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General PICU Flashcards

1
Q

Coagulopathy in Critical Illness - determining liver failure vs consumption

A

Check factors V, VII, VIII

Liver failure - low V/VII with normal VIII
Consumption - all low

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2
Q

Markers of Haemolysis

A

Decreased haptoglobulin (consumed by free Hb clearance)
Increased LDH
Increased reticulocytes
Blood film - fragmented RBC’s, reticulocytes
Coombs +/-

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3
Q

Cerebral complications of DKA - imaging

A

Cerebral oedema - plain CT head

Sinus venous thrombosis - need contrast CT

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4
Q

Compassionate Extubation

A

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

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5
Q

Initiating CVVH in acute on chronic renal failure/high urea

A

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
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6
Q

Conversion cmH2O to mmHg

A

1.3 cmH2O = 1 mmHg

10 cmH2O = 7 mm Hg

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7
Q

Intubating Long Segment Tracheal Stenosis

A

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

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8
Q

Role of HFOV in CDH

A

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

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9
Q

Mechanisms of Hyperinflation when Ventilating Asthmatics

A

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
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10
Q

management of acute laryngospasm

A

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
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11
Q

TPA administration

A

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

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12
Q

Jet Ventilation

A

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

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13
Q

VV-ECMO initiation

A

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

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14
Q

VV-ECMO disadvantages

A

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

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15
Q

VV-ECMO advantages

A

Preserves arteries

Maintains pulsatility - better solid organ function

Pulmonary oxygenation/circulation maintained

Efficient CO2 removal

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16
Q

VA-ECMO advantages

A

Provides CO and oxygenation

Efficient CO2 removal

SaO2 > 90, SvOw > 65%

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17
Q

VA-ECMO disadvantages

A

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

18
Q

Alveolar gas equation

A

PAO2 = (Patmospheric - Pwater) x FIO2 - PaCO2/resp quotient

PAO2 = (760 - 47) x FIO2 - PaCO2/0.8

19
Q

Oxygenation Index

A

OI = (FIO2 x MAP / PaO2) x 100

Rising OI indicates worsening lung disease.

Useful to track in cases of severe lung disease.

20
Q

Central Cyanosis - causes

A

Alveolar Hypoventilation

VQ mismatch

R to L shunt

Diffusion restriction

Abnormal Hb with decreased O2 affinity
- metHb

21
Q

Oxygen dissociation curve

A

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
22
Q

Lung Recruitment Neonates

A

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.

23
Q

TBI pathophysiology

A

Loss of autoregulatory mechanisms

  1. BP autoregulation lost first
  2. Oxygen responsiveness second
  3. CO2 responsiveness last

CO2 provides most predictable change in perfusion

24
Q

Extracranial causes raised ICP

A

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

25
Cerebral perfusion pressure targets
CPP targets: < 6yrs 45-55mmHg > 6yrs 50-60mmHg
26
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
27
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
28
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
29
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)
30
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
31
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
32
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.
33
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
34
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 ```
35
Toxidromes - cholinergic
Cholinergic: - pour fluid from all orifaces - diarrhoea, urination, salivation, vomiting - small pupils, bronchoconstriction, bradycardia organophosphates, mushrooms, carbamates
36
Toxidromes - anticholinergic
Anticholinergic: - dilated pupils, hyperthermia, tachicardia, hypertension, flushing, seizures, thirst, dry skin Atropine, TCA's, antihistamines
37
Toxidromes - sympathomimetic
Sympathomimetic: - hypertension, tachicardia, dilated pupils, hyperthermia, CNS excitation amphetamine, cocaine, ephidrine, caffeine
38
Toxidromes - narcotics
Narcotics - CNS depression, small pupils, apnoea/low RR, bradycardia, hypotension, pulmonary oedema Morphine, methadone, heroin
39
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
40
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
41
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
42
Glucose Infusion Rate calculation
GIR = dextrose % x rate (ml/hr) / 6 x weight (kg) = mg/kg/min

PICU (2 decks)

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