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ALS Flashcards

1
Q

When should an AED be used instead of a manual defibrillator

A

When someone trained to use a manual defibrillator is not immediately available

When only an AED is available

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2
Q

What is used to confirm correct tracheal tube placement during resus

A

Waveform capnography

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3
Q

If there is risk of cervical spine injury how do we initially secure the airway in an unresponsive patient?

A

Jaw thrust or chin lift in combination with manual in-line stabilisation (MILS) of the head and neck by an assistant. If airway obstruction persists add head tilt a small amount at a time until airway is open (oxygenation, ventilation prioritised over cervical spine injury)

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4
Q

Correct hand placement for chest compressions

A

middle of lower half of sternum

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5
Q

Features of high quality chest compressions

A

Depth 5-6cm
Rate 100-120 bpm
Chest recoil completely after each compression
Same amount of time for compression and relaxation
Minimise interruptions

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6
Q

Maximum time for chest compression interruption for endotracheal tube insetion

A

5s

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7
Q

Ventilation rate in resuscitation

A

10 breaths/min

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8
Q

Maximum time for chest compression interruption for pulse check

A

5s

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9
Q

What do you do if a patient is not breathing and has a pulse?

A

Ventilate/secure airway
Check for a pulse every minute
If any doubts about presence of a pulse, start compressions

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10
Q

What do you do in a monitored and witnessed cardiac arrest?

A

Confirm cardiac arrest
If VF/pVT, 3 successive (stacked) shocks
Check for pulse after each defibrillation attempt

If still no pulse after 3rd shock, start compressions (3 shocks counted as 1 shock in ALS algorithm)

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11
Q

When do you consider a precordial thump?

A

When it can be used without delay whilst awaiting on the arrival of a defibrillator in a monitored VF/pVT arrest

(Use ulnar edge of tightly clenched fist to delivver a sharp impact to lower half of the sternum from a height of 20cm, with immediate retraction of fist)

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12
Q

What proportion of cardiac arrests have shockable (VF/pVT) rhythms?

A

20%

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13
Q

Can cardiac arrest rhythms change into another arrest rhythm?

A

Yes - 25% of PEA/Asystoles can change into VF/pVT rhythms

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14
Q

Whilst charging the defibrillator what should happen?

A

Chest compressions should be continued

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15
Q

Where should pads be applied?

A

Under right clavicle anteriorly and on left mid-axillary line

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16
Q

What energy setting should shocks be given at in a cardiac arrest?

A

120-150J for 1st shock, then at same or higher settings for subsequent shocks

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17
Q

After a shock is given, what should happen?

A

Don’t stop for pulse check.

Immediately restart chest compressions

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18
Q

In shockable rhythm, which medications do you give and when?

A

Adrenaline 1mg IV after 3rd shock, then after every alternate shocks (approx 3-5minutes)

Amiodarone 300mg IV after 3rd shock, amiodarone 150mg IV after 5th shock

Lidocaine 1mg/kg can be used as alternative if amiodarone not available, but not to be given when amiodarone already given

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19
Q

Reversible causes of cardiac arrest

A

4Hs:
Hypoxia
Hypothermia
Hypo/hyperkalaemia, hypoglycaemia, hypocalcaemia, other metabolic disorders
Hypovolaemia

4Ts:
Tension
Thrombosis
Tamponade
Toxins

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20
Q

Dose of adrenaline

A

1mg IV

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21
Q

Dose of amiodarone

A

300mg IV, then 150mg IV after 5th shock

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22
Q

Why are compressions continued immediately after a shock?

A
  • Minimise chest compression interruptions
  • Even if shock successful, rarefor pulse to be immediately palpable (ROSC to palpable pulse may be longer than 2 minutes in 25% of shocks)
  • Even in ROSC, compressions do not increase chance of VF recurring
  • If shock resulted in asystole, compressions may usefully induce VF
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23
Q

In persistent VF/pVT arrest what should you also do?

A

Check positioning of pads after shocks and consider changing them to anterior posterior or other positions

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24
Q

When should PULSE checks be done?

A

Only when RHYTHM on monitor is compatible with a pulse, otherwise, don’t waste time

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25
Q

In a witnessed cardiac arrest with shockable rhythm, when do you give adrenaline and amiodarone

A

Give adrenaline after the ‘3rd’ shock (Ie the 5th shock including the 3 stacked shocks)

Give amiodarone after the initial stacked shocks

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26
Q

What is paramount in managing a PEA arrest?

A

Treating the reversible causes of cardiac arrests

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27
Q

What special consideration should be given when asystole is suspected during CPR?

A

Ensure ECG pads attached to chest, correct monitoring mode selected
Ensure gain setting appropriate
Check ECG carefully for presence of P waves, as if present they may be treated with cardiac pacing

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28
Q

When to give adrenaline in PEA/Asystole?

A

1mg IV immediately then every alternate cycle (3-5 mins)

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29
Q

When should chest compressions be interrupted for ventilation?

A

If excessive gas leakage causes inadequate ventilation of patient’s lungs, interrupt compressions to allow for 30:2 ratio

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30
Q

What is the key value measured by waveform capnography?

A

end-tidal PaCO2

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31
Q

What is waveform capnography used for?

A
  • Ensuring tracheal tube placement
  • Monitoring ventilation rate
  • Monitoring chest compression quality (high End-tidal PaCO2 with increase with increased ventilation rate and compression depth)
  • Identifying ROSC (increased end-tidal PaCO2 may help indicate ROSC)
  • Prognostication during CPR (lower end-tidalPaCO2 associated with ower ROSC rates, increased mortality)
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32
Q

Which sample is waveform capnography measuring?

A

A continuous sample of gas. (connector placed in breathing system usually on end of tracheal tube or supraglottic airway device)
- so end-tidal PaCO2 would be measuring the partial pressure of the gas in the airways just at the end of the expiratory phase

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33
Q

Normal range of end-tidal PaCO2?

A

4.3-5.5kPa

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34
Q

When would you suspect a Tamponade as the cause of a cardiac arrest?

A
  • Penetrating chest trauma
  • Post-cardiac surgery
  • Post-device implantation (eg pacemaker)
  • Post PCI
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35
Q

How would you treat cardiac tamponade?

A
  • Pericardiocentesis
  • Resuscitative thoracotomy
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36
Q

What should you do to exclude toxins as a cause of cardiac arrest?

A

Review drug chart and exclude any history suggestive of overdose

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37
Q

What should you beware of regarding intubation in the context of a possible tension pneumothorax?

A

Check tube position - intubation of right main bronchus may complicate tension pneumothorax further

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38
Q

How would you spot a tension pneumothorax in a cardiac arrest situation?

A

Clinically:
- Tracheal shift
- Unilateral chest expansion
- Subcutaneous emphysema

Investigations:
- Pleural ultrasound
- Chest X-Ray

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39
Q

What can you do for hypothermia

A

Active rewarming

If that fails, cardiopulmonary bypass if facilities available

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40
Q

What does hypovolaemic causes include?

A

haemorrhage, loss of fluids eg diarrhoea, sepsis, anaphylaxis

Basically many forms of hypovolaemic and distributive shock

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41
Q

4 types of shock

A

Hypovolaemic
Distributive
Cardiogenic
Obstructive

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42
Q

When does hypoxic brain injury start to set in?

A

Within 3 minutes of a VF/pVT cardiac arrest

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43
Q

Four non-technical skills that are essential in cardiac arrests

A

Situational Awareness
Leadership
Decision-making
Task management

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44
Q

How much flush is required for any peripherally injected drugs?

A

20ml Saline
Should also have elevation of the extremity for 10-20s to facilitate delivery of drug to central circulation

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45
Q

Where are the three recommended insertion sites for Intraosseous access?

A

Proximal Humerus
Proximal Tibia
Distal Tibia

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46
Q

Contraindications for intraosseous access

A

If at the target site there is:
- Trauma
- Infection
- Prosthesis

IO access attempt in the last 48 hours (including failed)

Failure to identify anatomical landmarks

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47
Q

What should you do after insertion of an intraosseous?

A
  • Confirm correct placement - attempt to aspirate IO blood (absence does not necessarily imply failure)
  • Flush needle to ensure patency, observe for leakage/extravasation (best done using extension set flushed with 0.9% saline attached to hub of needle before use)
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48
Q

How do you give medications via IO?

A

Pressure required - pressure bag or syringe to maintain flow rates

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49
Q

Complications of IO access

A
  • Extravasation into soft tissues surrounding insertion site
  • Dislodgement of needle
  • Compartment syndrome due to extravasation
  • Fracture/chipping of bone during insertion
  • Pain
  • Fat emboli
  • Infection/osteomyelitis
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50
Q

If PCI or angiography is required during a cardiac arrest, what is required?

A

Automated mechanical chest compression device and/or extracorporeal CPR to maintain circulation during procedure

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51
Q

How long should you continue CPR for if fibronolysis has been given with suspicion of PE?

A

60-90 minutes

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52
Q

How would you treat a PE-driven cardiac arrest?

A
  • Thrombolysis (eg alteplase),
  • CPR for 60-90 minutes post thrombolysis
  • Consider extracorporeal CPR
  • Consider surgical/mechanical thrombectomy
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53
Q

What is the recommended position for a focused ultrasound in cardiac arrests? (eg to exclude tamponade)

A
  • Sub-xiphoid probe position
  • Can do this just before chest compressions are paused for 10s
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54
Q

What conditions suggest benefit for extracorporeal CPR (ECPR)?

A
  • reversible causes of arrest
  • minimal comorbidities
  • witnessed arrest
  • immediate CPR started
  • ECPR started within 1 hr of collapse/arrest
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55
Q

In asystole, when is it generally accepted to stop CPR?

A

After 20 minutes in absence of reversible cause

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56
Q

How long should you observe the patient before confirming death after stopping CPR?

A

minimum 5 minutes

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57
Q

What should be done post-resus attempt?

A
  • Ongoing patient care with allocation of further roles, responsibilities, including handover
  • Documentation
  • Communication with relatives
  • Post-event debrief
  • Ensure equipment, drug trolleys are replenished
  • Ensure audit forms completed
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58
Q

Where is the commonest site of airway obstruction?

A

Pharynx (more often soft palate and epiglottis rather than tongue)

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59
Q

What can cause airway obstruction?

A
  • Vomit following regurgitation
  • Blood following trauma
  • Secretions
  • Foreign bodies
  • Oedema (burns, inflamation, anaphylaxis)
  • Bronchospasm
  • Tumours
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60
Q

What often causes laryngeal obstruction?

A

Oedema from:
- anaphylaxis
- burns
- inflammation

Laryngeal spasm from inhalation of foreign material or stimulation

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61
Q

What causes infra-laryngeal obstruction comonly?

A
  • excessive bronchial secretions
  • mucosal oedema
  • bronchospasm
  • pulmonary oedema
  • aspiration of gastric contents
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62
Q

What do you do for LOOK, LISTEN, FEEL?

A

Look for chest and abdominal movements
Listen and Feel for airflow at the mouth and nose

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63
Q

What sounds are audible in partial airway obstruction?

A

Inspiratory stridor
Expiratory wheeze
Gurgling
Snoring (pharyngeal)

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64
Q

Describe see saw breathing

A

Paradoxical chest and abdominal movement
Chest drawn in and abdomen expanding during inspiration and opposite during expiration

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65
Q

What features can you see in airway obstruction

A

See saw breathing
Use of accessory muscles
Intercostal and subcostal recession
Tracheal tug

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66
Q

What should you do if you suspect airway obstruction in patients with tracheostomies or permanent tracheal stomas

A

Remove any obvious foreign material from tube or stoma
Remove tracheostomy liner (inner tube) if one is present
I’d still not possible to ventilate, try to pass suction catheter. If this is successful, perform tracheal suctioning and attempt to ventilate. If it’s not successful, remove tracheostomy tube and exchange if possible

After tracheostomy tube removed, it might be possible to ventilate lungs by sealing stoma and using bag-valve applied to face or intubating orally (may not be possible if there was originally significant upper airway obstruction)

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67
Q

What to do when choking

A

Assess for signs of severe or mild airway obstruction
If mild, encourage to continue coughing
If severe, 5 back blows, (check each has resolved choking)
If fails, give abdominal thrusts

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68
Q

How do you give back blows

A

Stand slightly to side of patient and behind
Support chest with one hand, lean patient forward, 5 blows sharply between scapulae with other hand

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69
Q

How to give abdominal thrusts

A

Behind patient, arms around upper part of abdo, clenched fist under xiphisternum, pull sharply inwards and upwards

Repeat 5 times

Then alternate between back blows and abdo thrusts

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70
Q

How do you do a jaw thrust

A

Place index finger and other fingers behind angle of mandible, apply steady upwards and forward pressures to lift it

Also use thumbs to slightly open mouth and displace chin downwards

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71
Q

How do size an oropharyngeal airway

A

If in doubt put a bigger one in
Vertical distance between incisors and angle of jaw

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72
Q

Risk of oropharyngeal insertion

A

Tongue can be pushed backwards and obstruct further

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73
Q

How to insert an OPA

A

Insert backwards, advance until you hit junction of hard-soft palate then rotate 180 with advancement

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74
Q

What should you check for before an OPA insertion

A

Ensure no foreign bodies are there

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75
Q

What contraindicated an NPA

A

Basal skull fracture

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76
Q

What size should you use for an NPA

A

6-7mm (don’t go too big)
Traditional sizing unreliable

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77
Q

What FiO2 can a non-rebreather mask deliver at flow rates of 10Lmin-1

A

85%

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78
Q

What max FiO2 can a simple face mask deliver

A

50%

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79
Q

What max FiO2 can a self inflating (bag-valve) bag and mask give

A

85%

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80
Q

What FiO2 can a self inflating bag give if no oxygen or reservoir system attached?

A

21%

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81
Q

Risks of over inflation using bag valve mask

A

Gastric inflation and regurgitation that could lead to aspiration

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82
Q

What size is usually best for i-Gel SGA

A

Size 4

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83
Q

Limitations of iGel

A

Risk of significant leak in high airway resistance or poor lung compliance

Uninterrupted chest compressions can cause some gas leak- if evidenced, should do 30:2 instead

Theoretical aspiration risk

If not unconscious, coughing, straining, laryngeal spasm possible

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84
Q

What forms of syncope do not warrant admission

A

Situational (micturition, cough syncope)
Orthostatic hypotension
Uncomplicated faints

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85
Q

Which lead is best to see p waves

A

Lead II and V1

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86
Q

Which leads are best to spot atrial flutter

A

Inferior leads
II, III, aVF

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87
Q

What rate would atrial activity usually go at for atrial flutter

A

Around 300bpm

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88
Q

In atrial fibrillation what happens to p waves

A

You can’t see them but you can also see fibrillatory waves V1 where there is varying amplitude and duration of p waves

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89
Q

What would you see in retrograde activation of atria from the AV node?

A

Inverted p waves in leads II and aVF

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90
Q

What do you suspect if there is AF accompanied by a completely regular ventricular rhythm with a slow rate?

A

AV block

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91
Q

What two rhythm abnormalities can resemble VF?

A
  • polymorphic VT
  • pre-excitation syndromes such as WPW (which mimics polymorphic VT)
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92
Q

What happens when p waves are conducted to ventricles in VT?

A

Fusion or capture beats occur

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93
Q

What are fusion or capture beats?

A

P waves in VT that conduct to ventricles

Capture beat: normal looking QRS complex
Fusion beat: hybrid QRS caused by fusion of normal QRS from AV node with activity coming from ventricular focus causing VT

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94
Q

What should be avoided in Torsades de Pointes?

A

Drugs prolonging QTc, including amiodarone

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95
Q

In CHB, what determines the rate and QRS width?

A

The ventricle- stimulating pacemaker site:
- if in AV node or proximal bundle of His, intrinsic rate of 40-50 bpm or higher possible with narrow QRS
- if in distal His-Purkinje fibres or ventricular myocardium, rate 30-40 bpm or less with broad QRS (*more dangerous with greater likelihood of arrest and asystole)

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96
Q

What is an idioventricular rhythm?

A

Rhythm rising from ventricular myocardium, including ventricular escape rhythms from CHB.

Accelerated idioventricular rhythms have normal HR, observed often after successful thrombolyses or PCI (reperfusion arrhythmia) - these are not too worrying unless VT/VF develops

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97
Q

What are escape rhythms?

A

Cardiac depolarisation being initiated from subsidiary ‘pacemakers’, not the SA node

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98
Q

In escape rhythms, as a general rule, what influences the rate?

A

Location of pacemaker - distal more slow, proximal faster (ventricular escape rhythms slower than junctions rhythm from AV node or bundle of His)

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99
Q

What is an agonal rhythm?

A

Occurs in dying patients, slow, irregular, wide ventricular complexes of varying morphology

Becomes progressively broader before progressing to asystole

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100
Q

What is the anatomical threshold for a rhythm to be supraventricular?

A

Origin superior to bundle of His

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101
Q

Some causes of A Fib

A

HTN, Obesity, ETOH excess, Structural heart disease, hyperthyroid, LV impairment (acute or chronic, not usually due to direct ischaemia of atrial myocardium)

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102
Q

Causes of A Flutter

A

Usually right atrial issues, so from RHF related things, eg COPD, large PEs, congenital heart disease, CCF

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103
Q

Normal ranges of QTc

A

Up to 0.45s in men
Up to 0.47s in women

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104
Q

What QTc indicates high risk of cardiac arrest and sudden death?

A

0.5s or longer

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105
Q

List some causes of prolonged QTc

A

Acquired:
- Low potassium, calcium, magnesium
- Hypothermia
- Myocarditis
- Acute MI
- SAH
Drugs:
- amiodarone
- sotalol
- class 1a and class III anti-arrhythmics
- TCAs, SSRIs
- Others: methadone, chloroquine, terfenadine, erythromycin, haloperidol, ondansetron
Acquired:
- Jervell-Lange-Nielsen syndrome
- Romano-Ward syndrome

106
Q

How much does mortality increase by in the absence of bystander CPR per minute without defibrillation?

A

7-10%

107
Q

What 3 factors are essential for successful defibrillation?

A

1) time from onset to shock
2) continuity of chest compressions
3) short pre-shock pause

108
Q

If someone has a hairy chest what could you consider

A

Quickly finding a razor
If not, consider bi-axillary positioning
If pads stick, it’s no issue

109
Q

What other acceptable pad positions are there?

A
  • Antero-posterior (left precordium and just inferior to left scapula)
  • Postero-lateral (mid axillary line and just inferior to right scapula (V6 electrode placement))
  • bi-axillary (each on lateral chest wall bilaterally)
110
Q

In implantable medical devices, what should be done?

A
  • Look for medical alert bracelets
  • place electrode far away from device (at least 10-15cm) or use alternate positions
111
Q

What do you do with oxygen during defibrillation?

A
  • take off any oxygen mask or nasal cannula, place 1m away from patient’s chest
  • leave ventilation bag connected to tracheal tube or supraglottic airway device
  • or, disconnect ventilation bag from tracheal tube or supraglottic device and remove at least 1m (tbh you can just leave it)
  • if connected to ventilator, leave tubing connected
112
Q

When do you withhold adrenaline during CPR?

A

If there are signs of ROSC during CRP

113
Q

How is synchronised cardioversion delivered?

A
  • Synchronise shock with R waves of ECG by turning the switch
  • Anticipate delay between buttons and discharge of shock
114
Q

What should you do if synchronisation fails?

A
  • choose another lead and/or adjust amplitude
  • if in peri-arrest with VT give unsynchronised shock
115
Q

Where are ICDs usually placed?

A

Pectoral, left more often than right sided

116
Q

How much shock does an ICD usually discharge?

A

Approximately 40J (80J in S-ICD)

117
Q

How do you deactivate an ICD?

A

Using a ring magnet placed over the ICD

118
Q

Does deactivation of an ICD disable its pacemaking capability? (Eg in CRT-D)

A

No

119
Q

What can interrogation of a pacemaker or ICD achieve following an arrest?

A
  • Information about rhythm behaviour leading to arrest
  • an opportunity to check lead thresholds and device function
120
Q

What should be done with implantable loop recorders (ILR) in arrests

A
  • Careful pad placement due to risk of damage to device during arrest
  • interrogation of device afterwards
121
Q

Some causes of CHB from lower in the conducting system than the AV node

A
  • degenerative conducting tissue fibrosis
  • extensive anteroseptal myocardial infarction affecting all fibres of bundle branches
  • cardiomyopathies
  • calcific valve disease
122
Q

Usual cause of CHB at level of AV node

A

Acute MI

123
Q

What forms of pacing are there?

A

Invasive:
- Temporary Transvenous pacing
- Permanent pacing

Non-invasive:
- Percussion pacing (‘fist pacing’)
- Transcutaneous pacing

124
Q

What ECG feature makes pacing more likely to be successful?

A

Presence of p waves

125
Q

What current does capture usually happen at in transcutaneoous pacing?

A

50-100mA

126
Q

What can prevent successful pacing?

A
  • Hyperkalaemia
  • Movement artefact
127
Q

Does electrical capture and generation of a QRS complex ensure return of a pulse?

A

No - QRS complex does not guarantee myocardial contractiliy and absence of pulse means PEA

128
Q

In 3-lead monitoring, where should adhesive pads be applied?

A

Over bone than muscle to minimise interference from muscle artefact

129
Q

Is sodium bicarbonate recommended in acidosis?

A

No, adverse side effects include exacerbation of intracellular acidosis

130
Q

Does asystole present as a straight line?

A

Not a perfect straight line - that would indicate that the monitoring lead is disconnected

131
Q

What is the correct rate of adrenaline infusion in bradycardia?

A

Rate of 2-10mcg/min

132
Q

Are opioids contraindicated in bradycardia?

A

No

133
Q

If the patient has a serious infection what should you do before starting CPR?

A

Wear PPE

134
Q

What should the target PaCO2 be post ROSC?

A

Normocapnia, not excessively low PaCO2

135
Q

If someone is comatose after ROSC, what should you do?

A

Continuous monitoring of core temperature (pyrexia common 2-3 days post arrest)

136
Q

How does NaHCO3 exacerbate intracellular acidosis?

A

Generating CO2 within the blood, which diffuses intracellularly

137
Q

What should be considered to be given for TCA overdose?

A

50mmol, 50ml of 8.4% solution of sodium bicarbonate

138
Q

What does sodium bicarbonate do to the oxygen dissociation curve?

A

Shifts it to the left

139
Q

Should you start CPR in an unresponsive patient with agonal breathing?

A

Yes

140
Q

Adrenaline dose in anaphylaxis?

A

0.5mg IM (5ml of 1:1000)

141
Q

In cardiac arrests caused by asthma, what should you consider for defibrillation energies?

A

Higher defibrillation energies, due to thoracic impedence from hyperinflation

142
Q

What is the time cutoff for Primary PCI within onset of chest pain for a STEMI and what should you do if you cannot achieve this?

A

120 minutes
Do fibrinolysis instead if not available within 120 minutes

143
Q

What are the anterior-anteroseptal leads?

A

V1-V4

144
Q

What are the anterolateral leads?

A

V5-V6, I, aVL

145
Q

Which territory for an MI has the worst prognosis?

A

Anterior

146
Q

Inferior leads?

A

II, III, aVF

147
Q

Lateral leads?

A

V5-V6 and/or leads I and aVL, (sometimes aVL alone)

148
Q

How to spot a posterior STEMI?

A

Reciprocal ST depression in anterior leads
Dominant R waves in V1 and V2 reflects posterior Q wave development

You can confirm this by repeating ECG using posterior leads: place V8-10 in horizontal line around chest continuing from V6 (mid-axillary line) and V7 (posterior axillary line), V9 placed to left of spine, V8 halfway between V7 and V9, V10 to left of spine

149
Q

How to spot a right ventricular infarction?

A

ST elevation in V1 accompanying an inferior or posterior STEMI

150
Q

What variables is the GRACE score based on?

A
  • Age
  • Signs of HF
  • HR at presentation
  • BP at presentation
  • Creatinine conc
  • ECG changes
  • Troponin
  • ?cardiac arrest
151
Q

Contraindications to fibrinolysis?

A

Absolute:
- Previous haemorrhagic stroke
- Ischaemic stroke in last 6 months
- CNS damage/neoplasm
- Major surgery/trauma/head injury in last 3 weeks
- Active internal bleeding or GI bleeding in last month
- Known/suspected aortic dissection
- Known bleeding disorder

Relative:
- Refractory HTN (>180mmHg)
- TIA in last 6 months
- oral AC
- pregnancy or less than 1 week post-partum
- Traumatic CPR
- Non-compressible vascular puncture
- Active peptic ulcer disease
- Advanced liver disease
- Infective endocarditis
- Previous allergic reaction to fibrinolytic drug

152
Q

What indicates failed fibrinolysis in a STEMI?

A

Failure of ST elevation resolution by more than 50%

153
Q

What proportion of patients fail fibrinolysis?

A

20-30%

154
Q

What should be done during and after fibrinolysis?

A

Cardiac monitoring
Record ECG 12 lead 60-90 mins post fibrinolysis
If failed, transfer for rescue PCI

155
Q

What features indicate high probability of arrhythmic syncope?

A
  • in supine position
  • during/after exercise
  • no/brief prodromal symptoms
  • repeated episodes/unexplained
  • FHx of sudden death or inherited cardiac condition
156
Q

Causes of VF

A
  • ACS
  • hypertensive heart disease
  • valve disease
  • drugs (anti-arrhythmic, TCAs, antidepressants, digoxin)
  • inherited cardiac diseases (eg long QTc)
  • acidosis
  • electrolyte concentrations
  • hypothermia
  • electrocution
157
Q

What is the target glucose range post ROSC?

A

4-10

158
Q

What proportion of comatose patients have seizures?

A

one-third

159
Q

If motion artefact appears to be ihibiting the pacemaker, what should you do?

A

Switch to fixed-rate pacing

160
Q

What should you do if electrical capture has not occurred even with the highest current setting?

A

Change the electrode positions

161
Q

Can you do compressions with transcutaneous pacing?

A

Yes

162
Q

What is the usual transvenous pacing threshold?

A

<1V

163
Q

What are the usual reasons for failure for temporary transvenous pacing?

A
  • High threshold
  • Connection failure
  • Lead displacement
164
Q

What are the life-threatening features of arrhythmia?

A
  • Shock
  • Syncope
  • Heart Failure
  • Myocardial Ischaemia
  • Extreme heart rate
165
Q

If someone has life-threatening features of tachyarrhythmia, what do you do?

A

Synchronised cardioversion

166
Q

If synchronised cardioversion fails to terminate a tachy-arrhythmia what do you do?

A

IV amiodarone 300mg over 10-20 mins with an infusion of 900mg over 24hrs, then another synchronised cardioversion attempt (up to 3 attempts)

167
Q

What energy do you set for Atrial fibrillation DCCV?

A

maximum defibrillator output

168
Q

What energy do you set for Atrial flutter and non-atrial fibrillation narrow complex tachycardias

A

Start with 70-120J

169
Q

For atrial fibrillation and flutter, what position pads do you use?

A

Anteroposterior

170
Q

For broad-complex tachycardias what cardioversion setting do you use?

A

120-150J

171
Q

How do you treat torsade de pointes VT?

A
  • Stop all drugs known to prolong QTc
  • Correct electrolytes, especially K, Mg, Ca
  • GIve IV Mg 2g over 10 minutes
  • Obtain expert help afterwards to prevent relapse after successful initial treatment
  • Synchronised cardioversion if adverse features develop
172
Q

What doses of adenosine to give in stable SVT?

A

6, 12, 12 or 18 mg IV, flushed

173
Q

What to give if adenosine fails to terminate a regular narrow complex tachycardia?

A

Verapamil 2.5-5mg IV over 2 minutes
Or metoprolol 2.5-15mg IV in 2.5 mg bolus doses

174
Q

What to do in pulseless rapid narrow complex tachycardia if pulse very high >250

A

Start CPR
Give a synchronised shock - an exception to the PEA algorithm

175
Q

How long should anticoagulation be given for those with AF>48hr onset?

A

3 weeks

176
Q

In those with new AF where urgent cardioversion is required more urgently (not immediate), what should you do?

A

Give either LMWH or IV unfractunated infusion to maintain APTT 1.5-2 times reference value and then cardiovert.

Seek advice on duration of anticoagulation, but usually minimum of 4 weeks, often longer

177
Q

What drugs can be used for chemical cardioversion of new A fib <48hr onset and what are the contraindications?

A

Propafenone
Flecainide

Contraix:
- HF
- LV impairment
- IHD
- prolonged QTc

Can use amiodarone instead but may take longer to act

178
Q

In pre-excited AF (eg WPW) what should you do?

A

Seek expert help
Avoid using adenosine, diltiazem, verapamil, digoxin (AV node blockers that can cause relative increase in pre-excitation)

179
Q

Pharmacological bradycardia treatment

A
  • Atropine 500mcg IV repeat every 3-5mins to max of 3mg (caution in IHD)
  • Isoprenaline 5mcg/min IV
  • Adrenaline 2-10mcg/min IV
  • Dopamine 2.5-10mcg/kg/min
  • Glucagon IV if beta blocker or calcium channel blocker overdose suspeted
  • Consider digiband for dig toxicity

If Acute inferior wall MI, spinal cord injury or cardiac transplantation, consider slow IV aminophylline 100-200mg

180
Q

In bradycardia, what features confer risk of asystole?

A
  • Recent asystole
  • Mobitz II
  • CHB with broad QRS
  • Ventricular pause >3s
181
Q

If no response to pharmacological therapy and lifethreatning bradycardia, without access to pacing, what do you do?

A

Percussion pacing as interim measure - repeated thumps with closed fist over left lower edge of sternum at rate of 50-70bpm

182
Q

What happens to potassium with low pH?

A

increases, due to extracellular shift

183
Q

Causes of hyperkalaemia

A
  • Renal failure
  • Drugs (ACEi, ARBs, K sparing diuretics, NSAIDs, beta blockers, trimethoprim)
  • Tissue breakdown (tumour lysis, rhabdomyolysis, haemolysis)
  • Metabolic acidosis (DKA, renal failure)
  • Endocrine disorders( Addison’s)
  • Diet (esp in CKD)
  • Spurious (pseudo-hyperkalaemia in clotted blood samples when there is a long transit time to the lab)
184
Q

ECG features of hyperkalaemia

A
  • 1st degree HB
  • flattened/absent P
  • Tall T
  • ST depression
  • S and T merging
  • Widened QRS
  • VT
  • Bradycardia
185
Q

Main risks of hyperkalaemia treatment

A
  • Hypoglycaemia
  • Tissue necrosis from extravasation of IV Ca
  • Rebound hyperkalaemia after treatment effect has worn off - so need to monitor K for minimum of 24 hrs after episode
186
Q

Dose of calcium resonium in mild hyperkalaemia

A

15-30g

187
Q

Moderate hyperkalaemia treatment

A

10U actrapid + 25g glucose IV over 15-30mins
Give further 10% glucose at 50ml/hr for 5 hrs (250ml bag) in pre-treatment glucose of <7
Give calcium resonium as well

188
Q

Severe hyperkalaemia without ECG changes management?

A

10U actrapid + 25g IV glucose (+10% glucose in 250ml bag for 5 hrs if pre-treatment glucose <6) + calcium resonium

expert help
nebulised salbutamol 10-20mg
Consider sodium zirconium cyclosilicate (SZC eg 5-10g TDS up to 72hrs)
consider cardiac monitoring

189
Q

Severe hyperkalaemia with ECG changes management

A

In addition to everything, give calcium salts - 10% Ca Chloride IV 10ml over 2-5 minutes

190
Q

In cardiac arrests with hyperkalaemia what do you do?

A
  • confirm with blood gas
  • IV 10% 10ml Calcium chloride rapid bolus (consider repeating if refractory)
  • 10U Actrapid with 25g IV glucose injection, monitor blood glucose
  • Sodium bicarbonate 50mmol (50mL of 8.4% solution) IV by rapid injection (if severe acidosis or renal failure) - avoid mixing with CaCl (can cause precipitate)
  • Consider dialysis
191
Q

Causes of hypokalaemia

A
  • GI loss
  • Drugs
  • Renal losses (eg RTA, DI, dialysis)
  • Endocrine (Cushing’s, Conn’s)
  • metabolic alkalosis
  • Mg depletion
  • poor dietary intake
192
Q

Treating hypercalcaemia

A

IV fluids
furosemide 1mg/kg IV
hydrocortisone 200-300mg IV
pamidronate 30-90mg IV
treat underlying cause

193
Q

Treating hypermagnaesaemia

A

If Mg >1.75
CaCL 10% 5-10ml repeated
Ventilatory support if necessary
IVF with diuresis
haemodialysis

194
Q

Relative risk for cardiac arrests for patients on haemodialysis than general population

A

20 fold

195
Q

Special considerations for patients on haemodialysis for ALS

A
  • assign trained dialysis nurse ffor HD machine operation
  • stop dialysis and return patient’s blood volume with fluid bolus
  • disconnect from dialysis machine in accordance with international electrotechnical committee standards
  • leave dialysis access open to use for drug administration
  • dialysis may be required in early post-resus period
  • prompt management of hyperkalaemia
  • avoid excessive potassium and volume shifts
196
Q

Define septic shock

A

sepsis requiring vasopressors to maintain MAP>65 and lactate <2 despite adequate fluid resuscitation
has 40% mortality

197
Q

Persistence of what four features require urgent senior assistance after initial fluid resuscitation in sepsis?

A
  • Hypotension
  • Oliguria
  • Acute confusion
  • Lactate >2
198
Q

What does a low diastolic pressure suggest?

A

Arterial vasodilation - ?anaphylaxis ?sepsis

199
Q

What does a narrow pulse pressure suggest?

A

(should normally be 35-45mmHg)
Arterial vasoconstriction ?cardiogenic shock ?hypovolaemia ?rapid tachyarrhythmia

200
Q

How long do you apply cutaneous pressure to assess for CRT

A

5s

201
Q

In hypoglycaemia in an unconscious patient how do you treat?

A

50ml of 10% glucose IV
then further doses every minute until regained consciousness or total of 250ml 10% glucose

202
Q

How to calculate mean arterial pressure?

A

Diastolic + 1/3 of pulse pressure

203
Q

What can happen to temperature in drug overdose

A

hypo or hyperthermia

204
Q

Is routine gastric lavage recommended for poisoning?

A

no

205
Q

What can you give in poisoning to absorb drugs?

A

Activated charcoal in those where ingestion happened within 1 hr, in intact and protected airways
-multiple doses may be beneficial in carbamazepine, dapsone, phenobarbital, quinine, theophylline poisoning

206
Q

When do you consider whole-bowel irrigation in poisoning?

A

(using polyethylene glycol solution)
- sustained release or enteric-coated drug overdoses, oral iron poisoning and removal of ingested packets of illicit drugs

207
Q

Are laxatives and emetics recommended in poisoning?

A

No

208
Q

In moderate to severe salicylate poisoning, what can you look out for in the urine with treatment?

A

Urine alkalinsation (pH>7.5) by giving IV sodium bicarbonate

209
Q

What would haemodialysis in poisoning be used for?

A

drugs or metabolites with low molecular weight, low protein binding, small volumes of distribution, high water solubility

210
Q

What to give in opioid OD and doses per route?

A

Naloxone
IV: 400mcg
IM/SC: 800mcg
IN: 2mg

Large ODs require max dose of 10mg
duration of action 45-70 mins (but resp depression may persist to 4-5 hrs)

211
Q

What can acute withdrawal from opioids cause?

A

Sympathetic excess leading to pulmonary oedema, ventricular arrhythmia, severe agitation
use naloxaone with caution

212
Q

3 Features of benzo OD

A

LOC, Resp depression, low BP

213
Q

How to treat benzo OD?

A

Flumazenil (comp antag of benzos)
- To use only when no history or risk of seizures
- This can cause severe toxicity in dependence or co-ingestion of proconvulsant medications such as TCAs (seziure, arrhythmia, hypotension, withdrawal syndrome)

214
Q

Features of TCA OD?

A
  • Hypotension (alpha 1 receptor blockade)
  • Anticholinergic effects (dilated pupils, fever, dry skin, tachycardia, ileus, urinary retention)
  • seizures, coma
  • life-threatening arrhythmias (anticholinergic and sodium channel-blocking effects can cause broad complex VT)
  • Broad QRS and rRAD indicates greater risk of arrhythmias
215
Q

How to treat TCA OD?

A

sodium bicarbonate- aim for pH of 7.45 and 7.55

216
Q

What to consider in Local anaesthetic toxicity?

A

IV 20% lipid emulsion in addition to standard ALS, at 1.5ml/kg at 15ml/khg/hr - up to 3 boluses at 5 min intervals and continue infusion until patient stable or received max of 12ml/kg of lipid emulsion

217
Q

How to treat stimulant (eg Cocaine, amphetamine) OD?

A
  • small doses of IV benzodiazepines eg lorazepam
  • GTN and phentolamine if any coronary vasoconstriction (IV nitrates only as second line for myocardial ischaemia)
218
Q

How to treat organophosphate, carbamate or nerve agent poisoning causing bradycardia?

A

Follow ALS, atropine useful and large (2-4mg IV) and repeated doses may be required

219
Q

How much salbutamol do you give in severe asthma and how quickly?

A

5mg nebs repeated doses every 15-30 minutes
- or continuous doses 5-10mg/hr (requires special nebuliser)
- if nebs not available give via metered dose inhaler via large volume spacer device
- If inhaled therapy not possible, consider IV (250mcg IV slowly) and moitor lactate for toxicity

220
Q

Frequency of ipratropium bromide in severe acute asthma

A

nebs given 500mcg 4-6 hourly

221
Q

How much steroids in severe acute asthma?

A

Pred 40-50mg Oral, or Hydrocortisone 100mg IV 6hrly

222
Q

How much magnesium in severe acute asthma?

A

IV MgSO4 2g (8mmol) over 20 minutes

223
Q

Features of life threatening asthma

A

Any one of:
- PEF<33%
- normal PCO2
- PO2 <8
- SpO2<92%
- Reduced GCS
- exhaustion
- arrhythmia
- cyanosis
- low bp
- silent chest
- poor expiratory effect

224
Q

Features of severe asthma

A

Any one of:
- PEF 33-50%
- RR>25
- HR>110
- Inability to complete sentences

225
Q

Doses of aminophylline in severe asthma?

A

IV 5mg/kg loading dose over 20 mins + 500-700mcg/kg/hr

maintain conc below 20mcg/ml to avoid toxicity

226
Q

When to consider intubation in asthma?

A
  • Deteriorating peak flow
  • reduced GCS
  • worening hypoxaemia
  • worsening acidosis
  • severe agitation, confusion, fighting oxygen mask
  • progressive exhaustion, feeble respiration
  • arrest

(elevation of pCO2 alone does not indicate intubation)

227
Q

Special considerations for ALS in asthma

A
  • intubate early
  • consider increasing defibrillation energy if first shock unsuccessful due to dynamic hyperinflation in asthma
  • watch out for tension pneumothorax
228
Q

How comon are skin features in anaphylaxis?

A

over 80% of cases - can be subtle or dramatic

229
Q

What conditions may mimic anaphylaxis but don’t respond to adrenaline?

A
  • Inducible laryngeal obstruction
  • ACE inhibitor- induced angioedema (not life-threatening)
230
Q

What do you do if no response from giving adrenaline in anaphylaxis?

A

another dose of adrenaline and give IV fluid bolus

231
Q

If no response after 2 doses of IM adrenaline, what should you do? (refractory anaphylaxis algorithm)

A
  • Start adrenaline infusion (1mg adrenaline in 100ml of 0.9% saline, given at 0.5-1.0ml/kg/hr, titrate), with close monitoring
  • rapid IV fluid bolus
  • Give IM adrenaline every 5 mins until adrenaline infusion started
  • can consider nebulised adrenaline as adjunct (dose 5ml of 1mg mL (1:1000) adrenaline
232
Q

Doses of adrenaline by age group

A

age>12: 500mcg IM (0.5mL)
6-12: 300mcg
6 months to 6 yrs: 150mcg
<6months: 100-150mcg

233
Q

In cardiac arrests with suspectd anaphylaxis, what do you do with adrenaline?

A

Give standard 1mg dose of IV or IO adrenaline

234
Q

What investigation must be done for anaphylaxis and when?

A

Mast cell tryptase

Ideally 3 timed samples:
- 1st as soon as possible
- 2nd at 1-2 hrs (no later than 4 hrs post onset)
- 3rd at 24 hrs or in convalescence - provides baseline tryptase levels

235
Q

In pregnant Cardiac arrests, where should IV and IO lines preferably be put?

A

Above diaphragm due to IVC compression by gravid uterus

236
Q

What should you do with the uterus in pregnant cardiac arrests?

A

Displace it to left to minimise IVC compression

237
Q

Further reversible causes of collapse and cardiac arrest in pregnancy?

A

Haemorrhage
Drugs
Cardiovascular disease
Pre-eclampsia and eclampsia
Amniotic fluid embolism
PE

238
Q

4Ts of post-partum haemorrhage

A

Tone - uterine atony - give oxytocin/ergometrine/prostaglandins and uterine massage
Trauma
Thrombins - clotting screen and correction essential
Tissue - retained products of conception

239
Q

At what gestation shoud peri-mortem C section be considered?

A

Gestational age>20 weeks
(at <20 weeks, uterus not palpable above level of umbilicus, gravid uterus unlikely to compromise maternal cardiac output)

240
Q

Likely causs of cardiac arrest in traumas

A
  • Severe traumatic brain injury
  • Hypovolaemia from massive blood loss
  • Hypoxia from respiratory arrest/airway obstruction
  • Direct injury to vital organs + major vessels
  • Tension pneumothorax
  • Tamponade

(Generally have PEA and asystole as initial rhythms)

241
Q

What is ‘commotio cordis’

A

Actual or near cardiac arrest caused by blunt impact to chest wall over heart, causing VF/pVT

242
Q

How much TXA do you give in traumatic haemorrhage?

A

1g IV over 10 mins followed by 1g over 8hrs

243
Q

In In arrests caused by hypovolaemia, tamponade or tension pneumothorax, what is prioritised over compressions?

A

Treating cause (eg thoracotomy, controlling haemorrhage etc)

244
Q

In traumatic cardiac arrests, what is the approximate time when you can stop CPR if no response seen with all reversible causes excluded?

A

20 minutes

245
Q

How do you do haemorrhage control?

A
  • For compressible external haemorrhage, elevate and apply direct pressure, use tourniquets and topical haemostatic agents as required
  • For non-compressible haemorrhage, use splints, blood products, IV fluids and TXA, while moving to radiological/surgical control
  • For exsanguinating and uncontrollable infra-diaphragmatic torso haemorrhage, use immediate aortic occlusion, via resuscitative thoracotomy and cross-clamping of descending aorta or use of intravascular occlusion device (REBOA)
  • Be aware of neurogenic shock from spinal cord injury that can exacerbate hypovolaemia - treat with vasopressors
246
Q

Features of neurogenic shock

A

Warm, vasodilated peripheries, loss of reflexes below injured segment, severe hypotension with low heart rate

247
Q

Post-cardiac surgery cardiac arrests, what needs to be done and when?

A

Emergency resternotomy once all other reversible causes excluded and 3 shocks given

248
Q

How do you correct hypoxaemia in drowning?

A

Ventilation-only resuscitation

249
Q

When performing CPR on a drowned person, how do you start?

A

5 initial ventilations

250
Q

What is classified as severe hypothermia?

A

Less than 28 degrees (stage III)

250
Q

What level of hypothermia is irreversible?

A

Stage V: less than 11.8

251
Q

What temperature do patients need to be warmed to until cardioactive drugs can be given and what special precautions are required?

A

30 degrees - withold adrenaline until then and double dosing intervals compared ot normothermia

35 degrees- proceed as usual

252
Q

What considerations must be taken re: defibrillation in hypothermia?

A

Give 3 shocks in VF, but if it persists after 3 shocks delay attempts until temperature >30 degrees

253
Q

Triad of symptoms for heat stroke?

A
  • Severe hyperthermia >40 degrees
  • Neurological symptoms
  • Exposure to high environmental temperatures or recent strenous physical exertion
254
Q

Is rapid cooling in hyperthermia safe?

A

Yes

255
Q

What do you do in malignant hyperthermia?

A

Stop triggering agents, give oxygen, correct metabolic abnormalities, start active cooling

Give dantrolene

256
Q

How often do relapses occur in malignant hyperthermia?

A

Up to 25% in 72 hrs

257
Q

What are the post-cardiac arrest syndromes?

A
  • Brain injury
  • Myocardial dysfunction
  • Systemic ischaemia/reperfusion response
  • Persistent precipitating pathology
258
Q

What is the most effective treatment for post-cardiac arrest myocardial dysfunction?

A

Noradrenaline with or without dobutamine, with fluids (large volumes usually tolerated well)
- consider insertion of intra-aortic balloon pump if unresponsive

259
Q

List some sources of error with pulse oximetry

A
  • Presence of other haemoglobins (carboxyhaemoglobin, methaemoglobin, fetal haemoglobins, sickle cell)
  • Surgical/imaging dyes (eg methylene blue can give falsely low readings)
  • Nail varnish (esp blue, black, green)
  • High-ambient light levels (fluorescent and xenon lamps)
  • Motion artefact
  • Reduced pulse volume (hypotension, low cardiac output, vasoconstriction, hypothermia)

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