PICU Bri Flashcards
Airway
patent (stridor, obstruction)
protected (awake, breathing)
Breathing
RR, sats, WOB, A/E
Circulation
HR/BP/pulses CRT
Disability:
GCS, pupils, materializing signs, glucose
Exposure
undress the patient, temp
Resus station
PPE call for help, bring to resus room monitors O2 set of vitals ABCDE RN on PIV - if can't get in 5 minutes and child in shock, IO
8 year old in MVC, TBI. moaning, will not open his eyes, and flexes to pain
moaning - 2 verbal
won’t open eyes - 1
flexes to pain - 3
total = 6
decerebrate - NO BRAIN, extension is bad (weird)
Cushing’s Triad
hypertension
bradycardia
abnormal breathing
Monro-Kellie Doctrine
skull is fixed
if any of the compartments increases, the others can only decrease so much
if have a mass, increase in the space taken by the parenchyma, critical volume is where the ICP goes up
Evidence based TBI management - doesn’t mater what got you there
Guidelines for severe TBI
Normal - O2 sats, pCO2 (35-40 mmhg), BP >5th percentile, temperature (no hyperthermia, DO not COOL (trial shows that it is bad))
Avoid: hypoglycemia, seizures
Treat elevated ICP +/- impending herniation with hyperosmolar therapy
over 50% have an episode of hypotension/hypoglycemia
TBI management in PICU
ICP probe if GCS 20 for 5 minutes then (NORMAL ICP IS s triad, blown pupil)
ICP probe only in trauma
7 year old with CP involved in MVA and presents with GCS of 4, ICU x 1 week with no improvement despite aggressive management. Parents approach you regarding the withdrawal of treatment because of his underlying disability Which of the following is try:
not brain dead - because he has a GCS of 4
To be brain dead you need to have a GCS 3
Pediatric Brain death CLINICAL DIAGNOSIS
1) established aetiology capable of causing neurological injury in absence of reversible conditions
2) no confounders including:
- unresuscitated shock
- hypothermia (temp t do the above tests: MRA or CTA (nothing about EEG anymore)
Canadian guidelines are different from american
Who can perform neurological determination of death?
any licensed physician with the requisite knowledge and skill
Differences in kids
> 1 year old, same as adults
>30 day and < 30 days: minimum time from birth 48 hours, 2 exams separated by at least 24 hours
Procedural sedation for ortho, what are the 4 pieces of equipment you would want next to you ? 3 effects of ketamine?
Equipment: O2, suction, oral airway, BMV, airway cart, IV fluid
Ketamine: causes release of endogenous catecholamines: tachycardia, HTN, amnesia, analgesia, bronchorrhea, bronchodilation
ketamine good for hemodynamic unstable, no longer a problem for increased ICP
meds for intubation for kid with increased ICP
ketamine - maintains HR and BP
if hypertensive then use fentanyl with midaz
don’t use proposal, drops your BP
fentanyl most HD stable for the opioids
neuromuscular blockage
increases the chance of success in 1st attempt
always use it unless there is a reason not to (i.e. mediastinal mass)
SIDe effects of depolarizing NM blockade (ie succ)
hyper K - worse in renal failure, rhabdo
malignant hyperthermia
Neuromuscular disease - can cause worsening of symptoms in MD
Non depoolarizing - ie roc
blocks the receptor
less side effects but lasts up to one hour
3 month old with fever, HR 180, BP 50/30, unwell with poor pulses and delayed CRTI. How is this infants cardiac output compared to usual? What about SVR? What would be your IV doers
- CO decreased
- SVR increased
- 20 cc/kg NS push
best indicator of early hypovolemic shock in 3 year old
tachycardia is the first sign
oxygen delivery
cardiac output x arterial O2 content
Why do we need O2
anaerobic metabolism is not good
glycolysis
decreased ATP = failure of energy dependent processes
increased lactate = acidosis - cells don’t like->death
Shock types
1) distributie
2) cardiogenic
3) hypovolemic
4) neurogenic
Clinical markers of perfusion
- CRT
- pulses
- HR and BP
- u/o
Lab markers
lactate
mixed venous
acid-base
Septic Shock
warm shock
cold shock: cold, poor pulses, increased after load, lower cardiac output
has to do with how many vasodilator cytokines vs vasoconstriction
warm shock - toxic shock is most common - S. aureus/GAS, warm, cash cap refill, wide PP
loss of auto regulation
usually vasoconstrict/vasodilate based on demand
Shock:
recognize shock, O2, PIV 20 cc/kg/ NS x 3, 2nd PIV, start ABx, correct low BG and Ca cold shock = dopamine warm shock = norepi if catecholamine resistant = steroids
causes of cardiogenic shock
cardiomyopathy viral myocarditis post bypass coronary artery anomalies arrythmias etc signs and symptoms: cold shock+ poor perfusion + heart failure (Hepatomegaly, pulmonary/peripheral edema)
where spinal cord injury for neurogenic shock
T1 to L2
inappropriately nomal HR but hypotensive , treatment is vasopressors
Boy collapses at school. paramedic arrive and intubate, get IV access and use AED to defibrillate for wide complex tachycardia then continue CPR. On arrival you would:
1) defibrillate 2J/kg
2) defrillate 4J/kg
3) epi 1:10000 IV
4) continue CPR x 5 minutes
if using a manual defibrillator, then restart fresh at 2J/kg
if PEA or systole
don’t give a damn about your debrillator, you only have CPR and epi
management shock as soon as you can
CPR x 2 minutes, shock again THEN EPI (with the second shock)
once first epi then every 3-5 minutes after that
15:2 no advanced airway, no need to coodinate once intubated
epi dose: 0.01 mg/kg 1:10000 IV (going right to veins, vs muscle need more dose)
**we don’t know if epi helps in arrest
if you haven’t intubated need to co-ordinate (but not 1st priority if getting ventilation)
unconscious person
check pulse first
CAB
3 things you can tell the team to ensure good quality CPR
- push fast
- push deep
- minimize interruptions
- allow full chest recoil
- switch people
- no leaning (use a stool)
unstable SVT
synchronized cardioversion or adenosine (if have IV present)
0.5-1J/kg is the cardioversion dose
give them fentanyl first
SVT
stable - vagal, adenosine
unstable - cardiovert or adenosine
Wide complex tachy
unstable - pulseless arrest
stable - talk to cardiology
bradycardia HR<60 and compromised
usual ABCs
most commonly bradycardia is from hypoxia
if persists then start CPR, then give epi and atropine
if continues then do TC pacing
What is the does for anaphylaxis
1:1000 IM anterolateral thigh
don’t do it IV
if respiratory compromise
wheezing - ventolin
other - intubate
if need more than 3 IM epi then give infusion
H1/H2 antagonists, genadryl, ranitidine, steroids (prednisone)
tidal volume
regular breathing
functional residual capacity
lung still open, what is left
maximum inspiration
inspiratory reserve volume and expiratory reserve volume , total lung capacity without residual volume is your vital capacity
Where is breathing controlled
respiratory centres in brain
signals fo diaphram and heart
C345 diaphragm alive
ventilation CO2 clearance depends on what
minute ventilation
tidal volume x rr
5 year old 3 days of fluA with high ver, stridor and severe resp distress. First step in management? 2 likely organisms?
ABCs then secure airway
staph aureus, GAS
Symptoms of upper airway obstruction depends on where the obstruction is
negative intrathoracic pressure - collapses on inspiration , get symptoms of expiratory stridor
extrathoracic obstruction - should have collapse on inspiration
Upper airway obstruction
epiglottitis, bacterial tracheitis, croup, RPA, foreign body, airway anomaly
if in distress secure the airway
don’t give them sedatives or paralytics
consults anaesthesia or ENT
causes of hypercapnea
hypoventlation
obstructive lung disease (asthma, OSA)
neuromuscular disease
Respiratory acidosis
resp failure
bad vent settings
1:10 rule for acute resp acidosis, as you compensate closer to 3-4
metabolic alkalosis
vomiting
lasix/Bartters
respiratory alkalosis
secondary to something else
incorrect vent
Indications for intubation
- CNS: cannot protect airway (GCS <8, no airway reflexes), loss of control of breathing
- Resp: upper airway obstruction, hypoxemia, hypercapnea, severe WOB despite max medical tx
- CVS: hemodynamic instability, to decreased metabolic demand
4) logistics: transport, procedures
- small pneumo need a chest tube
pneumonic for intubation 7Ps
1) prepare
2) pre O2
3) premedicate -include atropine if <1 year old
4) paralysis
5) pressure on cricoid carilage (only if RSI)
6) placement of ETT (4+ age/4, depth = ETT size x 3)
7) post intubation care
equipment
1) mask
2) ETT
3) airway gadgets (oropharyngeal, LMA)
4) laryngoscope blade
5) stylet
6) suction catheter
7) syringe for cuff inflation
confirm ETT placement
1) ausculation
2) direct laryngoscopy
3) detect CO2 - BEST
4) CXR - BEST
5) condensation in the ETT
RSI - haven’t been fasted to higher risk of aspiration
preO2 before the BMV, want to limit the Positive pressure
minimize BMV as may distend stomach
Deep sedation and paralysis so increase chances of success
cricoid pressure to compress esophagus during laryngoscopy (controversial) BURP maneuver
Questions about changing the vent settings
Timing of the breath: synchronized, assist control, pressure support pressure or volume rate PEEP I/E time
low sats vented patient
DOPE, increased FiO2 or PEEP (increases SA)
high CO2 vented patient
increase minute vent with increased tidal volume or RR
1 month old with RSV, 22/6 FiO2 40% RR35 . first gas 7.20/75/23/70. next step
increase rate
increase PIP
12 year old old influenza pneumonia, sats 60% rule out new issues
increase the PEEP
3 year old female in ED for 4 hours with asthma, got ventolin q30 minutes, moderate distress on FiO2 40%
MgSO4 - reduces ICU admission
may need to give fluid with it
Status asthmaticus
failure to respond to initial bronchodilator
RFs for ICU in asthma
prior ICU, h/o increased bronchodilator use with no improvement, asthma exacerbation despite recent steroids, frequent ED visits, sats <92% despite O2
may need some adjuncts
no evidence for IV ventolin (do inhaled continuous first always)
ARDS
1) within 1 week of known clinical insult
2) bilateral lung opacities
3) not explained by CHF or fluid overload
P/F ratios with PEEP of at least 5
P/F ratios: mild 200-300, moderate 100-200, severe <100
Causes: sepsis, pneumonia, trauma, aspiration, TRALI
Tx: lung protective ventilation (high PEEP,low tidal volumes), early steroids, probing, ?NO, ?surfactant
Status epilepticus
acute symptomatic
prolonged febrile seizure
remote
idiopathic
management : ABCDs include BG
benzo q5 min x 2 )midaz and ativan best in CPS statement
fosphenytoin 20 mg/kg > 1 year old or phenobarb 20 mg/kg
then the other
if still seizing 10 minutes post then intubate with RSI and start midaz infusion
chance of 1st benzo stopping seizure
80% for first
20% for second
Differential for coma
vindicate
Burns
remove clothes and other exposures
ABCDEs 100% FIO2 and rapid trauma assessment (10% have other injuries)
wash burns with tepid water, flush chemical burns, cool minor burns with cool saline)
estimate % BSA involvement with partial /full thickness (don’t include 1st degree)
if >10% then at risk for SIRS response and fluid resuscitate with Parkland
What is Parkland
4cc/kg/percent BSA + maintenance crystalloid (1/2 in first 8 hour, 1/2 in 16 hours)
best indicator for volume resus is u/o
what concerns you about airway involvement in a burn patient?
soot in nares stridor carbonaceous sputum singed hair closed space, any resp distress intubate sooner rather than later if any respiratory involvement
Criter for refer to burn center
- partial or full thickness burns
>10% in pt 20% in other age groups
***get the rest from rbi slides
Trauma
C spine collar very important
exposure is a big one
log roll them and check their back
if bleeding then need to look for source as part of primary survey
long bone fractures splint them put them in a binder anything in abdomen that is suspicious tachycardia/hypotension ->look for sources of bleeding on primary survey secondary survey - full head to toe
chest tube
ant axillary 5th intercostal
tamponade
distended neck veins
good air entry
don’t get distracted by significant injuries
follow ABCDEs
best predictor of good survival after drowning
cardiopulmonary arrest (time for return of spontaneous circulation is the most important) quality CPR is the most importent if they are arrested; CPR at the scene is very important bad GCS when in hospital is less important electromechanical dissociation - PEA (a old word)
