pediatric cardiovascular problems in emergency setting 1 (5 feb- 2011)

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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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Page 1: Pediatric cardiovascular problems in emergency setting 1 (5 feb- 2011)

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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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

Cardiogenic shock

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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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LOGOCardiogenic Shock

1. Congenital heart diseases eg.

Ductal dependent lesion: Left sided obstructive lesions

Etiology:

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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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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,

Management of cardiogenic shock

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แสดงยาที่ใชใ้นการรกัษา cardiogenic shock

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aPVR , pulmonary vascular resistance; SVR, systemic vascular resistance; and PDE3, phosphodiesterase inhibitor.

Agent Site of action Dose (µg/kg/min) Effecta

Dopamine Dopaminergic

β

> β

0.5-4

4-10

11-12

Renal vasodilator

Inotrope

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

min then 0.375-0.75

µg/kg/min

Same as Amrinone

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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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RV LV

PVR SVR

PA AO

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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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Torsades de Points in Long QT syndrome

Polymorphic VT

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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

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

Fio2 = 0.21 Fio2 = 1.00

PaO2 PaO2

(% Saturation) (% Saturation) PaCO2

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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LOGOMajor 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/doseทุก 6-8 ชม.Maximum 6 mg/kg/day

arteriolar and venous

Competitive inhibition ofAngiotensin-convertingenzyme

Enalapril PO 0.1-0.2 mg/kg/dayทุก 12 or 24 ชม.

arteriolar and venous

Competitive inhibition ofAngiotensin-convertingenzyme

Hydralazine IVPO

0.1-0.5 mg/kg/dayทุก 6-8 ชม.0.25-1.0 mg/kg/dayทุก 6-8 ชม.Maximum 7 mg/kg/day

arteriolar Direct vasodilation by unknown mechanism

Prazosin PO 0.01-0.05 mg/kg/dayทุก 6-8 ชม.Maximum 0.1 mg/kg/dose

arteriolar and venous

Competitive blockade ofalpha-1 adrenergic receptors

Nitroprusside IV 0.5-6.0 µg/kg/minMaximum 10 µg/kg/min

arteriolar and venous

Direct vasodilation mediatedby changes in intracellular cGMP

Nitroglycerin IV 1-20 arteriolar and venous

Direct vasodilation

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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