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FRCS General Section 1/2 > Critical Care > Flashcards

Critical Care Flashcards

1
Q

How is Abdominal Compartment syndrome diagnosed?

A

Presence of IAP>20 measured 3 times 1-6 hours apart or Abdominal Perfusion Pressure <60

and

new organ dysfunction

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2
Q

What are the causes of Abdominal Compartment Syndrome?

A

Increased intra-luminal contents
Increased intra-abdominal contents (e.g. fluid/blood/abscess)
Capillary leak/fluid resuscitation
Miscellaneous (hernia repair, obesity)

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3
Q

How is Intra-abdominal pressure measured? (technique and criteria)

A

Technique
-Empty bladder, then 25ml of saline introduced
-Connect catheter to pressure transducer

Criteria
- End-expiration
- Supine
- Zeroed to mid-axillary line
- Abdominal muscular contraction absent/paralysed

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4
Q

How is Intra-Abdominal Hypertension graded?

A

Grade 1 12-15
Grade 2 16-20
Grade 3 21-25
Grade 4 >25

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5
Q

What are the pathophysiological changes associated with abdominal compartment syndrome? (5 categories)

A
  • Visceral - mucosal ischaemia
  • Renal - impairment at 15, oliguria at 20, anuria at 30
  • Pulmonary - splinting, decreased compliance/TVs, acidosis
  • CVS - decreased CO,BP,SV, increased SVR, DVTs
  • Cerebral - increased ICP, decreased CPP
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6
Q

What are risk factors for abdominal compartment syndrome?

A

Increased intra-luminal contents
Increased intra-abdominal contents
Capillary leak
Fluid resuscitation
Others (obesity, peritonitis, hernias)

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7
Q

What non-operative techniques should be used when abdominal compartment syndrome is suspected?

A
  • Sedation
  • Analgesia
  • NM blockade
  • Fluid optimisation
    -NG/rectal decompression
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8
Q

What factors intraoperatively increase the risk of abdominal compartment syndrome?

A

Long operating time
Lots of fluids
Electrolyte abnormalities
Trauma triad
Closure under tension

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9
Q

How is Acute Kidney Injury defined? (3)

A

Within 48 hours
1) Rise of creatinine of ≥26
2) Rise of creatinine between 150-200% of normal
3) UO <0.5ml/kg/hr for >6 hours

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10
Q

What are the causes of Acute Kidney Injury?

A

Pre-renal - shock (haemorrhage, septic, distributive), ACS
Intra-renal - ATN (Hypotension), nephrotoxins, GN
Post-renal - Catheter problems, bilateral ureteral problems/injury

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11
Q

What factors lead to oliguria in the sick surgical patient ?

A

Stress response –> ADH, Cortisol –> retain water
Catecholamines –> renal vasoconstriction
Sepsis –> relative hypovolaemia and decreased renal perfusion

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12
Q

What are the stages of Acute Kidney Injury?

A

Stage 1 - Creat 1.5-2 x normal/ UO≤0.5 >6 hours
Stage 2 - Creat 2-3 x normal/ UO≤0.5 >12 hours
Stage 3- Creat >3 x normal/ UO≤0.3 >24 hours

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13
Q

How can pre-renal and intrinsic renal failure be differentiated?

A

Pre-renal –> sodium conservation and concentrated urine
Urinary sodium/osmolality

Prerenal - <20mmol/l Na and osmolality >500
Renal - >40mmol/l Na and osmolality <350

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14
Q

What are the priorities in treatment of Hyperkalaemia? (4)

A

1) Identification - tall T waves, broad QRS and absent P
2) Stabilise myocardium with 0.5ml/kg CaGluconate 10%
3) Reduce intravascular potassium - Insulin dextrose (10u in 50mls 50%) + Salbutamol nebs (10mg)
4) Offload Potassium - Calcium resonium, stop drugs, ?furosemide ?RRT

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15
Q

What are the main indications for renal replacement therapy? (5)

A

1) Refractory pulmonary oedema
2) Refractory hyperkalaemia
3) Refractory acidosis <7.1
4) Symptomatic uraemia (encephalopathy/pericarditis)
5) Poisoning

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16
Q

What are the differences between haemodialysis and haemofiltration?

A

Dialysis - solute diffusion - cheaper, easier
Filtration - solute convection/ultrafiltration - better BP control, larger molecules (e.g. lipids, large cytokines), more physiological

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17
Q

How is ARDS defined?

A

1) Acute onset
2) pulmonary oedema
3) hypoxaemia despite PEEP ≥5cmH20
4) not caused by cardiac failure

Berlin Criteria

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18
Q

How is the severity of ARDS graded?

A

Mild - PaO2/FiO2 ratio 200-300mmHg (26.6-40kPa)
Moderate - PaO2/FiO2 ratio 100-200mmHg (13.3-26.6kPa)
Severe - PaO2/FiO2 ratio <100mmHg (<13.3kPa)

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19
Q

What is lung compliance?

A

Change in lung volume for a unit rise in pressure

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20
Q

What are the physiological changes seen in ARDS?

A

Reduced resting lung volumes
Increased V/Q mismatch
Decreased compliance
Increased work of breathing

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21
Q

What is ventilator induced lung injury?

A

Direct damage to alveolar tissue

Barotrauma - macroscopic injuries
Volutrauma - >10-15ml/kg –> ARDS
Oxygen toxicity –> >50%FiO2 free radical toxicity

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22
Q

What are the causes of ARDS?

A

-Pulmonary (infection, contusion, aspiration, drowning, smoke)

-Indirect (sepsis, major trauma, burns, pancreatitis, fat/amnion/thrombotic embolism)

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23
Q

What pathological processes are seen in ARDS?

A

1 ) Diffuse alveolar damage (Hyperacute) with damage to type 1 pneumocytes > type 2 pneumocytes
2) Acute inflammatory response
3) Proliferative/fibrotic phase

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24
Q

What are the principles of management of ARDS (5)?

A

-Low tidal volume ventilation (6-8ml/kg)
-PEEP
-Fluid management
-Proning
-ECMO or HFOV
-Permissive hypercapnia/acidosis (until myocardial depression)

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25
Q

What are the options for surgical airway insertion?

A

Surgical cricothyroidotomy – clip + use 5-7mm ET tube
Scalpel Bougie technique
Needle cricothyroidotomy

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26
Q

What is Atrial fibrillation?

A
  • Supraventricular tachcardia
  • Uncoordinated atrial activity
  • Irregularly irregular ventricular response if AV system intact
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27
Q

When should DCCV be considered for acute AF?

A

HR >150 with haemodynamic instability

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28
Q

What anti-arrhythmics can be used for AF?

A

Beta blockers esp where stopped prep
Amiodarone - central access only needs monitoring
Digoxin - less effective, more useful in chronic setting

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29
Q

What scoring systems might be used before starting anticoagulation for post operative AF?

A

HAS-BLED score (alcohol, meds, age, comorbidities)
CHA2DS2-VASc score >2 –> Anticoag

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30
Q

What are the goals of treatment for AF? (3)

A

Achieve ventricular rate control
Prevent thromboembolic events
Maintain sinus rhythm

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31
Q

When should anticoagulation be started after surgery?

A

Prophylaxis 6 hours
Treatment minor surgery 24 hours
Treatment major surgery 48-72 hours

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32
Q

What are the common congenital bleeding disorders?

A
  • Haemophilia A (VIII - x linked –> Desmopressin/F8 concentrate)
  • Haemophilia B (IX - x linked –> PCC /F9 concentrate)
  • Von Willebrands disease (AD – linked to platelet activation –> Cryo/F8/Desmopressin)
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33
Q

What are the common acquired bleeding disorders?

A
  • Vitamin K deficiency (II/VII/IX/X) from dietary, bile acid malabsorption, liver failure
  • Liver Failure - decreased synthesis of clotting factors (Except F8 which is increased) and Vitamin K
  • Platelet dysfunction - drugs, alcohol
  • Thrombocytopenia - decreased production/survival DIC (also factor consumption)
  • Renal failure
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34
Q

What are some common causes of AF?

A

PIRATES

Pulmonary Embolism
Ischaemia
Respiratory disease (pneumonia/atelectasis)
Atrial enlargement
Thyroid disease
Ethanol/Electrolytes
Sepsis/sleep apnoea

Also
-withheld drugs, hypovolaemia

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35
Q

What are the common acquired bleeding disorders?

A

Vitamin K deficiency (II/VII/IX/X) from dietary, bile acid malabsorption, liver failure
Liver Failure - decreased synthesis of clotting factors (Except F8 which is increased) and Vitamin K things
Platelet dysfunction - drugs, alcohol
Thromboyctopenia - decreased production/survival, DIC (also factor consumption)
Renal failure

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36
Q

What factors would make you suspicious of a hereditary thrombophilia?

A

History of recurrent VTE
History of idiopathic VTE (50%)
DVT <40
FH
Unusual site

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37
Q

What are the criteria for undertaking brainstem testing? (6)

A
  • Evidence of irreversible brain damage of a known aetiology
  • GCS 3 mechanically ventilated with apnea
  • No sedation
  • No muscle relaxation
  • Normothermic
  • Normal electrolytes/glucose
  • Cardiovascularly stable
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38
Q

Who can undertake brainstem death testing? (4)

A

-Two medical practitioners registered > 5 years
-At least one consultant
-Not member of transplant team
-No clinical conflict of interest

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39
Q

What are the criteria for diagnosis of brainstem death?

A

Establishing absence of brainstem reflexes
1) General examination to exclude voluntary/involuntary movement
2) Pupils fixed and non responsive (II/III)
3) No corneal reflex (Va/VII)
4) No vestibulo-cochlear reflexes (caloric test III, VI, VIII)
5) No response to supraoribital pressure (VII/Vc)
6) No gag/cough reflex (IX/X)

Apnoea test
- Pre oxygenate patient for 10 minutes
- Allow PaCO2 to rise to 6.0 with SBP >90 (6.5 for COPD)
- Disconnect from Ventilator for 5 minutes

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40
Q

How would you define a major burn and what fluid resuscitation is generally indicated?

A

Adult >15% TBSA, Child >10% TBSA, partial/full thickness

Assess size - Lund/Browder chart or Wallace rule of 9s or palm measurement

Parkland formula - %burn x kg x 4 in 24 hrs, half in first 8 hours

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41
Q

What criteria suggest transfer to a burns unit?

A

Extremes of age
2-3rd 10% in a child/15% adult
Inhalation injury
Special areas
Electrical/chemical burns
NAI
Escharotomy

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42
Q

When does the Parkland formula tend to under-estimate fluid requirements?

A

Inhalational injury
Delayed resuscitation
Hyperglycaemia
Alcohol intoxication

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43
Q

What is the pathophysiology of a burn?

A

Local effects
- protein denaturation (42) and cell death (45)
- Jackson’s zones - Coagulation, Stasis, Hyperaemia
Systemic effects
- Respiratory (ARDS)
- CVS - SIRS response
- Loss of skin function
- Increased BMR
-Immune suppression

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44
Q

What are the principles of resuscitation of burns?

A

First aid at scene - extinguish flame, remove chemical irritants, cool burn (15deg water)

ATLS approach especially airway and breathing and initial fluid resuscitation

Good Secondary Survey and covering of burns with simple dressings e.g. cling film

Burns fluid resuscitation

Adjuncts - NGT if >20%, Tetanus, Eye assessment, warming

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45
Q

How is DIC diagnosed?

A

Low platelets
Abnormal clotting
Raised D-dimer/FDPs
Low fibrinogen

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46
Q

What is HIT?

A

Reduction of platelet count of >30-50%, usually 4-14 days post heparin administration
Type 1 - transient fall, not immune related
Type 2 - autoimmune with antibodies against platelet factor-4/heparin complex

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47
Q

What anticoagulants are suitable for use in patients with HIT?

A

Argatroban (direct thrombin inhibitor)
Danaparoid (factor Xa inhibitor)
Fondaparinux (factor Xa inhibitor)

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48
Q

What are common causes of DIC? (6)

A

Anything that activates coagulation system
Commonly
- Severe sepsis (Gram-ve)
- Organ destruction (Pancreatitis/Burns)
- Trauma
- Transfusions
- Some obstetric emergencies
- Disseminated malignancy

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49
Q

When can an epidural be sited/removed? (Anticoagulant related)

A
  • 4 hours after Heparin
  • 12 hours after prophylactic LMWH
  • 24 hours after treatment LMWH

When Plt >100, INR <1.5

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50
Q

What are the fluid volumes in different compartments of a 70kg man

A

Intracellular (40% - 28L)
Extracellular (20% - 14 L),
- Interstitial ( 75% - 10.5L),
- Intravascular ( 20% - 3L),
- Transcellular (CSF, Intra-ocular 5% 0.5L)

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51
Q

What are the average daily fluid/electrolyte requirements?

A

NICE Guidelines

30ml/kg/day of fluid
1mmol/kg/day Na, K, Cl
50-100g/day glucose (avoid starvation ketosis)

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52
Q

What are the consequences of Duodenal and Jejunal high output fistulae?

A

Duodenum - Gastric/ Salivary - 4L/day –> Hypokalaemia/chloraemia
Jejunum - Variable, can be v high output can –> Hyponatraemia/kalaemia/ low bicarb (pancreas)

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53
Q

Why does gastric outlet obstruction cause aciduria?

A

Preferential preservation of Na+ in dehydration –> excretion of K+ and H+ ions

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54
Q

What is the typical dose of Octaplex?

A

25-50units/kg

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55
Q

What topical haemostatic agents can be used?

A

Biological - bovine albumin, fibrin glues, thrombin sealants (Floseal)
Dry matrix - gelatin matrix, oxidised regenerated methylcellulose (surgicel), veriset (PEG and cellulose)

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56
Q

What haemostatic drugs can be used to control intra-operative bleeding?

A

Anti-fibrinolytics (TXA, Aprotinin)
- TXA 1g over 1 mins then 1g over 8 hours
Recombinant factor VIIa
DDAVP

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57
Q

What is hepatorenal syndrome?

A

AKI with in patients with Acute/CLD

Usually associated with advanced CLD, cirrhosis and ascites, and up to 40% of patients with this will develop HRS

Two types - Type 1, rapid progressive decline in renal function, Type 2 moderate stable reduction

Prognosis poor

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58
Q

What is the pathogenesis of HRS?

A

Portal hypertension –> splanchnic vasodilation –> activation of RAAaxis –> renal vasoconstriction

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59
Q

What are the types of hyponatraemia?

A

True hyponatraemia (serum osmolality <280)
- Hypovolaemic (decrease in sodium > decrease in water, ECF decreased)
- Euvolaemic (increase in water, sodium unchanged, ECF decreased)
- Hypervolaemic (increase in water > Increase in sodium, ECF increased)

Pseudohyponatraemia (serum osmolality 280-295 caused by lipids or plasma proteins)

Translational hyponatraemia (serum osmolality >295 hyperglycaemia or mannitol)

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60
Q

How can different causes of hyponatraemia be classified and treated?

A

Treat underlying cause.
If hypovolaemic –> isotonic saline
Euvolaemic –> restrict water
Hypervoalaemic –> restrict water and diuretics

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61
Q

What common inotropes/vasopressors are used in critical care?

A

Noradrenaline α-1 agonist Vasopressor action, minimal effect on cardiac output

Adrenaline α and β receptor agonist Increases cardiac output and peripheral vascular resistance

Dopamine β1 agonist Increases contractility and rate (low dose renal vasodilation, med dose heart, high dose vasoconstriction)

Dobutamine β1 and β2 agonist Increases cardiac output and decreases SVR

Milrinone Phosphodiesterase inhibitor Elevation of cAMP levels improves muscular contractility, short half life and acts as vasodilator

Phenylepherine (pure alpha)
Metaraminol, Epheredine (sympathomimetics)
Vasopressin V1 for vasoconstriction and V2 for vasodilation (useful septic shock)

For Sepsis prob – NA + V

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62
Q

How can cardiac output be monitored non-invasively?

A

1) Analysis of arterial waveform (Lidco, PiCCO) –> area under systolic waveform = SV
2) Oesophageal doppler monitor (velocity of descending aortic blood flow)
3) Thoracic impedance/bioreactance techniques

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63
Q

What is a normal CVP?

A

Measured from sternal angle - 0-8mmHg
Tip of catheter at junction of SVC and RA

Indirect measure of volume status

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64
Q

What factors raise the CVP?

A

Increased intra-thoracic pressure (coughing, PEEP, CPAP)

Impaired right heart function (cardiac failure, tamponade, PE, SVC obstruction)

Decreased by hypovolaemia

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65
Q

How might CVP change with fluid resuscitation in hypovolaemic patients?

A

500ml fluid challenge:

Hypovolaemia –> non-sustained rise falling after 10 minutes
Normovolaemic –> rise above baseline with slow return
Overloaded –> persistent rise

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66
Q

What does a PA catheter measure?

A

Pulmonary artery wedge pressure - indirect measure of LV and diastolic (normally 8-12 mmHg)

Septic shock/hypovolaemia –> fall
Pulmonary oedema –> rise
ARDS –> normal

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67
Q

What is cardiac output?

A

Volume of blood pumped per minute == 5l/min

Indexed to BSA for cardiac index (2.2-3L/min/m2)

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68
Q

What is the Frank-Starling law?

A

Force of contraction/stroke volume increases with preload (up to a point)

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69
Q

What is the MAP?

A

DBP + 1/3 (SBP-DBP)

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70
Q

What is the mechanism of inotropes?

A

increased availability of calcium to cardiac myocytes by activation of adenyly cyclase leading to cAMP and calcium influx

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71
Q

What does a litre bag of Hartmanns contain?

A

131mmol/l Na
111mmol/l Cl
5mmol/l K
2mmol/l Ca
29mmol/l Lactate

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72
Q

What are colloids?

A

Large molecular weight containing infusatn usually >30000kda and exert oncotic pressure
Theory being they stay in the intravascular compartment longer

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73
Q

How should a high output stoma be managed?

A

Strict monitoring of input/output/electrolytes
Adequate IV fluid replacement including elecytolytes
Avoid hypotonic fluids and give balanced solutions
Fibre supplementation
Pharmacological treatments
Stoma nurse

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74
Q

What is DIC?

A

Consumptive coagulaopathy
Caused by release of free thrombin into circulation
Leading to widespread microvascular thrombosis

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75
Q

What is the pathohysiology of ARF with rhabdomyolysis?

A

Myonecrosis of postural muscles –> release of K+,PO4, CK-MM, LDH and myoglobin

Myoglobin binds to thick ascending limb of loop –> precipitate and tubular obstruction
Myoglobin = oxygen binding protein of muscle – source of O2 for muscle

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76
Q

What are the causes of rhabdomyolysis?

A

Direct muscle injury (Blunt trauma, reperfusion, burns, electrocution)
Excessive muscle contraction (status asthmaticus, taser injuries, statins)

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77
Q

How are hospital levels of care defined?

A

Level 0 - Normal <4hourly obs
Level 1 - At least 4 hourly obs, outreach support, additional monitoring or interventions e.g. chest drain
Level 2 - single organ support e.g. single agent vasopressor (not mechanical vent)
Level 3 - Advanced respiratory support or support of 2+ organ systems

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78
Q

How might level of care post operatively be decided (4)?

A

Local factors - e.g. some wards cannot manage epidurals
Patient factors e.g. comorbidities, risk calculation, CPET
Surgical factors e.g. flap observations, drains, continuous infusions, bleeding, major surgery)
Anaesthetic factors e.g. prolonged anaesthesia, need for vasoactive)

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79
Q

How do local anaesthetics work?

A

Block neuronal transmission by:
1) Sodium channel blockade
2) membrane expansion

Small fibres e.g. pain lost before touch sensation

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80
Q

What are the types of LA?

A

Ester - Cocaine, Procaine, Amethocaine
Amides
- Lidocaine (short acting 2 hours)
- Prilocaine (wide therapeutic index, used IV)
- Bupivicaine (long acting 4 hours)
- Levobupivicaine (less cardiotoxic/vasodilatory effects than bupivicanine)

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81
Q

How does adrenaline effect use of LAs?

A

Vasoconstriction reduces absorption, prolongs duration and reduces toxicity

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82
Q

In a crisis situation with life threatening haemorrhage what blood products would you administer?

A

If no grouped blood then O-ve x4 units (or O+ve for males)

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83
Q

How is massive haemorrhage defined?

A

1) >1 blood volume in 24 hours
2) >1/2 blood volume in 3 hours
3) >150ml/min
4) Transfusion of 10 units PRC in 24 hours with ongoing bleeding
5) Transfusion of 4 units PRC in 4 hours with ongoing bleeding

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84
Q

What does the major haemorrhage protocol comprise of?

A

20ml/kg PRC
20ml/kg FFP
10ml/kg Platelets
5ml/kg Cryo

In general

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85
Q

In practice what might a major haemorrhage pack comprise?

A

Pack 1
- 6 units PRC
- 4 units FFP
- optional platelets

Pack 2
- 4 units PRC
- 4 units FFP
- 1 unit platelets
- 2 pools of cryo

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86
Q

What lab parameters should be targeted in a major haemorrhage setting?

A

Hb. >80
INR <1.5
Plt >80 or 100 if multiple/CNS trauma

Fibrinogen >1g/L
Ionised calcium <1.13mmol/l

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87
Q

What are the complications of transfusion?

A

-Immune mediated (ABO/other, TRALI, immune modulation)
-Infectious (Hep, HIV, CMV, CJD)
-Metabolic (hypocalcaemia, hyperkalaemia)
-Volume related and idiosyncratic (TACO, thrombocytopenia, hypothermia, hypocalcaemia, hyperkalaemia, acidosis, coagulopathy)

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88
Q

What are some risk factors for nosocomial infection?

A

Patient factors (illness severity, comorbidity, nutrition, prolonged antibiotic use)
Environmental factors (poor hand hygiene, inadequate staff/space)
Organism factors (antibiotic resistance, pathogenicity)

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89
Q

How is a VAP diagnosed?

A

Systemic criteria (T<36 or >38 + WCC <4 or ≥12)
Pulmonary criteria ( new increased aspirates, worsening gas exchange, positive cultures, or radiography)

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90
Q

What organisms are associated with a VAP?

A

Gram-ve organisms (e.g. Gut)
Pseudomonas, Enterobacter, Kelbsiella, E.Coli

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91
Q

What factors can increase the risk of CVC infection?

A

Site
Poor technique
Multi-lumen
Poor hand hygiene
Frequent dressing changes

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92
Q

What factors can reduce the risk of CVC infection?

A

Aseptic technique
Early removal and regular review
Antiseptic/silver impregnated lines

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93
Q

Why is malnutrition important to surgical patients?

A
  • Impaired wound healing
  • Increased incidence of pressure ulcers
  • Overgrowth of bacteria in the GI Tract
  • Increases infective complications due immune dysfunction
  • Prolonged mechanical ventilatory support
  • increased muscle wasting
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94
Q

What are the benefits of enteral vs parenteral feeding?

A

Enteral
- Fewer infective complications
- Maintains normal gut mucosal integrity (stress ulcers, mucosal atrophy)
- Lower cost

Parenteral
- easier to provide full energy requirements
- does not require gut function/integrity

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95
Q

What are the negatives of enteral vs parenteral nutrition?

A

Enteral
- difficulty meeting requirements (absoprtion/ileus)
- diarrhoea
- increased risk of VAP
- aspiration

Parenteral
- Access related infections
- Liver dysfunction
- Trace element deficiency

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96
Q

What are the indications for PN?

A

Absolute - enterocutaneous fistula
Relative
- EN not possible
- Short bowel syndrome
- Prolonged bowel rest, obstruction
- Inflammatory states such as burns, trauma, pancreatitis if EN not possible

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97
Q

What is refeeding syndrome?

A

Metabolic disturbances that occur when introducing diet after a prolonged period of starvation.
- Hypophoshataemia, hypokalaemia and hypomagesaemia

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98
Q

What is the mechanism of refeeding syndrome?

A
  • Insulin levels rise and cause cellular uptake of K, PO4, Mg
  • Low PO4 depletes ATP and 2,3 DPG causing cellular dysfunction, resipratory and cardiac failure
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99
Q

Who is at risk of refeeding syndrome?

A

Any patients with poor intake for ≥5 days.
Specific
- Alcohol/drug abusers
- Chronically malnourished
- Anorexia

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100
Q

What are the typical daily requirements for components of TPN?

A

Water 30ml/kg
Calories 25-30kcal/kg (70% CHO, 30% Fat)
Protein 1-2g/kg
Sodium 1-2mmol/kg
Potassium 1mmol/kg
Calcium/Mg 0.1-0.3mmol/kg

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101
Q

How should sugars be managed in an ICU setting?

A

Tight glucose control is now less favoured
Aim for <10mmol/L

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102
Q

What are typical constituents of TPN?

A

Lipid emulsion 25% calories including essential fatty acids
CHO - Dextrose 75% calories
Protein 1-2g/kg (essential and non essential amino acids)
Water
Trace elements

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103
Q

What are the essential fatty acids?

A
  • Alpha linoelic acid
  • Linoleic acid
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104
Q

What is obstructive sleep apnoea?

A
  • Repeated episodes of partial/complete pharyngeal collapse –> upper airway closure during sleep
  • resultant T2RF leads to disruption of normal sleep cycle with awakening
  • occurs in about 5%, of whom 80% undiagnosed
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105
Q

What are the consequences of OSA?

A

Increased risk of:
- MI
- Arrhythmia
- L/RVH
- Pulmonary hypertension
- CVD
- HTN
- Diabetes

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106
Q

How is OSA diagnosed and classified?

A

Polysomnography (sleep study)
Apnoea hypopnea index (AHI) - number per hour

Severity
- None (<5/hr)
- Mild (5-15)
- Moderate (15-30)
- Severe (>30)

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107
Q

How can you assess for OSA at bedside?

A

STOP-Bang assessment
- Snoring
- Tired during day
- Observed apnoea
- Pressure (BP)
- BMI ≥35
- Age >50
- Neck circumference >40cm
- Gender (male)

≥3 predicts risk of moderate-severe OSA

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108
Q

How is death defined?

A

Irreversible loss of consciousness combined with the irreversible inability to breathe, can be by either neurological or circulatory criteria

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109
Q

How is death by circulatory criteria confirmed?

A

Asystole and lack of respiratory efforts for 5 minutes, with loss of light and corneal reflexes

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110
Q

What factors govern delivery of oxygen to patients?

A
  • Patient airway
  • FiO2
  • Adequate ventilation
  • Alveolar function
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111
Q

What adjuncts can be used to deliver oxygen to patients?

A

Variable performance:
Nasal cannula 2-4 L/min
Hudson face mask 5L/min

Fixed performance:
Venturi mask
Non-rebreather
High flow nasal cannula (optiflow)
CPAP
BIPAP
Invasive ventilation

112
Q

How to Venturi masks work?

A

Bernoulli principle
Entrainment of air to mix with oxygen

113
Q

What re the complications of oxygen therapy?

A

Absorption atelectasis (reduced nitrogen buffer)
Pulmonary toxicity
Hypercapnoea
Retinopathy in premature infants
Risk of fires

114
Q

What are steps of the WHO pain ladder?

A

Paracetamol/NSAID
Weak opiate (Tramadol,Codeine)
Strong opiate

115
Q

What are the components of general anaesthesia?

A

Hypnosis
Analgesia
Muscle relaxation

116
Q

What hypnotic agents are available?

A

IV - Propofol, Thiopentone, Ketamine, Etomidate
Volatile - Isoflurane, Sevo, Des, Halo

117
Q

What muscle relaxants are typically used?

A

Depolarising NMJ blockers (Suxamethonium) risk of Sux apnoea cholineseterase abnormality. Non-competitive blockade)

Non-depolarising NM blockers (Atrac, Roc). Competitive blockade. Can be reversed. Longer onset.

118
Q

What factors increase the risk of postoperative nausea and vomiting?

A

Patient - female, non-smoker, previous history
Anaesthetic - volatile agents, neostigmine, NO
Surgical - duration, type (gynae, Urol, bariatric)

119
Q

What is the mechanism of the vomiting reflex?

A
  • Vomiting centre located in medulla
  • Triggered by:
    —Chemoceptor triggering zone
    — Vagal pathway in GI tract
    — Neuronal pathways in vestibular system
    — Reflex afferents from the cerebral cortex
    — Afferents from the midbrain
120
Q

What is CPET?

A

Cycle ergometer
Baseline measurement of gas exchange and NIBP
Measured with increasing load while maintaining 60rpm
Terminated when cannot meet/continue

121
Q

What is the Anaerobic Threshold?

A

Surrogate marker of efficiency of lungs, heart and circulation
11ml/kg is general cut off

122
Q

What are the common ECG findings with PE?

A

Mostly none or sinus tachycardia
20% have signs of right heart strain = tall p waves, RBBB, RAD, S1Q3T3 or AF

123
Q

How does pulse oximetry work?

A

Beer-Lambert law
Oxygenated haemoglobin reflects different light wavelength to deoxygenated.

Pitfalls - Hypothermia, nail varnish, jaundice, abnormal haemoglobin e.g. carboxylate or methaem)

124
Q

How are PaO2 and FiO2 related?

A

Should be around 0.6 (normal 12kPa/21%)

125
Q

What does oxygen delivery depend upon?

A

Hb
CO
SaO2

126
Q

How is respiratory failure defined?

A

PaO2<8kPa on 21% FiO2

Type 1
-Hypoxaemic
-Damage to lung tissue, V/Q mismatch
- E.g. pneumonia, PE, asthma, ARDS, pulmonary oedema

Type 2
-Hypercapnoea
-Alveolar hypovenatilation
- E.g. reduced central drive, impairment of peripheral airway system such as COPD

127
Q

What are indications for failure of basic respiratory support?

A

RR >30
Increasing oxygen requirements to maintain SaO2
PaO2<8 or PaCO2 >6.5 with pH<7.35
Dyspnoea, exhaustion or low GCS

128
Q

What are indications for intubation?

A

Airway obstruction
Airway protection
Respiratory failure
Unconscious patients
Anaesthesia

129
Q

How does the body respond to a surgical insult?

A

Sympathetic activation (increased CO, glyoclysis and RAAA)
Endocrine response (ACTH –> Cortisol)
Acute phase response (cytokines, clotting cascade)
Vascular endothelium response

130
Q

What is the metabolic response to surgery/trauma?

A

Ebb phase (reduced EE for 24 hours and reduced BMR)
Flow phase (dramatic increase in BMR and catabolic state with negative nitrogen balance
Flow phase anabolic phase

131
Q

What is the role of lipids after trauma?

A

Principle source of energy
Lipolysis stimulated by SNS, ACTH, cortisol, glucagon
Ketones used by all tissues except blood/brain
FFA and glycerol –> gluconeogenesis

132
Q

how is carbohydrate metabolism affected by trauma?

A

-Insulin decreases, glucagon increases –> glycogenolysis/glycolysis
-Potentiated by increased insulin resistance from cortisol
-Glycogen stores last for 24 hours then gluconeogenesis from fats or AAs

133
Q

How can functional status be assessed?

A

METS - 2 flights of stairs = 4 METS = better outcomes
CPET
Exercise ECG
Dobutamine Stress Echo

134
Q

How is Jet Insufflation performed?

A

Oxygen for 1 s then expire for 4 s

Well oxygenated but poorly ventilated –> hypercapnoea

135
Q

What is the normal blood volume?

A

70ml/kg in adults
75ml/kg in children

136
Q

What strategies can be used to reduce the use of stored blood?

A

Intra-operative cell salvage (use within 4 hours, not contaminated, not malignant)
Pre-deposit autologous transfusion (rare)
Acute normovolaemic haemodilution

137
Q

What do FFP, PCC and Cryo contain?

A

FFP - all
PCC - 2,7,9,10
Cryo - fibrinogen, vWF, 8/13

138
Q

What is a TEG?

A

POCT for coagulopathies
R time - how long to clot - if long –> FFP
a-Angle - how fast a strong clot if formed if low –> Cryo
Amplitude - size of clot if low –> platelets
Ly30 - lysis - if high –> TXA

139
Q

Why are nutritional requirements higher in critically ill patients?

A

Response to injury/surgery
At risk of infection (SSI, lines, resistant organisms)
Ventilator –> increased work of breathing

Also have impaired use of glucose/fats (can normally be used by everything apart from erythrocytes and renal medulla) and enhanced protein breakdown to compensate for this

140
Q

What is the French scale of tubing?

A

Guage/3 == diameter in mm

141
Q

How is atelectasis best managed?

A

Supplemental O2 as required
Sit patient up
adequate analgesia
Regular chest physiotherapy

142
Q

What are the stages of hypovolaemic shock?

A

1 - <15%, Tachypnoea, mild tachycardia
2 - 15-30% tachycardia, narrowed pulse pressure, oliguria
3 - 30-40%, tachycardia, reduced blood pressure, ?confusion
4 - 40+%, extreme tachycardia, very reduced blood pressure, ?confusion/agression, anuria

143
Q

What compensatory mechanisms are employed with hypovolaemic shock?

A

Redistribution of blood flow to brain and heart
Baroreceptor inhibition –> sympathetic activation
SNS –> Splanchnic vasoconstriction and redistribution

Delayed activation of RAAS and ADH release

144
Q

How is lactate produced in metabolic acidosis?

A

hypoxia –> Blockade of citric acid cycle –> pyruvate –> lactate

145
Q

What are the physiological effects of acidosis?

A

negative inotropic effect
arteriolar dilatation
right shift of O2-Hb curve

146
Q

How is sepsis defined?

A

Sepsis 3 definitions JAMA 2016

Life threatening organ dysfunction caused by a dysregulated host response to infection

Organ dysfunction == increase in SOFA score by ≥2

147
Q

How is septic shock defined?

A

Sepsis 3 definitions JAMA 2016

Vasopressor requirement to maintain MAP ≥65mmHg + Lactate >2 + absence of hypovolaemia

Mortality >40%

148
Q

What is the qSOFA?

A

RR>22
SBP<100
GCS<15

in presence of suspected infection
high risk of mortality

149
Q

What fluids resuscitation should patients with sepsis receive?

A

At least 30ml/kg balanced crystalloid within 3 hours (?2Litres)

Consider albumin if received large volumes of crystalloids (not gelatine or starches)

Surviving sepsis Campaign guidelines 2021

150
Q

What is goal directed therapy in sepsis?

A

UO >0.5ml/kg
SVO2>70%
MAP >65
CVP >8

Rivers 2001
ProCESS, ARISE, ProMISe showed no benefit
Probably out of fashion - now guide by lactate and CRT

151
Q

What are the mechanisms of heat loss in surgical patients?

A

Radiation (40%)
Convection
Evaporation
Conduction
Respiration

152
Q

What are the clinical effects of hypothermia?

A

Increased oxygen consumption
Decreased oxygen delivery (left shifts)
CO fall
Arrhythmias
Metabolic acidosis
Wound infections

153
Q

What factors can reduce the incidence of VAP?

A

Intensive care society recommendations
Elevation of head of bed
Sedation level Assessment (daily)
Aspiration of subglottic secretions
Avoidance of routine circuit changes

Old recommendations - probably relevant
Tracheal tube pressure
Stress ulcer prophylaxis review (i.e. to stop)
Oral hygiene (teeth brushing, mouthwash)

Other standard
Standard infection control and monitoring
Reduce invasive ventilation
Enteral feeding post-pyloric

154
Q

What is the daily protein requirements?

A

0.8-1.5g/kg/day

No strong evidence for increase in sepsis

155
Q

What ABG findings are typically seen in patients with PE?

A

Type 1 RF
Respiratory alkalosis

156
Q

What comprises the MUST score?

A

BMI (18.5-20 = 1, <18.5 =2)
Unplanned weight loss (5-10% = 1, >10% = 2)
Acute illness and no nutritional intake for >5 days = 2

2 + points = high risk

157
Q

What are criteria for extubation?

A

Stable condition
No plans for return to theatre
Able to wean sedation so can follow commands and protect airway
Adequate oxygenation and gas exchange, FiO2<40% and PEEP 5-8

158
Q

What is the mechanism of TXA?

A

Reversible competitive inhibitor of plasminogen, prevents activation to plasmin and fibrinolysis

159
Q

How do topical haemostats work?

A

Biological - e.g Floseal - combination of gelatin and thrombin directly activate clotting cascade

Dry matrix e.g. Veriset - PEG and cellulose which acts as physical tamponade and recruits platelets and clotting factors to bleeding site

160
Q

What are the protein requirements of critically unwell patients?

A

Protein replacement should start at a low dose - 0.8g/kg/day
and increase to 1.2-2g/kg later

161
Q

What are the phases of wound healing?

A

Inflammation - lymphocytes, neutrophils and macrophages
Proliferation - fibroblasts, angiogenesis, type 3 collagen
Remodelling - up to a year, final scar, type 1 collagen

162
Q

How does dopamine work at low doses?

A

Dopamine has varying effects due to alpha-1, beta-1 and dopaminergic acitivity

Low does - <2ug/kg/min
- Mostly renal
- Increased blood flow (renal, cerebral, coronary and mesnteric due to vasodilatation (D receptors)

163
Q

How does dopamine work at intermediate doses?

A

Dopamine has varying effects due to alpha-1, beta-1 and dopaminergic acitivity

2-10ug/kg/min

Mostly Cardiac
B-1 –> increased contractility and HR
Increased CO and D effects –> increased mesenteric blood flow
Mild vasoconstriction

164
Q

How does dopamine work at high doses?

A

Dopamine has varying effects due to alpha-1, beta-1 and dopaminergic acitivity

10-20ug/kg/min

Vasoconstrictive (a1) and cardiac
May reduce renal and mesenteric blood flow

165
Q

What factors shift the oxygen-hb dissociation curve to the right?

A

Left shift = increased oxygen binding (decreased delivery)
Right shift = decreased oxygen binding (increased delivery)

CADET face right
CO2
Avid
DPG
Exercise
Temperature

166
Q

What are 5 inotropic agents used in critical care?

A

Noradrenaline α agonist Vasopressor action, minimal effect on cardiac output

Adrenaline α and β receptor agonist Increases cardiac output and peripheral vascular resistance

Dopamine β1 agonist Increases contractility and rate

Dobutamine β1 and β2 agonist Increases cardiac output and decreases SVR

Milrinone Phosphodiesterase inhibitor Elevation of cAMP levels improves muscular contractility, short half life and acts as vasodilator

167
Q

What is hiflow nasal oxygen and its characteristics?

A

Ultra high flow oxygen rates - 50-60l/min

  • humidified
  • well tolerated
  • T1RF (although can washout CO2)
  • applies some PEEP due to flow rate
168
Q

How does CPAP differ from BIPAP?

A

CPAP continuous pressure of 10 (PEEP) up to 40-50% FiO2 (nb risk of aspiration)
Helps for T1RF

BIPAP dual level - PEEP + and inspiratory
the added hilevel helps for CO2 blow off in T2RF

169
Q

What are the general indications for intubation? (4)

A

Lungs - O2, CO2, Work of breathing
Brain - aspiration risk or ICP control
Heart - failure or advanced support
Control - facilitate transfer/intervention

170
Q

How do you confirm successful intubation?

A

End tidal CO2

171
Q

How is cardiac output calculated?

A

CO = HR X SV

CO = MAP X SVR

172
Q

What are the indications for renal replacement therapy?

A

Diuretic resistant pulmonary oedema
Refractory hyperkalaemia
Metabolic acidosis
Symptomatic uraemia
Overdose of dialysable drugs

173
Q

What is the total body water composition in males?

A

60% of weight therefore 42kg of 70kg

2/3 intracellular
1/3 extracellular - 75% interstitial 25% intravascular

174
Q

which characteristics can be calculated from an art line?

A

Left ventricular contractility
Stroke volume
Peripheral vascular resistance
Fluid responsiveness

175
Q

What are some risk factors for PONV?

A

Female
Smoker
Previous history
Opiates
Hypotension
Ophthalmic/gynae surgery

176
Q

What are the characteristics of the ebb phase response to trauma?

A

-Increased sympathetic activity
-decreased BMR/energy expenditure
-increased gluconeogenesis/glycogenolysis

177
Q

What are the characteristics of the flow phase of response to trauma?

A

Catabolic phase for 1-2 weeks
Anabolic recovery phase for months
-Negative nitrogen balance
-Increased BMR/REE
-Increased gluconeogenesis
-Increased glucagon, insulin, cortisol, insulin resistance

178
Q

Which trace element is most important for wound healing?

A

Zinc

-copper less so

179
Q

Where is most Na/water absorbed in the sb?

A

Ileum

180
Q

What is the minimum obligatory length of jejunum proximal to a jejunostomy required to avoid supplementary fluid/nutrition

A

100cm.

181
Q

how does lidocaine work?

A

Blockade of axonal sodium channels

182
Q

How does bupivacaine work?

A

Binds to intracellular portion of sodium channels

Very cardiotoxic - contraindicated in regional

Levobupivicaine (chirocaine) less cardio toxic and causes less vasodilation

183
Q

What are the maximal doses of LAs?

A

Lidocaine 3mg/kg - max 200mg
Lidocaine + Adrenaline 7mg/kg - max 500mg
Bupivicaine 2mg/kg to max of 150mg

Calculated by IBW

184
Q

How is an LA overdose treated?

A

Stop injecting
High flow O2
CVS monitoring
Lipid emulsion (intralipid 20%) at 1.5ml/kg over 1 minute
Consider infusion at 0.25ml/kg/in

185
Q

What are the main stages of wound healing?

A

Haemostasis (platelets, fibrin rich clot)
Inflammation (neutrophils, Growth factors, fibroblasts, macrophages)
Regeneration (fibroblasts and epithelial cells, angiogenesis, looks like graduation tissue)
Remodelling (longest phase, fibroblasts –> myofibroblasts –> wound contraction)

186
Q

What is the difference between hypertrophic and keloid scars?

A

Excessive collagen not bound to original injury in keloid

187
Q

What are the three means of chronic inflammation?

A

Persistent infections (e.g. Mycobacterium TB)
Prolonged exposure to no biodegradable substances (suture, silica)
Autoimmune conditions

188
Q

What is the cellular difference between acute and chronic inflammation

A

Acute - neutrophil dominant
Chronic - macrophage, plasma cells and lymphocytes

189
Q

How can superficial partial thickness and deep partial thickness burns be differentiated?

A

no blanching with deep partial thickness

190
Q

When should burn fluid resus be instituted?

A

> 15% BSA involvement (2nd degree or more)

191
Q

What is the most accurate means of establishing burns coverage?

A

Lund Browder chart > Wallace rule of nines

192
Q

What are the indications for transfer to burns centre?

A

> 15% BSA
Face/hands/genitals affected
Deep PT or FT burns
Significant electrical or chemical burns

193
Q

What are the metabolic effects of adrenergic receptor agonism?

A

Alpha
-inhibits insulin release
-stimulates glycogenolysis
-stimulates glycolysis

Beta
-Stimulates glucagon
-Stimulates ACTH
-stimulates lipolysis

194
Q

What proportion of circulating cortisol is protein bound

A

90%

195
Q

How is the anion gap calculated?

A

(Na + K) - (Cl+HCO3)

Normal 10-18mmol/l

196
Q

What are some causes of normal anion gap metabolic acidosis?

A

GI HCO3 loss
Renal tubular acidosis
Drugs e.g. acetazolamide
Addisons disease

197
Q

What are some causes of a raised anion gap acidosis?

A

Lactate: shock
Ketone: diabetic ketoacidosis, alcohol
Urate: renal failure
Acid poisoning: salicylates, methanol

198
Q

What effect does chronic anaemia have on the O2Hb dissociation curve?

A

Shift to right as 2,3 DPG increased

199
Q

What ECG features may be seen with hypokalaemia?

A

U waves
Small/absent T waves
Prolonged PR interval
ST depression
Long QT interval

200
Q

What ECG features may be seen with hyperkalaemia?

A

Peaked T waves
P wave flattening
Prolonged PR Interval
Widened QRS

201
Q

Which respiratory measurements are reduced in the obese?

A

Tidal volume
Vital capacity
TLC
FRC

minute ventilation increased

202
Q

What are the types of opioid receptor?

A

δ (located in CNS)- Accounts for analgesic and antidepressant effects

k (mainly CNS)- analgesic and dissociative effects

Mu (central and peripheral) - causes analgesia, miosis, decreased gut motility

Nociceptin receptor (CNS)- Affect of appetite and tolerance to Mu agonists.

203
Q

What is the enzymatic sequence for the creation of adrenaline?

A

Tyrosine –> Dopamine (by DOPA decarboxylase) –> NA –> A

204
Q

What is the cause of toxic shock syndrome?

A

Exotoxin mediated illness most commonly by group A Strep (usually bad skin infection empyema, septic arthritis, new fasc) or Staph Aureus (more likely with tampons etc - menstrual vs non-menstrual)

205
Q

What are risk factors for toxic shock syndrome?

A

DM
Alcoholism
Injuries or surgical procedures

206
Q

What blood tests might be suggestive of necrotising fasciitis?

A

CRP>150
WCC>25
Creatinine >141
Glucose >10
Hb<110
Sodium <135

Laboratory risk indicator for necrotising fasciitis (LRINEC)

207
Q

In septic shock, when is Sodium bicarb indicated?

A

pH≤7.2 and AKI 2-3

208
Q

In sepsis when should enteral feeding be instituted?

A

within 72 hours

209
Q

Which muscle abducts the vocal cords?

A

Posterior cricoarytenoid (innervated by RLN)

210
Q

How are blood products stored?

A

PRC 35 days at 4 degrees
Platelets 5 days at 22
FFP 36 months at -25

211
Q

What clotting factors are made in the liver?

A

Hepatocytes - 2,5,7,9,10,11,12CS
Sinudoidal epithelial 8 and vWF

212
Q

What is the role of the liver in lipid metabolism?

A

TG —> glycerol and FAs
Glycerol —> glycolysis pathway
FAs —> beta oxidation into ketone bodies and can be used for energy

Also involved in lipogenesis and synthesis of VLDL

213
Q

What pressure is diagnostic of compartment syndrome?

A

Compartment pressure >30 (normal 0-8)
Perfusion pressure - DPB - CP <30

214
Q

What is the pressure of TED stockings?

A

18 at ankle
14 at calf
8 at popliteal

215
Q

How should patients with status epileptics be managed?

A
  • Initially protect patient, give oxygen + airway in inter-octal period, recovery position and IV access
  • Give Iv Lorazepam 4mg at 2mg/min (or 10mg IV diazepam or 10mg buccal midazolam) (0-10mins)
  • Then, measure glucose, consider thiamine, do bloods including gas, consider aetiology. If still fitting repeat once within 10-20minutes
    -Established status at 10-30minutes
  • 2nd line (ITU) –> Phenytoin (or valproate) –> GA
216
Q

How much energy is contained in Fat, Glucose and protein?

A

9.3kcal/g, 4.1kcal/g, 4.1kcal/g

217
Q

What are the advantages of jejunostomy over gastrostomy?

A

Less leakage
Gastric and pancreatic secretions reduced (Stomach bypassed)
Less nausea, vomiting or bloating
Reduced risk of pulmonary aspiration

218
Q

What is the lifetime risk of OPSI after splenectomy?

A

About 5%

219
Q

How is a ‘massive tranfusion’ defined?

A

> 10 units PRC in 24 hours (cf massive haemorrhage)

220
Q

How would you manage a blocked CVC?

A

Check simple things - Kinks, clamps, change bionector and see if positional.
Try and flush with 10mls N saline
Try and milk line with Heparinised saline (10u/ml)
Urokinase lock for 24 hours

221
Q

What are the common causes of acute severe hypercalcaemia and how does it present?

A

Malignancy (PTHRP from RCC, Lekaemias, Lymphomas and SCC Lung)
Hyperparathyroidism
Thyrotoxicosis, Milk-Alkali syndrome, Renal failure

When severe >3.5 –> lethargy, confusion, coma
Milder –> cognitive dysfunction, stone disease, constipation, pancreatitis, muscle weakness, dehydration

222
Q

How is acute severe hypercalcaemia best treated?

A

Aggressive fluid resuscitation –> NaCL (2-4L/day)
Check PTH +/- Urinary Calcium
Then Furosemide +/- calcitonin
If malignant –> Pamidronate (avoid if primary hyperparathyroidism)

223
Q

What are the causes of hypocalcaemia and how does it present?

A

Low PTH (Post op, autoimmune)
High PTH (vitamin D deficiency, CKD, psuedo - proteins, pH derangement, pancreatitis, sepsis, hypomagnesiamia, blood transfusion)

If severe - seizures, tetany, paraesthesia, psychiatric manifestations, carpopedal spasm (Trousseaus sign), Chovstek’s sign - tapping facial nerve –> contraction, QTc prolongation)

224
Q

What is the treatment of acute severe hypocalcaemia?

A

Confirm diagnosis, ECG, establish cause
IV replacement if symptomatic or ECG changes
1-2g of Ca Gluconate (preferred over chloride, reduced risk of tissue necrosis)

225
Q

What is the treatment of acute severe hypocalcaemia?

A

Confirm diagnosis, ECG, establish cause
IV replacement if symptomatic or ECG changes
1-2g of Ca Gluconate (preferred over chloride, reduced risk of tissue necrosis)

226
Q

What is PEEP?

A

pressure applied by ventilator at end one each breath to ensure that alveoli are not so prone to collapse

227
Q

What are the common causes of postoperative pyrexia?

A

Defined as >38 on 2 days or >39. Occurs in about 10% of patients

Immediate - malignant hyperthermia, bacteraemia, gas gangrene, FNHTR
Acute (1-3) - Pyretic response to surgery, atelectasis/pneumonia
Acute (5-7) - PE, thrombophlebitis, wound infection, anastomotic leak, UTI
Subacute (7-10) - Deep infection/abscess
Delayed - wound infection, viral infections

228
Q

How should a carotid puncture by CVC be managed?

A

Surgical repair if catheter ≥7Fr (i.e. all CVCs)
Risk of death 20% and Stroke 30%

Go to theatre, gain proximal and distal control, heparinise patient
Occlude vessels and remove catheter. Repair primarily or with vein patch

229
Q

What are the physiological consequences of pregnancy?

A

Pulmonary - increased TV and RR, respiratory alkalosis
CVS - increased CO, HR, Blood volume, decreased HCT/Hb

230
Q

What are specific considerations of the management of pregnant trauma patients?

A
  • Thoracostomy 1-2 spaces higher than normal
  • Higher threshold for vasopressors
  • Left lateral tilt (nb spinal cord)
  • If ≥23 weeks, foetal monitoring for at least 4 hours
  • do not delay imaging
  • anti-D immunoglobulin
231
Q

What are blood substitutes available?

A

Iron/TXA/Cell salvage
EPO
Volume expanders

no real alternatives - perfluorocarbons, synthetic haemoglobins - not licensed

232
Q

What is the INR?

A

Ratio of Prothrombin time to control
PTT = time to form clot by activating extrinsic pathway

233
Q

What clotting factors are involved in the extrinsic, intrinsic and common pathways?

A

Extrinsic - Tissue Factor (III) + VII –> Activation of X
Intrinsic - Damage - XII, XI, IX, VIII –> Activation of X

Common –> Xa+Va –> II, I, XIII

234
Q

What are the causes of a prolonged PT?

A
  • Warfarin, too high dose, interactions with meds
  • Liver disease (Factor production apart from 8)
  • Vitamin K deficiency
  • DIC
    -APS
235
Q

What is a resuscitative thoracotomy and its indications?

A

A left anterolateral or clamshell thoracotomy performed for life threatening injuries of the chest that gives rapid access to the thorax and the ability to treat:

-Pericardial tamponade
-Myocardial injuries
- Perform internal defibrillation/CPR
- Potentially hilar lung injuries

Indications
- Penetrating chest trauma with loss of vital signs and <15mins of CPR (10-15% survival)
- Blunt chest trauma with observed loss of vital signs (2-3% survival)

236
Q

How does velocity influence gun shot wounds?

A

GSW are high energy and can be divided into
High velocity - >2000ft/s - damage spread beyond track, more cavitation (pressure changes and bullet yawing)
Low velocity - <2000ft/s - damage limited to track

237
Q

What are the indications for laparostomy?

A

Abdominal compartment syndrome
Inability to close abdomen
Possible planned return to theatre (although risk of fascial retraction)

238
Q

How is neurogenic shock mediated and treated?

A

Usually high spinal cord injury leading to autonomic dystregulation (loss of sympathetic tone), can be seen in GBS, spinals, transverse myelitis

Treatment - haemodynamic stabilisation, fluid resuscitation, vasopressors/inortropes
If bradycardia then can hive atropine/glycopyrrolate as well

Prevention of further spinal cord injury

239
Q

What is the pathophysiology of OPSI?

A

Loss of opsonisation, less macrophages that recognised IgG/C3b bound bacteria

240
Q

How are pressure sores graded?

A

Grade 1 Skin discolouration
Grade 2 - Some tissue loss
Grade 3 - necrosis limited to skin
Grade 4 - necrosis extending deep to skin (tendons, joint or bone)

241
Q

What are the common causes of hypoalbuminaemia?

A

Liver disease
Heart failure
Malnutrition
Nephrotic syndrome
Protein losing enteropathies

Body produces about 10-15g/day, 40% Intravascular, half life of 30d

242
Q

How do TEDS work?

A

Pressure gradient from ankle upwards
Compresses veins in the leg and prevents them from expanding and pooling of blood, encouraging upwards flow
Replaces calf muscle pump

243
Q

What are the physiological consequences of obstructive jaundice?

A

Local effects - cholangitis, sepsis, chronically can progress to cirrhosis

Liver effects
– reduction of cholesterol/phospholipid secretion
– Backflow of substances secreted by liver - bile salts (reduces aerobic metabolism)
– inhibition of Cp450
–reduced synthesis of albumin, coagulation factors and immunoglobulins

GI effects - reduced mucosal integrity (bile salt blockage) –> sepsis/HRS
– endotoxin from endogenous bacteria

Other - ARF, coagulation disturbance, poor wound healing

244
Q

How can metabolic acidosis be classified?

A

4 causes - increased acid production, decreased acid secretion, loss of bicarbonate (renal/GI) or acid ingestion

Anion gap - Na - Cl + HCO3, normally 6-12 (can be affected by albumin)
High anion gap (usually lactate, but also DKA, methanol, other poisons)
Normal anion gap (loss of bicarbonate - diarrhoea/RTA)

245
Q

Examples of essential amino acids?

A

Leucine, Lysine, methionine

246
Q

What is the bodies response to fasting/starvation?

A

Early (12-24 hours)
- Glyogenolysis, gluconeogensis (Fa+ Glycerol)
- Glucose based energy consumption

Late (7 days)
- Gluconeogensis from AAs
- Ketogenesis from Fats
- Mixed energy consumption

Post-absorptive phase - gylogenolysis
Gluconeogenic phase - protein catabolism –> glucose for brain, others ketones
Protein conservation phase - decreased protein catabolism, FAs everywhere and ketones (CNS)

247
Q

What is the metabolic response to trauma?

A

Hyperacute Ebb phase - sympathetic driven, decreased BMR/perfusion/temp to preserve life in hypovolaemic shock, mediated by adrenals (all), fall in insulin and gluconeogensis

Flow catabolic (3-10 days) - maintenance of energy - increased BMR/Temp/O2 consumption, negative nitrogen balance), mediated by adrenals and insulin/glucagon

Flow anabolic (10-60) - replacement of lost tissue - +ve nitrogen balance, GH, IGH

248
Q

What is the aetiology of ileus?

A

Prolonged surgery, presence of sepsis, ?Open surgery, significant bleeding, prolonged starvation, bowel handling

Exclude mechanical obstruction

Treat with IVF/electrolytes, NGT decompression. No evidence for gastrograffin. May need to consider TPN

249
Q

What are the indications for tracheostomy?

A

Longer term ventilation
Airway obstruction
Failed intubation
Laryngeal trauma
Bilateral vocal cord palsies

250
Q

What are the problems with mechanical ventilation in patients with COPD?

A

Increased airway resistance/decreased compliance
Dynamic hyperinflation leading to auto-PEEP which increases work of breathing, compromises cardiac function

Predisposes to barotrauma and intrinsic lung injuries

251
Q

What are the problems with mechanical ventilation in patients with COPD?

A

Increased airway resistance/decreased compliance
Dynamic hyperinflation leading to auto-PEEP which increases work of breathing, compromises cardiac function

Predisposes to barotrauma and intrinsic lung injuries

252
Q

How can DIC be diagnosed?

A

ISTH score, combining Platelet count, PT, Fibrinogen, and FDP/D-dimer

253
Q

What is trauma triage?

A

Priority 1/Red - Immediate life saving intervention needed
Priority 2/yellow - significant intervention within 2 hours
Priority 3/green - care needed but can be delayed
Dead/black

254
Q

What are the differences between Type 1 and Type 2 pneumocytes?

A

Type 1 - gas exchange
Type 2 - surfactant secretion

255
Q

What criteria suggest readiness for extubation?

A

Complex, about 15% failed extubation

1) Determine disease resolution.
2) No imminent need for return to theatre
3) A/B - Adequate oxygenation and gas exchange (FiO2<40%)
4) C - stable on minimal drugs
5) D - rousable of sedation with GCS of at least >8 8
6) E - electrolytes, haemoglobin, sepsis controlled

256
Q

What is severe aortic stenosis?

A

AVA<1cm2, peak velocity of >4m/s or gradient of ≥40mmHg
Symptoms of angina, syncope, dyspnoea

Unable to increase outflow during stressor e.g. induction of anaesthesia leading to CV collapse. Also influenced by LVH due to pressure overload, low myocardial compliance and poor coronary reserve

Hypotension –> iscahemia and downward spiral

257
Q

What are the differences between epidural and spinals?

A

–Epidural placed in extradural space, spinal into subdural space, usually below L3 (where cord ends - conus medullar is)
– Spinal onset 5 vs 30 mins, duration 2-4 hours vs longer
– Spinal requires smaller doses of drug and better analgesia than epidural but single shot
– Spinal gives profound motor/sensory block below the injection

258
Q

After an epidural, what order are functions affected?

A

Unmyelinated fibres before myelinated fibres
B fibres –> Sympathetic
C fibres –> cold
Ad fibres –> pin prick
AB fibres –> touch
Aa fibres –> motor

259
Q

What drugs are typically used in a spinal or epidural?

A

Mostly local anaesthetics e.g. bupivicaine and opiates e.g. diamorphine/fentanyl that give prolonged duration of analgesia

260
Q

How does morphine produce analgesia?

A

Affinity for delta/kappa/mu opioid receptors

Net effect is activation of descending inhibitory CNS pathway from midbrain (mu) and inhibition of the peripheral nociceptive afferents

261
Q

How would you compare rectus sheath vs epidural?

A

Trial by Yassin 2017- RSA - early mobilisation but higher opiate usage
Krige BSJ Open 2022 - RSA higher pain score at 24 hours but less at 72 hours with lower opiate usage, hypotension/vasopressor dependence

262
Q

How should increasing pain with epidural be managed?

A
  • Exclude clinical problems
  • Involve pain team/anaesthetist
  • Consider increasing rate up to 25% and tilting if block uneven
  • Consider adjuncts
263
Q

How should epidural related hypotension be managed?

A
  • Exclude clinical problems
  • Involve pain team/anaesthetist
  • If 90-100, slow rate
  • If <90, stop epidural and lay flat + fluids

Caused by blockade of sympathetic afferents

264
Q

Where are baroreceptors located and what is their function?

A

Aortic arch (X) + Carotid sinus (IX)
Stretch sensitive mechanoceptors –> Low blood pressure leads to less activation of negative feedback loop relayed to NTS, decreased parasympathetic and increased sympathetic activity

Increased HR/SVR

265
Q

What are the investigations pertinent to carbon monoxide poisoning?

A

–COHb cannot be differentiated from OHb so SpO2 doesn’t work
–Identified on Hb usually 3-4% in non smokers –> 10% in smokers
– >20 adult/15 children significant

266
Q

What factors influence exercise tolerance?

A

Pulmonary gas exchange
Cardiovascular performance
Skeletal muscle metabolism

VO2Max = (SVMax x HR Max) x (CaO2 max - CvO2 max)

267
Q

What are important measurements in CPET?

A

AT <10 = high risk
AT 10-18 + VE/VCO2 slope ≥35 = high risk
AT 10-18 + VE/VCO2 slope <35 = moderate risk
AT >18 = low risk

268
Q

What values are measured in spirometry and what do they mean?

A

Forced vital capacity - FVC ≤80% predicted = abnormal (mean 4L)
Forced expiratory volume in 1 s (FEV1) <80% = normal (mean 3.5L)
FEV1/FVC ratio <0.7 = COPD (or FEV1<75%) NICE

269
Q

What are the CLOT and CATCH trials?

A

Showed LMWH > Warfarin for treatment of cancer associated VTE.

270
Q

What is the maximum peripheral potassium infusion rate?

A

Usually no more than 10mmol/hr, if >20mmol/hr will need cardiovascular monitoring

271
Q

How is shock defined?

A

Acute circulatory failure leading to inadequate tissue perfusion and cellular hypoxia

272
Q

How would you assess tissue perfusion?

A

Cool peripheries/CRT>2s
Poor vein filling
Increased RR
Poor UO <0.5ml/kg/hr
Restlessness/consufion
Metabolic acidosis

273
Q

What types of shock are common in postoperative patients?

A

Hypovolaemic/haemorrhagic - NBM, 3rd spacing, secondary haemorrhage
Septic
Cardiogenic - MI
Obstructive - PE

274
Q

How should postoperative patients with shock be assessed?

A

Assess for evidence of end-organ dysfunction and recent fluid balance
Resuscitation with fluid bolus unless evidence of cardiac failure
Initial investigations including blood tests, ABG, CXR, ECG
Assess response to fluid bolus - if brisk then likely sepsis/hypovolaemia
If overloaded will likely need CVC/HDU

275
Q

How can filling status/cardiac function be assessed?

A

Clinical markers of organ perfusion especially UO
CVP (should be >8, >15 = CHF)
A-Line –> LIDCO/PICCO (pressure waveform/AUC)
PAWP
TO-doppler

276
Q

What are the causes of postoperative ileus?

A

Impairment of basal electrical activity post procedure
Lack of stimulus of feeding (cf chewing gum)
Inhibition from anaesthetic agents, opioids, bowel handling

277
Q

What vaccinations are required for patients who have had a splenectomy?

A

Annual Flu
Pneumococcus + 5 yearly
HiB/MenC

Men B x 2
Conjugate Men ACWY

FRCS General Section 1/2 (13 decks)

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