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MRCS > Critical Care > Flashcards

Critical Care Flashcards

1
Q

How can local anaesthetics be classified?

A

Amides - lidocaine, bupivacaine, prilocaine

Esters - cocaine, procaine

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2
Q

What are the possible complications of local anaesthetics?

A

Neurological - personal & glossitis paraesthesia, light-headedness, drowsiness, seizures, tinnitus, tremors, confusion, coma
Cardiovascular - bradycardia, hypotension, VF, asystole

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3
Q

How would you manage a patient with lidocaine toxicity?

A

ALS approach
Primarily supportive
Seizure control with diazepam / midazlolam (phenytoin ineffective).
Cardiac monitoring

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4
Q

Which local anaesthetic is used in haematoma blocks?

A

Plain prilocaine, no adrenaline.

  • undergoes faster hepatic metabolism and has lower direct neurotoxicity
  • can cause methaemoglobinaemia
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5
Q

What are the safe maximum doses of local anaesthetic?

A

Lidocaine: 3mg/kg (7mg/kg with adrenaline)
Bupivacaine: 2mg/kg (3mg/kg with adrenaline)

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6
Q

What are the potential complications of spinal anaesthetics?

A

Hypotension & urinary retention

  • During insertion: direct neural injury, bleeding, haematoma, headaches
  • Due to catheter: block, dislodgement, infection, chronic fibrosis
  • During removal: haematoma, cord compression & paralysis. Anti-coags should be stopped prior to removal.
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7
Q

What is a burn injury?

A

Jackson’s burn model describes burns as ‘tri-zone injuries’

  • central area of coagulative necrosis
  • surrounded by static area of inflammation and ischaemia
  • further encircled by an area of hyperaemia
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8
Q

How would you classify burn injuries?

A

Depth: superficial, partial thickness, full thickeness
Cause: flash/flame, contact (hot/cold), friction, chemical, electrical, radiation

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9
Q

How do you assess burn size?

A
  • Patient’s palm ~1% TBSA
  • Wallace’s rule of nines: adult, head 9%, arm 9%, ant leg 9%, post leg 9%, ant trunk 18%, post trunk 18%, perineum 1%
  • Lund & Browder Chart: most accurate, adjusted for age
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10
Q

What fluid regime would you use to treat a burn injury?

A

Parkland formula = %TBSA x weight (kg) x 4ml in 24 hrs, first 50% given in first 8 hours post burn injury.

Required for adults with TBSA >15% or children with TBSA >10%

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11
Q

Which burns injuries should be referred to a burns unit?

A
  • full thickness TBSA >5%
  • partial thickness TBSA >10% in pts <10 or >50yrs
  • face, eyes, ears, hands, feet, genitalia & perineum
  • joints
  • inhalation, chemical and electrical
  • circumferential
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12
Q

Prognosis of burns patients?

A

Bull Chart estimates chance of survival based on age and %TBSA.
If patients age + %TBSA >100 survival is poor ~20%

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13
Q

How is a CVP line used to measure left atrial pressure?

A

Line inserted into SVC / right atrium to record right atrial pressure

  • assumed to be equal to left atrial pressure
  • if sides are asynchronous the assumption is no longer valid
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14
Q

How does cardiopulmonary bypass work?

A
  • right atrium cannula insertion
  • gravitational drainage of venous blood into reservoir
  • blood heparinisation
  • membrane oxygenator add O2 and removes CO2
  • heat exchanger controls blood temperature
  • oxygenated blood is passed through a bubble trap and microemboli filter
  • blood is returned to aortic circulation
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15
Q

What are the clinical indications for cardiopulmonary bypass?

A
  • Cardiothoracic surgery e.g. aortic surgery, CABG, valve repair / replacement, lung transplant, pulmonary thrombectomy
  • Neurosurgery e.g. basilar artery aneurysm repair
  • Supportive (critically ill pts) e.g. drug overdose, hypothermia
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16
Q

What are the complications of cardiopulmonary bypass?

A
  • immediate: air embolism, coagulopathy, hypothermia, inflammatory response, thrombocytopenia
  • early: ARDS, arrhythmia, AKI
  • late: coma, focal neurological deficit, mesenteric ischaemia, pancreatitis, seizures
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17
Q

What is the difference between primary and secondary brain injury?

A

Primary: occurs at time of injury e.g. direct brain cortex injury
Secondary: occurs after the injury, may be due to:
- Hypoxia
- Hypotension
- Hypercarbia
- High ICP

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18
Q

What is the Monro-Kellie doctrine?

A

Describes the intracranial pressure-volumes relationship as governed by: brain tissue, blood & CSF within a closed rigid box of fixe volume.
Change in 1 component must result in a compensatory change in another component in order to prevent a rise in ICP

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19
Q

What are the causes of increased intracranial pressure?

A
  • Medical: electrolyte imbalance, infection, stroke

- Surgical: haemorrhage / haematoma, oedema (contusions & DAI), tumour

20
Q

What is the cerebral perfusion pressure?

A

CPP = MAP - ICP

It is the pressure gradient which drives cerebral blood flow, O2 delivery and metabolite clearance.

21
Q

What are the key constituents of TPN?

A
  • carbohydrates >50%
  • fat >30%
  • amino acids
  • water
  • electrolytes
  • trace elements
  • vitamins
22
Q

Define acute and chronic renal failure

A
  • Acute: sudden, usually reversible impairment of functioning nephrons, resulting in reversible (usually) kidney function impairment
  • Chronic: progressive, permanent loss of functioning nephrons, resulting in irreversible kidney function impairment. CRF = advanced stage 4/5 CKD
23
Q

How is renal failure classified?

A

Pre-renal
- hypovolaemia (inadequate fluids, haemorrhage, burns, D&V)
- decreased cardiac output (HF, PE)
- hypotension (sepsis, anaphylaxis)
- vascular (renal artery or vein obstruction)
Intrinsic renal
- Drugs (gentamicin, NSAIDs)
- Glomerular (glomerulonephritis, antibody-mediated)
- Interstitial (pyelonephritis, sarcoid, lupus)
Post-renal (calculus, carcinoma for all)
- Ureteric
- Cystic
- Prostatic (BPH)
- Urethral (blocked catheter, stricture)

24
Q

What are the types of renal replacement therapy?

A
  • haemodialysis (works by diffusion)
  • haemofiltration (works by convection)
  • haemodiafiltration (combination of above)
  • peritoneal dialysis
25
Q

What are the indications for renal replacement therapy?

A
  • severe U&Es derangement e.g. refractive hyperkalaemia >6 or urea >35
  • severe acidosis e.g. ph <7
  • severe fluid overload e.g. resistant pulmonary oedema
  • uraemia complications e.g. encephalopathy & pericarditis
  • ESRF
  • cr clearance <10ml/min
  • removal of toxic drugs e.g. aspirin overdose
26
Q

What is the composition of Hartmann’s, Normal saline and dextrose-saline?

A

Hartmann’s: Na 131, Cl 111, Lactate 29 (metabolised to bicarb), K 5, Ca 2
Normal: Saline: Na 150, Cl 150
Dextrose-Saline: Na 30, Cl 30

27
Q

What are the fluid requirements of an average 70kg male of 24 hrs?

A

Maintenance: 2.5L water, 120-140 mmol Na, 70 mmol K

Insensible Losses: 600mls (skin), 400mls (lungs), 100mls (faeces)

28
Q

What are the normal reference ranges for PaO2 & PaCO2?

A

At sea-level:
PaO2 10-14 kPa
PaCO2 4.5-6 kPa

29
Q

How can you classify the causes of hypoxaemia?

A
  • Hypoxic (respiratory failure)
  • Anaemic (reduction or alteration of Hb)
  • Histotoxic (impaired mitochondrial respiration e.g. CN poisoning)
  • Stagnant (poor tissue perfusion e.g. CF, vascular obstruction
30
Q

What is acute lung injury and ARDS?

A

ALI and ARDS represent a spectrum of disease characterised by:

  • non-cardiogenic pulmonary oedema (diffuse pulmonary infiltrates on CXR)
  • progressive hypoxaemia
  • reduced lung compliance
31
Q

What are some causes of ALI & ARDS

A

FAT HIPS

  • Fat embolus
  • Aspiration pneumonia
  • Trauma & burns
  • Heart bypass
  • dIc
  • Pancreatitis
  • Sepsis
32
Q

How would you diagnosis ALI & ARDS?

A

Acute onset with diffuse pulmonary infiltrated on CXR. Pulmonary artery wedge pressure <18mmHg

  • PaO2 / FiO2 < 40 kPa - ALI
  • PaO2 / FiO2 < 26.6 kPa - ARDS
33
Q

What pathological changes occur in ALI & ARDS and what are the treatment principles?

A
  • inflammation / exudation due to cytokines, proteases, free-radicals. Interstitial alveolar oedema occurs & hyaline membranes formed. Supportive management and treat cause. PEEP & inverse & prone ventilation.
  • proliferation within 1-2 weeks of type II pneumocystis & fibroblasts. Granulation tissue narrows alveoli & vessels. Inhaled NO may help vasodilation and improve V?Q mismatch.
  • Fibrosis occurs over 2-4 weeks, steroids may be useful.
34
Q

What modes of ventilation are there?

A
  • IPPV: ventilator driven
  • PEEP: ventilator driven which ‘splints’ alveoli open and prevents collapse, helpful in ARDS.
  • CPAP: Patient driven and ‘splints’ alveoli open
  • SIMV (synchronised intermittent mandatory ventilation), ventilator kicks-in if inhalation missed whilst IPPV weaning
  • PSV (pressure support ventilation) patient ventilates spontaneously with added ventilator pressure support to ensure adequate tidal volume whilst IPPV weaning
35
Q

What are the complications of O2 therapy?

A
  • reduced hypoxic ventilatory drive (COPD)
  • pulmonary toxicity & fibrosis (free radical generation
  • absorption atelectasis (O2 flushes out N2 resulting in decreased alveolar ‘splintage’
  • retinopathy of prematurity (retrolenticular fibroplasia)
  • fire
36
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED

  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion venom
  • Hyper-calcaemia/lipidaemia
  • ERCP
  • Drugs e.g. azathioprine / furosemide
37
Q

How would you manage a patient with acute pancreatitis?

A

ALS approach - fluid resuscitation priority
Full history and thorough clinical examination
Prognostic blood tests and ABG
USS - assessment of gallstones
CT - between 3-10 days to delineate severity

38
Q

What are the modified glasgow criteria?

A

PANCREAS

  • PaO2 <8 kPa
  • Age >55
  • Neutrophils >15 x 10^9/L
  • Corrected Ca <2 mmol/L
  • Renal (Urea) >16 mmol/L
  • Enzymes (LDH) >600 U/L
  • Albumin <32 g/L
  • Sugar (glucose) >10 mmol/L
39
Q

What are the complications of acute pancreatitis?

A
  • Local: abscess, ascites, haemorrhage, necrosis, phlegmon, pseudocyst
  • Gastro: paralytic ileus
  • Haem: DIC
  • Hepatobiliary: CBD stricture, jaundice, portal vein thrombosis
  • Metabolic: hypo-albuminaemia/calcaemia/magnesaemia, hypoxaemia, hyperglycaemia
  • Renal: ARF
  • Respiratory: ARDS, pleural effusion
  • Other: chronicity, mortality ~10%
40
Q

What is SIRS?

A

2 or more of

  • temp <36 or >38
  • RR >20 or PaCO2 <4.3
  • HR >90
  • WCC <4 or >12 or >10% neutrophils
41
Q

What causes SIRS?

A

Progression of inflammation throughout the body: non-infective / infective

  • cardiovascular: major haemorrhage / infective endocarditis
  • GI: pancreatitis / bowel anastomosis leak
  • GU: ATN / UTI
  • Resp: Aspiration pneumonia / LRTI
  • Soft tissues: embolus -> ischaemia / nec fasciitis
  • General: Burns & trauma / sepsis
42
Q

What is MODS and MOFS?

A

Multiple organ dysfunction syndrome - reversible

Multiple organ failure syndrome - irreversible

43
Q

When would you consider patient admission to an ICU?

A
  • homeostatic failure: electrolytes / thermoregulation
  • high risk of MODS: pancreatitis
  • high risk procedure: AAA repair
  • intensive monitoring required: cardiovascular/neurological
  • mechanical support required: ventilation
  • pre-optimisation: pre-operative
  • severe condition: head injury / septicaemia
44
Q

What important conditions must be confirmed prior to diagnosing brainstem death?

A
  • patient comatose / ventilated
  • coma cause known
  • irreversible brain damage
  • reversible causes or coma excluded (alcohol, drugs, endocrine and metabolic disturbance, hypothermia, recent circulatory arrest)
45
Q

How would you diagnose brainstem death?

A 
Must be performed by 2 doctors (1 thats a consultant), both registered >5 yrs &amp; not part of transplant team.
The following must be tested and ABSENT
- pupillary light response
- occulovestibular reflex
- corneal reflex
- occulocephalic reflex
- gag reflex
- motor response to pain
- ventilatory effort following apnoea testing (PaCO2 rises to 6.65 kPa)

MRCS (6 decks)

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