Emergency Cardiovascular

Problems in Pediatrics

Jarupim Soongswang, M.D.

Professor in Pediatric Cardiology
Dept of Pediatrics, Faculty of Medicine
Siriraj Hospital, Mahidol University
Annual Meeting in Emergency Medicine
Feb 5, 2011
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Emergency cardiovascular problems in
pediatrics

 Cyanosis: hypoxic spell, ductal dependent pulmonary

circulation
 Dyspnea, tachypnea: congestive heart failure
 Hypotension: cardiogenic shock, low cardiac output,
cardiac tamponade, ductal dependent systemic circ,
pulmonary hypertensive crisis, VT
 Palpitation: SVT, atrial flutter
 Syncope: complete heart block, long QT syndrome, AS
 Chest pain: congenital coronary artery abnormal,
pericarditis
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Case 1
A seven-year-old boy presents with dyspnea,
tachypnea for 1 day. He has had upper
respiratory tract infection for 2-3 days with
rhinorrhea, low grade fever.
PE: T 36.5oC, RR 40/min, HR 140/min, BP 80/60,
dyspnea, capillary refilled 5 second,
restlessness
Lung: fine crepitation,
CVS: Normal S1,S2, S3 gallop, soft SM grade 2/6
at apex
Liver: 3 cm below RCM, rubbery consistency
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Cardiogenic shock

Definition: Inadequate CO and O2

transport to vital organs and functions.
Continuing process of CHF.
Life threatening condition.
Requires aggressive and prompt
treatment.
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Cardiogenic shock
Physiology :
CO = HR X SV
SV = EDV X (EDV-ESV)
EDV
CO = HR X EDV X EF
Oxygen delivery = CO x Hb X SaO2 x 13.9

CO: cardiac output, HR: heart rate, SV: stroke volume,

EDV: end diastolic volume, ESV: end systolic volume, EF:
ejection fraction, HB: hemoglobin, SaO2: oxygen
saturation
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Cardiogenic shock

Clinical manifestations
 Low cardiac output
• Grayish color
• Poor peripheral perfusion
• Hypotension
• Conscious change
• Urine output decrease<0.5-1 ml/kg/hr.
• Metabolic acidosis
• Decrease oxygen saturation in venous
blood gas
• Increase serum lactate
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Signs and symptoms of low cardiac outputs

Organ System  CO CO Shock

CNS - Restless, apathetic Agitated-confused,

Respiration - Ventilation Ventilation
Metabolism - Compensated Uncompensated
mtabolic academia metabolic academia
Gut -  Motility lleus
Kidney Specific gravity, Oliguria Oliguria-anuria
volume
Skin Delayed capillary Cool extremities Mottled, cyanotic,
refill cold extremities
CVS Heart rate Heart rate, Heart rate, blood
Peripheral pulses pressure, central
pulses only

CNS, central nevous system; CVS, cardiovascular system;,slightly increases;

 ,greatly
increased; , slightly decreased; , greatly decreased.
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Minimum blood pressure to diagnose hypotension

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Cardiogenic Shock
Etiology:
1. Congenital heart diseases eg.
Ductal dependent lesion: Left sided obstructive lesions
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Right sided obstructive lesions

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Cardiogenic shock

Etiology
2. Myocardial diseases:

myocarditis, cardiomyopathy

3. Cardiac dysrhythmia

4. Cardiac tamponade
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Management of cardiogenic shock

 Specific: correct causes eg arrhythmia,

tamponade, PGE1, etc.
 Supportive and symptomatic treatments:
• Augment contractility: inotropes
• Afterload: vasodilators
• Decrease O2 consumption: sedate, bed
rest, respiratory support
• O2 supplement
• Correct metabolic: electrolytes, sugar,
anemia,
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แสดงยาที่ใช้ในการรักษา cardiogenic shock
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Agent Site of action Dose (µg/kg/min) Effecta

Dopamine Dopaminergic 0.5-4 Renal vasodilator

β 4-10 Inotrope
>β 11-12 Peripheral vasoconstriction
Increased PVR
Dysrhythmias

Dobutamine β 1 and β 2 1-20 Inotrope

Vasodilation (β2)
Lowers PVR
Weak a-activity
tachycardia
and extrasystoles
Isoproterenol β 1 and β 2 0.05-2.0 Inotrope
Vasodialtation
Lowers PVR
MVO2
Dysrhythmias

Norepinephrine >β 0.005-2.0 Profound constrictor

Inotrope
MVO2, SVR 

Amrinone PDE3 inhibitor 1-20 Inotrope

Chronotrope
Vasodilatation

Milrinone PDE3 inhibitor Load 50 µg/kg > 10 Same as Amrinone

min then 0.375-0.75
µg/kg/min

aPVR , pulmonary vascular resistance; SVR, systemic vascular resistance; and PDE3, phosphodiesterase inhibitor.
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Management of cardiogenic shock

 Monitoring: Intensive care

 Invasive arterial blood pressure:
 Central venous pressure:
 Pulmonary artery wedge pressure:
 Urine output:
 Arterial blood gas, venous gas
 Serum lactate
 Blood chemistry: liver function, kidney
function, sugar, electrolytes
 Non-invasive monitoring : ECG, O2 sat, RR, T
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Case 2
 A one-year-old boy with history of cyanotic
heart disease presents with deep cyanosis
after crying for 15 min.
He develops dyspnea and unconscious
PE: RR 30/min, PR 120/min, BP 80/65, deep
cyanosis, O2 sat 40-50%,
Heart: normal S1, S2, SM grade 1/6 LUSB
Lung: clear
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Hypoxic spell

 Definition: Sudden and transient

uncompensated hypoxia in cyanotic heart
diseases (Rt to Lt shunt)
 TOF is the prototype
 Majority is self limited in 15-20 mins.
 Depend on balance between pulmonary and
systemic pressure and resistance
 Precipitating factors: crying, defecation etc.
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PA AO

PVR SVR

RV LV
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Pathophysiology of hypoxic spell
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Hypoxic spell

Signs and symptoms: Increase in

cyanosis, hyperpnea, conscious
change, decrease intensity of SEM,
syncope, +/- convulsion
Management:
 Knee chest position
 O2
 Sedate
 NaHCO3
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Hypoxic spell

Continue management
 Propanolol IV: 0.1 mg/kg/dose dilute IV slowly
(monitor HR)
 Correct hypoglycemia: 25% glucose 1-2
cc/kg/dose IV push
 Keep normal systemic BP
 Correct Hct: PRC infusion (anemia), blood
letting (polycythemia; Hct >65%)
 Paralyze and ventilate
 Emergency shunt surgery
 Closed FU. blood gas, correct acidosis etc.
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Case 3

 Ten-year-old girl presents with

palpitation, and chest pain for 10
hours.
PE: BP 100/70, HR 200 /min, RR 18/min,
capillary refill 2 sec, no dyspnea
Lung: clear
Heart: no murmur
Liver: 3 cm rubbery consistency.
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Cardiac Dysrrhythmia

Tachyarrhythmia: Abnormally fast HR and rhythm

HR>220 in infants,
HR>180/min in children < 8 yo.
HR>160/min in children > 8 yo.
1. SVT: tachyarrhythmia which originates
from or involve pathways mostly above bifurcation
of His
2. VT: tachyarrhymia which originates from
myocyte or Purkinje fiber below bifurcation of His.
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Mechanism of SVT in WPW syndrome

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Two syringe technique

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Management of SVT

 Physiological treament:
 Vagal maneuver - Ice pack
 Gag reflex - Carotid massage

 Medical treatment
 Adenosine: 0.1-0.3 mg/kg/dose: 2 syringe
 technique, max 12 mg
 Propanolol: 0.1 mg/kg/dose, dilute, IV slowly
 Verapamil: 0.1 mg/kg/dose, dilute, IV slowly
 Amiodarone: 5-10 mg/kg IV drip in 1-2 hrs.
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Management of SVT

Electrical treament
 Direct current synchronous mode
0.5-2 J/kg, max 4 J/kg
 Overdrive pacing
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Convert with adenosine

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Electrical Cardioversion
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Tachyarrhythmia

Ventricular tachycardia
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Polymorphic VT

Torsades de Points in Long QT syndrome

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Management of VT

 Mechanical: resuscitation
 Electrical treatment: DC shock or
synchronized mode 2-4 J/kg
 Medical:
 Lidocaine:1 mg/kg IV bolus, follow by IV
infusion
 Amiodarone: 5 mg/kg IV in 20-60 min , follow
by IV infusion
 Procainamide 15 mg/kg IV drip in 30-60 mins
 MgSO4: 25-50 mg/kg IV, max 2 gm
 Correct hypoMg, hypoCa, hypo&hyperkalemia
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Cardiac dysrrhythmia
 Bradyarrhythmia: abnormally slow heart and rhythm
 complete heart block: congenital, acquired (post
operative CHD)
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Temporary pacemaker
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Case 4

A 3-day-old boy was brought to the ER

due to develop cyanosis 1 hour ago.
PE: RR 65/min, PR 150/min, BP 58/30
O2 sat 60%, active, no dyspnea,
cyanosis,
no dysmorphic features
CVS: normal S1, S2 single, no murmur
Abd: liver just palpable
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Differential Diagnosis

Cyanotic heart diseases with decrease

pulmonary blood flow eg.
 VSD with pulmonary atresia supply by
PDA (closing)
 Complex heart diseases with pulmonary
atresia
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Cyanotic heart disease with parallel

circuit eg.
 D-transposition of great arteries with
inadequate mixing
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Obstructed total anomalous pulmonary
venous connection
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Interpretation of oxygen challenge test

Fio2 = 0.21 Fio2 = 1.00
PaO2 PaO2
(% Saturation) (% Saturation) PaCO2
Normal 70 (95) >200 (100) 35
Pulmonary disease 50 (85) >150 (100) 50
Neurologic disease 50 (85) >150 (100) 50
Methemoglobinemia 70 (85) >200 (85) 35
Cardiac disease
Separate circulation <40 (<75) <50 (<85) 35
Restricted PBF <40 (<75) <50 (<85) 35
Complete mixing 50 (85) <150 (<85) 35
without restricted PBF

Persistent pulmonary hypertension Preductal Postductal

PFO (no right-to-left shunt) 70 (95) <40 (<75) Variable 35-50
PFO (with right-to-left shunt) <40 (<75) <40 (<75) Variable 35-50

Adapted J Pediatr. 1970;77:484; Peiatr Rev. 1982;4:13; and Arch Dis Chid. 1976;51:667.
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Management

PGE1 IV drip rate 0.01-0.1 mcg/kg/min

gradually titrate – accept O2 sat > 70%,
PaO2 >30 mmHg
Maintain airway, breathing, metabolic
status and vital signs
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Modified Blalock-Taussig shunt

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Major changes in new CPR guideline 2010
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Major changes in PALS 2010
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Thank you
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Case 4

 A 1-year-old boy with atrioventricular septal

defect and severe pulmonary hypertension,
underwent total repaired.
 4 hours PO. he develops hypotension,
 PE: On ventilator, BP 60/40, CVP 13 mmHg,
PA pressure 80/55, HR 150/min
O2 sat 98%
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Pulmonary hypertensive crisis

 Def: Decrease pulmonary blood flow from

sudden increase in pulmonary vascular
resistant with result in inadequate cardiac
output.
 Clinical manifestations:
 Low cardiac output: hypotension, tachycardia,
decrease urine output
 Increase CVP
 Decrease LA pressure
 Metabolic acidosis
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Management of PHT crisis

 Sedate, paralyze with ventilatory support

 Keep serum alkalosis
 Pulmonary vasodilator:
 Milinone
 NO
 Iloprost: inhale, IV
 Sildenafil
 Keep dry:
 Decrease pulmonary vasoconstrictor:
adrenaline, high dose dopamine
 Correct metabolic disturbance
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Pathways of anti-pulmonary hypertensive drug

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แสดงขนาดและกลไกการออกฤทธิ์ของ Vasodilator แต่ละชนิด
Medication Route Dosage Site action
Captopril PO 0.1-2.0 mg/kg/dose arteriolar and Competitive inhibition of
ทุก 6-8 ชม. venous Angiotensin-converting
Maximum 6 mg/kg/day enzyme
Enalapril PO 0.1-0.2 mg/kg/day arteriolar and Competitive inhibition of
ทุก 12 or 24 ชม. venous Angiotensin-converting
enzyme
Hydralazine IV 0.1-0.5 mg/kg/day arteriolar Direct vasodilation by unknown
PO ทุก 6-8 ชม. mechanism
0.25-1.0 mg/kg/day
ทุก 6-8 ชม.
Maximum 7 mg/kg/day
Prazosin PO 0.01-0.05 mg/kg/day arteriolar and Competitive blockade of
ทุก 6-8 ชม. venous alpha-1 adrenergic receptors
Maximum 0.1 mg/kg/dose
Nitroprusside IV 0.5-6.0 µg/kg/min arteriolar and Direct vasodilation mediated
Maximum 10 µg/kg/min venous by changes in intracellular
cGMP
Nitroglycerin IV 1-20 arteriolar and Direct vasodilation
venous
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Tachyarrhythmia

Atrial flutter: reentry circuit in atrium

- Congenital atrial flutter

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Emergency in Pediatric Cardiovascular
Conditions

Cardiogenic shock
Congestive heart failure
Hypoxic spells
Cardiac arrhythmia:
 Tachyarrhythmia
 Bradyarrhythmia
Pulmonary hypertensive crisis
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Normal conducting system