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Icu Flashcards

1
Q

Indications for artificial ventilation in adult at rest

A

VC 10ml/kg
RR >35
AA gradient over 300mmhg

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2
Q

Types of ventilator associated lung injury

A 
Volutrauma 
Barotrauma 
Atelectatrauma 
Biotrauma (inflam) 
Sheer stress
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3
Q

Ventailator associated lung injury can appear like ARDS

A

True both can present bilateral infiltrates on CXR

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4
Q

How to set PEEP in VALI

A

Set PEEP at the lower inflection point (I.e the point that alveolar recruitment happens in inflation)

Note peep improves oxygenation but not mortality

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5
Q

Indications for artificial ventilation in gbs

A

VC <15ml/kg

Reducing trend

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6
Q

Clinical features of tricyclics antidepressant overdose

A 
Tachycardia 
Hypotension 
Flushed 
Raised temperature 
Dry mouth 
Dry skin 
Dilated pupils 
Seizures 
Agitation 
Reduced conscious level 
Urinary retention
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7
Q

ECG features of tricyclics antidepressants

A 
Sinus tachycardia
Short pr interval 
Wide qrs 
Long QT 
AV block
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8
Q

What is proposed mechanism for intralipid I’m drug toxicity ieLAST and TCA

A

Intralipid acts as lipid sink. Binds to free lipid soluble drug and reduces the free plasma concentration. Drug then redistributes from the tissues and is excreted as normal

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9
Q

Specific changes to ALS protocol in poisoning secondary to TCA or LAST

A

Administer hco3
Prolonged resuscitation
Use intralipid

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10
Q

Initial approach to poisoning

A 
ABCDE approach 
100% o2 
PPE 
Secure airway if GCS <8 
IV access and bloods for Fox inc paracetamol salicylate alcohol 
Toxbase 
Identify agent or toxidrome 
Specific antidote if available
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11
Q

Scoring tool by trauma audit and research network to measure overall severity of injury

A

Injury severity score
Out of 75
If any area gets a score of 6 (unsurvivable) they are automatically given score of 75
Injury severity score more than 15 is major trauma

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12
Q

3 core principles of damage control resuscitation

A 
Permissive hypotension (first clot is best) 
Haemostatic resuscitation with early use of blood 
Damage control surgery
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13
Q

Aims of damage control surgery

A 
Control haemorrhage 
Prevent triad of death 
Restore physiology 
Prevent contamination 
Return to theatre at later date to restore anatomy
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14
Q

What is triad of death in trauma

A

Coagulopathy
Hypothermia
Metabolic acidosis

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15
Q

Mechanism of action of TXA

A

Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin

Therefore prevents plasmin induced fibrinolysis

Stabilises the clot

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16
Q

Dose of TXA

A

1 gram immediately (less than 3 hours)

1 gram over 6-8 hours

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17
Q

What evidence supports use of TXA

A

CRASH 2
Benefit if transexamic used less than one hour
Poor outcome more than 3 hours
Mortality reduced

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18
Q

Indications for tracheostomy (grouped)

A

Indications for trache grouped into

  • requirement for prolonged mechanical ventilation
  • provision of pulmonary toilet
  • protection of airway
  • management of upper airway obstruction
  • as part of a surgical procedure
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19
Q

Considerations choosing tracheostomy tube

A

Type and size (appropriate internal diameter remembering That inner tube may significantly reduce the diameter )

Subglottic suction required

Longer or extended tube size (obesity or anatomy may result in needing adjustable flange)

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20
Q

Checking position of trache on insertion

A

Capnography

Endoscope

Neutral head position

Leak test to 20-30cm h2o

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21
Q

NAP 4 most common reason for trache critical incident

A

Displaced trache

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22
Q

Project that audits and teaches re tracheostomy

A

National tracheostomy safety project

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23
Q

National tracheostomy safety project algorithm patent upper airway

A
  1. Call for help, look listen feel mouth and tracheostomy, mapleson c may help if available and capnography
  2. If breathing - high flow o2 to mouth and stoma
    (If not breathing cpr)
3. Assess tracheostomy patency 
Remove speaking valve 
Remove inner tube 
Try pass suction catheter 
If unable to pass deflate cuff 
Look listen and feel/map c/ capnography 
Is patient improving.
  1. If not improving remove trache tube
    Look listen feel/map c
  2. Is patient breathing
    No call resuscitation team, cpr if no pulse
  3. Primary emergency oxygenation
    Oral airway manoeuvres and cover stoma
    Or tracheostomy stoma ventilation

7, secondary Emergency oxygenation.
Oral intubation prepared for difficult intubation
Intubation of stoma

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24
Q

Complications of tracheostomy

A

Early
Haemorrhage
Pneumothorax
Failed

Short term 
Blockages 
Tube displacement 
Surgical emphysema 
Tracheal necrosis 
Tracheal arterial fistula

Long term
Tracheomalacua
Tracheal stenosis
Decannulation issues

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25
Q

Bedside signs in tracheostomy

A 
Size 
When was inserted 
(Tracheostomy vs laryngectomy)
Why Inserted 
How ie surgical vs percuatneous 
Any sutures in place 
Any issues with airway and how was managed
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26
Q

Bedside equipment tracheostomy

A

Spare tube and inner cannula
Suction
Stitch cutters
Emergency bell

Fibreoptic scope nearby

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27
Q

Bleeding trache

A

Causes abberant vessels…. rarely Inominate artery fistula

Suction
External compression surgical clips or cautery
Gauze soaked in adrenaline or tranexamic acid around bleeding site
Consider hyperinflating cuff to tamponade

Surgical exploration and repair

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28
Q

Types of RRT

A

Peritoneal dialysis
IHD
CVVHF CVVHD CVVHDF
SLED (sustained low efficiency dialysis)SCUF (slow continous ultrafiltration)

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29
Q

Aims of RRT

A

Solute and water removal
Correction electrolyte abnormalities
Normalisation a die base

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30
Q

Basics how RRT works

A

Diffusion (hd)or convection (hf)
Extracorpeal curcuit filled with blood
Roller lumps control speeds of flow towards memebrane
Por size of membrane effects what can pass through
Middle molecules are preferentially cleared by convective measures
Small molecules better cleared by diffusion

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31
Q

Describe haemofiltration in terms of CVVHF

A

Haemofiltration is a comvective process where a hydrostatic pressure gradient is used to filter plasma, water and solute across a membrane

Solute drag where appropriately sized molecules are pulled along with mass movement of solute

Convective transport is independent of solute concentration but determined by magnitude or transmembrane pressure

Ie higher flow rate equals increased UF

Measures that increase negative pressure across membrane including pump in effluent line can have marked effect - high volumes effluent discarded and circulating volume of patient replaced with balanced crystalloid buffer

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32
Q

Describe haemodilaysis as in CVVHD

A

Hamodilaysis solute clearance is achieved by diffusion across the membrane
Space outside the blood containing fibres within the filter is filled with dialysate which is pumped counter current to flow.
Diialysate is reconstituted to include a buffer and essential electrolytes
Diffusion occurs down a concentration gradient to equilibrium - countercurrent maintains a waste solute gradient

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33
Q

Types of RRT membrane

A

Cellulose

Synthetic

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34
Q

Types of filter fluid in RRT

A 
Lactate based (lactate accumulation in hepatic dysfunction) 
Hco3 based

Can be added before filter (reduces risk of filter clotting) or mixed with blood in venous drip chamber ( increases clearance solutes)

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35
Q

Positives of continuous RRT in icu

A

Enhanced haemodynamic stability
Superior management of fluid balance
Enhanced clearance of inflammatory mediators
Better preservation cerebral perfusion

No difference in survival benefit
Kdigo favours CRRT for haemodynamic instability

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36
Q

Classical indications for initiating RRT

A 
Refractory hyper Kalaemia over 6.5 
Refractory fluid overload 
Refractory metabolic acidosis 
Certain drug and alcohol intoxication’s 
Signs of uraemia ie pericarditis or encephalopathy 
Temperature control
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37
Q

Risks of RRT

A 
Cannula insertion 
Biocompatibility 
Fluid shifts 
Altered drug metabolism 
Nursing workload 
Cost
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38
Q

Discontinuation RRT

A

When kidney function improving
Ie UOP
Creatinine clearance

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39
Q

Dosing RRT

A

Continuous technieques dosing is sum of effluent in ml per kg per hour

Initial high rates used but now dosing 20-25ml/kg/hr

40
Q

Vascular access choices RRT kdigo

A

1) Right IJ
2) Femoral
3) Left IJ
4) Subclavian
In order.

41
Q

Anticoagulation in RRT

A

Systemic or regional anticoagulation

Systemic heparin most common cheap but risk of haemorrhage and heparin resistance and HIT

Systemic with heparnoids ie danaparoid especially if HIT

Regional anticoagulation with citrate but as chelates calcium (inhibiting platelet aggregation) require calcium infusions, and potential metabolic complications (alkalosis and acidosis hypocalc and hypomagnesia)

Regional prostacyclin

42
Q

What percentage those with aki and RRT never regain full renal function

A

40

43
Q

Classifications of renal failure

A

RIFLE (risk injury failure loss esrf)
AKIN (aki network)

Based in serum creatinine and urine output

44
Q

Causes of non specific aki

A 
Sepsis 
Critical Illness 
Circulatory shock 
Burns 
Trauma 
Cardiac surgery 
Nephrotixic drugs 
Radiocontrast agents
45
Q

Susceptibilties to aki

A 
Dehydration 
Age 
Female 
Black 
CKD 
DIABETES 
cancer 
Anaemia
46
Q

Traumatic and non traumatic causes Rhabdo

A

Traumatic causes
Crush injury
Burns esp electrocution
Compartment syndrome

Non traumatic 
Injection 
MH 
Serotonin syndrome 
Drug related 
Exertional 
Status 
Metabolic ie DKA
47
Q

Clinical findings traumatic rhabdo

A 
Signs of compartment syndrome ie 
Swelling tense 
Pallor 
Pain 
Myalgia
48
Q

Tests for rhabdo

A

Urine for myoglobin
Lactic acidosis
CK over 5000

49
Q

Principles of managing a patient with rhabdo

A

Aggressive fluid rehydration aiming for UOP more than 3ml/kg/hour

Early surgical fixation cause

Treat hyperk

Alkalise urine

Renal replacement therapy

Early enteral nutrition
MDT involvement

50
Q

Electrolytes values for brain stem death

A

Na 115-160
K more than 2
Phosphate and mag 0.5-3
Glucose 3-20

51
Q

Brain stem tests and CN

A 
Pupillary light II III
Corneal V and VII 
Ocvestibular reflex VIII and III,IV,VI
Painful stimuli V VII 
Gag IX X
Cough XX
52
Q

Apnoea test

A

Increase fio2 to 1
ABG to calibrate ETCO2
Reduce minute volume until ETCO2 is 6 and ph 7.4 (sats 95%)
Disconnect and apneoic ventilation 5 mins either with oxygen or CPAP
Confirm increase paco2 more than 0.5kpa

53
Q

Drugs used prior to organ donation

A

Vasopressin
Methylprednisolone 15mg/kg
T3

54
Q

Absolute contraindications to donation

A 
Cjd 
HIV disease 
Metastatic cancer 
Melanoma unless sumo,e 
Untreated TB 
Ages over 85
55
Q

Vasopressin functions physiologically

A 
Reabsorb water at collecting duct (plasma osmolality) 
Maintains circulating volume 
ACTH release 
Thermoregulation
Circadian rhythm
56
Q

Vasopressin receptors

A

V2 kidney at CD
V1 sm arteriolar (vasoconstriction)
Oxytocin like receptors in myometrium (vasoconstriction)
ACTH receptors pituitary (increase acth)

57
Q

Pharm agents derived from vasopressin

A

Desmopressin DI VWD

Terlipressin varicella bleeding

Argipressin hypotensive or septic shock

58
Q

Delirium

A

Delirium is acute syndrome
Deficits in attention and cognitive function
Hyper or hypo psychomotor activity
Disordered sleep wake cycle

59
Q

Features of hyperactive delirium

A

Agitation
Delirium
Can’t follow commands
Hallucinations

60
Q

How many types delirium

A

Hyper
Hypo
Mixed

61
Q

Screening tools delerium

A

Cams ICU
4 AT
Delerium detection score

62
Q

Patient factors predisposing to delerium

A 
Increased age 
Dementia 
Depression 
Alcohol or drug withdrawal 
Visual impairment
63
Q

Critical illness factors predisposing to dementia

A 
Acidosis 
Hypothermia 
Sepsis 
Anaemia 
Metabolic disturbances
64
Q

Apart from pharmacological management what other management of delerium

A 
Orientation ie clocks 
Sleep hygiene 
Maintain physiological homeostasis 
Management of withdrawal phenomenon 
Medications review
65
Q

Types of critical illness weakness

A

Polyneurpathy
Myopathy
Neuromyopathy

66
Q

Things to rule out before diagnosis of CIW

A 
GBS 
CNS infection
Anterior spinal artery stroke 
MG 
LEMS 
Porphyria 
Drug induced weakness
67
Q

Patient factors contributing to CIW

A 
Age 
Female 
Multiple comorbidities 
Infection 
Mof
iPpv 
Hyperglycemia 
Low albumin
68
Q

Pharm factors contributing to CIW

A

Neuromuscular blockade
Long term steroids
Aminoglycosides
RRT

69
Q

Motor findings in CIW

A

Symmetrical weakness
Reduced reflexes
Facial sparing

Mrc scale out of 60- 48 suggests a diagnosis

70
Q

Investigations of weakness in icu

A

LP for csf
Nerve conduction
MRI
Muscle biopsy

71
Q

Symptoms PE

A

Sob
Cp
Collapse

72
Q

Signs of pe

A

Cyanosis
Tachycardia
Lous s2

73
Q

Investigations in pe and what would be looking for

A

ECG sinus tachycardia Rv strain
Echo rv dikation , tricuspid regurgitation
Ctpa filling defect
Vq mismatch

74
Q

Management massive PE

A 
Fluid resuscitation 
Consider intubation and ventilation 
Thrombolysis is hypotension and RVF 
Dobutamine 
MDT input ie cardiology 
Therapeutic anticoagulati’n 
Thrombectomy
75
Q

Point of care ultrasound in icu

A 
Airway and vascular use pre tracheostomy 
Diagnostic lung ultrasound 
Poc echo 
Placement of drains 
Oesophageal Doppler 
Trasncranial doppler
76
Q

Indications for tracheostomy

A 
Airway obstruction 
Airway protection 
Pulmonary toilet 
Long respiratory wean 
Laryngectomy
77
Q

Benefits of percutaneous tracheostomy technique

A

Avoid transfer
Reduced wound infection
Reduced early complications

78
Q

Things to check or do pre tracheostomy

A 
Who checklist 
Check coagulation 
NG stopped 6 hours 
US neck 
Check airway equipment 
Check laryngoscopy view
79
Q

Complications of tracheostomy early & management to help

A

Bleeding - use la with adrenaline
Airway loss - 2 person procedure
Pneumothorax - under direct vision
Misplacement - under direct vision

80
Q

What is nec fasc

A

Nec fasc is a subcutaneous infection through fasciae layers rapidly spreading leading to potential life threatening emergency

81
Q

Risk factors nec fasc

A 
Diabetes
IVDU 
Malignancy 
Renal disease 
Obesity 
Peripheral vascular disease
82
Q

Classification nec fasc

A

Anatomical

Type 1 poly microbial
Type 2 monomicrobial
Type 3 grams negative
Type 4 fungal

83
Q

Diagnosis nec fasc

A

Clinical - pain more than expected, crepitus, bullae

Investigations raised inflammatory markers raised CK low calcium
CT air in fascia layers

84
Q

Treatment nec fasc

A

Early diagnosis
Broad spectrum antibiotics including clindamycin for endotoxins
Debridement
Hyperbaric oxygen
Immunoglobulin (strep and staph)
Organ support fluid resus and vasopressors

85
Q

Benefits early nutrition

A 
Reduced mortality 
Reduced length of stay 
Improved muscle function 
Reduced duration weaning 
Psychosocial 
Reduced wound breakdown 
Reduced infection
86
Q

Energy requirements per kg by artificial nutrition

A

Energy 25kal per kg

Carb 2 gram per kg 
Protein 1 
Fat 1 
 Sodium 1-2 mol kg day 
Potassium 1 mol kg  day 
Calcium and magnesium 0.1 
Phosphate 0.4

Micronutrients ie zinc
Immune modulators

87
Q

Positives enteral nutrition

A

Cheap
Reduced risk ileus
Reduced risk gastric ulcers Reduced infection

88
Q

Negatives enteral nutrition

A

Micro aspiration
Displacement
Peg if more than 4 weeks

89
Q

Define acute liver failure

A

Specific liver condition that evolves rapids,h into life threatening illness

Hallmarks are coagulopathy
Hepatic encephalopathy

90
Q

Hyper acute vs acute vs subacute liver failure

A

Hyperacute less than 7 days is rapidly evolving but also offset faster

Acute 7-28 days

Subacute 28 days to 12 weeks - more insidious BUT prognosis often poor by time diagnosed

91
Q

Grades encephalopathy

A

Grade 1 mild
Grade 2 disorientated
Grade 3 incoherent, somnolence
Grade 4 coma

92
Q

Tests in acute liver failure

A

Intrahepatic tests ie LFTs, coagulation, ammonia

Extra hepatic ie u&e, Fbc

For cause 
Viral screen 
Autoantibodies ie ana for aih or anti mitochorndrial psc 
Paracetamol levels 
Pregnancy test
93
Q

Management ALF

A

Early intubation and ventilation
Lung protective strategies but need to be balanced with cerebral protection

Fluids and vasopressors. Avoid terlioressin in acute use norad

Early renal replacement therapy if aki continous proffered

Treat intracranial hypertension and seizur3s

Coagulation abnormalities use TEG

Sepsis most common cause death so prophylactic antibiotics especially if on urgent transplant ,list

Treat hyperglycemia
Early enteral feeding as protein catabolism

Specific treatments

Refer to specialist centre early

NAC for paracetamol ( cysteine precursor of gluthione which neutralises NAPQI)
Steroids for autoimmune
Hep b lamivudine
Wilson’s penicillamine

? Plasma exchange
? Mechanical assist

Liver transplant definitive

94
Q

Kings college criteria for paracetamol overdose liver transplant

A

Ph less than 7.25
Create more than 300
Inr more than 6.5 or PT more than 100
Grade 3 or 4 encephalopathy

95
Q

Kings college non paracetamol guidelines

A

Inr more than 6.5 PT more than 100

Biki over 300
Jaundice to encephalopathy more than 7 days
Seronegative

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