Pediatric Advanced Life Support (PALS)

A set of life-saving protocols and skills that

extend Pediatric Basic Life Support (PBLS)
to further support the circulation and
provide an open airway and adequate
ventilation, in manage efficiently and
effectively the critically ill infants and
children, resulting in improved outcomes
1. Prevention
2. Early cardiopulmonary resuscitation (CPR)
3. Prompt access to the emergency response system
4. Rapid pediatric advanced life support (PALS)
5. Integrated post cardiac arrest care
 The principle aim of pediatric
advanced life support (PALS)
To prevent cardiopulmonary failure through
early recognition and management of
respiratory distress, respiratory failure, and
shock.
 Components of PALS
Recognition and treatment of
cardiopulmonary arrest;
Pediatric assessment;
Respiratory management;
Defibrillation and synchronized
cardioversion;
Intraosseous access and fluid bolus
administration; and
Resuscitation team
Oxygen
Use 100% oxygen during
resuscitation
Stable: wean supplementary
oxygen but ensure adequate
oxygen delivery by
appropriate monitoring
Humidify oxygen to prevent
mucosal drying and
thickening of pulmonary
secretions
 Endotracheal Tube Size
Roughly equal the size of childs little
finger
Uncuffed endotracheal tube size (mm ID)
=(age in years/4) + 4
Cuffed endotracheal tube size (mm ID)
= (age in years/4) + 3
Ready with 0.5 mm smaller and 0.5 mm
larger than the size estimated
 ET tube size, Suction catheter and
Laryngoscope blade
Age ID Tube Suction Laryngoscope blade
size Catheter
Newborn 3.0 6 Fr No. 0, Miller straight blade
18 mos 4.0 8 Fr No. 1, Miller straight blade
3 years 4.5 8 Fr No. 2, Miller straight blade
5 years 5.0 10 Fr No. 2, Miller straight blade
8 years 6.0 10 Fr No. 2, Miller straight blade or
MacIntosh curve blade
12 years 6.5 10 Fr No. 3, MacIntosh curve blade
16 years 7.0 12 Fr No. 3, Miller straight blade or
MacIntosh curve blade
 Rapid Sequence Intubation (RSI)
Requires special training
Cuffed endotracheal tube is as safe as an
uncuffed tube
Chose appropriate size
Use sedatives, neuromuscular blocking
agents
Verify tube position and secure the tube
after intubation
Keep cuff inflation pressure <20 cm H2O
Maintain the patients head in a neutral
position
 Laryngeal inlet

Courtesy of Joshua Nagler, MD.

 Verification of Endotracheal Tube
Placement
Look for bilateral chest movement
Listen for equal breath sounds over both
lung fields
Listen for gastric insufflation sounds over
the stomach
Check oxygen saturation with a pulse
oximeter
Perform direct laryngoscopy if still
uncertain
Perform chest x-ray to verify tube position
Deteriorates ?? Consider DOPES !!
Displacement from the trachea
Obstruction
Pneumothorax
Equipment failure
Stomach (Gastric distension)
 Bag-Mask Ventilation
(Healthcare Providers)
Effective and safer in providing ventilation for
short periods and out-of-hospital setting
Select the correct mask size
Use self-inflating bag with volume 450-500 mL
Supplementary oxygen may attached
Opening the airway
Making a tight seal between the mask and face
Delivering effective ventilation
Assessing the effectiveness of ventilation
Pause after compressions to give 2 ventilations
Avoid hyperventilation
E-C clamp technique
 Excessive ventilation
Increases intrathoracic pressure and
impedes venous return -- decreases
cardiac output, cerebral blood flow,
and coronary perfusion.
Causes air trapping and barotrauma in
patients with small airway obstruction.
Increases the risk of regurgitation and
aspiration in patients without an
advanced airway.
 Gastric Inflation and Cricoid Pressure
Gastric inflation interfere effective
ventilation and cause regurgitation
Avoid excessive peak inspiratory
pressures (eg, ventilate slowly)
Apply cricoid pressure in an unresponsive
victim (Sellick's maneuver)
 Defibrillators
Manual or automated (AED), with mono or
biphasic waveforms
Paddle size:>10 kg=8-10 cm;<10 kg=4.5 cm
Interface: gel pads, self-adhesive
monitoring-defibrillation pads, electrode
cream, paste
Paddle position: on right side of the upper
chest and the apex of the heart; or on the
left sternum and below the scapula
Energy dose:2-4 J/kg (up to 9 J/kg)
 "Nonshockable Rhythm
(Asystole,Pulseless Electrical Activity/PEA)
Asystolic and bradycardia are the most
common ECG findings in infants and
children in cardiac arrest (90 %)
PEA: organized electrical activitymost
commonly slow, wide QRS complexes
without palpable pulses
 "Shockable Rhythm
(VF/Pulseless VT)
5% to 15% of all pediatric victims of out-of-
hospital cardiac arrest
Up to 20% of pediatric in-hospital arrests
Defibrillation is the definitive treatment
for VF with an overall survival rate of 17%
to 20%
 During CPR
Correct reversible causes*
Check electrode position and contact
Attempt/verify:
IV/IO access
airway and oxygen
Give uninterrupted compression
when airway secure
Give adrenalin every 3-5 min
Consider:amiodarone, atropine,
magnesium
 Reversible causes*
Hypoxia
Hypovolemia
Hypo/hyperkalaemia/metabolic
Hypothermia
Tension pneumothorax
Tamponade, cardiac
Toxins
Thrombosis (coronary or pulmonary)
 Continuous recording during an episode of ventricular
fibrillation that progresses to asystole

At the onset of ventricular fibrillation (VF), the QRS complexes are regular, widened, and of
tall amplitude, suggesting a more organized ventricular tachyarrhythmia. Over a brief
period of time, the rhythm becomes more disorganized with high amplitude fibrillatory
waves; this is coarse VF. After a longer period of time, the fibrillatory waves become fine,
culminating in asystole.
 Vascular access
Peripheral proximal upper extremity is the
location of choice for IV administration
IO vascular access in the proximal tibia or distal
femur should be initiated if peripheral access
cannot be achieved in 3 attempts or 90 seconds
in a child younger than 6 years of age
IO access is a rapid, safe, and effective route for
the administration of medications and fluids
Central venous access (preferably femoral)
should be obtained, if IO access is unsuccessful
or if the child is over six years of age
 Intraosseous (IO) access
Easily to achieved
Recommended in cardiac arrest if no IV
access in place or fail to achieve quickly
Commonly used at distal femur, proximal
tibia, and distal tibia (medial malleolus)
Proximal tibia is the most common
Often successful and relatively free
complications
Potential problems : failure to place the
needle, fracture, infection, and compartment
syndrome (extravasation of fluid)
 Fluids
Use isotonic crystalloid solution (eg,
lactated Ringers solution, normal saline)
or colloid (eg, albumin)
Fluid boluses, 20 mL per kg rapidly until
the shock is resolved (delivered in less
than 20 minutes)
Use a glucose-containing solution to only
treat documented hypoglycemia
 Algorithm of hemodynamic support
in infants and children (1)
0
Recognize decreased mental status and perfusion. Begin high flow
O2. Establish IV/IO access.
5
Initial resuscitation:
If 2nd PIV
Push boluses of 20 cc/kg isotonic saline or colloid up to & over 60 start
cc/kg until perfusion improves or unless rales or hepatomegaly inotrope.
develop. Correct hypoglycemia & hypocalcemia. Begin antibiotics.
Shock not reserved?
15
dose range:
Fluid refractory shock: dopamine up
Begin inotrope IV/IO. Use atropin/ketamine IV/IO/IM to obtain to 10 mcg/
central access & airway if needed. Reserve cold shock by titrating kg/min,
epinephrine
central dopamine or, if resistent, titrate central epinephrine.
0.05 to 0.3
Reserve warm shock by titrating central norepinephrine. mcg/kg/min

Shock not reserved?

60
min Catecholamine resistant shock:
Begin hydrocortisone if at risk for absolute
adrenal insufficiency
 Inotropes/Vasoactive Agents
DRUGS DOSAGES
Dopamine 1-5 mcg/kg/min: dopaminergic; 5-15 mcg/kg/ min:
more beta-1; 10-20 mcg/kg/min: more alpha-1
Dobutamine 2.5-15 mcg/kg/min; mostly beta-1, some beta-2

Epinephrine 0.05-0.1 mcg/kg/ min: mostly beta-1, some beta-2;

>0.1 to 0.2 mcg/ kg/min: alpha-1
Nor-epinephrine 0.05-0.2mcg/kg/ min; Use up to 1mcg/kg/min; only
alpha and beta-1
Milrinone 50mcg/kg load then 0.375-0.75 mcg/kg/min;
Phosphodiesterase inhibitor; results in increased
inotropy and peripheral vasodilation (greater effect
on pulmonary vasculature)
TQ