PALS

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PALS
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  1. PALS primary assessment differs a bit from other assessment algorithms we have presented in that it also includes ______________. In other assessment algorithms including PHTLS, we have included “that” as a first step in the secondary assessment.[page 11]
    VS / SpO2
  2. PALS “Identify” step in their assessment process includes identification of four types of respiratory problems. What are they? [Page 11]
    Upper Airway Obstruction,Lower Airway Obstruction, Lung Tissue Disease, Disordered Control of Breathing.
  3. PALS “Identify” step in their assessment process includes identification of four types of circulatory problems. What are they?
    Hypovolemic Shock, Obstructive Shock, Distributive Shock, Cardiogenic Shock
  4. PALS categorizes the respiratory condition of the patient as either respiratory ________ or respiratory ___________. [page 11]
    Distress, failure
  5. ***************************************
  6. PALS categorizes the cardiovascular condition of the patient as either _______ shock or__________ shock. [page 83]
    Compensated or hypotensive (decompensated)
  7. ***************************************
  8. PALS suggests that the proper positioning of the patient is helpful to manage the airway. In cases whereyou are not required to perform a head tilt-chin lift or jaw thrust, howshould you position the child? [page 12]
    position of comfort / least distress
  9. What are the five parts of the PALS breathing assessment? [page 13
    rate, effort, depth (chest expansion-air movement), lung and airway sounds, O2 saturation by pulse oximetry
  10. PALS suggests that you evaluate the child’s respiratory rate ______ you perform other assessments. [page 13]
    Before
  11. PALS suggests that you count the child’s respiratory rate for ____ seconds. [page 13]
    30
  12. Why do they suggest that you count for 30 seconds? [page 13]
    In the case of sleeping infants, the pattern is irregular---remember that the actual rate may not be as helpful as an assessment of their effort
  13. If you have a child patient who was tachypneic but has now slowed their breathing rate, how do you know if that patient is improving or getting worse? [page 13 and 14]
    If their rate is slowing but their LOC is dropping, that indicates things are worse than if their rate slows while they seem to calm down and wake up
  14. PALS primary assessment differs a bit from other assessment algorithms we have presented in that it also includes ______________. In other assessment algorithms including PHTLS, we have included “that” as a first step in the secondary assessment.[page 11]
    fever, pain, sepsis, anemia, dehydration / DKA or other metabolic causes
  15. Why is it true that quiet tachypnea occurs? [page 14]
    the increased rate is in anattempt to normalize metabolic acidosis rather than to address hypoxia
  16. We usually don’t use the term “bradypnea”. PALS mentions it as a key assessmentpoint and notes several causes. List them. [page 14]
    causes that suppress the neuro system’s respiratory drive (meds, infection,hypothermia, CNS injury) or simply that the patient has worn out fromrespiratory muscle fatigue
  17. List as many signs of increased respiratory effort as you can. [page 14]
    retractions, nasal flaring,head bobbing, see-saw breathing, use of accessory muscles, grunting,open-mouth breathing, gasping, prolonged expiratory phase
  18. What are retractions and why are they important to detect? [page 15]
    retractions show that the child is using chest muscles to try to move air into the lungs---they appear as inward chest movements on inspiration (see page 42 also)
  19. What is grunting and why is it important to detect? [page 16]
    ”low pitched” and “short”sound made at the end of expiration in an attempt to prevent atelectasis---provides some PEEP---similar to pursed-lip breathing in COPDers
  20. What is head bobbing and why is it important to detect? [page 15]
    chin lifts and neck extends during inspiration in an attempt to get accessory muscles involved in inspiration---more common in infants than older kids
  21. What is see-saw breathing and why is it important to detect? [page 15, 42]
    chest retracts and abdomen extends during inspiration---accessory muscles trying to help on inspiration----likely related to upper airway obstruction or really bad lower airway obstruction---weaker chest muscles than adults so the expansion of the chest is less and the negative intrathoracic pressure generated by the belly muscles overcomes the weak chest muscle’s abilityto keep the chest expanded
  22. What is stridor and why is it important to detect? [page 16]
    severe distress sign---high pitched sound on inspiration and sometimes also on expiration---upper airway obstruction from swelling or foreign body
  23. When auscultating to detect the effectiveness of air movement, where does PALS suggest that you listen? [page 16]
    over the anterior AND posterior chest because the chest is so small that sounds are transmitted easily from side to side----listen front and back to help you try to decide where the abnormal sounds are coming from.
  24. In a patient with bronchiolar obstruction, what abnormal lung sound would you suspect and why? [page 17]
    wheezes caused by narrowed bronchioles that act to make a whistle when air movementoccurs
  25. Will all patients with bronchiolar obstruction produce wheezes? Which ones may not?
    If the child is not moving any air through the obstructed bronchiole, there won’t be any air movement to make the whistle and so wheezes will not be heard. Be sure you arehearing clear air movement rather than no air movement. Also, as your bronchodilators begin to work, the child will wheeze louder in many cases but that’s GOOD.
  26. What conditions cause stridor?
    Upper airway obstruction from swelling or foreign body
  27. What conditions cause grunting?
    State leading to atelectasis
  28. What conditions cause gurgling? [page 17]
    Secretions / blood / vomit etc in the upper airway
  29. What conditions cause crackles?[page17]
    fluid in the alveoli and / or the alveoli popping open
  30. What conditions cause wheezing? [page17]
    • Bronchiolar obstruction “essentially",  narrowed
    • bronchioles that act to make a whistle when air movement occurs
  31. PALS lists two types of crackles---what are they and what do they suggest? [page 17]
    fluid in the alveoli and / or the alveoli popping open
  32. What is hypoxia? [page 38]
    Low oxygen in the TISSUES.
  33. What is hypoxemia? [page38]
    Low oxygen in the BLOOD.
  34. Does pulse oximetry detect hypoxemia or hypoxia? [page 38]
    Hypoxemia
  35. Does pulse oximetry help you assess ventilation? Why or why not?[page 17, 40]
    Not really. EtCO2 is better at assessing ventilation but you must make sure that the metabolism and perfusion are normal before you start making decisions about ventilation based on capnometry. Pulse Ox readings that are low indicate hypoxemia----one cause of that would be inadequate ventilation but there are many causes.
  36. Can a patient be hypoxemic but not hypoxic? How? [page 38]
    Sure.Hypoxemia indicates low oxygen levels in the blood but if cardiac output is increased to compensate, then there is more blood moving past the tissues and even though it's not carrying its usual O2 load, the tissues can still get the O2 they need. By the way, can you be hypoxic without being hypoxemic?Sure---low perfusion---the blood had plenty of O2 but its just not gettingdelivered to the tissues. It sounds like a word game but the point here is that pulse oximetry measures HYPOXEMIA!
  37. How can you evaluate the accuracy of a pulse oximetry reading? [page17]
    Watch the signal strength indicator on the pulse ox and match the HR on the pulse ox with the patient’s HR.
  38. What conditions can give you false readings on pulse oximetry? [page 18]
    • Poor perfusion, cold (poorly perfused) skin where the probe is placed, Carbon
    • Monoxide, methemoglobinemia.
  39. How do you assess capillary
    refill? [page 19]
    • Normothermic
    • environment---raise just above level of heart---doesn’t have to be a
    • nailbed.
  40. What is the value of using
    capillary refill for an assessment? [page 19]
    • Faster than a blood pressure. Gives some
    • qualitative info. Similar to presence of peripheral pulses.
  41. Is capillary refill a
    reasonably accurate measure in infants and children? [page 20]
    • If its present in pediatrics,
    • its reasonable to consider that perfusion is not normal but its absence
    • does NOT guarantee normal perfusion.
  42. What
    is considered a delayed capillary refill time? 
    [page 19]
    • less
    • than or equal to 2 seconds or the time it takes you to say “capillary refill”
  43. *********************************************************************************************************************
  44. What is mottling and what
    does it tell you? [page 20]
    • Irregular or patchy
    • discoloration of the skin. Uneven combination of pink, bluish, gray, or
    • pale skin tones.
  45. What is pallor and what does
    it tell you? [page 20]
    • paleness,
    • lack of normal color in the skin or mucous membrane. May be caused by decreased
    • blood supply to the skin (cold, stress, shock, hypovolemic and cardiogenic);
    • decreased number of red blood cells (anemia); decreased skin pigmentation.
  46. What is peripheral cyanosis
    and what does it tell you?
    • Page 20, Bluish discoloration
    • of the hands and feet. Can be caused by diminished O2 delivery to the
    • tissues.may be seen in shock, CHF, or peripheral vascular disease, or
    • conditions causing venous stasis.
  47. What is central cyanosis and
    what does that tell you?
    • Page 20, blue color of the
    • lips and other mucous membranes.
  48. How do you know what a normal
    HR, RR or BP is for an infant or child?
    Chart, page 21
  49. Your
    patient is hypovolemic. Why is she tachycardic?
    • Page 74---a decrease in
    • central perfusion pressure is sensed by the baroreceptors and the brain
    • orders an increase in cardiac output which includes an increase in HR 50.
  50. What if your hypovolemic
    patient who was tachycardic starts to have her HR decrease---what does
    that mean?
    • Compensation has
    • failed---likely the myocardium has become hypoxic from prolonged
    • hypotension and so the HR slows. Arrest is imminent.
  51. Make a chart (from memory) of
    the GCS for adults. Now add children and infants to it---what is the main
    difference for infants on motor response compared to other ages?
    • Page 24 infants response to
    • touch and to pain is different than others.
  52. Do children have a higher or
    lower need for O2 to support metabolism compared to adults in terms of ml
    / kg per minute? How much difference is there?
    • Page 38 peds have a much
    • higher (about twice as high) need for O2
  53. In a pediatric patient with
    hypoxia, what would you expect their HR and RR to do compared to normal
    while they are compensating?
    • Increase
    • initially (Page 38
  54. In a pediatric patient with hypoxia, what
    would you expect their HR and RR to do compared to normal while they are
    decompensating?
    • Page 38----decrease in both
    • as a late sign that indicates failure to compensate and imminent arrest
  55. ***************************************
  56. ***************************************
  57. If your patient was initially agitated and anxious with a low pulse oximetry reading and you gave supplemental oxygen that has now improved the pulse oximetry reading to above 90% and it is still climbing and the child seems MUCH more calm and,actually, really seems to be pretty tired and listless, is this a problem? If so, what is the problem and how will you fix it?
    Page 40 This is a big problem and may be due to hypercarbia (condition of having the presence of an abnormally high level of carbon dioxide in the circulating blood) and so ventilation needs to be increased to eliminate CO2. The child may also be too fatigued to continue without support.
  58. Explain why the same amount
    of airway edema / inflammation in an adult will have a much less significant
    impact than that same amount in an infant.
    • Page
    • 40 Adults have larger airways reducing airway resistance; children have smaller
    • airways making it more difficult with narrowed passages.
  59. What is lung compliance?
    • Page
    • 41 the change in lung volume produced by a change in driving pressure across
    • the lung. When lung compliance is high, the lungs are easily distended.
    • Children with low lung compliance, the lungs are stiffer; more effort is needed
    • to inflate the alveoli
  60. What causes decreased lung
    compliance?
    • Page 41 Pneumothorax, pleural
    • effusion.
  61. How can gastric distention
    impact ventilation?
    • Page
    • 42 Impedes
    • diaphragm movement.
  62. What impact is there from the
    difference in chest wall compliance in very young patients compared to
    older children or adults?
    • Page 42. Also, see see-saw
    • breathing, 
    • chest retracts and abdomen
    • extends during inspiration---accessory muscles trying to help on
    • inspiration----likely related to upper airway obstruction or really bad
    • lower airway obstruction---weaker chest muscles than adults so the
    • expansion of the chest is less and the negative intrathoracic pressure
    • generated by the belly muscles overcomes the weak chest muscle’s ability
    • to keep the chest expanded
  63. Inspiration is normally an
    active process (requires energy) while expiration is normally passive
    (simple relaxation---minimal energy consumed). What can cause expiration
    to also become active and therefore increase the work of breathing
    potentially leading to respiratory muscle fatigue?
    • Page 44. Upper or Lower
    • Airway obstruction or Lung Tissue Disease
  64. Explain how breathing rate is
    regulated by the nervous system.
    • Page 42. Brainstem
    • respiratory centers issue out involuntary breathing, can be overwritten by
    • manual control from the cerebral cortex.
  65. Pediatric
    patients who are working hard to exhale will generate higher than normal
    intrathoracic pressure which may lead to what problem?
    Page 44. Bronchiolar collapse
  66. What are signs of an upper
    airway obstruction?
    • Page 44. Tachypnea, increased
    • inspiratory respiratory effort (eg, inspiratory retractions, nasal
    • flaring); change in voice (eg, hoarseness), cry, or presence of a barking
    • cough; stridor (usually inspiratory but may be biphasic)
  67. What are signs of a lower
    airway obstruction?
    • Page 44. Tachypnea, wheezing
    • (most commonly expiratory, but may be inspiratory or biphasic), prolonged
    • expiratory phase associated with increased effort (expiration is active
    • rather than a passive process), and cough
  68. What are signs of “lung
    tissue disease” according to PALS?
    • Page 45. Tachypnea (often
    • marked); increased respiratory effort; grunting; crackles (rales);
    • diminished breath sounds; tachycardia; hypoxemia (may be refractory to
    • administration of O2)
  69. What are signs of “disordered
    control of breathing” according to PALS?
    • Page 45. Variable or
    • irregular respiratory rate (tachynpea altering with bradypnea); variable
    • respiratory effort; shallow breathing (frequently resulting in hypoxemia
    • and hypercarbia); central apnea (ie, apnea without any respiratory
    • effort).
  70. In a pediatric patient who is
    not in cardiac arrest, what is your first priority in management?
    • Page 49-- “evaluation of
    • airway and breathing”
  71. Your pediatric patient has a
    cough suggestive of croup and is having trouble swallowing and so they are
    drooling and have lots of upper airway secretions. Why is suctioning
    something you should do with caution?
    • Page 50. Suctioning may
    • increase a child's agitation and may increase respiratory distress.
  72. Upper airway edema is best
    treated with what?
    • Page 51--nebulized
    • epinephrine (“racemic epinephrine”)
  73. Your pediatric patient has an
    anaphylactic reaction for some reason. Describe your management of the
    patient in terms of any medications or fluid therapies.
    • Page
    • 52. Administer epinephrine by autoinjector or regular syringe every 10-15
    • minutes as needed. Repeated doses may be needed. Treat bronchospasms (wheezing)
    • with albuterol by MDI or nebulizer.
  74. ***************************************
  75. Your pediatric patient is
    drowsy, bradycardic, has quiet lung sounds, see-saw breathing and a pulse
    oximetry reading of 85%. Describe your management and explain what is the
    likely field diagnosis.
    • She has a severely increased
    • work of breathing (see-saw) and now she is hypoxic (85% sat). Severely
    • hypoxic enough to be drowsy (probably hypercapnic too) and she’s in
    • trouble because bradycardia is NOT what I was expecting---tachycardia
    • should have been the compensation but she’s probably soooooo hypoxic that
    • her myocardium is ischemic and she’s about to code. To be working that
    • hard to breathe and yet not have enough air movement to make many sounds
    • indicates that her problem is respiratory. This is not “quiet tachypnea”
    • because the increased effort of breathing is not part of that---and
    • “quiet” means clear lung sounds rather than diminished or absent. She
    • needs an airway and immediate bag mask ventilation. Once that is in place,
    • we need to assess her for shock---it might be all related to the brady
    • rhythm but that’s not nearly as likely as some other cause of hypoxia. I’m
    • assuming bilaterally decreased lung sounds and no reason to worry about
    • tension pneumos. Regardless, first thing is to ventilate and oxygenate
    • while we investigate.
  76. According to PALS, what is
    the role of CPAP in pneumonia?
    • Page 55. Noninvasive
    • ventilation.
  77. What is the difference
    between CPAP and BiPAP?
    • CPAP is a continuous pressure
    • where BiPAP is two different levels of pressure
  78. Your pediatric patient has
    crackles in his lungs and is very drowsy. You decide that CPAP is not
    indicated because of his decreased level of consciousness. What should you
    do?
    He needs positivepressure ventilation and if non-invasive (CPAP) is not an option thenthat leaves invasive (ET intubation and Bag-Mask). However, standard Bagto ET tube ventilation doesn’t keep any positive pressure at the end ofexpiration (PEEP) so you need a PEEP valve on your BVM.
  79. What is PEEP?
    Page 56. PositiveEnd Expiratory Pressure
  80. What does PEEP do for your
    patient?
    Page 56---helpsprevent alveolar collapse (atelectasis) and reduces work of breathing /alveolar strain or trauma---recall the pressure needed to blow up aballoon when it is collapsed completely compared to the pressure neededto inflate that same balloon it it is not allowed to fully collapse---PEEPkeeps the alveoli from fully collapsing.
  81. How do you deliver PEEP with
    non-invasive ventilation?
    CPAP
  82. How do you deliver PEEP with
    invasive ventilation (after ET intubation)?
    PEEP valveattached to the exhalation port
  83. When would you use PEEP?
    PEEP keeps thealveoli from fully collapsing.
  84. What is Cushing’s Triad and
    what does it suggest?
    Page 57.Hypertension, bradycardia and irregular respiration that suggest elevatedICP (increased intracranial pressure)
  85. When is intentional
    hyperventilation appropriate and why and how do you do it?
    • Page 57---careful and
    • controlled increase in ventilatory rate and depth that is best judged by a
    • target EtCO2 (20 is a typical goal)---the theory is that the increase in
    • breathing produces a decrease in CO2 which causes vasoconstriction which
    • allows for a bit more space inside the skull---one of the three allowable
    • occupants of the skull is blood inside vessels and so vasoconstriction may
    • produce a little space for swelling to continue before the brainstem gets
    • squeezed out the foramen magnum. If there are signs of brainstem
    • herniation, controlled hyperventilation remains a desperate
    • option----think about it---vasoconstriction in the brain should reduce
    • cerebral perfusion and that is never good. The trade-off between bad and
    • badder stuff here is that if you don’t stop the herniation, you won’t have
    • a need to perfuse.
  86. In a patient with elevated
    ICP, you MUST prevent any episode of ________ OR ______________.
    Hypoxia;Hypotension
  87. What is the impact of
    hyperthermia on ICP?
    Increases ICP
  88. What is the role of agitation
    on ICP?
    Increases ICP
  89. Name two bronchodilators for
    delivery by nebulizer and explain their action.
    Albuterol is asympathetic agonist (Beta 2 mostly) and so it causes bronchodilation, Ipratropium is a parasympathetic antagonist and so it inhibitsbronchoconstriction
  90. Your asthma patient has not
    responded to nebulized bronchodilators, what are some other possible
    interventions?
    Page 53(terbutaline, steroids, mag)
  91. What tools or techniques are
    useful to place your patient in the sniffing position for airway
    management?
    Ramping withblankets / towels / pillows / head of bed
  92. How do you assess whether you
    have achieved the sniffing position when doing airway management?
    • Ear to sternal notch line
    • parallel with the ground. Page 63!!!!
  93. Is hypotension the same as
    hypoperfusion? Why or why not? Give examples or explain.
    Page 69. NOT the same. Hypoperfusion occurs WELL BEFORE hypotension in most cases.
  94. Name some conditions that
    would contribute to shock even when the patient has not lost volume, has
    no pump malfunction and the container is the appropriate size? Why is this
    the case?
    Page 69 and70---fever / infection, injury / pain, respiratory distress all add tothe metabolic demands of the patient and therefore their need for oxygen
  95. What is anaerobic metabolism
    and why do we need aerobic metabolism?
    Page 70 Anaerobicis neither efficient enough so sufficient to meet the cell’s energy
  96. ***************************************
  97. Explain preload and the
    impact of reduced or increased preload on cardiac output.
    • Page 71 Preload is the amount
    • of blood available to the heart to pump---blood that has returned from the
    • peripheral circulation. Increased preload equals increased cardiac output
    • as long as contractility, heart rate and afterload remain the same.
    • Decreased preload equals decreased cardiac output with the same
    • conditions.
  98. Explain afterload and the
    impact of reduced or increased afterload on cardiac output.
    • Page 71 Afterload is the
    • systemic vascular resistance or “blood pressure” against which the left
    • ventricle must pump. This is usually due to hypertension and, naturally,
    • this is usually not an issue with pediatrics. Vasoconstriction increases
    • afterload though.
  99. How can cardiac output be
    increased?
    • Page 71 Increased heart rate,
    • increased strength of contraction, increased preload, decreased afterload.
  100. As shock develops, list four
    things that you body does to try to maintain O2 delivery to the tissues of
    the vital organs.
    • Page 72. Increased cardiac
    • output by increased rate and strength of contraction PLUS increased
    • preload from an increase in systemic venous tone to, in effect, shrink the
    • container and squeeze blood back to the heart PLUS an increase in arterial
    • smooth muscle tone (increased afterload) to effectively shrink the
    • container.
  101. What signs and symptoms do
    each of those three things produce usually?
    • Page 73 Cool / pale / moist
    • skin, tachycardia, nausea (blood shunting away from the gut), delayed cap
    • refill and weak peripheral pulses as a result of vasoconstriction. Note
    • also that the pulse pressure may narrow as the diastolic pressure is
    • increased by the vasoconstriction.
  102. Tachycardia has its limits as
    a compensatory mechanism. As the rate increases past some point, cardiac
    output actually decreases. Why is this the case? (consider number 103 and
    104)
    • Inadequate ventricular filling
    • time due to a shortened diastole occurs with very rapid heart rates. In
    • addition, since the myocardium is perfused during diastole, a rapid heart
    • rate shortens diastole to the point that the myocardium becomes ischemic
    • and function drops----and eventually heart rate drops as well. (Right
    • before arrest!) pages 121 and 122
  103. ***************************************
  104. ***************************************
  105. How do you tell if a patient
    is in compensated or uncompensated shock?
    • Page 73---measure their
    • systolic BP---hypotension = uncompensated (decompensated)
  106. What is the most common cause
    of distributive (container) shock in pediatrics?
    Page 75, 76, 77 septic
  107. In terms of cardiac output
    and systemic vascular resistance, how is distributive shock different from
    the other three types of shock?
    Page 75-77Vasodilation occurs instead of vasoconstriction so the cool / pale /moist skin caused by vasoconstriction is not usually seen in the initialphases. This is “warm”
  108. Why does volume replacement
    help in distributive shock?
    Page 86 Volume fills the space in the inappropriately large container.
  109. ***************************************
  110. What is pulse pressure?
    Systolic minus diastolic pressure
  111. ***************************************
  112. Explain how the compensatory
    mechanisms of the body tend to work to make cardiogenic shock worse.
    Page 78 Compensatory tachycardia increases the myocardial oxygen consumption of the alreadyfailing heart while vasoconstriction increases preload at a time when theheart is unable to pump out what its already supposed to be handling.Also, vasoconstriction increases afterload and makes the heart have towork harder to pump out blood---again, at a time when it can’t handle whatit already has to do.
  113. Initially, tachycardia can
    increase cardiac output and compensate for loss of blood volume or
    inappropriate vasodilation. Eventually, bradycardia occurs which usually
    leads rapidly to cardiac arrest. Why does this happen?
    Tachycardia causes increased myocardial O2 consumption and decreased filling / perfusing time---allthese can lead to myocardial ischemia which shows as bradycardia.
  114. Most shock types are
    initially treated with volume replacement. For hypovolemia and
    distributive shock, the fluid bolus for pediatrics is ______ ml/kg.
    Page 86 (20)
  115. For pediatric patients in
    ______________ shock, the volume replacement fluid bolus amount is 25% of
    the initial fluid volume treatment at 20 ml/kg.
    Page 86(cardiogenic)
  116. Why is that true during
    cardiogenic shock, the volume replacement fluid bolus amount is 25% or the
    standard fluid bolus?
    • Small increases in preload
    • may stretch the ventricles (Frank-Starling mechanism----”rubber band”)
    • whereas large increases are more likely to overload an already struggling
    • or failing ventricle.
  117. How can you assess the
    difference between cardiogenic and hypovolemic shock? (think about
    tachypnea)
    Page 86Cardiogenic shock is often accompanied by pulmonary vascular congestionwhich turns into pulmonary edema with an increased work of breathing.(think CHF). PALS uses the term “quiet tachypnea” to refer to those caseswhere an increased respiratory rate is occurring but without increasedwork of breathing. In hypovolemia, the patient would be “quietlytachypneic” in order to help compensate for the reduced amount of bloodcirculating (what is left needs to be loaded with O2 to the maximumamount possible so rapid breathing).
  118. List three things that can
    cause obstructive shock in adults (not counting supine hypotensive
    syndrome) and pediatrics. Then list a fourth cause that is peculiar to
    infants.
    Page 79Tamponade, Tension Pneumo, Pulmonary Embolus (think “H’s and T’s”) Ininfants, some sort of “ductal dependent congenital cardiac defect” isanother option. Remember, in women in their late 2nd and 3rd trimester ofpregnancy, supine hypotensive syndrome is a form of obstructive shock.Obstructive shock in Cardiac Tamponade occurs when the ventricles areobstructed from filling. Obstructive shock in Tension Pneumo occurs whenthe vena cava is obstructed by the “air bubble” and preload is reduced---andwhen the ventricles are obstructed from filling. Pulmonary Embolus is anobstruction in the pulmonary arterial flow which obstructs blood gettingthrough the pulmonary system and back to the heart---so reduced leftsided preload and increased right sided afterload.
  119. What is pulsus paradoxus and
    how would you measure it?
    Page 80 Manually,slowly, carefully and with attention to the breathing cycle and its impact on blood pressure---related to increased intrathoracic pressure causing crimping of the vena cava and therefore reduced preload.
  120. ***************************************
  121. In tension pneumothorax, list
    the two main things that lead to hypoxia and hypoperfusion.
    Page 81Compression of a lung and compression of the heart / vena cava.
  122. ***************************************
  123. ***************************************
  124. Of all the metabolic issues
    that can compound shock, hypoglycemia is probably the only one that we can
    really deal with in the field. Describe how treatment of hypoglycemia in
    pediatrics is different from adults.
    Page 95 DilutedD50
  125. ***************************************
  126. ***************************************
  127. In adults, we treat shock by“lay them down, keep them warm, give high flow O2, control external bleeding and transport rapidly.” Which of those is potentially different for pediatrics and why?
    The “lay themdown” part---position of comfort (their comfort, not yours) is best. The sickest ones will let you lay them down though.
  128. In adults, when we have patients in shock, most paramedics give a minimal “radio report” that consists of basically an alert rather than a full patient description and rarely is a physician consult involved. How is that different for pediatrics or is it the same?
    Expert consultation is suggested by PALS---early and often.
  129. After about one hour,approximately how much of the Normal Saline fluid bolus that you gave your patient is still in the intravascular space?
    25%
  130. Other than cardiogenic shock,PALS suggests that there is one other group of pediatric patients in shock who should receive less than the usual fluid bolus volume. Who are they?
    Beta blocker or Ca Channel Blocker overdose / poisoning
  131. The usual fluid bolus is given over how many minutes?
    5-10
  132. ***************************************
  133. You have a 5 year old patient who was struck by a car and initially was anxious, crying, HR 130, BP 90/50, RR 30. You rapidly package the patient, lay him supine on a backboard and cover him with blankets, give him a NRBM at 15lpm with a good mask seal even though you have to keep him from taking it off,control the minor bleeding from his lower leg wound and begin rapid transport. You had a 7 minute scene time and a 25 minute trip to a traumacenter. During transport, you attempt an 18 gauge IV and get it with little fight from the patient. His BP is 80/60 and HR 150 with RR now 16.What can you determine from this repeat assessment?
    His HR is up, his BP is down and the pulse pressure is narrowing plus he’s dropping his mental status (didn't fight me on the IV!!!!!!) and even his RR is declining---he’s getting MUCH worse.
  134. ***************************************
    Get expert consult on these cases. Most rational protocols won’t go this deep anyway.
  135. First line treatment of anaphylactic shock is medication or fluid therapy?
    Epi
  136. d
  137. List the treatments for anaphylactic shock in order---include steroids, histamine blockers,epinephrine, fluids, bronchodilators and oxygen in your list. (Page 103)
    Epinephrine by IM epinephrine(1:1000) or autoinjection. Repeat as needed in severe cases with a seconddose or epinephrine infusion.

    Aminister isotonic crystalloid fluid boluses as needed.

    • Albuterol as PRN for bronchospasms
    • Antihistamines such as H1 blocker (diphenhydramine); consider H2 blocker (ranitidine or famotidine).A combination of an H1 and 2 may be more effective than either givenalone.

    Corticosteroids such as methylprednisolone or equivalent. 

    For hypotension unmanageableto epi and fluid, use vasopressors.
  138. Does PALS ever suggest the use of CPAP in the management of shock? If so, when? If not, why not?
    Page 105 In cardiogenic shock with pulmonary edema causing increased work of breathing along with interference with diffusion (fluid / swelling in the alveolar / capillary membrane), “non-invasive positive pressure ventilation” (CPAP in English)may be a consideration. EXPERT consultation is the best plan but don’tforget to mention this option to the Expert. The Expert is usually expertin treating kids---maybe not in paramedics treating kids. They may notknow what we have or what we can do and so their urge is to “just get thekid to me”. CPAP may make a huge difference in that uncommon pedscardiogenic shock patient.
  139. ***************************************
  140. Why does PALS differentiate primary from secondary bradycardia?
    Page 114 and 119---because you treat them differently! Primary Brady gets Atropine (Sinus Brady + AVblock 1 and Mobitz I)---Secondary Brady gets Epi.
  141. What is the difference from primary and secondary bradycardia?
    Primary Brady (Sinus Brady +AV Block First, Second (Mobitz I)) gets Atropine (slow heart rate)---Secondary Brady gets Epi (av block)
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  143. ***************************************
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  145. What is the ratio of chest compressions to ventilations for various ages of patients?
    Varies based on how many of you are working it and what age but remember these two things: it is ALWAYS 30:2 when you are by yourself and it is ALWAYS 30:2 on adults so.....the only time it CAN be 15:2 is when you are working an infant or child with a helper.
  146. What is the depth of chest compressions for various ages of patients?
    Always 1/3 the“chest depth” (the anterior-posterior dimension) which comes out to 1.5 inches for infants, 2 inches for children and at least 2 inches for adults but nobody can agree on what is 2 inches anyway plus you can’t tell how deep you are going in inches---so the proportion of 1/3 the chest depth (and till you make a pulse?) works
  147. Would you ever do chest compressions on a patient with a pulse and why or why not?
    You should compress the chest of a severely bradycardic pediatric patient (<60)who is hypotensive. Page 117.
  148. Name three ways to differentiate ST from SVT in pediatric patients.
    Page 134 and 135 P-waves present / normal vs absent or abnormal; rate varies with activity/ simulation versus rate remains the same; rate > or < 180 for children and > or < 220 for infants. PALS also mentions history /onset info if valid history can be obtained quickly enough.
  149. In pediatric patients, a wide-complex tachycardia should be treated by:
    Page 134 and 137 WCT in peds is usually VT (like adults)
  150. List the vagal maneuvers suggested by PALS.
    Page 127 bag of ice to the face, valsalva if they can understand how (blow through a straw may work) and carotid sinus massage
  151. List the additional vagal maneuver suggested by Dr. Womack.
    Gag with tongue depressor etc.
  152. ***************************************
  153. ***************************************
  154. Describe how you would administer adenosine to a patient with SVT who measures in the Blue area on the Broselow. Be specific on how much volume of the medication you would give.
    Page 111 gives us an estimated 20kg weight and Page 200 tells us 0.1mg/kg initial dose so that’s 2mg initial dose and Adenocard comes in 6mg preloads. Now.....I suppose you could just push one-third of that preload and then save the other two-thirds for a repeat dose if needed.
  155. List the indications for the use of magnesium sulfate according to PALS.
    Page 221 The usual---if you know they are low on magnesium by some miracle and the“zebra” ECG (torsades de pointes) AND maybe for asthma that is not responding to anything else----anyone know why that would work????? Think of the three causes of bronchiolar obstruction (asthma) and so......will Mag help with mucous or inflammation or will it relax the smooth muscle in the bronchiole that is spasmed shut!
  156. ***************************************
  157. ***************************************
  158. When you are doing CPR by yourself, what is always the ratio of compressions to breaths?
    30:2 If I had said “rate” instead of “ratio”, what would you have said????
  159. When you are doing CPR on an adult, regardless of how many of you are working it, what is always the ratio of compressions to breaths?
    30:2
  160. When you have an advanced airway in place, what is always the rate of ventilations?
    Page 149 “8-10 breaths per minute” “one breath every 6-8 seconds”
  161. What counts for an “advanced airway” for number 160?
    ET tube,Combitube, King LT, LMA (all flavors)
  162. What are rescue breaths and what is the rate for them in the various age groups?
    Rescue breaths are given when the patient is in respiratory arrest but not (yet) in full cardiac arrest. The rate differs for peds (a breath every 3-5 seconds)compared to adults (every 6-8 seconds). That’s because these patients are in imminent danger of cardiac arrest and it is believed that peds patients have hypoxic arrests most commonly and so....even though there is real danger of reduced afterload with frequent or deep positive pressure breaths, it seems prudent to maximize the likelihood of oxygenation with ventilation.
  163. What does PALS say about Lidocaine versus Amiodarone for pediatric cardiac care?
    Page 153 Basically, no evidence to prove much but it seems reasonably likely that Amio is a better bet. Stay tuned.
  164. What does PALS say about when to use pediatric pacing / defib electrodes and when to use adult?
    Page 157 Read that closely---its talking about paddles (which some of you have never seen!) but it also refers to pads and it seems to suggest that adult pads should be used on anyone over 10kg. They note that those patients areusually one year olds or older. But....they say to check with the manufacturer. So, you better know this one ahead of time because you don’t have time to sort it out on the scene and that Zoll owner’s manual is a big one!
  165. What does ZOLL say about that question in number 164?
    less than 8 yearsof age and weighs less than 55 lbs (25 kg) so, on page 111, the Broselow color chart for Orange (Large Child) ranges from 24-29kg
  166. ***************************************
  167. If you have to use the ET tube route for drug administration, how is the dose modified for various drugs?
    Page 151 Recommended dose for Epi is 10 times the amount by IV/IO, and other drugs 2-3 times more.
  168. What is the dose of Amiodarone for a patient measured in the Yellow area on the Broselow for cardiac arrest?
    Page 111 says 13kg is the mid-range on Yellow and Page 204 says 5mg/kg for Amio first dose and so.....that’s 65mg. Assume your Amio comes in 50mg/ ml vials.How much in volume (in ml’s) do you need to draw up???? About 1.3 ml? If you can’t do that in your head----you’d better get a good reference chart ready or figure it out ASAP. Somebody’s kid may need you to know it.
  169. What does PALS suggest for resuscitation of the drowning patient?
    Page 164.Consider c-spine when you are doing airway; consider hypothermia (treat like a trauma code and RUN to where somebody can do some “House” stuff) and then also realize that they will vomit sooner rather than later.
  170. What does PALS suggest about needle decompression in traumatic arrest for pediatric patients?
    Page 163“Consider empiric” bilateral needles which means just do it.
  171. What does PALS suggest for ET intubation for patients with anaphylaxis?
    Page 164---at least get ready with a smaller size tube than you anticipate before you go looking around since the swelling will likely force you down a size or so on tubes. But....you should have that tube out anyway.
  172. Describe PALS recommendations for family presence during resuscitation.
    Page 166 Let them watch and watch what you say.
  173. Would you consider termination of a pediatric cardiac arrest in the field? Why or why not?
    Nope. No way. Not going to happen. I didn't say “not start”---I said terminate. Too many bad things will happen. Take them to the Doctor. Remember, no such thing as a slow code---its no code or full code.
  174. What is ROSC?
    Return Of Spontaneous Circulation
  175. PALS suggests that pediatric patients who have achieved ROSC may have elevated EtCO2 readings and they give instructions on how to manage that situation. What are their recommendations and explain why they suggest that practice?
    Page 173 and 174 PALS says you need to chill out on this. Work SLOWLY to normalize EtCO2.Don’t assume a high reading is all that abnormal. Consider metabolism and perfusion as well as ventilation. Both metabolism and perfusion have been very poor prior to ROSC. Further, if you get all excited about ventilating the patient just to get that EtCO2 down to where YOU can tolerate it, you will likely over-ventilate your patient and increase their intrathoracic pressure and thereby decrease their preload and thereby decrease their perfusion and you might end up back where you started on this. THEY can tolerate the high EtCO2 for quite a while.
  176. When your intubated patient suddenly deteriorates, you should check for four things and the Mnemonicfor that is DOPE. What are the things you should immediately check?
    Page 176 (If you have them on a ventilator, TAKE THEM OFF as soon as they get bad until you figure out if the Vent was the problem)

    Displacement of Tube; Obstruction of the Tube; Pneumothorax; Equipment failure
  177. ***************************************
  178. ***************************************
  179. ***************************************
  180. Shockable
    • 0 min CPR Epi 1mg
    • 2 min CPR Amio 300mg
    • 4 min CPR Epi 1mg
    • 6 min CPR Amio 150mg
    • 8 min CPR Epi 1mg
  181. Not Shockable
    • 0 min CPR Epi 1mg
    • 2 min CPR  
    • 4 min CPR Epi 1mg
    • 6 min CPR  
    • 8 min CPR Epi 1mg
  182. H
    • Hyperkalemia/hypokalemia
    • Hypovolemia
    • Hypoxia
    • Hydrogen Ion (Acidosis)
    • Hypothermia
    • Hypoglycemia
  183. T
    • Toxins
    • Tamponade
    • Tension pneumothorax
    • Thrombosis
    • Trauma

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