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High Yield Facts for the Final FRCA > Resuscitation > Flashcards

Resuscitation Flashcards

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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
Which criteria are used for the diagnosis of serotonin syndrome?
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
26
What are the three components of serotonin syndrome?
Mixture of mental status change, neuromuscular abnormalities, and autonomic hyperactivity Occurs within 24 - 48 hours of trigger, usually a change in medications
27
How many serotonin receptor types are there and how do they work?
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
28
What is the Rule of Nines for estimating burn surface area?
Head and neck - 9% Chest and abdomen - 18% Back - 18% Upper limbs - 9% each Lower limbs - 18% each Genitalia - 1%
29
What are the priorities of immediate management in a patient presenting with septic shock?
Oxygen Antibiotics (broad spectrum until cultures back) Blood cultures Fluid challenge Lactate and haemoglobin measurement Urine output measurement
30
What is the definition of massive pulmonary embolism?
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
What are the absolute and relative contraindications to thrombolysis?
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
What is the only intervention proven to improve survival rates after cardiac arrest with return of spontaneous circulation?
Therapeutic hypothermia
33
What is the METHANE acronym for declaring a major incident?
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
What are the management priorities in a major trauma patient with limb injuries and major haemorrhage?
- 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
What are the functions of the spleen?
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
What are the benefits of non-operative management in minor splenic injury?
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
What are the causes of distributive shock?
- Sepsis - Anaphylaxis - Neurogenic shock - Acute adrenal insufficiency
38
What signs may be seen in methyl alcohol poisoning?
Metabolic acidosis Kussmaul breathing Papilloedema Low bicarbonate
39
What is methyl acohol metabolised to?
d-formaldehyde and formic acid
40
What are your immediate pharmacological options for managing intraoperative bronchospasm?
- 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
What other actions might you take while treating intraoperative bronchospasm?
- 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
What are the chronic pathophysiological changes seen in asthma?
- Chronic inflammation - Mucosal oedema - Bronchial smooth muscle contraction and hypertrophy - Infiltration of inflammatory cells
43
What are the potential triggers for intraoperative bronchospasm?
- 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
What is the classic triad of fat embolism?
Acute respiratory distress Neurological derangement Petechial rash
45
What is anaphylaxis?
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
What are the other possible causes, apart from anaphylaxis, of high airway pressures?
Bronchospasm Asthma Endobronchial intubation Tension pneumothorax Pneumoperitoneum causing diaphragmatic splinting Blockage or kinking of tubing
47
What is the immediate management of anaphylaxis?
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
What are the recommended doses for adrenaline in paediatric anaphylaxis?
>12 years old - 500mcg IM 6-12 years old - 300mcg IM <6 years old - 150mcg IM
49
According to the sixth national audit project (NAP 6) what are the four most common causes of perioperative anaphylaxis?
Antibiotics Muscle Relaxants Chlorhexidine Patent blue dye
50
What is pulsus paradoxus and in what conditions is it seen?
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
Do you know any diagnostic criteria for malignant hyperthermia?
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
Which drugs are known triggers of malignant hyperthermia?
Halothane Isoflurane Enflurane Sevoflurane Desflurane Suxamethonium
53
Which common anaesthetic drugs are considered safe in malignant hyperthermia?
Propofol and all other intravenous induction agents Nitrous Oxide Benzodiazepines Non-depolarising muscle relaxants Local anaesthetics Opioids All analgesics Glycopyrrolate Atropine Metoclopramide Neostigmine
54
What are the late signs of malignant hyperthermia?
Rise in body temperature Rise in CK Generalised rigidity Myoglobinuria DIC Cardiac arrhythmias
55
What is the differential diagnosis for malignant hyperthermia?
Inadequate depth of anaesthesia Anaphylaxis Sepsis Thyrotoxicosis Ischaemia Phaeochromocytoma Myopathy
56
How would you anaesthetise a patient with a family history of malignant hyperthermia?
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
How can you test for malignant hyperthermia?
Genetic testing Muscle biopsy Caffeine halothane contracture test Note that genetic testing cannot rule out susceptibility to MH
58
What are the clinical features of malignant hyperthermia?
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
What is the genetic defect in malignant hyperthermia?
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
What is the immediate management of malignant hyperthermia?
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
What are the Association of Anaesthetists recommendation for use of intraoperative cell salvage?
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
What are the complications of allogenic blood transfusion?
Febrile reactions Anaphylaxis Haemolysis Transfusion associated circulatory overload (TACO) Transfusion associated lung injury (TRALI) Transmission of infection Immunosuppression
63
What are the waste products of cell salvage?
Plasma Clotting factors Anticoagulant Free haemoglobin White cells Platelets Bone fragments Fat Bacteria Squames
64
What are the complications of cell salvage?
Air embolism Fat embolism Electrolyte disturbance Febrile reactions Microemboli Infection Haemolysis and release of haemoglobin causing AKI Salvaged blood syndrome
65
What is 'salvaged blood syndrome'?
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
What substances should not be suctioned during cell salvage?
Chlorhexidine Iodine Antibiotics that cannot be given IV Topical clotting agents Orthopaedic cement Glue
67
What are the steps of cell salvage?
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
What are the advantages of using cell salvage over donor blood?
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
What medications should be given in acute severe asthma?
Oxygen to aim for sats >94% Back to back salbutamol nebulisers 2.5 - 5 mg Ipratropium nebulisers 500 mcg Magnesium sulphate IV 2g over 20 minutes Hydrocortisone 100 - 200mg IV or Prednisolone 50mg PO Aminophylline 5mg/kg at 25mg/min Consider IM adrenaline 0.5mg
70
What are the features of life threating asthma?
PEFR <33% predicted Silent chest Normal or raised PaCO Bradycardia Arrhythmia Hypotension Exhaustion Confusion or reduced GCS
71
What are the benefits of ketamine in asthma?
Bronchodilation via NMDA antagonism Maintains cardiovascular stability Preserves respiratory drive Allows a DSI approach to facilitate monitoring and preoxygenation
72
What is dynamic hyperinflation?
The bronchoconstriction reduces airway diameter This increases resistance to airflow This makes inspiration harder It also makes expiration much slower, leading to gas trapping when the ventilator delivers the next breath too soon You can see this on your ventilator flow diagram, as the flow doesn't return to zero before the next breath is delivered This needs a much smaller I:E ratio (such as 1:4 or 1.5) to allow that gas to escape What are the risks? Rising intrathoracic pressure → reduced venous return → hypotension and cardiac arrest Barotrauma → pneumothorax Worsening gas exchange → hypercapnia and hypoxia What do I do about it? Reduce respiratory rate Increase expiratory time Lower tidal volumes Monitor for auto-PEEP
73
What initial ventilator settings should you use for an intubated asthmatic?
PEEP <5cmH2O Resp rate 8 - 10 I:E ratio at least 1:4 up to 1:8 Pmax <35cmH2O 6 ml/kg IBW Tidal volume Permissive hypercapnia
74
What should you do if an intubated asthmatic's airway pressures are rising and blood pressure is dropping?
You're probably either looking at a tension pneumothorax or dynamic hyperinflation. Have a listen both sides and look at the chest expansion Look with ultrasound if immediately available and you have the requisite skillset If one side quieter and more inflated, consider needle decompression If bilaterally hyperinflated then consider detaching from the vent and manually decompressing with firm steady pressure over the anterior chest wall Either way a fluid bolus is probably a good idea too.
75
What are the risks of mechanical ventilation in asthma?
Barotrauma Dynamic hyperinflation Dyssynchrony ITU weakness (after prolonged neuromuscular blockade and steroids)
76
How do β-Agonists treat asthma?
Bind to G-protein coupled receptors on bronchial smooth muscle Activates adenylate cyclase Increased conversion of ATP to cAMP This sets off a cascade with the following results: Inhibits myosin phosphorylation Lowers intracellular calcium Inhibition of mast cell degranulation Hyperpolarisation of smooth muscle cells
77
What intravenous agents can be used to treat bronchospasm?
Adrenaline 10 - 100mcg Salbutamol 100 - 250mcg Magnesium 2g Ketamine 20 - 30mg Aminophylline 5mg/kg Hydrocortisone 200mg
78

High Yield Facts for the Final FRCA (22 decks)

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