpm in children

ST or SVT SVT - Management

• Valsalva maneuvre

• IV Adenosine
100 mcg/kg
200 mcg/kg
maximum 1st dose 6mg, 2nd dose 12mg

• Amiodarone in refractory SVT

• DC cardioversion – for decompensated children

Ventricular Tachycardia Ventricular Tachycardia Causes

• Congenital HD & surgery

• Poisoning (TCAs/Tricyclic Antidepressants),

Quinidine)

• Brugada syndrome / Long QT interval

• Renal Disease / Hyperkalemia

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VT - management Long QT - congenital

• Normal QTc < 400ms, > 460 ms abnormal
• Easiest to reproducibly measure in II & V5
• Channelopathy
• Genetic mutations identifies in 90% familial cases
• Subtypes 1-14
• Risk of torsades and VF
• May present with syncope (VT), risk greatest with QT >
500ms
• Ask about family history of syncope, sudden death and
epilepsy
• European registry 1993; 8% 5 yr mortality
• Treatment with BB

Atrial Flutter Atrial Fibrillation

Atrial Flutter and Fibrillation Pre-excitation syndromes

• Most common in WPW
• Rare
• Ventricular Pre-excitation in SR,
• Underlying CHD, status post-open heart surgery
short PR and delta wave
• Cardioversion in decompensated
• Commonest arrhythmia is
• In hemodynamically stable children, amiodarone orthodromic AV re-entry
or elective cardioversion tachycardia

• Antidromic less common

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The collapsed infant

COLLAPSE • Wide differential (means that there are many possible
explanations for the observed symptoms)
• Always cover for sepsis

Congenital heart disease

• May present as lethargy, poor feeding, "not right",
cyanosis to complete cardiovascular collapse

Congenital heart disease Congenital heart disease

Fetal PVR>SVR; blood bypasses
lungs through ductus arteriosus • Failure of normal development or
and foramen ovale

DA usually closes 24-36hrs post

• Persistence of fetal circulation
birth – may be much longer
• 7-9% live births
FO closes when left atrium volume
increases
• Acyanotic or Cyanotic heart disease

Acyanotic Heart Disease Cyanotic Heart Disease

• VSD (25%) • Tetralogy of Fallot

• ASD • Transposition of the great
• PDA arteries
• PV stenosis • Tricuspid atresia
• CoA • TAPVD (Total Anomalous
• AS Pulmonary Venous
• Hypoplastic left heart Drainage)
• HOCM
• Dextrocardia

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VSD and ASD

Acyanotic Heart Disease

AV and PV stenosis PDA and CoA

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Cyanotic Heart Disease

TAPVD (Total Anomalous Pulmonary

Transposition of the great arteries Venous Drainage)

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Congenital heart disease Cyanosis

Common presentations: • Cyanosis – ~4-5g/dL of deoxygenated blood

• Cyanosis • Cardiac cause – ‘comfortably blue’, worse with

crying, minimal improvement with O2
• Heart failure
• Primary pulmonary disease; no R-L sats diff
• Heart murmur • Primary cardiac; 5-10 % R-L sats diff
• Sepsis; no diff

Failure Innocent murmurs

• Common in children
• Sweating • Never diastolic
• Poor feeding • Soft, Short, midsystolic, low intensity
• Hepatomegaly • Localised
• SOB • Often vibratory or musical
• Tachycardia • Increase with output, (fever)
• No thrill/ heave or radiation
• Asymptomatic
• May resolve in few months
• Commonest at lower left sternal edge
• Venous hum

Evaluation ED management
• Pre-natal (USS) • ABC – sats 75-85%
• Family history • Correct metabolic acidosis and shock with fluid and
bicarb
• Birth history (birth state, trauma, risk infection)
• 2 lines/ UVC (Umbilical Venous Catheter) if possible
• Is this cardiac? (murmur + cyanosis + absent pulses) • Antibiotics
Pre- and post ductal oxygen saturations
• Gentle handling
ABG • Keep warm
4 limb BP (>10mmHg difference suggests coarctation) • Prostoglandin – ductal patency
ECG • Inotropes
CXR • Ventilate – in air if possible, PEEP (Positive End-
Echo Expiratory Pressure) 4-6cmH2O

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Prostaglandin
Prostaglandin
• PGE2 infusion (dinoprostone)
Possible Adverse Effects Administration
• In duct dependent lesion
• Hyperoxia test suggestive, femoral pulses • Apnea • Intravenous infusion
diminished, metabolic acidosis persistent after
• Hypotension • Consider intubation
volume and inotropes
• Hyperthermia (transient)
• Ensure antibiotics given! • Dose
• Tachycardia
• Beware of apnea. May cause hypotension, • 0.01 – 0.1 mcg/kg/min
• Bradycardia
jitteriness and jerks • Seizures
• No absolute contraindications • Diarrhea
• Skin flush

Hyperoxia test

• 10 mins on 100% O2 ACQUIRED HEART DISEASE

PaO2 <20 KPa, cyanotic heart disease likely
Pao2 <27KPa but >20, equivocal
PaO2 >27 KPa, respiratory disease

Caution, severe pulmonary disease

Care duct dependent lesions

CASE STUDY Diagnosis?

• 18 month old girl
• 6 days of high fever
• Miserable
• Swollen hands and feet with pain and redness

Immediate action?
Investigations?
Working diagnosis?
Further management?

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Kawasaki Disease Diagnosing Kawasaki disease

• Commonest cause of acquired heart disease in
children in the UK
• Febrile, exanthematous, multi-system vasculitis in
children <5y
• Coronary arteritis with aneurysm formation in 20-
30% in untreated patients
• Fever of 5 days plus any 4 physical exam findings:
Ø Rash
Ø Cervical lymphadenopathy (at least 1.5 cm in
diameter)
Ø Bilateral conjunctival injection
Ø Oral mucosal changes
Ø Peripheral extremity changes

Kawasaki disease Any Questions?

• Admission as in-patient
• ECG, ECHO
• IV immunoglobulins
• Aspirin high dose
• Pediatric/Cardiology F/U (repeat ECHO at 6 weeks)

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