General PICU Flashcards
Coagulopathy in Critical Illness - determining liver failure vs consumption
Check factors V, VII, VIII
Liver failure - low V/VII with normal VIII
Consumption - all low
Markers of Haemolysis
Decreased haptoglobulin (consumed by free Hb clearance)
Increased LDH
Increased reticulocytes
Blood film - fragmented RBC’s, reticulocytes
Coombs +/-
Cerebral complications of DKA - imaging
Cerebral oedema - plain CT head
Sinus venous thrombosis - need contrast CT
Compassionate Extubation
Wean ventilation prior to extubation
- allows CO2 to rise - avoids sudden stimulus to breathe
- creates somnolent state
Premedicate prior to extubation
- negates sudden feeling of lack of support/panic
- opiate and benzodiazepine
Titrate to comfort post extubation
Initiating CVVH in acute on chronic renal failure/high urea
High urea = high risk of disequilibrium syndrome
Use CVVHDF - dialysate decreases risk Pre commencement - give mannitol Decrease clearance - aim 1L/m2 BSA/hr - standard clearance 2L/m2/hr - enhanced clearance > 3L/m2/hr Dialysate rate = preblood flow rate Start with low blood flow rate
Conversion cmH2O to mmHg
1.3 cmH2O = 1 mmHg
10 cmH2O = 7 mm Hg
Intubating Long Segment Tracheal Stenosis
Avoid intubation if at all possible - NIV, heliox, cautious sedation
ETT position best just below cords - don’t push beyond stenosis as makes lumen even narrower
Avoid muscle relaxation - active exhalation is helpful
Ventilate with high peak pressures and low RR, ensure full expiration
Role of HFOV in CDH
CO2 clearance at lower mean airway pressures
If need HFOV for oxygenation then probably unsurvivable lesion
cf Conventional use HFOV for recruitment of lung and oxygenation in severe ARDS
Mechanisms of Hyperinflation when Ventilating Asthmatics
Breathing near TLC
- mechanical ventilation increases volume further
Insufficient time to exhale
- increased end exp lung volume and auto peep
Dynamic hyperinflation adaptive initially
- increased airway diameter and elastic recoil
- over time becomes pathological - alveolar distension
management of acute laryngospasm
Deal with laryngospasm:
- PEEP - hold sustained PEEP with bag mask
- Jaw thrust - open airway
- Muscle relax if above fails and intubate
Remove perpetuating stimuli:
- sedate
- suction oropharynx
- check iCa
- decompress stomach
TPA administration
Give 10ml/kg FFP prior
- source of fibrinogen
- ensure normal INR
Normalise coagulation - INR < 1.6 - fibrinogen > 2 - plts > 100 Grp and Hold current
Reduce IV heparin infusion by half 30mins prior, continue during TPA infusion
TPA 0.5mg/kg/hr x 6hrs
Increase heparin to therapeutic at end of infusion
Neuro obs Q1H, coagulation blds Q2H
Jet Ventilation
Suction catheter - cut off tip
- insert one end into O2 tubing 15L/min flow (10 in babies)
- insert end into cricoid cannula - use suction port to provide intermittent O2 flow
Size 3 ETT cap into cannula
Size 7 ETT cap into 3ml syringe
VV-ECMO initiation
Avoid rapid normalisation pCO2
- brain ischaemia
- slow increase flows
Slow weaning of ventilation
- high pressures pre ecmo
- rapid decrease can result in air bubble formation
- match slow vent wean to slow rise in flows
- wean to rest settings 10/10/10
Slow initiation also reduces haemodynamic effects on other organs
VV-ECMO disadvantages
No systemic BP support
Recirculation
- increased SvO2, decreased SaO2
- < 10% diff SaO2:SvO2 makes recirculation likely
Lower SaO2 and PaO2 than VA-ECMO
- sats 75-85%, SvO2 > 65%
Complex cannulation - dual venous cannula or double lumen cannula
VV-ECMO advantages
Preserves arteries
Maintains pulsatility - better solid organ function
Pulmonary oxygenation/circulation maintained
Efficient CO2 removal
VA-ECMO advantages
Provides CO and oxygenation
Efficient CO2 removal
SaO2 > 90, SvOw > 65%
VA-ECMO disadvantages
Arterial cannulation
- requires reconstruction or ligation
- late stroke risk
Cardiac standstill - emergent LA vent
May not generate sufficient flows in sepsis - cool, muscle relax, run sats at 80
Alveolar gas equation
PAO2 = (Patmospheric - Pwater) x FIO2 - PaCO2/resp quotient
PAO2 = (760 - 47) x FIO2 - PaCO2/0.8
Oxygenation Index
OI = (FIO2 x MAP / PaO2) x 100
Rising OI indicates worsening lung disease.
Useful to track in cases of severe lung disease.
Central Cyanosis - causes
Alveolar Hypoventilation
VQ mismatch
R to L shunt
Diffusion restriction
Abnormal Hb with decreased O2 affinity
- metHb
Oxygen dissociation curve
Left Shift:
- alkalosis
- low pCO2
- cold temp
- decreased 2,3DPG
- fetal Hb
Right Shift: decreased oxygen affinity - increased oxygen delivery to tissues
- fever
- acidosis
- increased 2,3DPG
Lung Recruitment Neonates
Difficult to recruit lungs
- compliant chest walls
- relative surfactant deficiency
- underdeveloped pores of cohn, can’t take advantage of time constants/differential alveolar filling
Increase minute volume to improve oxygenation
- small fast breaths
PEEP/staircase recruitment limited value until develops pores of cohn.
TBI pathophysiology
Loss of autoregulatory mechanisms
- BP autoregulation lost first
- Oxygen responsiveness second
- CO2 responsiveness last
CO2 provides most predictable change in perfusion
Extracranial causes raised ICP
Ventilation issues
- Increased PEEP, high CO2, PaO2 < 60
Hyperthermia
Obstructed cerebral venous return
DKA
Hepatic Failure
Metabolic crisis - high ammonia
Toxins/medications - lead, doxycyclin, tetracycline, rofecoxhib
Cerebral perfusion pressure targets
CPP targets:
< 6yrs 45-55mmHg
> 6yrs 50-60mmHg
Vasospasm post SAH
Occurs several days post SAH, peak severity at 1 wk
Presentation:
- unilateral change neuro exam or increased somnelance
Represents ischaemia, expect normal ICP. Raised ICP suggests irreversible infarction
Prevention:
- avoid hypovolaemia/ hyponataemia
- Hb > 9g/dL
- nimodipine - prevents increase in intracellular Ca, neuroprotective
Management of Cerebral Vasospasm
Ensure adequate cerebral perfusion pressure
Triple H therapy - hyperhydrate, hypertension, haemodilution
- titrate BP to resolution of symptoms - target increase systolic BP 20mmHg
Vasodilation - milrinone
Nimodipine - neuroprotective effect seondary to reduced Ca metabolism in vulnerable brain
Interventional - balloon angioplasty
CVP wave
A - atrial contraction
C- TV closure, TV bulges as ventricle starts to contract
V - filling of RA during diastolic phase
x decent - atrial relaxation and change in ventricular geometry
y decent - opening of TV and atrial emptying
Adequate Cardiac Output on ECMO
Normal cardiac output
- 2.2 - 2.5L/min/m2
2 ventricle heart - usually achieved with 100ml/kg/min
Single ventricle heart - requires higher flows to maintain same cardiac index
- 150-180ml/kg/min
- higher flows also mitigate risk of shunt thrombosis (high haematocrit in cyanosed pt, high risk thrombosis)
HFOV physiology
Higher MAP’s tolerated when lungs poorly compliant - not transmitted to cardiovascular structures
Lower Hz has greater lung excursion, increased risk barotrauma
- best to set Hz as high as tolerated, and continue to increase as lungs improve
Congenital Diaphragmatic Hernia - prognosis
Prenatal LHR (lung head ratio) - predicts adequate lung for gas exchange < 1 = poor 1-1.4 = associated with 38% survival > 1.4 = improved survival
Preductal sats > 80-85R on FIO2 < 0.6 indicates adequate lung tissue
Predictors poor prognosis;
- liver in chest
- inability to clear CO2
- post natal diagnosis
- FETO study - 1/10 survival
Congenital Diaphragmatic Hernia - management
Aim preductal sats > 85%
Minimal ventilation
- HFOV
- subphysiological TV
- PIP < 22
PGE if RV strain/PHT
Low dose epinephrine infusion
iNO often not helpful - vascular bed not reactive. Document improved oxyenation and RV function.
Airway Cast Management
Dornase Alpha
- breaks down cellular material
Inhaled heparin/urokinase/TPA
- breaks down fibrin
N-acetylcystine
- breaks down mucin
Trial agents to find most effective one
Can do ex-vivo testing on retrieved casts
High Anion Gap Metabolic Acidosis
Anion gap = Na - (Cl + HCO3)
normal = 11
C carbon monoxide, cyanide A alcohol, alcoholic ketoaciosis T toluene M metformin, mehtanol U uremia D DKA P phenformin, propylene glycol I iron, isoniazid L lactic acidosis E ethylene glycol S salicylates
Toxidromes - cholinergic
Cholinergic:
- pour fluid from all orifaces
- diarrhoea, urination, salivation, vomiting
- small pupils, bronchoconstriction, bradycardia
organophosphates, mushrooms, carbamates
Toxidromes - anticholinergic
Anticholinergic:
- dilated pupils, hyperthermia, tachicardia, hypertension, flushing, seizures, thirst, dry skin
Atropine, TCA’s, antihistamines
Toxidromes - sympathomimetic
Sympathomimetic:
- hypertension, tachicardia, dilated pupils, hyperthermia, CNS excitation
amphetamine, cocaine, ephidrine, caffeine
Toxidromes - narcotics
Narcotics
- CNS depression, small pupils, apnoea/low RR, bradycardia, hypotension, pulmonary oedema
Morphine, methadone, heroin
Serotonin Syndrome
Excessive stimulation of serotonin receptors
CNS - anxiety, agitation, confusion
Autonomic - diarrhoea, flushing, hypertension, hyperthermia, sweating, tachicardia, dilated pupils
Neuromuscular - clonus, hyperreflexia, increased tone, myoclonus, tremour, rigidity
SSRI, MAOI’s, amphetamines, lithium
Desaturation during Lung Recruitment
Decreased venous return secondary to high ITP
- worsening SmvO2, desaturation
Increase blood flow through shunt
- overinflation of baby lung, increased PVR with blood diverted to non-recruited non-ventilated lung
Pneumothorax
Acid Base Interpretation
Anion Gap = Na - (Cl + HCO3)
normal = 11
Normal AG - renal losses or GI losses
Urinary AG - (Na + K) - Cl
- positive uAG = renal RTA
- negative uAG = GI losses, NaHCO3
- NH4 excreted with Cl - measured Cl will rise if kidney working appropriately
Raised AG - MUDPILES
Osmolar Gap = 2x Na + BUN + glucose
Glucose Infusion Rate calculation
GIR = dextrose % x rate (ml/hr) / 6 x weight (kg)
= mg/kg/min
