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Diploma in Anaesthesia > ACLS > Flashcards

ACLS Flashcards

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1
Q

What are the ACLS updates 2015 versus 2010

A

Any intervention: compression interruption < 5 seconds
Waveform capnography included
Stepwise airway management dependent on patient factors and rescuer skill

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2
Q

Is mechanical chest compression (LUCAS) indicated in the 2015 guidelines?

A

Some circumstances (patient transfer)

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3
Q

Is peri-arrest ultrasound indicated

A

In certain situations in providers with appropriate training

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4
Q

What do the guidelines say about Extracorporeal Life Support techniques

A

May be useful in certain patients where standard measures have failed

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5
Q

What two possible intra-operative conditions require deviation from standard cardiac arrest algorithm

A

Local anaesthetic toxicity

Anaphylaxis

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6
Q

What is the incidence of intraoperative cardiac arrest primarily attributable to anaesthesia

A

1 in 10 000

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7
Q

Classify the the major causes of perioperative cardiac arrest

A

Primary bleeding (Truama/coagulopathy/surgical vessel rupture)

Primary cardiac (MI/Dysrhythmia/block)

Other

  • PE (air/fat/thrombus)
  • Anaphylaxis
  • Hypoxia (Airway/ventilatory complications
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8
Q

What circumstances constitutes cardiac arrest considered to be directly attributable to anaesthesia?

A

Immediate arrest following drug administration

Airway complications and mishaps

(Unstable patients arresting on induction were not considered having arrested primarily due to anaesthesia)

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9
Q

List in descending order the survival to hospital discharge the rhythms with best survival to hospital discharge

A

pVT/VF (41.8 %)
Asystole (30.5 %)
PEA (26.4 %)

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10
Q

What action should be taken if there is loss of SaO2 signal and ETCO2 reading diminishing

A

Pulse check (PEA arrest possible)

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11
Q

How is management of intra-operative VF different from the ALS algorithm

A

Stacked shocks - 2 x successive shocks –> CPR and algorithm

Precordial thump - if defibrillator not available

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12
Q

How is management of intra-operative asystole different from the ALS algorithm

A

EXCLUDE lead disconnection (completely straight line)
STOP VAGAL STIMULATION and TRY ATROPINE 0.5 MG
Most likely cause: excessive vagal tone
- Stop surgeon
- Administer atropine 0.5 mg titrated up to effect
If no immediate ROSC: CA algorithm

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13
Q

How is management of intra-operative PEA different from the ALS algorithm

A 
Start CPR
Give fluid (unless certain of normovolaemia)
Vasopressor - Adrenalin 1mg is too much - give a small dose of adrenalin or another vasopressor initially --> if this fails to restore cardiac output, increase the dose
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14
Q

Cardiac arrest in a prone patient - how to do chest compressions

A

Compress on the back with or without sternal counter pressure

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15
Q

Describe the immediate management of a patient once anaphylaxis has been diagnosed

A
  1. Help
  2. Convert to ETT with FiO2 100%
  3. Adrenalin 0.5mg IM (50 ug titrated boluses IV anaesthetists)
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16
Q

Describe Early management (after immediate Rx) of a patient once anaphylaxis has been diagnosed

A

Fluid (500 ml or 20 ml/kg)
Chlorphenamine 10 mg IV
Hydrocortisone 200mg IV

If bronchospasm is significant -
Intravenous bronchodilators:
- Salbutamol (5 - 20 ug/min)
- Magnesium Sulphate (2g over 20 minutes)
- Aminophylline (load with 5.7 mg/kg if naive)

17
Q

Describe late management (after early Rx) of a patient once anaphylaxis has been diagnosed

A

ICU
Tryptase levels: immediate, 2 hours and > 24 hours
Ensure allergy/immunology clinic referral

18
Q

What is used in the treatment of cardiac arrest associated with local anaesthetic toxicity? Describe the proposed mechanism for its effect

A

Intralipid 20%

It has been suggested that the local anaesthetic partitions into the lipid which reduces the concentration in the myocardium.

19
Q

What are the clinical findings suggestive of local anaesthetic toxicity

A

Precipitous CVS and or CNS disruption

CVS
Sinus brady/blocks/asystole/ventricular tachyarrhythmias

CNS
Severe agitation/LOC ± seizures

20
Q

Does local anaesthetic toxicity occur immediately after administration of toxic dose?

A

There may be some delay after the initial injection

21
Q

Describe the immediate management of LA toxicity

A
  1. Help and fetch intralipid bag
  2. ETT and FiO2 100%
  3. Rx seizures with increments of propofol/thiopental/benzo
  4. CPR if necessary ALS protocols (consider cardiopulmonary bypass if available)
  5. Administer Intralipid
22
Q

What is the maximum cumulative dose of intralipid?

A

12ml/kg

23
Q

How is intralipid administered in the setting of local anaesthetic toxicity?

A
  • 1.5mg/kg bolus over 1 minute (3 boluses 5 minutes part if CVS not stabilized)
  • 15mg/kg/hr infusion (double to 30 after 5 mins if CVS not stabilized)

For a 70 kg man

  1. 100ml bolus with infusion at 1000ml/hr for 40 mins
    After 5 mins CVS instability remains
  2. 100 ml bolus with infusion 2000 ml/hr for 20 mins
    After 5 mins CVS instability remains
  3. 100 ml bolus with infusion at 2000ml/hr for 16 mins

Maximum cumulative dose is 840 mls - this determines the infusion duration

24
Q

How long should CPR continue in the setting of cardiac arrest caused by LA toxicity

A

Recovery from LA induced CA may take > 1 hour

Consider cardiopulmonary bypass

25
Q

Is propofol a suitable substitute for 20% lipid emulsion

A

NO

26
Q

How should hypotension/bradycardia and tachyarrhythmia be treated in the context of LA toxicity

A

Use conventional therapies and algorithms except exclude lidocaine as an antiarrythmic

27
Q

What tests should be done in in the subsequent two days if ROSC is obtained

A

Exclude pancreatitis - Lipase and amylase daily

28
Q

Summarize post-resuscitation care

A

Airway and breathing

  • Advanced airway with waveform capnography
  • SaO2 94 - 98%
  • ETCO2 5 - 5.5kPa

Circulation

  • SBP > 100 mHg (IABP/Vasopressor)
  • Normovolaemia
  • 12 lead ECG

Disability

  • Rx seizures
  • Optimize sedation

Exposure

  • Tb: 32 -36 deg C
  • Control shivering

Investigation
Likely Cardiac –> Coronary angiography/PCI
Unlikely cardiac –> CTB/CTPA

29
Q

What is post cardiac arrest syndrome?

A

Comprised of 4 components

  1. Post CA brain injury (coma/seizures/myoclonus/neurocognitive dysfunction and brain death)
  2. Post CA myocardial dysfunction
  3. Systemic ischaemia and reperfusion response (Activation of immune and coagulation pathways –> multiple organ failure and risk of infection)
  4. Persistent precipitating pathology
30
Q

Why is survival to hospital discharge significantly higher in patients who suffer CA in the perioperative setting

A

A reversible cause is more likely in this setting and intervention is often immediate

31
Q

Considering the higher likelihood of survival from CA in the perioperative setting, how does this influence the management of the patient with a DNACPR order

A

Counsel patient beforehand to establish preference with regard to whether they would like to maintain DNACPR for the procedure or not

32
Q

In what % of perioperative cardiac arrests is there a primary cardiac cause?

A

44%

33
Q

What is the survival to hospital discharge for a perioperative cardiac arrest that occurs due to bleeding

A

10.3 % survival

34
Q

What is the survival to hospital discharge for a perioperative cardiac arrest that occurs due to a primary cardiac cause

A

42%

35
Q

What is the survival to hospital discharge for a perioperative cardiac arrest that occurs due to a ‘other’ causes (non bleeding and non cardiac)

A

> 57%

36
Q

Of the cardiac arrests caused directly by drugs, which drugs are the most common cause

A

Neuromuscular blockers are the most common cause of drug-induced cardiac arrest directly attributable to anaesthesia.

37
Q

What % of perioperative cardiac arrests survive to hospital discharge

A

34.5%

Diploma in Anaesthesia (73 decks)

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