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RESP 5017 > 12. Paediatric Advanced Life Support (PALS) > Flashcards

12. Paediatric Advanced Life Support (PALS) Flashcards

1
Q 
Age classification for:
premature neonate
neonate
infant
child
A

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

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2
Q

What are the components of the PALS assessment overview?

A

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

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3
Q

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

A

hold assessment, treat underlying problem

evaluate, identify, intervene

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4
Q

What are the 3 components of the initial impression?

A

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

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5
Q

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

A 
A - airway
B - breathing
C - circulation
D - disability
E - exposure
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6
Q

Describe how to assess the airway.

A

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

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7
Q

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

A

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

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8
Q

Describe how to assess breathing.

A

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

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9
Q

define apnea.

A

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

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10
Q

What can increase respiratory effort?

List signs of increased effort.

A

conditions that increase resistance or decrease compliance

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

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11
Q

describe how to assess circulation.

A

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

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12
Q

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

A

when peripheral vasoconstriction occurs

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13
Q

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

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

A 
decreased skin perfusion (dehydration, shock, hypothermia)
hemodynamically compromised (warm shock)
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14
Q

What does pallor or paleness indicate? Mottling?

A

decreased blood supply to the skin (shock), anemia

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

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15
Q

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

A

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

*refer to tables on slide 26

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16
Q

Describe how to assess disability.

A

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)

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17
Q

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

A

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

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18
Q

What should you observe for in relation to exposure?

A

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

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19
Q

How would you perform a secondary assessment?

A

focused history/physical exam

ISAMPLE

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20
Q

What are the components of ISAMPLE?

A 
immunizations
sign and symptoms
allergies
medications
past medical history
last food, fluid intake
events
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21
Q

Work through the ABCDE for upper a/w obstruction.

A

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

22
Q

Work through the ABCDE for lower a/w obstruction.

A

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

23
Q

Work through the ABCDE for lung tissue disease.

A

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

24
Q

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

A

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

25
Q

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

A

bronchiolitis - nasal sxn, neb epi, HFNC, bronchodilator, hypertonic N/S trial

asthma - ventolin +atrovent, corticosteroids, mag sulphate, IV ventolin

26
Q

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

A

pneumonia/pneumonitis - ventolin (if wheeze), antibiotics, NIV, ventilation

pulmonary edema/ARDS - NIV, ventilation, vasoactive drugs, diuretics

27
Q

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

A

inadequate oxygen delivery to tissues

tachy, increased SVR, increased contraction

compensated = maintain BP
uncompensated = unable to maintain BP
28
Q

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

A

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

29
Q

What is distributive shock? what are the 3 types?

A

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

30
Q

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?

A

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

31
Q

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

A

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

32
Q

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

A

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

33
Q

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?

A

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

34
Q

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

A

physical obstruction of blood flow

cardiac tamponade, tension pneumo, ductal dependent heart lesions, massive pulmonary embolism

35
Q

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?

A

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

36
Q

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?

A

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

37
Q

pulmonary embolism: what is it? pathophysiology?

work through ABCDE.

A

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

38
Q

Management of shock:

List some components of general management.

A

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

39
Q

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

A

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

40
Q

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

A

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

41
Q

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

A

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

42
Q

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

A

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

43
Q

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

A

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

44
Q

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

A

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

  1. 01mg/kg (0.1ml/kg of 1:10,000) Q3-5M, max single dose 1mg
  2. 1mg/kg (0.1ml/kg of 1:1,000) Q3-5M
45
Q

Atropine:

classification? action? indications? brady IV/IO dose?

A

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

46
Q

amiodarone:

classification? action? indications? VF/pulseless VT dose?

A

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)

47
Q

adenosine:

classification? action? indications? SVT IV/IO dose?

A

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)

48
Q

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?

A

brief pause of CPR

5ml peds
2ml infants

5 rapid PPV

Naxolone, Atropine, Vasopressin, Epi, Lidocaine

49
Q

What is primary brady a result of? specific examples?

What is secondary brady a result of? specific examples?

A

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

50
Q

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

A 
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

RESP 5017 (19 decks)

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