12. Paediatric Advanced Life Support (PALS)

Question 1

Age classification for:
premature neonate
neonate
infant
child

Answer 1

prem neo - < 37 weeks
neo - up to 1 month
infant - 1 month - 1 year
child - 1 year - 18 years

Question 2

What are the components of the PALS assessment overview?

Answer 2

initial impression - “end of bed” quick observation
primary assessment - hands on ABCDE + vital signs
secondary assessment - focused medical history + physical exam
diagnostic tests

Question 3

if you identify a like threatening problem, what you you do?

Answer 3

hold assessment, treat underlying problem

evaluate, identify, intervene

Question 4

What are the 3 components of the initial impression?

Answer 4

appearance (LOC, ability to interact), breathing (WOB, effort, sounds w/o auscultation), circulation (skin colour)

Question 5

What does each letter of the ABCDE acronym stand for in the primary assessment?

Answer 5

A - airway
B - breathing
C - circulation
D - disability
E - exposure

Question 6

Describe how to assess the airway.

Answer 6

determine if patent, look for movement, listen for movement

may be obstructed if: increased insp. effort with retractions, abnormal inspiratory sounds, no a/w or breathing sounds despite inspiratory effort

Question 7

If the a/w is obstructed, what should we do?

Answer 7

child in position of comfort, allow for patency, head tile/chin lift, a/w adjunct, CPAP, intubation, relief of FBO

Question 8

Describe how to assess breathing.

Answer 8

RR, effort, chest expansion/air movement, breath sounds, O2 sat

Question 9

define apnea.

Answer 9

cessation of breathing for 20 s or more and accompanied by bradycardia, and cyanosis

Question 10

What can increase respiratory effort?

List signs of increased effort.

Answer 10

conditions that increase resistance or decrease compliance

nasal flaring, retractions, head bobbing, seesaw respirations, abdominal breathing, tracheal tug

Question 11

describe how to assess circulation.

Answer 11

HR/rhythm, pulses, skin colour/temp, BP, end organ perfusion (urine output, LOC, tone)

Question 12

When would there be an exaggerated difference between central and peripheral pulses?

Answer 12

when peripheral vasoconstriction occurs

Question 13

What does a prolonged cap (> 3 s) refill suggest?

what does a fast cap (< 2 s) refill suggest?

Answer 13

decreased skin perfusion (dehydration, shock, hypothermia)
hemodynamically compromised (warm shock)

Question 14

What does pallor or paleness indicate? Mottling?

Answer 14

decreased blood supply to the skin (shock), anemia

vasoconstriction/irregular supply of blood to the skin caused by hypoxemia, hypovolemia, and/or shock

Question 15

What is BP dependent on? How is hypotension in a newborn measured? How is hypotension measured after the newborn period?

Answer 15

child’s age
based on gestational age (=MABP)
systolic BP and age

*refer to tables on slide 26

Question 16

Describe how to assess disability.

Answer 16

AVPU response scale: Alert, Voice, Painful, Unresponsive
TICLS - tone, interactiveness, consolability, look/gaze, speech/cry
GCS
Papillary response to light (size, equality of size, response to light)

Question 17

What do pinpoint pupils suggest? dilated pupils? unilaterally dilated pupils?

Answer 17

narcotic ingestion
sympathomimetic ingestion (cocaine), anticholinergic ingestion (atropine), increased ICP
herniation, increased ICP

Question 18

What should you observe for in relation to exposure?

Answer 18

rash, burns, bleeding, signs of trauma, petechiae, pupura

Question 19

How would you perform a secondary assessment?

Answer 19

focused history/physical exam

ISAMPLE

Question 20

What are the components of ISAMPLE?

Answer 20

immunizations
sign and symptoms
allergies
medications
past medical history
last food, fluid intake
events

Question 21

Work through the ABCDE for upper a/w obstruction.

Answer 21

A - partial/complete obstruction
B - increased RR/effort, stridor, barking cough, hoarseness, decreased air movement
C - tachy (early), brady (late), pallor/cool skin (early), cyanosis (late)
D - anxiety/agitation (early), lethargy/unresponsiveness (late)
E - variable temp

Question 22

Work through the ABCDE for lower a/w obstruction.

Answer 22

A - patent unless decreased LOC
B - increase RR/effort, wheezing, prolong exp., decreased air movement
C - tachy (early), brady (late), pallor/cool skin (early), cyanosis (late)
D - anxiety/agitation (early), lethargy/unresponsiveness (late)
E - variable temp

Question 23

Work through the ABCDE for lung tissue disease.

Answer 23

A - patent unless decreased LOC
B - increase RR/effort, grunting, crackles, decreased b/s, decreased air movement
C - tachy (early), brady (late), pallor/cool skin (early), cyanosis (late)
D - anxiety/agitation (early), lethargy/unresponsiveness (late)
E - variable temp

Question 24

List some ways to manage upper a/w obstruction (croup, anaphylaxis, foreign body aspiration).

Answer 24

croup - neb epi, oral corticosteroids, inhaled steroids, mool mist

anaphylaxis - IM epi, ventolin, neb epi, antihistamine, corticosteroids

foreign body aspiration - position of comfort, ENT consult

Question 25

List some ways to manage lower a/w obstruction (bronchiolitis, asthma).

Answer 25

bronchiolitis - nasal sxn, neb epi, HFNC, bronchodilator, hypertonic N/S trial asthma - ventolin +atrovent, corticosteroids, mag sulphate, IV ventolin

Question 26

List some ways to manage lung tissue disease (pneumonia/pneumonitis, pulmonary edema/ARDS)

Answer 26

pneumonia/pneumonitis - ventolin (if wheeze), antibiotics, NIV, ventilation pulmonary edema/ARDS - NIV, ventilation, vasoactive drugs, diuretics

Question 27

How do you recognize shock? What are some compensatory mechanisms? Difference between compensated vs. uncompensated?

Answer 27

inadequate oxygen delivery to tissues tachy, increased SVR, increased contraction ``` compensated = maintain BP uncompensated = unable to maintain BP ```

Question 28

In hypovolemic shock, volume loss occurs from what? What are the 2 types? Work through ABCDE. How will preload, contractility, and afterload be affected?

Answer 28

diarrhea, vomiting, hemorrhage, inadequate fluid intake, osmotic diuretics, third space losses, burns hemorrhagic and non hemorrhagic ``` A - patient unless decreased LOC B - quiet tachypnea C - tachy, N systolic BP w narrow pulse pressure OR systolic hypotension with narrow pulse pressure, delayed cap refill, cool/pale/ mottles/diaphoretic, dusky/pale distal extremities, oliguria D - changes in LOC E - extremities cooler than trunk ``` decrease preload, normal/increased contractility, increased afterload

Question 29

What is distributive shock? what are the 3 types?

Answer 29

inappropriate distribution of blood volume with inadequate organ/tissue perfusion septic (warm/cold), anaphylactic, neurologic

Question 30

What is the most common form of distributive shock? How is CO and SVR effected in cold/warm shock? Work through ABCDE. How is preload, contractility, and afterload affected?

Answer 30

septic shock cold - low CO, high SVR warm - high CO, low SVR A - patent unless decreased LOC B - quiet tachypnea, unless pneumonia, ARDS, etc. C - tachy, oliguria warm shock - warm, flushed skin peripherally, hypotension with wide pulse pressures, bouding peripheral pulses, brisk cap refill cold shock - pale mottled skin, hypotension with narrow pulse pressure, weak peripheral pulses, delayed cap refill D - changes in LOC E - fever or hypothermia, extremities warm or cool, petechial or purpuric rash decrease preload, normal/decreased contractility, variable afterload

Question 31

Distributive shock - anaphylactic shock: pathophysiology? Work through ABCDE. How is preload, contractility, and afterload effected?

Answer 31

venodilation, arterial vasodilation, increased capillary permeability, pulmonary vasoconstriction A - angioedema (face, lips, tongue) B - resp distress, stridor + wheezing C - tachy, hypotension with wide pulse pressure, delayed cap refill D - anxiety/agitation, changes in LOC, nausea/vomiting E - urticaria (hives), swelling/edema, itching, redness/rash decrease preload, variable contractility, afterload: decreased for LV, increased for RV

Question 32

Distributive shock - neurogenic shock: results from? pathophysiology? work through ABCDE. How is preload, contractility, and afterload effected?

Answer 32

cervical/upper thoracic injury that disrupts the SNS innervation of the blood vessels and heart uncontrolled vasodilation, inhibition of compensatory tachy A - affected by LOC B - increased RR, may affect resp muscles and diaphragm C - normal HR or brady, hypotension with wide pulse pressure, delayed cap refill D - changes in LOC E - injury decreased preload, normal contractility, decreased afterload

Question 33

cardiogenic shock: inadequate tissue perfusion secondary to what? list specific examples. what is the compensatory mechanism? work through ABCDE. how is preload, contractility, and afterload effected?

Answer 33

myocardial dysfunction e.g. CHD, myocarditis, cardiomyopathy, arrhythmias, sepsis, myocardial injury vasoconstriction (to maintain BP) and has detrimental effects as the heart now has to work harder A - patent unless decrease LOC B - tachypnea, increased resp effort from pulmonary edema C - tachy, N or decreased BP with a narrow pulse pressure, weak/absent peripheral pulses, normal/weak central pulses, delayed cap refill, signs of CHF, cyanosis, cool/pale/mottled/diaphoretic D - changes in LOC E - extremities cooler than trunk variable preload, decreased contractility, increased afterload

Question 34

in obstructive shock, how is CO impaired? what are the 4 types?

Answer 34

physical obstruction of blood flow | cardiac tamponade, tension pneumo, ductal dependent heart lesions, massive pulmonary embolism

Question 35

cardiac tamponade: where does fluid/blood/air accumulate? what does this impede? what can it progress to? where is it often seen? work through ABCDE. how is preload, contractility, and afterload effected?

Answer 35

pericardial space systemic/pulmonary venous return (reducing ventricular filling and SV/CO) PEA trauma, cardiac surgery, infection, tumor A - patent unless decreased LOC B - resp distress with increased rate/effort C - tachy, poor peripheral perfusion (weak distl pulses, cool extremeties, delayed cap refill), muffled/diminished heart sounds, narrow pulse pressure, pulsus paradoxus, distended neck veins, dampened QRS, tachycardia progressing to bradycardia D - changes in LOC E - extremities cooler than trunk variable preload, N contractility, increased afterload

Question 36

tension pneumothorax: how does the high intrathoracic pressure effect the heart? what can it progress to? when should this be suspected? work the ABCDE. how is preload, contractility, and afterload effected?

Answer 36

compresses heart/great vessels impeding venous return PEA chest trauma or rapid deterioration when receiving PPV A - variable, advanced a/w may already be in place, tracheal deviation B - resp distress with increased rate/effort, hyperresonance, hyperexpansion, diminished BS C - pulsus paradoxus, distended neck veins, rapid deterioration in perfusion, tachy to brady D - changes in LOC E - extremities cooler than trunk variable preload, contractility, increased afterload

Question 37

pulmonary embolism: what is it? pathophysiology? | work through ABCDE.

Answer 37

total/partial obstruction of PA/branches V/Q mismatching, hypoxemia, increased PVR, RH failure, decreased LV filling/CO/ETCO2 A - patent unless decreased LOC B - resp distress with increased rate/effort C - tachy, cyanosis, hypotension, systemic venous congestion and RH failure, chest pain D - changes in LOC E - extremities cooler than trunk

Question 38

Management of shock: | List some components of general management.

Answer 38

oxygen, IV/IO, ECG monitoring, POC glucose testing, A/W management

Question 39

List the management strategies for hypovolemic shock (hemorrhagic vs. non hemorrhagic)

Answer 39

control external bleeding, 20mL/kg NS bolus, repeat 2-3x PRN, transfuse PRBCs 10mL/kg (HB <70) NON: 20 mL/kg bolus, repeat PRN, consider colloid therapy

Question 40

List the management strategies for distributive shock (septic vs. anaphylactic vs. neurologic)

Answer 40

septic: 20mL/kg bolus, repeat ++, ABx, inotropes anaphylactic: IM epi, 20mL/kg, repeat PRN, ventolin/neb epi, antihistamines, corticosteroids, epi infusion neurologic: 20mL/kg NS bolus, repeat PRN, fluid refractory hypotension (epi/norepi), maintain temp

Question 41

list the management strategies for cardiogenic shock (brady/tachy arrhythmia vs CHD, myocarditis, cardiomyopathy, poisoning)

Answer 41

brady/tachy: specific protocol CHD blah blah blah: normotensive with pulmonary congestion: diuretics, cardiogenic shock: 5-10mL/kg NS SLOW bolus, dopamine/dobutamine/milirinone, expert consultation

Question 42

list the management strategies for obstructive shock (tension pneumo vs cardiac tamponade vs pulmonary embolism)

Answer 42

tension pneumo: needle decompression, chest tube tamponade: percardiocentesis, 20mL/kg NS bolus embolism: 20 mL/kg NS bolus, repeat PRN, consider thromobolytics, anticoagulants, expert consultation

Question 43

What does IO access provide access to? Why? What are the common peds sites? Contraindication?

Answer 43

noncollapsible marrow venous plexus, to administer drugs/fluids during resuscitation proximal 1 to 3 cm below proximal tibial tuberosity and slightly medial, distal tibia fractures/crush injuries, conditions of fragile bone, previous attempts in same bone

Question 44

Epinephrine: classification? action? indications? Brady IV/IO dose? neb croup dose? cardiac arrest IV/IO dose? cardiac arrest ETT dose?

Answer 44

catecholamine, vasopressor, inotrope alpha/beta adrenergic activity anaphylaxis, brady, croup, cardiac arrest, shock 0.01mg/kg (0.1ml/kg or 1:10,000) Q3-5M, max single dose 1mg <1 year = 2.5ml 1:1,000 and >1year 5ml 1:1,000 0. 01mg/kg (0.1ml/kg of 1:10,000) Q3-5M, max single dose 1mg 0. 1mg/kg (0.1ml/kg of 1:1,000) Q3-5M

Question 45

Atropine: | classification? action? indications? brady IV/IO dose?

Answer 45

parasympatholytic, anticholinergic blocks acetylcholine/muscarinic agonists parasympathetic neuroeffector sites, increases HR/CO by blocking vagal stimulation, reduces saliva, cause mydriasis brady caused by increased vagal tone, cholinergic drug toxicity, primary brady, 2nd degree (type I and II) and 3rd degree block 0.02mg/kg, min dose 0.1mg, max single dose 0.5mg, may repeat dose once

Question 46

amiodarone: | classification? action? indications? VF/pulseless VT dose?

Answer 46

class III antiarrhythmic prolongs action potential duration and effective refractory period, slow sinus rate, prolongs PR and QT interval VF/pulseless VT 5mg/kg dose rapid bolus (max 300mg), may give up to 3 doses (max daily 15mg/kg)

Question 47

adenosine: | classification? action? indications? SVT IV/IO dose?

Answer 47

antiarrhythmic stimulates adenosine receptors in the heart and transiently blocks conduction through the AV nose allowing return of NSR SVT first dose - 0.1mg/kg rapid push (max 6mg) second dose - 0.2mg/kg rapid push (max 12mg)

Question 48

When instilling drugs down ETT: pause vs no pause in CPR? volume of flush for peds vs infants? how many PPV breaths following? What 5 drugs can be given this way?

Answer 48

brief pause of CPR 5ml peds 2ml infants 5 rapid PPV Naxolone, Atropine, Vasopressin, Epi, Lidocaine

Question 49

What is primary brady a result of? specific examples? | What is secondary brady a result of? specific examples?

Answer 49

congenital/acquired heart condition - congenital abnormalities of hearts conducting system, surgical injury to heart conducting system, cardiomyopathy, myocarditis noncardiac condition that alters normal function of the heart - hypoxia, hypotension, drug effects, acidosis, hypothermia

Question 50

How are peds tachy with pulses and poor perfusion classified? Describe sinus tachy. Describe supraventicular tachy.

Answer 50

``` width of QRS: narrow complex (< 0.09 sec) = sinus tachy/supraventricular tachy wide complex (>0.09 sec) = ventricular tachy ``` sinus tachy - rate faster than ECG rate for age, develops in response to bodies need to increase CO, varies with activity and factors increasing O2 demand supraventricular tachy - rapid regular rhythm that often appears abruptly and may be episodic, prolonged undiagnosed SVT may cause CHF