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High Yield Facts for the Final FRCA > Resuscitation > Flashcards

Resuscitation Flashcards

1
Q

A 42 year old male with no known allergies is undergoing an emergency laparotomy for a perforated diverticulum.

After induction of anaesthesia and intubation, you administer co-amoxiclav, soon after which the patients heart rate increases to 174 bpm and his blood pressure falls to 44/26mmHg.

What is the appropriate immediate management for this patient?

  1. IV adrenaline 50mcg
  2. IM adrenaline 500mcg
  3. Fluid resuscitation with 250ml Plasmalyte
  4. Chlorphenamine 10mg IV
  5. Start cardiopulmonary resuscitation
A
  1. Start cardiopulmonary resuscitation

This is anaphylaxis, for which adrenaline is the key treatment, however according to the AAGBI guidelines, if the systolic blood pressure drops below 50mmHg then CPR should be started immediately.

Fluid resuscitation is also important, but should be given after adrenaline.

Chlorphenamine plays no role in the immediate management of anaphylaxis.

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2
Q

A 49 year old woman with a previous medical history of hypertension, hypercholesterolaemia and heavy smoking undergoes insertion of a central venous catheter while on the intensive care unit, to facilitate administration of concentrated potassium and vasopressors.

She becomes suddenly breathless and a portable chest xray demonstrates a pneumothorax measuring 1.8cm at the hilum. What is the most appropriate management for this pneumothorax?

  1. Insert surgical chest drain
  2. 100% oxygen for 48 hours and repeat chest xray
  3. Insert 8-14Fr Seldinger chest drain
  4. Aspirate with 16-18 gauge cannula
  5. Observe closely and repeat chest xray in 24 hours, or if becomes more symptomatic
A
  1. Aspirate with 16-18 gauge cannula

This woman has a heavy smoking history, making this a secondary pneumothorax.

Since it measures less than 2cm at the hilum, it should first be aspirated with a 16-18 gauge cannula, with total volume aspirated less than 2.5 litres.

A chest drain is only required if this does not resolve the pneumothorax.

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3
Q

What are the endogenous ketone bodies?

A

3-beta-hydroxybutyrate
Acetoacetate
Acetone

3-beta-hydroxybutyrate is the main ketone body and is the one tested for when treating DKA.

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4
Q

What are the serious complications of diabetic ketoacidosis

A
  • Hypokalaemia
  • Hypoglycaemia
  • Acute Kidney Injury
  • Cerebral oedema
  • Death
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5
Q

What ECG changes can occur in diabetic ketoacidosis?

A
  • Peaked T waves
  • Broad QRS
  • Absent P waves
  • Ventricular fibrillation
  • Asystole
  • ST Elevation
  • Ectopic beats
  • Escape rhythm
  • Bundle branch block
  • Sine wave
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6
Q

What is the immediate management of diabetic keto acidosis with Hyperkalaemia?

A
  • 10ml of 10% calcium gluconate or chloride
  • 50ml of 50% dextrose with 10 units insulin
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7
Q

How does diabetic ketoacidosis develop?

A

Lack of insulin means cells cannot take glucose up from the body, and there is an increase in glucagon, growth hormone and cortisol release as a result.

This leads to increased gluconeogenesis and glycogenolysis.

Lipolysis increases, resulting in beta-oxidation of fatty acids to produce ketoacids.

These dissociate to produce a high anion gap metabolic acidosis.

The concentration of glucose in the blood exceeds the proximal convoluted tubule’s ability to reabsorb glucose, and this results in glycosuria.

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8
Q

What are the diagnostic features for diabetic ketoacidosis?

A

Blood sugar >11mmol/litre
Ketones >3mmol/litre
Bicarbonate <15mmol/litre or pH <7.30

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9
Q

What is the Parkland Formula?

A

This is equal to 4ml per kilogram bodyweight, per % surface area burned

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10
Q

What are the anaesthetic concerns in a burns patient?

A

Airway compromise
Hypothermia
Blood loss
Overactive metabolism
Severe pain
Changes in pharmacokinetics and drug handling
Monitoring difficulties

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11
Q

What are the risk factors for increased mortality in burns patients?

A

Elderly patients
More significant burns
Airway compromise
Significant comorbidities

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12
Q

What are the commonest causes of death in burns patients?

A

Multiple organ failure
Sepsis
Burn shock
Inhalational injury

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13
Q

What are the indications for early intubation in burns patients?

A

GCS less than 8 or airway reflexes not intact
Added sounds such as snoring or stridor
Inadequate oxygenation with hypoxaemia
Inadequate ventilation with hypercapnoea
Deep facial or neck burns
Any evidence of swelling of the oropharynx

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14
Q

What muscle relaxant should you use in burns patients?

A

The one you are most confident with!
Rocuronium is safe in burns patients
Suxamethonium is safe in the first 24 hours after the burn injury
Between 24 hours and 1 year after the injury, the upregulation of extra-junctional receptors gives a greater risk of potentially fatal hyperkalaemia

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15
Q

What are the three components of airway injury in burns?

A

Upper airway thermal injury

  • The mouth, tongue, pharynx and epiglottis can receive a huge amount of thermal energy by the inhalation of superheated fumes, causing them to swell significantly, leading to the following clinical signs:
    – Stridor
    – Hoarse voice
    – Swollen Uvula

Lower airway thermal injury

  • This is caused less by the direct heating that is seen in the upper airway, and more by the inhaltion of material that is still burning. This strips the epithelium of the trachea and large airways, stimulating production of mucus and release of inflammatory mediators.
    This can lead to bronchospasm and mucus plugging, with airway obstruction and alveolar collapse.
    Signs and symptoms include:
    – Very productive cough
    – Wheeze
    – Shortness of breath
    – Mucosal hyperaemia and ulceration

Noxious gas poisoning
- particularly carbon monoxide

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16
Q

What are the symptoms of carbon monoxide poisoning?

A

Headache
Nausea and vomiting
Reduced consciousness
Collapse
Convulsions

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17
Q

What effects does carbon monoxide have on tissue oxygenation?

A

Left shift in the oxyhaemoglobin dissociation curve, reducing haemoglobin’s ability to deliver oxygen to the tissues
Uncoupling of oxidative phosphorylation, producing a histotoxic hypoxia
A persistent lactataemia in a patient that has received adequate fluid resuscitation should make you think of cyanide poisoning

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18
Q

How can you calculate how much of the body has been burned?

A

Total body surface area
Depth
Lund and Browder Chart
Rule of Nines in adults

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19
Q

In which three locations is serotonin made?

A

Enterochromaffin cells of GI tract
Serotoninergic CNS neurons
Platelets

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20
Q

What metabolite of serotonin can be found in the urine?

A

5-hydroxyindole acetic acid (5-HIAA)

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21
Q

What CNS effects does serotonin have?

A

Modulates pain transmission at spinal level
 
Contributes to hypothalamic/sympathetic regulatory mechanisms
 
Modulates chemoreceptor trigger zone/vomiting centre
 
Influences arousal, muscle tone, mood, and memory

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22
Q

What cardiovascular effects does serotonin have?

A

Splanchnic, renal, pulmonary, and cerebral vasoconstriction

Amplification of local actions of noradrenaline, angiotensin II, and histamine
 
Increased vascular permeability and platelet aggregation

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23
Q

What is thought to be the underlying pathophysiological trigger for serotonin syndrome?

A

Thought to be from hyperstimulation of 5-HT1a and 5-HT2 receptors in medulla and central grey nuclei

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24
Q

What is the treatment for serotonin syndrome?

A

Stop any drugs that increase serotonin
Supportive therapy
Self-resolves within 24 hours - rarely fatal - usually good prognosis if spotted early
Benzodiazepines for anxiolysis and seizures
Cyproheptadine has also been used (antihistamine that also has anti-serotonin activity)

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25
Q

Which criteria are used for the diagnosis of serotonin syndrome?

A

Sternbach criteria

Four major or (3 major + 2 minor) features

Major:

Confusion
Elevated mood
Coma
Fever
Sweating
Clonus
Hyperreflexia
Tremor
Rigidity
Shivering

Minor:

Hyperactivity
Agitation
Restlessness
Insomnia
Tachycardia
Tachypnoea
Labile blood pressure
Flushing
Incoordination
Mydriasis
Akathisia
Ataxia

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26
Q

What are the three components of serotonin syndrome?

A

Mixture of mental status change, neuromuscular abnormalities, and autonomic hyperactivity

Occurs within 24 - 48 hours of trigger, usually a change in medications

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27
Q

How many serotonin receptor types are there and how do they work?

A

7 classes 5HT1–7 with different subtypes e.g. 5-HT2a

Over 14 different subtypes

All act via G-Proteins and cAMP, apart from 5HT-3, which acts via a ligand-gated ion channel

5HT-3 receptors act in GI tract and CNS to generate emetic response, hence inhibitors of 5HT-3 receptors (like ondansetron) are effective antiemetics

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28
Q

What is the Rule of Nines for estimating burn surface area?

A

Head and neck - 9%
Chest and abdomen - 18%
Back - 18%
Upper limbs - 9% each
Lower limbs - 18% each
Genitalia - 1%

29
Q

What are the priorities of immediate management in a patient presenting with septic shock?

A

Oxygen
Antibiotics (broad spectrum until cultures back)
Blood cultures
Fluid challenge
Lactate and haemoglobin measurement
Urine output measurement

30
Q

What is the definition of massive pulmonary embolism?

A

Massive pulmonary embolism (PE) is defined as

PE with hypotension
- either systolic BP <90mmHg or
- a pressure drop ≥40 mmHg for more than 15 minutes
- that is not caused by a
cardiac arrhythmia, hypovolaemia or sepsis.

31
Q

What are the absolute and relative contraindications to thrombolysis?

A

Absolute

  • Anticoagulated or coagulopathic patient
  • Recent major surgery or head injury within 3 weeks
  • Stroke within 6 months
  • Previous haemorrhagic stroke
  • GI bleed within 1 month
  • Aortic dissection
  • Any CNS disorder such as tumour
  • Acute pancreatitis
  • Bacterial endocarditis or pericarditis

Relative

  • BP >180mmHg systolic or >100mmHg diastolic
  • Long CPR duration
  • Known GI ulcer
  • Pregnancy or within 1 week of post partum
32
Q

What is the only intervention proven to improve survival rates after cardiac arrest with return of spontaneous circulation?

A

Therapeutic hypothermia

33
Q

What is the METHANE acronym for declaring a major incident?

A

Major incident to be declared
Exact location
Type of incident
Hazards, both current and potential
Access and approach routes
Number of casualties and type
Emergency services already present and required

34
Q

What are the management priorities in a major trauma patient with limb injuries and major haemorrhage?

A
  • Primary survey
  • C spine immobilisation
  • IV access - wide bore x2
  • Major haemorrhage resuscitation with blood products - O negative blood until matched blood available
  • Cross match blood and matched blood transfusion as soon as possible
  • Permissive hypotension
  • Oxygen
  • Analgesia
  • Neurovascular examination of injured limbs
  • Warming
  • Tranexamic acid
35
Q

What are the functions of the spleen?

A

Storage

  • 250ml of blood
  • 30% of platelets
  • Iron

Metabolism

  • Clearance of old red blood cells
  • Platelet clearance
  • Cleavage of haem from haemoglobin

Immune

  • Lymphocyte storage
  • Macrophage storage
  • Antigen presentation

Synthetic

  • Production of opsonins
  • Haematopoeisis in early foetal life
36
Q

What are the benefits of non-operative management in minor splenic injury?

A

Avoids risk of surgery
Preserves splenic function
Avoids risk of post-operative infection
Reduced cost
Reduced morbidity and mortality
Fewer intra-abdominal complications
Reduced need for transfusion

37
Q

What are the causes of distributive shock?

A
  • Sepsis
  • Anaphylaxis
  • Neurogenic shock
  • Acute adrenal insufficiency
38
Q

What signs may be seen in methyl alcohol poisoning?

A

Metabolic acidosis
Kussmaul breathing
Papilloedema
Low bicarbonate

39
Q

What is methyl acohol metabolised to?

A

d-formaldehyde and formic acid

40
Q

What are your immediate pharmacological options for managing intraoperative bronchospasm?

A
  • Increase volatile agent concentration, if not using desflurane
  • Salbutamol - 8-10 puffs into circuit or 2.5-5mg nebuliser, or 250microgram slow IV bolus
  • Ipratropium 500mcg nebuliser
  • Aminophylline 5mg/kg slow IV
  • Adrenaline 10-100mcg titrated to effect
  • Ketamine 10-20mg bolus or 1-3mg/kg/hour infusion
  • Magnesium 1.2-2g
  • Hydrocortisone 100-200mg

Note that antihistamines play no role in management of bronchospasm.

41
Q

What other actions might you take while treating intraoperative bronchospasm?

A
  • Call for skilled assistance
  • Increase FiO2 to 100%
  • Increase I:E ratio or respiratory rate
  • Manual ventilation
  • Alert surgeon to stop or deflate abdomen
  • Auscultate chest to rule out pneumothorax
42
Q

What are the chronic pathophysiological changes seen in asthma?

A
  • Chronic inflammation
  • Mucosal oedema
  • Bronchial smooth muscle contraction and hypertrophy
  • Infiltration of inflammatory cells
43
Q

What are the potential triggers for intraoperative bronchospasm?

A
  • Inadequate depth of anaesthesia
  • Airway manipulation
  • Desflurane
  • IV drugs
  • Anaphylaxis or anaphylactoid reactions
  • Neostigmine reversal of paralysis
  • Pre-existing LRTI
  • Histamine release from IV drug
  • Aspiration
44
Q

What is the classic triad of fat embolism?

A

Acute respiratory distress
Neurological derangement
Petechial rash

45
Q

What is anaphylaxis?

A

Anaphylaxis is a life-threatening systemic allergic reaction
It is a type 1 immediate hypersensitivity reaction induced by IgE antibodies
The trigger cross-links IgE on mast cells, causing degranulation and release of histamine and other eicosanoids and cytokines

46
Q

What are the other possible causes, apart from anaphylaxis, of high airway pressures?

A

Bronchospasm
Asthma
Endobronchial intubation
Tension pneumothorax
Pneumoperitoneum causing diaphragmatic splinting
Blockage or kinking of tubing

47
Q

What is the immediate management of anaphylaxis?

A

Stop the administration of all agents likely to have caused the anaphylaxis
Call for help
Maintain the airway and give 100% oxygen
Lie the patient flat with the legs elevated
Give adrenaline*
IV crystalloid boluses fluid, understanding that adult patients may require up to 2–4 litres
*This may be given:
IM 0.5–1 mg (0.5–1 ml of 1:1000) - repeated every 10 min as required
IV 50–100 µg i.v. (0.5–1 ml of 1:10 000) over 1 min

48
Q

What are the recommended doses for adrenaline in paediatric anaphylaxis?

A

> 12 years old - 500mcg IM
6-12 years old - 300mcg IM
<6 years old - 150mcg IM

49
Q

According to the sixth national audit project (NAP 6) what are the four most common causes of perioperative anaphylaxis?

A

Antibiotics
Muscle Relaxants
Chlorhexidine
Patent blue dye

50
Q

What is pulsus paradoxus and in what conditions is it seen?

A

Pulsus paradoxus is the exaggerated fall of stroke volume, systolic blood pressure and pulse wave amplitude seen during inspiration in conditions such as:

  • Asthma
  • Cardiac tamponade
  • Constrictive pericarditis
  • Cardiomyopathy
  • Amyloidosis
51
Q

Do you know any diagnostic criteria for malignant hyperthermia?

A

A 1994 consensus conference came up with the following:

  • Respiratory acidosis (end-tidal CO2 above 7.32 kPa or arterial pCO2 above 7.98 kPa)
  • Unexplained tachycardia or arrhythmia
    Metabolic acidosis (base excess lower than -8, pH <7.25)
  • Muscle rigidity
  • CK >20,000 or myoglobinuria, or K >6 mmol/litre
  • Rapidly increasing temperature >38.8 °C
  • Other (rapid reversal of MH signs with dantrolene, elevated resting serum CK levels)
  • Family history

Any 6 and MH is very likely.

52
Q

Which drugs are known triggers of malignant hyperthermia?

A

Halothane
Isoflurane
Enflurane
Sevoflurane
Desflurane
Suxamethonium

53
Q

Which common anaesthetic drugs are considered safe in malignant hyperthermia?

A

Propofol and all other intravenous induction agents
Nitrous Oxide
Benzodiazepines
Non-depolarising muscle relaxants
Local anaesthetics
Opioids
All analgesics
Glycopyrrolate
Atropine
Metoclopramide
Neostigmine

54
Q

What are the late signs of malignant hyperthermia?

A

Rise in body temperature
Rise in CK
Generalised rigidity
Myoglobinuria
DIC
Cardiac arrhythmias

55
Q

What is the differential diagnosis for malignant hyperthermia?

A

Inadequate depth of anaesthesia
Anaphylaxis
Sepsis
Thyrotoxicosis
Ischaemia
Phaeochromocytoma
Myopathy

56
Q

How would you anaesthetise a patient with a family history of malignant hyperthermia?

A

Use regional anaesthesia wherever possible
New breathing circuit
Flush with 100% oxygen maximal flows for 20-30mins
Remove all vaporisers
Use charcoal filters
TIVA

57
Q

How can you test for malignant hyperthermia?

A

Genetic testing
Muscle biopsy
Caffeine halothane contracture test
Note that genetic testing cannot rule out susceptibility to MH

58
Q

What are the clinical features of malignant hyperthermia?

A

Hypermetabolism
Tachycardia
Hypercapnoea
Lactic acidosis
Tachypnoea
Hypoxaemia
Hyperthermia
Rhabdomyolysis
Hyperkalaemia
Cardiac arrhythmia
Myoglobinuria
Acute kidney injury
Disseminated intravascular coagulation
Muscle rigidity
Masseter spasm
Hypertension

Note that an isolated pyrexia in recovery is not concerning for MH if CO2 and heart rate were normal during the operation - the other two must be present for MH to be possible.

59
Q

What is the genetic defect in malignant hyperthermia?

A

Mutation of ryanodine receptor
Usually on the long arm of chromosome 19
Uncontrolled calcium release from sarcoplasmic reticulum into the cell after exposure to a triggering agent - suxamethonium or volatile agent

60
Q

What is the immediate management of malignant hyperthermia?

A

Stop the vapour and call for lots of help
100% oxygen and hyperventilate
Grab a new breathing circuit and stick the charcoal filters from the MH kit on
Keep asleep with propofol and use non-depolarising muscle relaxant
Delegate someone to start drawing up dantrolene
Start cooling the patient down - cool IV fluid, irrigation of body cavities, send someone to get ice, remove blankets and drapes (dialysis and bypass can be used as well if immediately available)
Administer 2.5 mg/kg dantrolene and keep giving up to 10mg/kg - aiming to see a normalisation of heart rate, ETCO2 and temperature

61
Q

What are the Association of Anaesthetists recommendation for use of intraoperative cell salvage?

A

The use of cell salvage is recommended if it is believed it will reduce the need for donor blood, or will avoid severe postoperative anaemia

There should be cell salvage equipment available 24/7 in any hospital where major haemorrhage may be expected, as well as the staff trained to use it

Use of ‘collect only’ mode can be condsidered if blood loss might exceed 500ml or >10% circulating volume or >8ml/kg in children over 10kg

Every hospital should have a nominated clinical lead and coordinator for cell salvage

The patient should be consented appropriately if planning to use cell salvage in surgery for malignancy or infection

The use of leucodepletion filters should be considered for cancer surgery or in cases of sepsis

Cell salvage should not routinely be used in caesarean section, unless clearly anaemic before surgery or at high risk of bleeding

62
Q

What are the complications of allogenic blood transfusion?

A

Febrile reactions
Anaphylaxis
Haemolysis
Transfusion associated circulatory overload (TACO)
Transfusion associated lung injury (TRALI)
Transmission of infection
Immunosuppression

63
Q

What are the waste products of cell salvage?

A

Plasma
Clotting factors
Anticoagulant
Free haemoglobin
White cells
Platelets
Bone fragments
Fat
Bacteria
Squames

64
Q

What are the complications of cell salvage?

A

Air embolism
Fat embolism
Electrolyte disturbance
Febrile reactions
Microemboli
Infection
Haemolysis and release of haemoglobin causing AKI
Salvaged blood syndrome

65
Q

What is ‘salvaged blood syndrome’?

A

This is due to white cell and platelet activation in the centrifuge. Any activated cells that get reinfused can then trigger intravascular coagulation and a SIRS-type response leading to AKI and lung injury

66
Q

What substances should not be suctioned during cell salvage?

A

Chlorhexidine
Iodine
Antibiotics that cannot be given IV
Topical clotting agents
Orthopaedic cement
Glue

67
Q

What are the steps of cell salvage?

A

Collection (via suction or washing swabs) and anticoagulation
Filtration
Separation and washing of red cells
Disposal of waste
Cell salvage (storing prepared red cells in bag for infusion)
Re-infusion

68
Q

What are the advantages of using cell salvage over donor blood?

A

No need to use donor blood (which is in short supply)
Reduced risk of infection transmission
No ABO incompatibility
Superior oxygen delivery as cells are not refridgerated and normal 2,3-DPG levels
Inflammatory cytokines removed
Less postoperative anaemia than when convential transfusion thresholds used
Reduced post operative transfusions on the ward
Lower risk of immunological side effects
No risk of sensitisation to Kell, Duffy or Lutheran antigens
Much lower risk of acute transfusion reaction
Can be used if donor blood not acceptable to the patient
Can be used if rare patient blood group

69
Q
A

High Yield Facts for the Final FRCA (22 decks)

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