PART 4 OF PALS DESCRIBE PEDIATRIC SHOCK AND ARRHYTHMIA

1. PEDIATRIC ADVANCED
LIFE SUPPORT 2017
GUIDELINES-PART 4
DR. SAYED ISMAIL,MD
PROFESSOR AND CONSULTANT OF PEDIATRIC
ALAZHAR UNIVERISITY

2. Objectives
• Pediatric advanced life support 2017 guidelines are
presented in 4 parts presentations
• To provide up to date management of life threatening
conditions
• To help the pediatricians and emergency physicians to
pass the PALS examination

3. Shock
Part 4

4. The child in shock
• Shock is an acute circulatory dysfunction resulting in
inadequate delivery of oxygen and other nutrients to meet
tissue metabolic demands.
• The final pathway is a failure of both substrate delivery and removal
of metabolites leading to a state of acute cellular oxygen deficiency .
This in turn leads to anaerobic metabolism and cellular acidosis,
culminating in loss of normal cellular function, cell death, organ
dysfunction and eventually death, if not recognised and
appropriately treated.
Introduction

5. Pathophysiology of shock
• Shock is a progressive state which can be divided into :
• Types of shock
1. Compensated = poor tissue perfusion
2. Hypotensive shock
= poor tissue perfusion + hypotension

6. Maintenance of adequate tissue perfusion and oxygen supply depends
on blood volume, cardiac output and arterial oxygen content.
Cardiac output = heart rate X stroke volume, and is directly
proportional to preload (venous return), afterload (systemic vascular resistance) and
cardiac contractility.
Blood pressure = COP X SVR ( systemic vascular resistance )

7. Physiology of Compensated shock
• In this early phase, compensatory mechanisms maintain vital
(i.e. brain, heart and kidneys) organ perfusion.
• Sympathetic nervous system reflexes increase systemic arterial
resistance, divert blood away from nonessential tissues,
constrict the venous reservoir and increase the heart rate to
maintain cardiac output.
• The systolic blood pressure remains normal, whereas the
diastolic pressure may be elevated due to the increased systemic
arterial resistance.
• Increased secretion of angiotensin and vasopressin allows the
kidneys to conserve water and salt, while reduced renal
perfusion leads to reduced urine output, and intestinal fluid is
reabsorbed from the digestive tract.

8. The clinical signs of compensated shock
• The clinical signs = Signs of poor perfusion :
– mild agitation or confusion
– skin pallor, cold skin
– increased heart rate, weak peripheral puse
– decreased capillary return
– reduced urine output.
– Early recognition is crucial as appropriate
therapeutic interventions at this stage can
completely reverse shock.

9. Hypotensive shock
• If shock is untreated in the early stage, it progresses further and the
compensatory mechanisms fail to support the circulatory system.
• Poorly perfused tissue leads to Anaerobic metabolism produces
lactate and acidosis . Acidosis reduces myocardial contractility and
impairs the response to circulating catecholamines.
• A further result of anaerobic metabolism is the failure of the
energy‐dependent sodium–potassium pump, which maintains the
normal homeostatic environment for optimal cellular function.
Lysosomal, mitochondrial and membrane functions deteriorate
without this homeostasis.
• Sluggish blood flow and chemical changes in small vessels lead to
platelet adhesion and may produce damaging chain reactions in the
kinin and coagulation systems, heralding the onset of disseminated
intravascular coagulation (DIC).

10. The clinical signs of hypotensive shock
• Hypotension
• Tachycardia,
• Prolonged capillary refill,
• Cold peripheries,
• Acidotic breathing,
• Depressed cerebral state and severely
• Reduced or absent urine output.
• Blood gases reveal metabolic acidosis and blood
lactate is increased.

11. Causes of shock
Hypovolemic Haemorrhage
Gastroenteritis,
Intussusception, volvulus
Burns
Peritonitis
Cardiogenic Arrhythmias
Heart failure (cardiomyopathy, myocarditis)
Distributive Septicaemia
Anaphylaxis
Spinal cord injury
Obstructive Congenital cardiac (coarctation, hypoplastic left heart,
aortic stenosis)
Tension pneumothorax
Flail chest
Cardiac tamponade
Pulmonary embolism

12. signs of compensated shock include
• Tachycardia
• Weak peripheral pulses compared with central pulses
• Normal systolic blood pressure
• Cooland pale distal extremities
• Prolonged (>2 seconds) capillaryrefill
• Agitation , confusion
• Decreased urine output
Signs of decompensated shock
• In addition to the above, these signs include
• Weak central pulses
• Hypotension.
• Depressed mental status
• Metabolic acidosis ( rapid deep breathing)
• Tachypnea
• Deterioration in color (eg,mottling, )

13. • ˂ 60 mmHg in infant less than one month
• ˂ 70 mmHg in infant ˂ 1 year
• After that = age X 2 + 70 till 10years age
• <90 mm Hg in children 10 years of age
Hypotension =

14. Distributive and (Septic) shock
• Wide pulse pressure due to decreased peripheral systemic
resistance, increase blood flow to skeletal muscles and
decreased to vital organs heart, brain, liver and kidney
• In neurogenic shock there is loss of sympathetic tone , so no
tachycardia and no vasoconstriction ( normal HR or
bradycardia + severe hypotension)
• Specific signs : variable
– May Bounding pulse or weak
– Skin warm or cold -- warm shock , cold shock )
– Tachycardia or bradycardia

15. Clinical Features Of Septicemia
History
• Fever
• Poor feeding
• Miserable
• Lethargy
• History of focal infection, e.g. meningitis, osteomyelitis,
gastroenteritis, cellulitis
• Predisposing conditions, e.g. sickle cell disease, immunodeficiency
Examination
• Fever
• Purpuric rash (meningococcal septicaemia)
• Irritability
• Shock
• Multi-organ failure

16. Anaphylactic shock
• A – angioedema , swelling in the face , lip..
• B- stridor , wheezing , resp distress
• C hypotension , tachycardia
• D -agitation
• E- urticarial rash

17. Cardiogenic shock
Is characterized by RD ,grunting , chest retractions
Lung crepitations
Cardiomegaly
Hepatomegaly
Congested neck veins
Gallop , murmur
Narrow pulse pressure
Cyanosis
+ Signs of poor perfusion

18. Obstructive shock
• Cardiac tamponade
• Tension pneumothorax
• Congenital Obstructive left heart syndrome
• TAPVR
c/p in cardiac tamonade :
– systemic and or pulmonary congestion + s/s of shock +
– RD ,muffled heart sounds
– Pulsus paradoxus ( decrease BP >10mmhg during
inspiration )

19. • In pneumothorax
– tracheal deviation ,
– Hypo expansion of affected side with diminished breath sound ,
– distended neck veins
• In duct depended lesions
– higher preductal vs. post ductal PB and o2 sat (more than 3-4%)
– Absence of femoral pulse
– + cardiomegaly
– hepatomegaly

20. Primary assessment and resuscitation in shock
Airway
● Ensure airway is open: consider airway‐opening manoeuvres, airway adjuncts or urgent
induction of anaesthesia and intubation to secure the airway.
Breathing
● if Adequate airway: give high‐flow oxygen through a face mask with a reservoir,
(nonrebreathing mask)
● Hypoventilating: support with oxygen via a bag–valve–mask device and seek experienced,
senior help for early tracheal intubation and mechanical ventilation.
Circulation
● Gain intravenous (IV) or intraosseous (IO) access:
● Insert two wide‐bore IV cannulae if possible, immediately proceed to IO access if
peripheral venous access is difficult.
• Give isotonic crystalloid boluses
● Femoral venous access can be used in situations where peripheral or IO access is impossible and
experienced help is available.
● Take blood for blood gas , chemistry including lactate, , renal and liver function tests, (CRP)
or procalcitonin , blood culture, meningococcal/streptococcal polymerase chain reaction
(PCR), cross‐match and coagulation studies …..continu

21. Secondary assessment : Key features of the child in shock
• A history of vomiting and/or diarrhoea points to fluid loss either externally (e.g.
gastroenteritis) or into the abdomen (e.g. volvulus, intussusception,ruptured appendix)
• The presence of fever and/or rash points to septicaemia
• The presence of urticaria, angioneurotic oedema or history of allergen exposure points to
anaphylaxis
• The presence of cyanosis unresponsive to oxygen or a grey colour with signs of heart
failure in a baby under 4–6 weeks points to duct‐dependent congenital heart disease
• The presence of heart failure in an older infant or child points to cardiomyopathy or
myocarditis
• A history of sickle cell disease, abdominal pain and enlarged spleen points to acute splenic
sequestration
• An immediate history of major trauma points to blood loss and, more rarely, tension
pneumothorax, haemothorax, cardiac tamponade or spinal cord transection
• The presence of severe tachycardia and an abnormal rhythm on the ECG points to a cardiac
cause for shock
• A history of polyuria and acidotic breathing and a very high blood glucose points to
diabetes ketoacidosis
• A history of drug ingestion points to poisoning

22. • begins with boluses of up to 20 ml/kg crystalloid over 5–10
minutes, (repeat as needed boluses )titrated to reversing
hypotension, increasing urine output (>1 ml/kg/h), and attaining
normal capillary refill, peripheral pulses and level of consciousness.
• Reassess the patient after each fluid bolus to look for signs of
improvement.
• If signs of shock persist after the first bolus, give a second fluid
bolus of crystalloid or colloid
• In patient with crystalloid refractory hemorrhagic shock , give
transfusion PRBCS 10ml/kg
Specific treatment of shocks :-
Hypovolemic shock

23. Guide to fluid bolus in shock
Type of shock Volume Rate
Hypovolemic
Distributive
20ml/kg bolus
Repeat as needed
Over 5-10min
Cardiogenic shock
Posoining
5-10ml/kg
Repeat as needed
Over 10-20min
DKA 10-20ml/kg 1-2hour
Indication of blood product administration
Give Packed RBC If 2-3 isotonic boluses not improve hypovolemic shock due to
blood loss ,Give gross matched , or type specific or group 0- ve
Pals

24. Approach to the child with septic shock
• Septic shock is defined as sepsis with cardiovascular end‐organ
dysfunction.
• Septic shock is the classic example of a combination of several
factors contributing to the shock.
• These include hypovolaemia (fever, often associated diarrhoea,
vomiting and anorexia, together with capillary leakage),
• cardiogenic (impaired cardiac function due to hypovolaemia and
direct myocardial suppressive factors from infecting organisms and
the host inflammatory response),
• distributive (alterations in vascular tone with vasoconstriction
in some vascular beds and vasodilatation in others)
• and dissociative (there is a non‐specific sepsis‐induced
mitochondrial dysfunction impairing cellular oxygen utilisation)
elements.

25. Organisms
• Neisseria meningitidis is the commonest cause of
community‐acquired septicaemia in infants and children.
• group B streptococcal infection in neonates and young
infants,
• Gram‐negative sepsis in relation to underlying urinary tract or
gut problems
• infection of long‐term indwelling devices (such as venous
catheters) is becoming increasingly prevalent
• The cardinal sign of meningococcal septicaemia is a purpuric
rash in an ill child.

26. • In toxic shock syndrome the initial clinical picture includes:
– a high fever, diffuse erythema, headache, confusion, conjunctival
and mucosal hyperaemia (strawberry tongue), scarlatiniform rash,
subcutaneous oedema, vomiting and watery diarrhoea.
• Findings may also include a trivial injury such as an infected
wound, minor burn or scald, surgical wound infection or
coexistent deep‐seated infection such as pneumonia or
bone/joint infection.
– Early administration of anti‐staphylococcal/ streptococcal
antibiotics, concurrent with initial resuscitation, is vital.
– Intravenous immunoglobulin should be considered along with
urgent drainage of any localised pus.

27. Treatment of septic shock
Treatment in the first hour (Pre-ICU)
• Airway and Breathing
• Oxygen high flow by non rebreathing mask
• Ventilation IF > 60ml/kg fluid in first hour is given.
• 40% of cardiac output is used to power work of breathing – so intubation and ventilation
can reverse shock.
• IO access if IV access is not obtained within minutes
• Fluid bolus isotonic crystalloid 20ml/kg immediately if no hepatomegaly or lung
creps. If hepatomegaly or creps, give fluid bolus more cautiously, and consider
other diagnoses (heart disease, metabolic disease, pneumonia)
• Antibiotic is given as soon as possible, preferably after doing a blood culture.
• Repeat fluid bolus to achieve normal CRT and BP. 60ml/kg or more is often
required in paediatric sepsis in the first hour.
• Fluid refractory shock – add adrenaline or dopamine (cold shock) or
noradrenaline (warm shock)
• Start hydrocortisone after obtainng random cortisol if there is clinical suspicion
of adrenal suppression, or if shock is adrenaline/noradrenaline refractory.
Continue
Pals

28. • Give Antibiotics
– Cefotaxime or ceftriaxone
– Antipyretics
– If hospital acquired or neutropenic,
consider tazobactam.
• If previous culture of resistant
organism, give appropriate
antibiotic (e.g. methicillin‐resistant
Staphylococcus aureus (MRSA): add
vancomycin; extended‐spectrum
β‐lactamases (ESBL): meropenem).
• If vascular access device has been
used for more than 48 hours add
vancomycin.
Continue …Treatment of septic shock
• Monitoring
– pulse oximeter
– continuous ECG
– BP
– Temperature
– Urine output
• Therapeutic endpoints:
– CRT ≤ 2secs
– normal peripheral and central
pulses
– warm extremities
– >1ml/kg/hr urine output
– normal mental status
– normal bp

29. Continue …Beyond the first hour (PICU)
Monitoring … insert central lines
• CVP
• Invasive BP monitoring – pay attention to pulse
pressure (wide in warm shock, narrow in cold
shock)
• SCVO2 > 70%
• Pulse oximetry
• ECG
• Core temperature
• Urine output
• Lactate, glucose, coags ….

30. Fluids
• Requirement for boluses may be required for days
• If Hb < 10g/dL, give blood
• If coags abnormal give FFP – but not as a push bolus
Cold normotensive shock
• SCVO2 < 70% continue epinephrine , fluids add Milrinone
• If low bp add Noradrenaline
Warm shock
Low BP, SCVO2 > 70%
Noraderenaline
Add Vasopressin 2nd line
Continue …

31. Approach to the child with anaphylaxis
• Common triggers include certain foods, especially nuts, egg and
shellfish, and drugs such as penicillin, anaesthetic agents and
radiographic contrast media.
• shock, is due to acute vasodilatation and fluid loss from the
intravascular space caused by increased capillary permeability.
Any of these may lead to collapse and respiratory or cardiac
arrest.

32. Symptoms and signs in allergic reaction
Symptoms Signs
Allergic
reactions
Burning sensation in mouth,
itching of lips, mouthand throat,
coughing, feeling of warmth,
nausea, abdominal pain, loose
bowel motions,
sweating
Urticarial rash, angio‐oedema,
conjunctivitis
Anaphylaxis Difficulty breathing,
noisy breathing,
cyanosis,
agitation,
collapse
Wheeze, stridor, tachycardia
with hypotension,
poor pulse volume and pallor,
respiratory arrest
or cardiac arrest

33. Treatment of anaphylactic shock
• A rapid, ABC assessment with immediate and concurrent
administration of IM epinephrine (1st and most
important)
• All patients with signs and symptoms of anaphylaxis
should receive rapid administration of IM epinephrine.
Pals
ABCDE

34. Pharmacological management of anaphylaxis
Drug and route of
administration
Frequency Dose
(maximum dose)
Epinephrine (1:1000)
IM
Immediately, then every 5–15 min as
required
0.01 mg/kg (0.5 mg)
Diphenhydramine IM/IV Every 4–6 h as required for cutaneous
manifestations
1 mg/kg/dose (50 mg)
Ranitidine PO/IV Every 8 h as required for cutaneous
manifestations
1 mg/kg/dose (50 mg)
Corticosteroids: prednisone
PO or methylprednisolone IV
Every 6 h as required 1 mg/kg PO (75 mg) or
1 mg/kg IV (125 mg)
Nebulized Albterol
Nebulized epinephrine
For bronchospasms
Every 20 min to 1 h for symptoms of upper
airway obstruction (stridor)
2.5–5 mL by nebulization
Epinephrine IV (infusion Continuous infusion for hypotension –
titrate to effect
0.1–1 µg/kg/min
(maximum 10 µg/min)

35. Treatment of neurogenic shock
Hypotension , bradycardia and hypothermia
Management :
1- position the patient flat with head down
2- bolus fluid therapy , if no response give
3- vasopressor : norepinephrine , epinephrine
Pals
ABCDE

36. Treatment of cardiogenic shock
• O2 , consider ppv ventilation (to decrease o2 consumption)
• Optimize preload : Give 5-10ml/kg isotonic infusion slowly 10-
20min , repeat PRN
• Assess for pulmonary edema
• Drugs : to increase contractility by inotropes and decrease SVR
(afterload) are main therapy , e.g. Contractility is supported with
inotropes. Milrinone is often used to decrease peripheral
vascular resistance
• Order labs and other studies to determine the underlying causes
• Obtain expert advise (E)
• Consider mechanical circulatory support
Pals
ABCDE

37. Cardiac shock
1. the preload 5-10ml NS
2. heart contractility by inotropes, Dopamine
3. VR by vasodilator e.g. milrinone
in obstructive shock give fluid, inotropes and
relieve the obstruction

38. • N.B : Be cautious in primary cardiogenic shock and in those with
signs of raised intracranial pressure (ICP): the first group may still
benefit from a judicious fluid bolus (5–10 ml/kg) to optimise
preload. It is important to seek the urgent advice of a paediatric
cardiologist for further treatment.
• Give inotropes if hypotension does not respond to initial fluid
resuscitation or if hepatomegaly or new respiratory crackles
develop.
• For improved circulation, peripheral IV or IO access can be used for
inotrope infusion when a central line is not available.

39. Class Medication Effects
Inotropes Dopamine
Epinephrine
dobutamine
Increase cardiac
contractility
Increase HR
Variable on SVR
Inodilators Milrinone Decrease the SVR
Improve coronary blood
flow
Improve contractility
Vasodilator Nitroglycerin
nitropruddide
Decrease the SVR
Vasopressors Dopamine > 10mcg/kg/ min
Epinephrine > 0.3mcg/kg/ min
Norepinephrine
Vasopressin
Increase the SVR
Increase heart
contractility except
vasopressin
Vasoactive drugs

40. • Expert advice regarding intubation and ventilation should be sought in
patients who have received more than 40 ml/kg fluid with signs of ongoing
shock. Mechanical ventilation decreases the energy requirements of the heart and
respiratory muscles, allows delivery of adequate concentrations of oxygen and
helps reduce the risk of development of pulmonary oedema.
• Renal perfusion should be monitored with a urinary catheter and hourly
urine output measurement as it is an important marker of renal perfusion.
• Give an antibiotic such as ceftriaxone or cefotaxime for those with an
obvious or suspected diagnosis of septicaemia, e.g. in the presence of a
purpuric rash, or in those where the aetiology is unknown. Blood cultures
should be obtained before administering antibiotics when possible but this
should not delay administration of antibiotics.
• If the tachyarrhythmia is supraventricular tachycardia (SVT) then this can be
treated with IV/IO adenosine as this can often be administered more
quickly than a synchronous electric shock.
• If a tachyarrhythmia is identified as the cause of shock, up to three
synchronous electric shocks at 1.0, 2.0 and 2.0 J/kg should be given
• If anaphylaxis is obvious give adrenaline 10 micrograms/kg IM or 150
micrograms (<6 years), 300 micrograms (6–12 years) or 500 micrograms
(>12 years).
TREAT THE CAUSE of shock :

41. Treatment of obstructive shocks
• Cardiac tamonade
• Tension pneumothorax
• Duct depended congenital heart disease
• Massive pulmonary embolism
Recognize and treat the underlying cause
ABCDE

42. Duct depended congenital heart disease
• Neonates with duct‐dependent systemic circulation (e.g. critical
aortic stenosis, hypoplastic left heart syndrome,) usually present
in the first few days of life with inability to feed, breathlessness, a
grey appearance and collapse with poor peripheral circulation
and cardiogenic shock. These infants are severely ill with signs of
poor organ perfusion with severe metabolic acidosis, poor urine
output and decreased conscious level.
• Pulses can be difficult to feel in these patients because of
left‐sided obstruction to cardiac output and a difference may be
noticed in the upper and lower limb pulses and blood pressure
depending on the site of the lesion.

43. Emergency treatment of duct‐dependent congenital heart disease
Reassess ABC
● Oxygen therapy will often provide limited benefit. Since it may
accelerate duct closure, use oxygen judiciously or discontinue if
there is no effect.
• Keep a low threshold for tracheal intubation and mechanical
ventilation in patients with cardiogenic shock. This decreases
metabolic demands of the body and assists cardiac function.
• Give an IV infusion of prostaglandin E2
• transfer to a paediatric cardiology unit.
• Monitor pre‐ and post‐ductal saturations.
Investigations
●Chest X‐ray
●ECG
●Full blood count, arterial blood gases, urea and electrolytes (including calcium),
glucose and lactate
● Blood cultures since differential diagnosis with sepsis might be difficult

44. Pediatric Dysrhythmias

45. Pediatric dysrhythmias
Treatment not required Treatment is required
Sinus arrhythmia Supraventricular tachycardia
Wandering atrial pacemaker
Isolated premature atrial
contractions
Isolated premature ventricular
contractions
Ventricular tachycardia
First degree AV block Third degree AV block with
symptoms
Reproduced from Zitelli’s Atlas of Pediatric physical diagnosis, 2007, pg 140.

46. Etiology in general
• Congenital:
channelopathy ,abnormal conduction or fetal
inflammation as in maternal SLE
• Acquired:
Myocarditis , cardiomyopathy ,toxins, after
surgical correction of CHD , Rheumatic fever
• 6 H , 5 T

47. Presentations of arrhythmias in children
• Poor feeding (pre‐verbal child)
• History of palpitations (verbal child)
• Heart failure
• or shock
• Signs of poor perfusion = compensated shock
– pallor, cyanosis, cool mottled extremities, prolonged capillary refill,
– thready ,weak, or absent peripheral pulses,
– irritable,lethargic, confused, or have decreased level of consciousness.

48. BRADYCARDIA
• Bradycardia is a heart rate below normal range for age .
• There are several types of bradyarrhythmias including :
–Sinus bradycardia
–Atrioventricular (AV) block.

49. Bradyarrhythmias - Causes
• Primary : Abnormal pacemaker/conduction system (congenital or
postsurgical injury), cardiomyopathy, myocarditis
• Secondary : Reversible Hs & Ts:
– Hypoxia – Hypotension– H+ ions (acidosis)
– Heart block – Hypothermia – Hyperkalemia
– Trauma (head)
– Toxins/drugs (Ca++ channel blockers, β-adrenergic blockers,
digoxin, opioids)

50. The heart rate slows down in , athetes , sleep or vagally-induced sinus bradycardia during
the Valsalva maneuver. Lone sinus bradycardia in a normal heart usually does not require any
type of intervention.
On the other hand, patients with (ASD), complex congenital heart defects,, those who
underwent heart surgery will require further work-up to determine if a pacemaker is
indicated, especially if there are associated symptoms

51. First degree AV block
• PR interval is greater than upper limits of normal for a given age
• Generally does not cause bradycardia since AV conduction remains intact
• Diseases that can be associated with first degree AV block: rheumatic
fever, rubella, mumps, hypothermia, cardiomyopathy, electrolyte
disturbances

52. Second degree heart bock

53. Third degree AV block
• Most common cause of abnormal bradycardia in infants and
children
• Can be congenital – in this case it is strongly associated with
maternal SLE
• Mom of an infant should be worked up
• Most common structural heart defect associated is corrected
transposition of great vessels
Complete disassociation between P waves and QRS complexes

54. Third degree AV block
• May be asymptomatic – follow clinically
• Slower the heart rate, and wide QRS escape
rhythms place into high risk group
• May need implantable pacemaker:
– significant bradycardias,
– syncope, exercise intolerance,
– ventricular dysrhythmias, or ventricular
arrhythmias, structural disease

55. 1st degree heart block
2nd degree heart block, Mobitz I
2nd degree heart block, Mobitz
II
3rd degree heart block

56. Arrhythmias: The First Step
• Connect the child to an
ECG machine
• Get a 12 lead ECG
• If the child is
uncooperative, at least
get the limb leads

57. Treatment of bradycardia
• A-Open airway using head tilt-chin lift method
• B-Supplemental 100% oxygen ,Assist ventilation as needed using
Bag-Valve-Mask
• Treat the the underlying cause : hypoxia , hypothermia , ..
• If acutely deteriorating head injury, ventilate
• If heart block or post heart transplant, apply transcutaneous pacer
• C- connect to monitor ,ECG
• initiate chest compressions if heart rate remains < 60 beats/
minute despite oxygenation , ventilation and signs of severe
cardiopulmonary compromise persist
• D- Epinephrine (1:10,000) 0.01 mg/kg (Max 1 mg) IV/IO
OR, if no IV/IOM
ABCDE

58. • Epinephrine (1:1,000) 0.1 mg/kg (Max 2.5 mg) diluted in 5 ml of
NaCl via endotracheal tube; give 5 manual ventilations after drug
administered
– Repeat dose every 3-5 minutes until either the bradycardia or
severe cardiopulmonary compromise resolves
• Atropine at 0.02 mg/kg via IV, IO, or Endotracheal tube (if given via
ETT dilute in 5 ml of 0.9% NaCl and administer 5 ventilations after
drug given)
– Minimum dose is 0.1 mg; Maximum individual dose is 0.5 mg
– May repeat once after 3-5 minutes
– Use if bradycardia due to increased vagal tone or AV block
• If severe cardiopulmonary compromise persists despite Epinephrine
or Atropine apply transcutaneous pacemaker

59. A
B
C

60. Bradycardia with poor perfusion
If pulse is less than 60 /min and these are signs of poor
perfusion (pallor , mottling ,cyanosis..
Despite support of ventilation --- start CPR
Bradycardia is usually a pre‐terminal rhythm

61. Tachyarrhythmias

62. Tachyarrhythmias - Classification
• Narrow complex:
– sinus tachycardia,
– supraventricular tachycardia,
– atrial flutter
• Wide complex:
– ventricular tachycardia,
– supraventricular tachycardia with aberrant
intraventricular conduction

63. Narrow QRS <0.09
second
Usually stable hemodynamics
• Supraventricular
• Sinus tachycardia
Wide QRS > 0.09 sec
Often unstable hemodynamics
• Ventricular tachycardia
• supraventricular with
abnormal conduction
Classification of tachyarrhythmia

64. Tachyarrhythmias - 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,
– shock

65. Tachyarrhythmias - Causes
• 1ry: Underlying conduction abnormalities
• 2ry: Reversible Hs & Ts
– Hypovolemia – Toxins
– Hypoxia – Tamponade (cardiac)
– H+ ions (acidosis) – Tension pneumothorax
– Hypoglycemia – Thrombosis (coronary, pulmonary)
– Hypothermia – Trauma
– Hypo/Hyperkalemia

66. • Sinus tachycardia
– Usually <220 bpm in infants, <180 bpm in
children
– P waves present and normal (upgoing in I, II,
AVF), narrow QRS, beat to beat variability
– Response to body’s need for increased cardiac
output or oxygen delivery (ie: hypoxia,
hypovolemia, fever, pain, anemia)

67. Sinus Tachycardia: A Cause Can
Almost Always be Found
• Hypovolemia
• Anxiety
• Fever
• Hypovolemia
• Hyperthyroidism
• Bronchodilators

68. Treatment of ST
• Sinus tachycardia
• Infants: rate usually <220/min
• Children: rate usually <180/min
• Identify and treat possible causes
MPORTANT NOTE: An absolute contraindication to adenosine is sinus tachycardia (ST).
Dehydrated patients, especially infants and young children with fever, failure to thrive
and/or an infection may appear to be in SVT, when in fact they’re barely compensated with
a sinus tachycardia with a rate that may be greater than 180-200 bpm.

69. Supraventricular tachycardia
• Most common abnormal tachycardia seen in pediatric
practice
• Most common arrhythmia requiring treatment in pediatric
population
• Most frequent age presentation:
– 1st 3 months of life,
– 2nd peaks @ 8-10 yr. and in adolescence
• Supraventricular tachycardia (SVT) is a common non-
arrest dysrhythmia seen in children

70. SVT
Supraventricular tachycardia. Note a normal QRS complex tachycardia at
a rate of 214 beats/minute without visible P waves.
S/S of SVT
• Tachypea ,Rales , wheezing if CHF develop
• s/s of poor perfusion ( cold skin , weak pulse ,hypotension ..

71. Sinus Tachycardia SVT
Onset
History
Gradual
Fever , dehydration
Sudden onset
tachypnea, poor feeding , CHF s/s
Heart
rate
infant < 220 bpm;
Child < 180 bpm
 220 bpm
 Child> 180 bpm
ECG • Variable R-R waves
• P waves present and
upright
Non-variable R-R waves
The P waves may be non-identifiable, If P waves
are present, they will likely be inverted i
Causes
CXR
Dehydration
Hypovolemia (most
common)
Fever
Hypoxia , Anemia
Shocks
Small heart
• Reentry with an accessory pathway (WPW) OR
Spontaneous depolarization of pacemaker sites
• Cardiac pathology (i.e: Ebstein's anomaly)
• medications containing sympathomimetic amines,
caffeine)
• hyperthyroidism, etc.)
• Large heart , pulmonary edema

72. SVT - Treatment
• Vagal maneuvers in stable patients(successful in 80%)
– Ice pack on face for infants
– Carotid sinus massage
• Adenosine if IV access readily available(Rx of choice)
– Stop conduction through AV node
– 0.1 mg/kg (max 6 mg), repeat 0.2 mg/kg ( max 12 mg) in line
closest to central circulation
– Need continuous ECG and BP monitoring
• Synchronized cardioversion in unstable patient
• Amiodarone, or Procainamide if above unsuccessful
• Transesophageal atrial pacing can also be performed

73. • Vagal manoeuvers
• Ice bag on face for infants
• In older children : Carotid sinus massage,
• supine valsalva

74. Supraventricular tachycardia with pulse and poor
perfusion
• Consider vagal manoeuver (no delay)
• If vascular access is available:
– Adenosine 0.1 mg/kg (Maximum individual dose 6 mg) IV
rapid bolus , Repeat Adenosine twice at 0.2 mg/kg if needed
(Maximum individual dose 12 mg)
• If Adenosine is unsuccessful and patient is unstable :
– Synchronized Cardioversion at 0.5- 1 J/kg
– If unsuccessful and severe symptoms persist repeat
Synchronized Cardioversion at 2 J/ kg (Maximum individual
dose 360 joules)
• Pediatric cardiac consultation

75. Administering Adenosine
Adenosine 50-200
mcg/kg, fast push
Saline bolus,
fast push
Reliable proximal IV
line
10 cm extn.

76. AV nodal re-entrant tachycardia: Sudden termination with adenosine
Response to Adenosine
Tachycardia Sinus

77. Response to DC Shock

78. Ventricular tachycardia
• Regular wide complex tachycardia
• Life threatening arryhthmia
• Most patient has underlying heart disease (long QT
syndrome ,myocarditis , cardiomyopathy , channelopathy ,
cardiac surgery…)
Monomorphic VT
ECG Characters of VT : wide QRS 0.09 sec , no P wave , inverted T wave

79. SVT - WPW
If difficult to DD SVT with abnormal conduction and
VT , assume the tachycardia with wide QRS as VT
Figure 5-43 Wolff-Parkinson-White syndrome. Note the characteristic findings of a short P-R
interval, slurred upstroke of QRS (delta wave), and prolongation of the QRS interval.

80. V-Tach
• Treatment: IV amiodarone ,procainamide,
• If critically ill: synchronized cardioversion
• Pedia cardiac consultation : Long term: meds, ablation, or
defibrillator

81. Polymorphic VT
Early identification of this VT is important because may rapidly deteriorate to VF

82. Ventricular tachycardia with a pulse
• If the patient is stable provide supportive care
• Early consultation with ped. cardiacologst
• Treatment: IV, amiodarone , procainamide ,lidocaine,
• If the patient becomes unstable (hypotension and acutely altered
mental status):
– Synchronized Cardioversion at 0.5- 1 J/kg
– If unsuccessful and severe symptoms persist repeat Synchronized
Cardioversion at 2 J/ kg (Maximum individual dose 360 joules)
• If Torsades de Pointes is suspected:
– Magnesium Sulfate 50 mg/kg IV over 5-10 minutes