The goal of Pediatric Advanced

Life Support (PALS) is to save a

life.

For a child or infant

experiencing serious
injury or illness, your
action can be the
difference between life
and death
PALS Course/What content is taught
in the PALS Classroom Course?
Recognition of Recognition of
High-quality Child patients who do cardiopulmonary
Apply team
CPR AED and Infant and do not require arrest early and
dynamics
CPR immediate application of CPR
intervention within 10 seconds

Differentiation
Differentiation Early interventions between Early interventions
between respiratory for respiratory compensated and for the treatment of
distress and failure distress and failure decompensated shock
(hypotensive) shock

Clinical
Differentiation
characteristics of
between unstable Post–cardiac arrest
instability in
and stable patients management
patients with
with arrhythmias
arrhythmias
Audience/Who is the target audience for the PALS
Course?

• Healthcare providers who either direct or participate in the management of

respiratory and/or cardiovascular emergencies and cardiopulmonary arrest in
pediatric patients.

• Personnel in emergency response, emergency medicine, intensive care, and

critical care units

• Physicians, nurses, paramedics, and others who need a PALS course

completion card for job or other requirements.
Core Case Testing Stations/What are the course
completion requirements for the PALS Course?

The 12 required case scenarios are:

1. Upper Airway Obstruction

2. Lower Airway Obstruction
3. Lung Tissue Disease
4. Disordered Control of Breathing
5. Hypovolemic Shock
6. Obstructive Shock
7. Distributive Shock
8. Cardiogenic Shock
9. Supraventricular Tachycardia
10. Bradycardia
11. Asystole/PEA
12. VF/Pulseless VT
Skills Stations/What are the course completion
requirements for the PALS Course?

Required skills stations include:

• Child CPR and AED

• Infant CPR
• Management of Respiratory Emergencies
• Rhythm Disturbances/Electrical Therapy
• Vascular Access
 Exam/What are the course completion
requirements for the PALS Course?

The minimum course completion requirements include:

• Participation in the classroom course, including completion of all learning stations

• Completion of the open-resource written exam with a minimum score of 60 %

• Passing the 1- and 2-Rescuer Child BLS With AED and 1- and 2-Rescuer Infant BLS
Skills Tests

• Passing 2 PALS core Case Scenarios (1 cardiac and 1 respiratory or shock) as a

team leader, providing appropriate medical treatment and demonstrating
effective team dynamics
Elaborate cognitive and psychomotor
course objectives

• Identification and treatment of problems that place the child at risk

for cardiac arrest
• Timely recognition and interventions required to prevent cardiac or
respiratory arrest
• Application of a systematic approach to pediatric assessment
• Use of the “evaluate-identify-intervene” sequence
• Use of PALS algorithms and flowcharts
• Demonstration of effective TEAM dynamics
• Key elements of post resuscitation management
BLS
Infant BLS
Systemic approach
Initial Impression
• The algorithm begins with the “Initial Impression.” The initial impression
consists of a quick assessment of three characteristics:

• Consciousness:
Unresponsive, irritable, or alert.

• Breathing:
Rate, Abnormal breathing Patterns, Abnormal breath Sounds, and Accessory
muscle use.

• Color:
Visual characteristics that indicate poor perfusion and/or oxygenation such
as cyanosis, pallor, or mottling.
• This initial impression of consciousness, breathing, and color
helps to answer the following question: “Is the child
unresponsive with no breathing or only gasping?” This
question is the first decision point of the algorithm.
• The left side of the algorithm leads into the Pediatric Cardiac Arrest Algorithm.

• The right side of the algorithm flows into the Evaluate-Identify-Intervene

Sequence.

• The right side of the algorithm is where the effective treatment of the critically
ill child occurs.
• The goal of treatment is to keep the child away from the left branch of the
algorithm.

• Prevention of cardiopulmonary arrest using the Evaluate-Identify-Intervene

Sequence is central to PALS.

• This sequence of Evaluate-Identify-Intervene allows you to carry out the best

treatments based upon ongoing assessment.
1) Evaluation

Three assessment tools:.

• Primary assessment:
ABCDE evaluation tool to evaluate respiratory, cardiac, and neurological
function. Vital signs are also included in this assessment.

• Secondary assessment:
Focused history and a focused physical exam.

• Diagnostic tests:
advanced tests that can help identify the cause of the pediatric emergency.
Examples include ABG, x-ray, and laboratory blood tests.
• Evaluation portion of the Evaluate-Identify-Intervene Sequence
provides you with the information you need to move forward into
the next portion of the sequence which is Identify.
2) Identification

• Identification of the specific problem that caused the pediatric

emergency is essential for improving outcomes.

• Specific problems within PALS are broken down into 4 categories:

Respiratory problems
Circulatory problems
Cardiopulmonary failure
Cardiac arrest.
3) Intervention

• Interventions for the treatment of the critically ill child include

both general interventions and specific interventions. These
interventions for the management of the critically ill child are
thoroughly reviewed throughout this course.
• Once the sequence is complete, the sequence starts again with
an evaluation of the child’s clinical. This Evaluate-Identify-
Intervene Sequence is carried out until the child is stable .
 SYSTEMATIC APPROACH. SUMMARY

• Initial Impression/Assessment
• Cardiac Arrest
• Evaluate/ Identify/ Intervene

• Evaluate
• Primary Assessment/ ABCDE
• Secondary Assessment/ Focused Exam/ SAMPLE
History
• Tertiary Assessment/ Diagnostic Tests
• Identify
• Respiratory > Severity > RD/RF
• Circulatory > Severity > CS/UCS
• Intervene
Teamwor
k
CODE Team Positions During CPR
Closed Loop Communication
ADVANCED LIFE
SUPPORT
Systemic approach to
seriously ill child
 Apply the evaluate-identify-
intervene sequence

Systematic
Explain the purpose and
approach components of initial impression

to
seriously ill Describe the ABCDE components of
the primary assessment
child
Interpret clinical findings during the
primary assessment
 Infants and
Children, most
cardiac arrests
Rapid results from
progressive
respiratory failure,
Interventi shock or both.

on to
Prevent
Cardiac Outcome is poor
even with optimal
resuscitation once
Sudden collapse
without warning

Arrest
occur less
Cardiac arrest
commonly.
occurs.
Initial Impression
• Consciousness
• Level: Unresponsive, irritable, alert

• Breathing
• Increased work of breathing, absent or
decreased respiratory effort, or abnormal
sounds heard without auscultation.

• Color
• Abnormal skin, color, such as cyanosis, pallor
or mottling.
Circulation
Disability
Exposure

• Undress seriously ill or injured child

• Keep child comfortable

• Check temperature—Hypothermia / hyperthermia

• Use blankets

• Look for signs e.g. petechial rash, purpura, bruising, lines, patterned
bruises--NAI
Secondary Assessment
History
Diagnostic testing

• O2 saturation
• VBG
• CBC
• Electrolytes, Calcium, Mg, Phos
• Lactic acid
• CXR
• EKG
• Echo
• CVP
Evaluate-Identify-Intervene
Evaluate
Clinical Brief Description
Assessment
Primary A rapid, hands on ABCDE approach to evaluate
Assessment respiratory, cardiac and neurological function;
this will include assessment of Vital signs and
Pulse oximetry.
Secondary A focused medical history and a focused
assessment physical exam.

Diagnostic Tests Lab, radiographic and other advanced tests

that help to identify the child physiological
condition and diagnosis.
Identify
Type Severity
Respiratory Upper airway Respiratory Distress
Obstruction
Lower airway Respiratory Failure
Obstruction
Lung tissue disease
Disordered control of
breathing
Circulatory Hypovolemic shock Compensated shock
Distributive shock
Cardiogenic shock Hypotensive shock
Obstructive shock

Cardiopulmonary Failure
Cardiac Arrest
Intervene

• Positioning the child to maintain a patent airway

• Activating emergency response
• Starting CPR
• Obtaining the code cart and monitor
• Placing the child on a cardiac monitor and pulse
oximeter
• Administering O2
Intervene
• Supporting Ventilation
• Starting medications and fluids (e.g. nebulizer
treatment, IV/IO fluid bolus)

• Remember to repeat the evaluate-identify-intervene

sequence until the child is stable
• After each intervention
• When the child’s condition changes or deteriorates.
Early Intervention

Respiratory Distress

Respiratory Failure/Shock

Cardiopulmonary
Failure

Cardiopulmonary
Arrest
Continuous Sequence

• Till child is stable

• Re-assess before and after intervention
• Oxygen- re-evaluate
• Breathing easier
• Color and mental status improving
• Fluid bolus- improving?
• Determine if the problem is
• Life threatening
• Not Life threatening
• Life threatening; then initiate the Emergency Response
system
• If not then continue with Systemic Approach.
Life Threatening problems
Air way Complete or Severe airway
Obstruction

Breathing Apnea, significant increased

work of breathing , bradycardia

Circulation Absence of palpable pulses, poor

perfusion, hypotension,
bradycardia

Disability Unresponsiveness, decreased

level of consciousness

Significant hypothermia,
Exposure significant bleeding, petechiae,
or purpura consistent with septic
shock.
Respiratory Distress /
Respiratory Failure
Signs of respiratory distress

• Tachypnea
• Tachycardia
• Grunting
• Stridor
• Head bobbing
• Flaring
• Inability to lie down
• Agitation
• Retractions
• Accessory muscles
• Wheezing
• Sweating
• Prolonged expiration
• Apnea
• Cyanosis
Signs of respiratory failure

• Reduced air entry

• Severe work

• Irregular breathing or apnea

• Cyanosis despite oxygen delivery

• Altered level of consciousness

• Diaphoresis
Signs of circulatory compromise
• Tachycardia

• Cool skin

• Weak peripheral pulses

• Changes in level of consciousness

• Delayed capillary refill time

• Decreased urine output

• Changes in skin color (pallor, mottling, cyanosis)

Causes of respiratory Failure
Scenario
Scenario
Scenario

A young mother presents to the ED with a 12-month-old boy who has had
constant vomiting for 24 hours. The infant is lying still and has poor muscle
tone. He is irritable if touched, and his cry is weak. There are no abnormal
airway sounds, retractions, or flaring.
Cardiac Arrhythmias in Pediatrics
Bradycardia
Conduction Pathway
E.C.G
What Things You Need To Notice

• Rate
• Rhythm
• Intervals
• Waves
• Segments
Recognize bradycardia

• Heart rate slower in comparison with a normal heart rate range

for the child’s age and level of activity.
Bradyarrhythmia - Symptoms

• General:
Altered LOC, fatigue, lightheadedness, dizziness,
syncope

• Hemodynamic instability:
Hypotension, Poor end-organ perfusion,
Respiratory distress/failure, Sudden collapse
Bradyarrhythmias - Causes

• 1º:
• Abnormal pacemaker/conduction system
(congenital or postsurgical injury), cardiomyopathy,
myocarditis

• 2º:
• Reversible Hs & Tso:
• Hypoxia – Hypotension – H+ ions (acidosis)
• Heart block – Hypothermia – Hyperkalemia

• Trauma (head)
• Toxins/drugs (cholinesterase inhibitors, Ca++ channel blockers, β-
adrenergic blockers, digoxin, central α2-adrenergic agonists, opioids)
Bradyarrhythmias - Types

• Sinus bradycardia
• Physiologic (ie: sleep, athletes) vs.
• Pathologic (ie: abnormal lytes, infection, drugs,
hypoglycemia, hypothyroidism, ↑ICP)

• Sinus node block

• Subsidiary pacemakers lead to atrial,
junctional, & idioventricular escape rhythms

↓Junctional beat
1st degree heart block

2nd degree heart block,

Mobitz I

2nd degree heart block,

Mobitz II

3rd degree heart block

Sinus bradycardia
Bradyarrhythmias - Management

• Stable patients:
• ABC, O2, 12 lead EKG, Labs, Consult
cardiology

• Unstable patients:
• ABCs, O2, CPR, Defib, IV Access
• PALS Pediatric Bradycardia Algorithm

• Address reversible causes (Hs & Ts)

When bradycardia requires immediate
intervention

• Decreased level of consciousness

• Hypotension
• Shock
• Poor end organ function
• Respiratory distress or failure
• Sudden Collapse
Describe initial steps to stabilize a child
with acute cardiopulmonary
compromise

• Airway, Breathing, Circulation

• O2 inhalation
• Attach an ECG monitor/defibrillator
• Obtain vascular access
Recognize when to start CPR in a child with
bradycardia

If heart rate <60 beats per minute with poor

perfusion despite effective ventilation with oxygen,
start CPR.
Select appropriate medications treatment of symptomatic bradycardia

• Continue to support airway, ventilation,

oxygenation, and chest compressions.

• If bradycardia persists or responds only

transiently,
• Epinephrine IV (or IO) 0.01 mg/kg (0.1 mL/kg of
1:10,000 solution) or

• if IV/IO access not available, give endotracheal 0.1

mg/kg (0.1 mL/kg of 1:1,000 solution).
Select appropriate medications treatment of symptomatic bradycardia

• If bradycardia is due to increased vagal tone or

primary AV conduction block (i.e., not secondary
to factors such as hypoxia),

• give IV/IO atropine 0.02 mg/kg or

• an endotracheal dose of 0.04 to 0.06 mg/kg.
When to use pacing?
• Emergency transcutaneous pacing may be
lifesaving

• if the bradycardia is due to complete heart block or

sinus node dysfunction unresponsive to ventilation,
oxygenation, chest compressions, and medications,

• especially if it is associated with congenital or

acquired heart disease.

• Pacing is not useful for asystole or bradycardia due

to post-arrest hypoxic/ischemic myocardial insult or
respiratory failure.
Reversible causes
6 Hs 5 Ts -Search for Reversible Causes

• Hypoxia or ventilation problems

• Hypovolemia
• Hypothermia
• Hypoglycemia
• Hypo /hyper kalemia
• Hydrogen ion (acidosis)

• T amponade, cardiac
• T ension pneumothorax
• T oxins – poisons, drugs
• T hrombosis – coronary (AMI)
• T hrombosis – pulmonary (PE)
Reversible Causes
Hypoxia:
Give high conc. Of supplemental O2 with
assisted ventilation
Acidosis:
Provide ventilation to treat respiratory
acidosis sec to hypercarbia: consider sodium
bicarbonate in sever metabolic acidosis
Hyperkalemia :
Restore normal Potassium conc .
 Reversible Causes

• Hypothermia:
Warm the child as needed, avoid hyperthermia, if the pt
has experienced a cardiac arrest.
• Heart Block:
For AV block, consider atropine, chronotropic drugs and
electrical pacing, obtain expert opinion
Toxins, poisons and drugs:

Treat with specific antidote and provide

supportive care.
Some toxicological causes of bradyarrythmias
are

• Cholinesterase inhibitor (organophosphate,

nerve agents)
• Ca channel blockers
• Badrenergic blockers
• Digoxin and other cardiac glycoside
• Opoids
• Succinylcholine
Reversible Causes: Trauma
• Head Trauma :
• Bradycardia in child with head trauma is
ominous sign of raised ICP
• Provide oxygenation, ventilation
• Obtain expert opinion
Return of spontaneous
circulation (ROSC)/Post
resuscitation care
Post resuscitation care

Aims:
• Optimize ventilation and circulation
• Preserve organ/tissue function
• Maintain blood glucose level
• Minimize the risk of deterioration
Post resuscitation care
Children who have been resuscitated from cardiorespiratory
arrest may die hours or days later from multiple organ failure
sec to hypoxia /ischemia and inflammatory mediators

• Re perfusion injury : Cellular damage continues after

spontaneous circulation has been restored, caused by
• Depletion of ATP
• Entry of calcium into cells
• Free fatty acid metabolism activation
• Free radical O2 production
Respiratory
• Chest x-ray to verify ET tube placement
• ABGs acid base balance
• Heart rate and rhythm
• End tidal CO2
• Maintain good oxygenation
• Adequate ventilation pco2 between 35to 45
• Control pain
CVS
• ABGS
• HR rhythm
• BP
• CVP
• UOP
• Chest x-ray
• Ecg
• Echo
• Maintain intravascular volume
• Adequate oxygenation
• Correct metabolic abnormality
Neurological
• Elevate head of bed (cerebral perfusion)
• Temperature(avoid hyperthermia)
• Maintain blood glucose
• Neurological exam
• Consider CT/EEG
• HTN, bradycardia, respiratory distress or apnea may
indicate cerebral herniation
Renal
• UOP
• Routine blood chemistries
• ABGs
• Urine exam
• Cardiac output
Hematology
• CBC
• Coagulation profile
• Blood chemistries
GI
• NGT
• Abdominal exam
• Abdominal USG OR CT
• Liver panel, coagulation
• Gastric perfusion, liver protection
• Early introduction of feed
• Calories – Feeds / TPN
Post resuscitation care: Labs

• Cbc, blood group and save

• U/e, ca, mag, po4, blood /sugar
• Renal and hepatic function
• ABG, VBG
• Lactate
• Blood c/s
• X ray chest
• echocardiography
PALS course
DAY-2
Fluids and Electrolytes
in Pediatrics
Introduction
• Enteral feeds are the ultimate goal

• Patients who are NPO require “maintenance” fluids, unless severe volume overload is
present.

• Patients may require additional “replacement” fluids to address excessive ongoing

losses (e.g. NG output).

• In addition, many patients require “volume resuscitation” due to intravascular volume

depletion.
Indication of IV fluid replacement

Replace extracellular fluid volume losses

Maintain fluid and electrolyte balance

Correct existing electrolyte or acid-base disorders

Provide a source of glucose

 Tonicity

• Net vector of force on cells

relative to a semipermeable
membrane when in solution

• Infused isotonic fluids do not

result in osmotic shifts

• Cellular expansion occurs during

immersion in hypotonic fluids

• Hypertonic fluid immersion: free

water shifts out of the cells,
leading to cellular contraction
Osmolality
• Osmolality is measured as osmoles of solute per kilogram of solvent.

• Serum osmolality can be estimated by the following formula:

2 × Na(mEq / L) + BUN (mg / dL)/2.8+glucose (mg/dL)/18

Types of fluids
• Isotonic fluid has a sodium concentration similar to plasma (135–144 mEq/L).
• Plasma:
• 93% aqueous and 7% anhydrous
• sodium concentration in the aqueous phase of plasma of 154 mEq/L
• osmolarity of 308 mOsm/L
• similar to that of 0.9% sodium chloride (NaCl).

• hypotonic fluid has a sodium concentration lower than that of the aqueous phase of
plasma.
• Hartmann solution (sodium concentration 131 mEq/L; osmolality 279 mOsm/L)

• PlasmaLyte (sodium concentration 140 mEq/L; osmolarity 294 mOsm/L)

• Lactated Ringer solution (sodium concentration 130 mEq/L; osmolarity 273 mOsm/L),
 Composition of commonly used intravenous fluids

Osmolalit Tonicity Na+ Cl− K+ Mg2+ Ca2+ Buffera

y
Plasma 288 Referenc 140 103 4.5 1.25 2.5 24
e
0.9% 308 Isotonic 154 154 0 0 0 0
NaCl
Lactated 279 Hypotoni 130 111 4.0 0 2.7 29
Ringer’s c
PlasmaLy N/A Isotonic 140 98 5.0 1.5 0 50
te
Sterofun 309 Isotonic 140 127 4.0 1.0 2.5 29
din
5% 278 Hypotoni 0 0 0 0 0 0
Glucose c
1.4% 333 Hyperton 167 0 0 0 0 167
NaHCO3 ic
Assessment
• Perfusion—central / peripheral • selection of IV fluid therapy:
• Heart rate • blood pressure
• Urine volume/ colour/ specific • acid-base status
gravity/osmolality
• kidney function
• Serum lactate/ sodium
• presence of diabetes
• plasma osmolality
• Body weight/ total body weight
Maintenance fluid volume for a 24-hour period:​

• Weight less than 10 kg − 100 mL/kg​

• Weight >10 kg to 20 kg − 1000 mL for first 10 kg of body weight plus 50 mL/kg for any increment of
weight over 10 kg​

• Weight >20 kg - 1500 mL + 20 mL/kg for every kg over 20 (up to a maximum of 2400 mL daily)
Neonatal IV hydration
• From birth to day 1: 50–60 ml/kg/day

• Day 2: 70–80 ml/kg/day

• Day 3: 80–100 ml/kg/day

• Day 4: 100–120 ml/kg/day

• Day 5–28: 120–150 ml/kg/day

Complications
Typical type of IV fluid Complication

Normal saline Hyperchloremic metabolic acidosis,

worsening hypertension

Hypotonic IV fluids Hyponatremia

Hypertonic or isotonic IV fluids Hypernatremia

Usually isotonic IV fluids Fluid overload

Hyper hydration when needed
Risk of tumor lysis
• Cancer mass

• Cell lysis potential/Chemo-sensitive tumors

• Presenting features—nephropathy, dehydration, hypotension, exposure to

nephrotoxin
Tumor lysis syndrome
• Hyperuricemia​ urate nephropathy/ xanthine nephropathy

• Hyperkalemia​ cardiac dysrhythmia

• Hyperphosphatemia​ intravascular calcium phosphate salt  AKI

• Hypocalcemia​ cardiac dysrhythmia / neuromuscular irritability

Why Hyperhydration
• to rapidly improve renal perfusion and glomerular filtration

• to minimize acidosis (which lowers urine pH and promotes the precipitation of uric acid
crystals)

• prevent oliguria
• 3L/m2/24 hours= 125ml/m2/hour​

• 4L/m2/24 hours= 170ml/m2/hour​

• 4.5L/m2/24 hours= 200ml/m2/hour​

• Vitals sign, respiratory/pulse rate to be monitored vigilantly as hyper hydration can lead to
overload​
Insensible losses in children plus other losses
• fever
• Sweating
• Burns
• Tachypnea
• gastro-intestinal losses
• Drains
• polyuria
Normal maintenance water requirements:
• IWL = 45
• Renal = 50
• Stool = 5
Total 100 cc/100 Cal/day
Electrolytes replacements: Na, K, HCO3, Ca, Mg
Dextrose
• Initial bolus – Give dextrose, 0.20 to 0.25 grams/kg of body weight (maximum single dose, 25
grams) =2.5 mL/kg of 10 percent dextrose solution,

• higher concentrations of glucose will lead to severe local tissue damage if extravasation occurs. The
bolus should be administered slowly (2 to 3 mL/min), regardless of the patient's age.​
​
• The dextrose is given slowly to avoid acute hyperglycemia, which can cause rebound hypoglycemia
​
• Subsequent infusion – After the bolus, plasma glucose should be maintained by an infusion of
dextrose at 6 to 9 mg/kg per min​
Hypocalcemia

IN THE SETTING OF TUMOUR LYSIS, CALCIUM MUST NOT BE GIVEN AS RENAL

FAILURE MAY BE PRECIPITATED.

Phosphate binders & hemofiltration / dialysis may be required in this situation -discuss with
consultant on call and renal team, especially if phosphate >2mmol/l

In an arrest situation calcium gluconate (10%) 0.5ml/kg may be given stat and neat.
Hyponatremia
• Serum sodium of less than 125 mEq/L are at high risk for serious central nervous system symptoms;
lethargy followed by seizures is common

• The volume of 3% sodium chloride is determined by the sodium deficit, which is calculated using the
following equation:

(desired serum sodium concentration – current serum sodium concentration) × 0.6 × (weight in kg)

• Multiplying the sodium deficit by 2 gives the volume of 3% sodium chloride needed. This is generally
given over a few hours, with serum sodium checks done throughout in order to avoid hypernatremia.

• Serum sodium should not be corrected faster than 12 mEq/L within 24 hours
Hyperkalaemia
• Serum potassium of greater than 6 mEq/L
• ECG changes
• How the blood was acquired

Treat:
• Remove K from IV fluids, continuous ECG monitoring

• Calcium gluconate 10% 0.5ml/kg = 0.1mmol/kg IV, maximum 20ml slow bolus over 5-10 minutes. (Central
access: give neat. Peripheral access: Dilute 1ml in 4ml 0.9% NaCl.)
Calcium is used in symptomatic patients for cardioprotective effects, as it antagonizes the membrane effects of
potassium

• Give insulin & dextrose AND salbutamol TOGETHER (40-50% of patients are non-responders to salbutamol
alone so avoid monotherapy)
Hypomagnesaemia

• Mg < 0.6 mmol/l +/-ECG changes Arrhythmias egg Torsades

• Magnesium glycerophosphate PO

• Magnesium sulphate: 0.2mmol/kg IV 12 hourly (<12yrs)

or 4mmol IV 12 hourly (>12yrs) over 30min-2 hours
(dilute to a 10% solution with 5% dextrose or 0.9% saline)
Sodium Bicarbonate
• The routine use of sodium bicarbonate is not recommended because of lack of convincing evidence
of beneficial effects and potential adverse effect.​

• The American Heart Association (AHA) recommends that sodium bicarbonate be considered only in
children with prolonged cardiac arrest and documented severe metabolic acidosis who fail to
respond to oxygenation, ventilation, fluids, and chest compressions combined with epinephrine in
recommended doses.
Recognition of Shock
Definition of shock
• Shock is a critical condition that results from inadequate tissue
delivery of O2 and nutrients to meet tissue metabolic demand.

• Shock is often characterized by inadequate peripheral and end

organ perfusion

• In children, most shock is characterized by low cardiac output;

however, in some types of such as distributive shock, cardiac
output may be high.
Shock and Blood Pressure
• The definition of shock does not require presence of hypotension
• Shock can occur with a normal, increased, or decreased systolic blood
pressure.
Contributing factors
• Conditions that increase tissue demand for O2 and
nutrients
Fever
Infection
Injury
Respiratory distress
Pain
Whether due to inadequate supply, increased
demand, or a combination of both, Oxygen and
nutrient delivery to tissue is inadequate relative
to metabolic needs.
Types of Shock
Signs of
Shock
Pathophysiology of Shock
• When O2 delivery is inadequate to meet tissue demand, cells use
anaerobic metabolism to produce energy.

• Lactic acid produced as a by product.

• Anaerobic metabolism can only maintain limited cell function.

• If O2 delivery is not restored, organ dysfunction or failure will

result.
Factors influencing O2 delivery

Preload
Contractility Stroke Volume
Afterload x Cardiac Output
Heart Rate x
Adequate O2 delivery depends O2 content
on:
1. Sufficient O2 content in the
blood.
2. Adequate blood flow to the
O2 Delivery
tissue (CO).
3. Appropriate distribution of
blood flow to the tissues.
Effect on Blood Pressure
• Blood pressure is determined by cardiac output and
systemic vascular resistance(SVR).

• As cardiac output decreases blood pressure can be

maintained by an increase in SVR.

• In children with shock this compensatory mechanism can be

so effective that systolic blood pressure may initially remain
normal or even slightly elevated.

• Pulse pressure
• Narrow- compensated shock
• Wide- sepsis

• When SVR cannot increase further, BP starts to fall. At that

point delivery of oxygen to vital organs is severely
Compensated Shock
Compensated shock is a clinical state in which there
are clinical signs of inadequate tissue perfusion, but
patient blood pressure is in normal range.
Compensatory Area Sign
Mechanism
Increased HR Heart Tachycardia
Increased SVR Skin Cold, pale,
mottled,
diaphoretic
Peripheral Delayed capillary
circulation refill
Pulses Weak peripheral
pulses; narrow
pulse pressure
Increased Kidney Oliguria
renal and (decreased urine
splanchnic output)
vascular Intestine Vomiting, ileus
Hypotensive Shock
• Hypotensive shock is characterized of impaired
perfusion that will rapidly progress to cardiac arrest if
not corrected.

• Hypotension is a late finding in most types of shock

and may signal impending cardiac arrest.

HYPOTENSION FORMULA
1-10yrs: Hypotension is present if SBP is less than
70 mm Hg + [child’s age in years x 2] mm Hg
Once hypotensive shock is identified, it
may be minutes before a child arrests
Compensated shock

Hypotensive shock

Cardiac Arrest
 Hypovolemic Shock
Primary Finding
Assessment
A Patent unless low GCS • Diarrhea
B Quiet tachypnea
C • Tachycardia
• Vomiting
• Narrow Pulse pressure
• Weak or absent peripheral • Hemorrhage
pulses
• Normal or weak central pulses • Inadequate fluid
• Delayed capillary refill
• Cool to cold, pale, mottled, intake
diaphoretic skin
• Dusky/pale distal extremities • Osmotic diuresis
• Changes in level of
consciousness • Third space losses
• Oliguria
D Changes in level of • Large burns
consciousness
E Extremities often cooler than trunk
 Distributive Shock
Primary Finding
Assessme
nt
A Patent unless low GCS
B Quiet tachypnea unless pneumonia, ARDS • Septic shock
or cardiogenic pulmonary edema
C • Tachycardia • Anaphylactic shock
• Bounding peripheral pulses
• Brisk or delayed capillary refill • Neurogenic shock
• Warm flushed skin peripherally
Or
• pale mottled skin with vasoconstriction
• Hypotension with a wide pulse pressure
Or
• Hypotension with a narrow pulse
pressure
Or
• Normotension
• Changes in level of consciousness
• Oliguria
D Changes in level of consciousness
E Fever or hypothermia
Extremities warm or cool
 Cardiogenic Shock
Primary Finding
Assessment
A Patent unless low GCS
B Tachypnea • Congenital heart
Increased effort resulting from
pulmonary edema disease
C •
•
Tachycardia
Normal or low BP with
• Myocarditis
•
narrow Pulse pressure
Weak or absent peripheral
• Cardiomyopathy
pulses
• Normal -> weak central • Arrhythmias
pulses
• Delayed capillary refill with • Sepsis
cool extremities
• Signs of CHF • Poisoning or toxicity
• Cyanosis
• Cold, pale, mottled,
diaphoretic skin
• Myocardial injury
• Changes in level of
consciousness
• Oliguria
D Changes in level of
Obstructive Shock
Cardiac tamponade:
Cardiac tamponade is caused by
accumulation of fluid, blood, or air in
the pericardial space. Increased
intrapericardial pressure and
compression of heart impede
systemic and pulmonary venous
return.
Cardiac Tamponade
Primary Finding
Assessment
A Usually patent unless level of consciousness is
significantly impaired
B Respiratory distress

C • Tacycardia
• Poor peripheral perfusion
• Muffled heart sounds
• Pulsus paradoxus
• Distented neck veins
D Changes in level of consciousness.

E Extremities often cooler than trunk.

Tension Pneumothorax
• Tension pneumothorax is caused by an entry of air into
pleural space and accumulations under pressure.

Primary Finding
Assessme
nt
A • Variable depending upon on situation and
primary cause of respiratory distress.
• Tracheal deviation toward contralateral
side .

B • Respiratory distress.
• Hyper resonance of affected side.
• Diminished breath sounds.
C • Distended neck veins.
• Pulsus paradoxus .
• Rapid deterioration in perfusion.

D Changes in level of consciousness.

Pulmonary Embolism
• Pulmonary embolism is a total or partial
obstruction of the artery or its branches by a blood
clot, fat, air, amniotic fluid, catheter fragment, or
injected matter.
Primary Finding
assessment
A Usually open unless level of consciousness is
significantly impaired.
B Respiratory distress
C  Tachycardia
 Cyanosis
 Hypotension
 Systemic venous congestion and right
heart failure
 Chest pain
D Changes in level of consciousness
E Extremities may be cool and mottled.
Recognition of Shock Flowchart
Clinical Signs Hypovolemic Shock Distributive Cardiogenic Obstructive
Shock Shock Shock
A Patency Airway open and maintained/not maintainable
Respiratory rate Increased
B
Respiratory effort Normal to increased Labored
Breath sounds Normal Normal Crackles, grunting
(+/- crackles)
Systolic BP Compensated shockHypotensive shock
Pulse pressure Narrow Variable Narrow
Click to add text
C Heart rate Increased
Peripheral pulses Weak Bounding or Weak
weak
Skin Pale, cool Warm or cool Pale, cool
Capillary refill Delayed Variable Delayed
Urine output Decreased
D Level of Irritable early, Lethargic late
consciousness
E Temperature Variable
CASE 1
Introduction You enter the room of a 3 Years old girl who was brought to the EAR with
a h/o vomiting and diarrhea with poor oral intake.

General Assessment You see a child who appears listless. She is lying on the
bed and does not respond to her parents. She is breathing rapidly
without retractions or respiratory distress. Her color appears mottled.

Primary Assessment You start oxygen. HR 210/min, RR 50/min, BP 60/43, Temp

36.1. SPO2 monitor is not picking up the pulse consistently, but when a
reading is obtained it is 99-100%. Weak brachial and femoral pulses are
palpated, but distal pulses are absent. Heart sounds are normal. Extremities
are cool and mottled below the elbows and knees. Capillary refill time in
the foot is >5sec. During the examination child moans occasionally but
otherwise has little response to verbal or painful stimuli.

Is this shock?

What type?
CASE 2
Introduction A mother brings her 4 year old girl to the OPD. The child has a
history of increasing lethargy, fever, and dizziness when she tries to
stand up. There is no history of vomiting or diarrhea. Her oral intake has been poor
over the last 12 hours. Typical chicken pox lesions developed 5 days ago.
Over the last 18 hours, several lesions on her abdomen have become red,
tender, and swollen.

General Assessment You note that the child is lying supine and appears listless.
She is breathing rapidly and quietly. Her skin is mottled.

Primary Assessment You start oxygen and note that the child seems confused. She
responds to your voice and tries to answer questions but does
not know where she is and does not seem to understand what people are
saying. HR 165/min, RR 60/min, BP 90/30, Temp 39.4. You hear a regular, rapid
heart beat with a short systolic ejection murmur. Extremities are warm and bright
red; central pulses are full and bounding; peripheral pulses are palpable but
feel thready. Capillary refill is about 2 sec. The skin lesions on her abdomen
are bright red and tender. SPO2 is 100% while the child is on O2.

Is this shock?

What type?
CASE 3
Introduction A 3 month old girl is brought to the EAR because of poor oral
intake and listless behavior that has worsened over the past 6 hours. She
had a several day history of vomiting and watery diarrhea, but those
symptoms had resolved yesterday. Despite the improved diarrhea and no
vomiting, she is still not taking liquids well.

General Assessment You see an infant who appears listless. She is breathing
rapidly with moderate retractions. Her color appears mottled.

Primary Assessment You start oxygen. HR 210/min with regular rhythm, RR

50/min, BP 55/43, Temp 36.1. On examination, the infant has little
response to verbal or painful stimuli. There is increased respiratory effort
with moderate retractions. Auscultation reveals reduced distal air entry and
scattered inspiratory moist crackles at both bases. The cardiac rhythm
is rapid and regular without identifiable murmur, but heart sounds are
difficult to hear secondary to her breathing noises and rapid heart rate. Her
brachial and femoral pulses are weakly palpable and the distal pulses are
absent. Extremities are cool and mottled. Capillary refill time in the foot is
>6sec. The skin is mottled without any rashes.

Is this shock?

What type?
CASE 4
Introduction You are called to see a 15 year patient who has developed
acute chest pain and respiratory distress. He was admitted
3 days ago after being struck by a car while crossing the
street. His injuries include a fractured left femur and
multiple contusions and abrasions. His femur fracture was
stabilized with external fixation and was overall doing well
until this episode.

General Assessment You see a boy who appears anxious. He has tachypnea
and appears diaphoretic. He is alert with mottled skin.

Primary Assessment RR 32/min with deep respirations and mild retractions. HR

135/min with thready distal and weak central pulses. On
EKG he has NSR without arrhythmias. BP 88/62, Temp
37.7 and SPO2 is 92% on RA. There are scattered wheezes
and a few moist crackles noted. His skin is cool and clammy
without rash. He is anxious and alert. He answers questions
appropriately and tells you he does not feel well.

Is this shock?

What type?
Tachyarrhythmia
Tachycardia

• Tachycardia is heart rate that is fast than normal

range of heart rate for that specific child’s age.

• Rhythm remains normal

age Awake heart rate

New-born to 3 months 85 to 205

3 months to 2 years 100 to 190

2 to 10 years 60 to 140

>10 years 60 to 100

Tachyarrhythmia - Symptoms

• General:
Palpitations, syncope, fatigue, SOB, chest pain

Infants: poor feeding, tachypnea, irritability, sleepiness,

pallor, vomiting
• Hemodynamic instability:
Respiratory distress/failure, hypotension, poor
end-organ perfusion, altered LOC, sudden
collapse
Tachyarrhythmia - Causes

• 1º:
Underlying conduction abnormalities

• 2º:
Reversible Hs & Ts
• Hypovolemia – Toxins
• Hypoxia – Tamponade (cardiac)
• H+ ions (acidosis) – Tension pneumothorax
• Hypoglycemia – Thrombosis (coronary)
• Hypothermia – Thrombosis (pulmonary)
• Hypo/Hyperkalemia – Trauma
Tachyarrhythmia - Classification
Narrow Complex
Tachycardia
Sinus Tachycardia

• Usually <220 bpm in

infants, <180 bpm in children
• P waves present and normal (up going in I, II,
AVF), narrow QRS, beat to beat variability
• Response to body’s need for increased cardiac
output or oxygen delivery (i.e.: hypoxia,
hypovolemia, fever, pain, anemia)
Supraventricular tachycardia

• Narrow Complex, >220 bpm in infants, >180

bpm in children
• Abrupt onset; occurs intermittently
• Usually narrow QRS, absent or abnormal P
waves, no beat to beat variability
• Caused by accessory pathway reentry (i.e.:
WPW), AV nodal reentry, ectopic atrial focus
Symptoms

• In infants:
Poor feeding, tachypnea, irritability, sleepiness, pallor,
vomiting
• May go undetected in infants for long periods of time
until cardiac output is significantly impaired

• In children:
Palpitations, SOB, chest pain, dizziness, lightheadedness,
fainting
ECG

• No beat to beat variability

• Usually >220 bpm in infants, > 180 bpm in children
• Absent or abnormal P waves
• PR Interval - Short or not seen
• RR Interval - Constant
• QRS usually - Narrow, <0.09
(wide complex uncommon and difficult to diagnose
without careful analysis of 12 lead EKG; unless child is
known to have aberrant conduction it is best to presume
wide complex tachycardia is VT)
 1- Ice bag on face

Vagal Fill a mixture of ice and water in

a plastic bag and apply it to the
maneuvers upper half of face for 15 sec.
Do not occlude nose or mouth

2-Valsalva Maneuver
Blowing through a narrow straw

3- Carotid sinus message

4- Ocular pressure ?
SVT- Management

• SVT with adequate perfusion

• Vagal maneuvers while preparing adenosine

• SVT with poor perfusion

• Immediate adenosine or cardioversion

• Consider vagal maneuvers if no delay

• Adenosine
• Rapid bolus then flush using proximal PIV or CVL
• 0.1 mg/kg; max 1st dose 6 mg; additional 0.2 mg/kg if needed
(max 2nd dose 12 mg)

• Cardioversion (0.5-1 J/kg; next 2J/Kg,sedate if possible)

Atrial Flutter

• Saw tooth pattern on EKG

• Atrial rate 350-400/min; ventricular rate varies
Wide Complex
Tachycardia
Ventricular Tachycardia

• Wide QRS (>0.08 sec), P waves may be

unidentifiable or not related to QRS

• Caused by underlying heart disease, post-heart

surgery, myocarditis, cardiomyopathy, ↑QTc, ↑K+,
↓Ca++, ↓Mg++, drug toxicity
Signs/Symptoms

• Tachycardia >120 b/min <200 b/min

• Tachypnea (according to age )
• CHF signs
• JVP (older children)
• Enlarged ,tender hepatomegaly
• Basal crackles
• With or without pulse
ECG

• Heart rate
• >120 <200/min, regular
• QRS complex
• wide >0.09
• P wave
• often not identified
• T wave
• Typically opposite in polarity from QRS
Torsade's de Pointes

• Variable polarity & amplitude of QRS, appearing

to rotate around the EKG isoelectric line
• A type of polymorphic VT
• Caused by long QT syndromes, ↓Mg++, drug
toxicities (including antiarrhythmic)
• Can deteriorate to ventricular fibrillation
Tachyarrhythmia vs. Artifact

• Differentiating arrhythmia from artifact:

• Sharp spikes from QRS complexes
superimposed on “arrhythmia”
• Wandering baseline
• Normal QRS complexes
in some leads

• Causes of artifact:
• Simultaneous use of other equipment,
muscle contractions, movement
Tachyarrhythmia - Management

• General
• ABC, O2
• Attach monitor/defibrillator, pulse ox;
• Establish vascular access
• Obtain appropriate labs (i.e.: blood gas, lytes)
• Identify & treat any reversible causes

• Torsade de Pointe or VT due to ↓Mg++

• Magnesium sulfate
Tachyarrhythmia - Management

• ABCs
• If pulse → PALS tachycardia algorithms

• Poor perfusion → Pediatric Tachycardia With

Pulses and Poor Perfusion algorithm

• Adequate perfusion → Pediatric Tachycardia

With Adequate Perfusion algorithm

• If no pulse → PALS Pediatric Pulseless Arrest

algorithm
Cardiac Arrest
Recognising Cardiac Arrest
Blood Gases Interpretation
Objectives
Learn to read and interpret blood gases
L
Components of blood gas
 pH
 Partial carbon dioxide level (PCO2)
 Total carbon dioxide level tCO2 or
 Partial pressure of oxygen (PO2)
 Oxygen saturation
 HCO3
 BE
 Other information
pH/PCO2/PaO2/HCO3-
pH = power of Hydrogen defined by the Henderson-Hasselbalch equation:
pH=pK+log ([HCO−3]/0.03 PCO2)
pH/PCO2/PaO2/HCO3-
 Respiratory component of blood gas: Dissolved CO2

 When PCO2 changes, pH changes to the same degree but in the opposite direction
 CO2 Acidosis
 CO2 Alkalosis
pH=pK+log ([HCO−3]/0.03 PCO2)

 Cerebral Vasodilatation
 Pulmonary vasoconstriction
pH/PCO2/PaO2/HCO3-
 Normal blood PaO2 value is 80-100 mmHg.
 Physiological causes of hypoxia:
• Hypovolemia
• Right to left shunt
 Diffusion limitation
• Interstitial/pulmonary edema
• Pneumothorax pleural effusion
• Atelectasis
• Pneumonia
pH/PCO2/PaO2/HCO3-
 Normal level in venous blood is 22-26
 Physiological buffer, maintained mainly by kidneys
 Bicarbonate values outside the normal range are usually influenced by metabolic
conditions or in response to changes in acid base balance.
 In an effort to maintain normal pH, the kidneys excrete or retain bicarbonate.
 When pH decreases, the kidneys will compensate by retaining bicarbonate.
 As the pH rises, the kidneys will excrete bicarbonate through the urine.

pH=pK+log ([HCO−3]/0.03 PCO2)

 Arterial pH values are 0.05 greater than venous

 Arterial PCO2 is 10 mmHg less than the venous blood

 Lower oxygen content in venous blood is less due to oxygen consumption

 Bicarbonate levels in arterial and venous blood will yield the same result
Examine the pH

Acidemia vs Alkalemia

 PH < 7.35  Acidosis

 PH > 7.45  Alkalosis
Primary Disorder?
 Acidosis
Metabolic Acidosis
Respiratory Acidosis

 Alkalosis
Metabolic Alkalosis
Respiratory Alkalosis
 Acidosis
Any process which

increases PCO2

OR

decreases HCO3

pH=pK+log ([HCO−3]/0.03 PCO2)

 Alkalosis
Any process which

decreases PCO2

OR

increases HCO3

pH=pK+log ([HCO−3]/0.03 PCO2)

 Compensation

Acidosis or alkalosis produced by body’s homeostatic mechanisms to correct

pathological acid-base disturbance.
Metabolic or Respiratory?
 Metabolic HCO3 is altered

 Respiratory PCO2 is altered

Case 1
1. Respiratory Acidosis

2. Respiratory Alkalosis

3. Metabolic Acidosis

4. Metabolic Alkalosis
Case 2
1. Metabolic alkalosis with respiratory compensation

2. Metabolic acidosis with respiratory compensation

3. Respiratory acidosis with metabolic compensation

4. Respiratory alkalosis with metabolic compensation

1. Metabolic acidosis

2. Respiratory acidosis

3. Metabolic acidosis and respiratory acidosis

Anion Gap

Help differentiate between acid H+ gain

Or
HCO3 loss

 Anion gap=[Na+]−([Cl−]+[HCO−3])
 Normal gap 8−12 mEq/L
 Anion gap acidosis: gap> 12mEq/L

 Caused by decrease in HCO3 balanced by increase in unmeasured

acid ions, not by increase in Cl

 Causes include salicylates, methanol, paraldehyde, ethylene glycol,

lactic acidosis, ketoacidosis (from diabetes or starvation), and
uraemia.
 Non–anion gap acidosis: gap 8 to 12 mEq/L

 Caused by decrease in HCO3 balanced by increase in Cl

 Causes include renal tubular acidosis, carbonic anhydrase inhibitor,

and diarrhoea.
Resuscitation Tools
Medical Devices
Intraosseous needle
• OPENPediatrics

• https://learn.openpediatrics.org/learn/course/3004/
play/51001/chapter-8-documentation
Tracheostomy care
Neuro-observation
Bag Mask ventilation
SEPSIS
SIX