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Advanced Life Support (ALS) > Chapter 12: Resuscitation in Special Circumstances > Flashcards

Chapter 12: Resuscitation in Special Circumstances Flashcards

1
Q

What happens to potassium in acidosis?

A

Serum K+ increase as it moves from cells to serum

H+/K+ pump

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2
Q

How is hyperkalaemia defined and what classifies as severe?

A

K+>5.5mmol/L

Severe >6.5mmol/L

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3
Q

What can cause hyperkalaemia?

A

Renal failure
Acidosis
DKA
Drugs - Spironolactone, ACEi, amiloride, ARB, NSAID’s, B blockers, trimethoprim
Endocrine - Addison’s disease
Tissue breakdown - rhabdomyolysis, TLS, haemolysis

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4
Q

How may hyperkalaemia present?

A

Arrhythmia

Weakness –> flaccid paralysis, paraesthesia, depressed tendon reflexes

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5
Q

What ECG changes do you see with hyperkalaemia?

A 
Absent/small p waves
Long PR
Tall tented t waves
Wide QRS
Can see ST segment depression

S and T merging
VT
Bradycardia
Cardiac arrest

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6
Q

How is hyperkalaemia treated?

A

STOP DRUGS/K+ fluids

  • IV Calcium chloride - 10ml/10% over 2-5 mins
  • Insulin/Dextrose - 10 units in 250ml of 10% 15-30min
  • Sodium bicarbonate - 50mmol IV bolus - severe acidosis or renal failure
  • Salbutamol nebulised 10-20mg
  • Dialysis
  • K+ binder - calcium resonium 15-30g or Sodium Polystyrene Sulfonate
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7
Q

What do you do for each stage of hyperkalaemia?

A

Mild: 5.5-5.9

  • Address cause
  • Calcium resonium or sodium polystyrene sulfonate

Mod: 6.0-6.4

  • Insulin dextrose
  • as above

Severe: 6.5+

  • Expert help
  • Calcium chloride
  • Shifting agents
  • Remove K+ - dialysis
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8
Q

What are the main risks associated with hyperkalaemia treatment?

A

Hypoglycaemia - monitor BM

Tissue necrosis - secondary to extravasation of intravenous calcium salts - Ensure secure vascular access

Intestinal necrosis and obstruction - K+ exchange resin - avoid prolonged use and give laxative

Rebound hyperkalaemia - after drug treatment warn off - monitor for at least 24hr

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9
Q

What is important to know about cardiac arrest in haemodialysis patients?

A 
Sudden cardiac death most common cause
Usually ventricular arrhythmia
Stop ultrafiltration, give fluid and return pt blood volume
Disconnect dialysis machine
Use dialysis access for drugs
Early defib
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10
Q

How is hypokalaemia defined?

A

<3.5mmol/L

Severe = <2.5mmol/L

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11
Q

What can cause hypokalaemia?

A 
GI losses
Alkalosis
Drugs - loop diuretics, thiazides, laxatives, steroids
Renal losses
Cushings/hyperaldosteronism
Mg depletion
Poor intake

Overtreated High K+

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12
Q

How can you recognise hypokalaemia?

A
  • Rule out in all arrhythmia/cardiac arrest
  • Seen at end of haemodialysis or in peritoneal dialysis
    Symptoms:
  • Fatigue
  • Weakness
  • Leg cramps
  • Constipation

If severe:

  • Rhabdomyolysis
  • Ascending paralysis
  • Resp difficulties
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13
Q

What ECG features are seen in hypokalaemia?

A 
U waves
Small t waves
ST segment changes
Arrhythmia's
Cardiac arrest
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14
Q

How should K+ be replaced?

A

Gradually
Max 20mmol/L per hour

More rapid infusion indicated in unstable arrhythmia - 2mmol/L/min for 10 mins then 10mmol over 5-10 mins

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15
Q

What can cause hypercalcaemia?

A

Primary/tertiary hyperparathyroid
Malignancy
Sarcoid
Drugs

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16
Q

How does hypercalcaemia present?

A 
Confusion
Weakness
Abdo pain
Hypotension
Arrhythmia
Cardiac arrest
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17
Q

What ECG changes are seen in hypercalcaemia?

A 
Short QT
Wide QRS
Flat t waves
AV block
Cardiac arrest
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18
Q

How is hypercalcaemia treated?

A 
Fluid replacement
Furosemide - 1mg/kg
Hydrocortisone 200-300mg
Pamidronate 30-90mg
Treat underlying cause
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19
Q

What can cause hypocalcaemia?

A 
Chronic renal failure
Pancreatitis
Calcium channel blocker OD
Toxic shock syndrome
Rhabdomyolysis
TLS
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20
Q

How does hypocalcaemia present?

A 
Paraesthesia
Tetany
Seizures
AV block
Cardiac arrest
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21
Q

What ECG changes are seen for hypocalcaemia?

A

Prolonged QT
T wave inversion
Heart block
Cardiac arrest

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22
Q

What can cause hypermagnasaemia?

A

Renal failure

Iatrogenic

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23
Q

How does hypermagnasaemia present?

A 
Confusion
Weakness
Resp. depression
AV block
Cardiac arrest
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24
Q

What ECG changes are seen for hypermagnasaemia?

A

Prolong PR and QT
T wave peak
AV block
Cardiac arrest

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25
Q

How is hypermagnasaemia managed?

A

Calcium chloride 10ml 10%
Ventilatory support if req.
Saline diuresis - furosemide 1mg/kg+0.9% saline
Haemodialysis

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26
Q

What can cause hypomagnasaemia?

A 
GI loss
Polyuria
Starvation
Alcohol
Malabsorption
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27
Q

How does hypomagnasaemia present?

A 
Tremor
Ataxia
Nystagmus
Seizures
Arrhythmia - torsades 
Cardiac arrest
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28
Q

How does hypomagnasaemia present on ECG?

A 
Prolong PR and QT
ST depression
T wave inversion
Flat p waves
Wide QRS
Can get polymorphic VT - torsades
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29
Q

How is hypomagnasaemia managed?

A

2g 50% MgSo4 (4ml 8mmol/L)

  • severe = over 15 mins
  • torsades = over 1/2 mins
  • Seizure = over 10 mins
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30
Q

How is septic shock defined?

A

Lactate >4mmol/L
Hypotension unresponsive to fluid resus

50% mortality

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31
Q

What are the common causes for mortality in poisoning?

A

Airway obstruction and respiratory arrest secondary to decreased conscious level - early tracheal intubation

Drug induced hypotension - usually respond to IV fluids but may need vasopressor support

Electrolytes, BM and ABG’s should be checked as they commonly cause mortality

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32
Q

What modifications are required to resus in poisoning?

A

Avoid mouth to mouth breathing in presence of cyanide, hyrogen sulphide, corrosives and organophosphates

Check for hypo/hyperthermia

Be prepared for long resus time and consider ECLS

Seek expert advise and consult TOXBASE

Focus on correcting hypoxia, hypotension, acid/base and electrolytes

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33
Q

What specific treatments are available for poisoning?

A

Skin exposure - remove clothes

Gastric lavage and laxatives not used

Activated charcoal - <1hr and intact airway. Useful for carbamazepine, dapsone, phenobarbital, quinine and theophylline

Whole bowel irrigation using polyethylene glycol - sustained release/enteric coated drugs, oral iron poisoning, removal of ingested packets illicit drugs

Sodium Bicarb IV - salicylate poisoning

Haemodialysis - Drugs with low molecular weight, low protein binding, small volume of distribution, high water solubility

Specific antidotes

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34
Q

What is the specific antidote for paracetamol?

A

N-acetylcysteine

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35
Q

What is the specific antidote for organophosphate poisoning?

A

High dose atropine

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36
Q

What is the antidote for cyanides poisoning?

A

Sodium nitrite
Sodium thiosulphate
Hydroxocobalamin
Amyl nitrite

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37
Q

What is the antidote for digoxin poisoning?

A

Digibind - digoxin specific Fab antibodies

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38
Q

What is the antidote for benzodiazepines?

A

Flumazenil if no risk of seizure

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39
Q

What is the antidote for opioid poisoning?

A

Naloxone 400mcg IV, 800mcg IM, 800mcg SC or 2mg Intranasal

Non IV may be quicker - save time getting access

Duration of action not as long as respiratory depression persist - give increments until breathing adequately

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40
Q

What does opioid poisoning cause?

A

Resp depression
Pinpoint pupils
Coma following resp. arrest

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41
Q

What happens if opioids are withdrawn acutely in poisoning?

A

State of sympathetic excess leading to complications:

  • Pulmonary oedema
  • Ventricular arrhythmia
  • Severe agitation

Use naloxone cautiously in patients with dependence

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42
Q

What can a benzodiazepine OD cause?

A

Loss of consciousness
Respiratory depression
Hypotension

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43
Q

What can reversal of benzodiazepine OD with flumazenil lead to in patients with dependence or have coinjested pro-convulsants?

A

Seizure
Arrhythmia
Hypotension
Withdrawal syndrome

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44
Q

Is flumazenil used in comatose patients?

A

No

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45
Q

What can tricyclic antidepressant OD cause?

A

Hypotension
Seizure
Coma
Life-threatening arrhythmia - commonly shockable
Anti-cholinergic effects - mydriasis, fever, dry skin, delirium, tachycardia, ileus, retention

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46
Q

What may indicate that a TCA overdose will lead to arrhythmia?

A

Wide QRS
Right axis deviation

Consider sodium bicarb

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47
Q

When can you get local anaesthetic toxicity?

A

Regional anaesthesia - enters artery or vein

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48
Q

What issues can you get with local anaesthetic toxicity?

A

Severe agitation

Loss of consciousness with or without tonic-clonic convulsions

Sinus Bradycardia/ Conduction blocks/Asystole/VT

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49
Q

How can local anaesthetic toxicity be treated?

A

Resus measures

IV 20% lipid emulsion

  • initial 1.5mL/kg/hr bolus in 1 min followed by 15mL/kg/hr infusion
  • Give upto 3 boluses at 5 min intervals
  • Max 12mL/kg emulsion
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50
Q

What should you do following lipid emulsion rescue for local anaesthetic toxicity?

A

Exclude Pancreatitis - daily amylase or lipase assays for 2 days

Safe. transfer to clinical area

Report cases to National Patient Safety Agency

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51
Q

What can cocaine toxicity cause?

A

Sympathetic overstimulation:

  • agitation
  • symptomatic tachycardia
  • hyperthermia
  • hypertensive crisis
  • myocardial ischaemia with angina
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52
Q

What can be done to treat cocaine toxicity?

A

Small dose IV benzo (midazolam, diazepam, lorazepam)

GTN and phentolamine - reverse coronary vasoconstriction

Can consider beta blockers and anti-arrhythmics - best unclear

Use normal adrenaline dose if arrest

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53
Q

How is drug induced severe bradycardia managed?

A

Atropine - organophosphate, carbamate, nerve agent poisoning or acetylcholinesterase inhibitors

2-4mg IV repeated doses

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54
Q

What can be used to treat bradycardia due to beta blockers or calcium channel blockers?

A

Can use Isoprenaline at high dose if refractory bradycardia due to beta blockers

Vasopressors, inotropes, calcium, glucagon, phosphodiesterase inhibitors and high dose insulin-dextrose-potassium infusions

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55
Q

Which asthmatic patients are at highest risk for near fatal attacks?

A
  • Hx of req. intubation and mechanical ventilation
  • Hospitalisation/emergency care in last year
  • Low or no use of inhaled ICS
  • Increased use/dependence on SABA
  • Anxiety, depression and/or poor compliance
  • Food allergy
56
Q

What can cause cardiorespiratory arrest in asthmatic patients?

A
  • Severe bronchospasm and mucous plugging –> asphyxia
  • Hypoxia –> cardiac arrhythmia. Can also be due to drugs or electrolyte abnormalities
  • Dynamic hyperinflation in mechanically ventilated - reduced venous return and BP
  • Tension pneumothorax
57
Q

What signs indicate acute severe asthma?

A
  • PEFR 33-50%
  • RR >25
  • HR >110
  • Inability to complete sentence in 1 breath
58
Q

What signs indicate life-threatening asthma?

A 
Altered conscious level
Exhaustion
Arrhythmia
Hypotension
Cyanosis
Silent chest
Poor resp effort

PEFR<33
SpO2 <92%
PaO2 <8kPa
‘normal’ PaCO2 - 4.6-6

59
Q

What indicates asthma mat be near fatal?

A

Raised PaCO2 and/or mechanical ventilation with raised inflation pressures

60
Q

What may absence of wheezing in asthma indicate?

A

Critical airway obstruction

Increased wheezing may indicate + response to therapy

61
Q

What can happen to SpO2 in SABA therapy of asthma?

A

May initially decrease as beta agonists cause bronchodilation and vasodilation - increased intra pulmonary shunting

62
Q

How can acute asthma attacks be managed?

A
  • High flow O2 - sats of 94-98%
  • Salbutamol 5mg neb - repeat every 15-30 mins or cont. 5-10mg/hr
  • Add neb ipratropium bromide 500mcg 4-6hr
  • Prednisolone 40-50mg PO or hydrocortisone 100mg IV

Can give IV Magnesium sulphate 2g (8mmol) over 20 mins
Consider IV salbutamol 250mcg if inhaled not possible

Senior advice for aminophylline - 5mg/hr IV 20 min then 500-700mcg/kg/hr infusion (max dose 20mcg/mL to avoid toxicity)

63
Q

What can beta agonist and steroid therapy in asthma cause?

A

Hypokalaemia - correct

64
Q

When should tracheal intubation and controlled ventilation be considered in asthma?

A 
Deteriorating peak flow
Reduced conscious level
Persisting/worsening hypoxaemia
Worsening resp. acidosis
Severe agitation, confusion and fighting against o2 mask
Progressive exhaustion
Cardioresp. arrest

Role of non invasive ventilation unclear - only considered in ICU setting

65
Q

How is ALS modified in acute asthma?

A
  • Intubate early - high risk of GI inflation and hypoventilation if ventilate without tracheal tube
  • RR 10 breaths and normal tidal volume
  • If dynamic hyperinflation - compress chest wall + disconnect tracheal tube
  • Be aware of tension pneumothorax
  • Consider extracorporeal life support
66
Q

Which 3 criteria are indicative of anaphylaxis?

A

1 Sudden onset and rapid progression of symptoms
2 Life threatening airway and/or breathing and/or circulatory problems
3 Skin and/or mucosal changes - flushing, urticaria, angioedema

67
Q

What is important to remember about recognising anaphylaxis?

A

Skin and mucosal changes alone not a sign

Skin and mucosal changes can be subtle/absent

Can be GI symptoms

68
Q

How is anaphylaxis managed in an adult?

A 
Remove trigger
Lie down
IV Fluid challenge 500-1000ml
IV chlorphenamine 10mg
IV hydrocortisone 200mg
IM Adrenaline 0.5mg (0.5ml of 1:1000) - anterolateral middle thigh
69
Q

How is anaphylaxis managed in children?

A

Fluids:
- Crystalloid 20ml/kg

Child 6-12:

  • IM adrenaline 0.3mg
  • IV chlorphenamine 5mg
  • IV hydrocortisone 100mg

Child 6 month to 6 yo:

  • IM adrenaline 0.15mg
  • IV chlorphenamine 2.5mg
  • IV hydrocortisone 50mg

Child <6 months

  • IM adrenaline 0.15mg
  • IV chlorphenamine - 250mcg/kg
  • IV hydrocortisone 25mg
70
Q

When can IV adrenaline be used in anaphylaxis?

A

Only by specialists

Can cause hypertension, tachycardia, ischaemia, arrhythmia if spontaneous circulation

May be used if repeated IM doses

Max 50mcg in adults and 1mcg/kg in children

71
Q

How can anaphylaxis be investigated?

A

Mast cell tryptase - 3 timed samples:

  • ASAP after resus
  • 1-2hr after start of symptoms
  • 24hr after
72
Q

What can cause cardiac arrest in pregnancy?

A 
Cardiac disease
PE
Psychiatric disorders
Hypertensive disease - eclampsia/pre-eclampsia
Sepsis
Haemorrhage
Amniotic fluid embolus
Ectopic
73
Q

How do you initially treat a distressed/compromised pregnant patient?

A

Left lateral position/manually displace uterus - relieve pressure on IVC

High flow O2

Fluid bolus

74
Q

How is cardiac arrest management modified in pregnancy?

A

Summon help immediately
Start CPR - hand may be slightly higher
Establish IV access above diaphragm
Manually displace uterus/left lateral tilt 15-30 degrees
Prep for C-Section
Early tracheal intubation
May need alternative pad positions for defibrillation

75
Q

How is haemorrhage in pregnancy managed in cardiac arrest?

A

Fluid Resus

Tranexamic acid and correct coagulopathies

Oxytocin, ergometrine, prostaglandins and uterine massage for uterine atony

Uterine compression sutures, packs or intrauterine balloon devices

Surfical control - aortic cross clamp/compression and hysterectomy. Placenta percreta may req. intra-pelvic surgery

76
Q

How is pre-eclampsia treated?

A

Magnesium sulphate - prevent eclampsia in labour

77
Q

How are amniotic fluid emboli managed?

A

Supportive

Correct coagulopathies

78
Q

Should fibrinolysis be given in PE in pregnancy?

A

Must be carefully considered

If diagnosis suspected and maternal cardiac output can’t be restored then yes

79
Q

When is peri-mortem C-section considered?

A

<20 weeks - not considered
20-23 weeks - Initiate emergency delivery to permit successful resus of mother not for survival of infant
>24 weeks - initiate for both mother and infant

80
Q

What is important in post resus care for pregnant patients?

A

Targeted temperature management with fetal heart monitoring

ICD’s can be used

81
Q

What are the key causes of cardiac arrest in trauma patients?

A 
Severe traumatic brain injury
Hypovolaemia
Hypoxia
Tension pneumothorax
Direct injury to vital organs
Cardiac tamponade
82
Q

What is commotio cordis?

A

Actual or near arrest caused by blunt impact to chest wall over the heart

If coincide with t wave, can lead to VF

83
Q

What factors are associated with survival from traumatic cardiac arrest?

A 
Presence of reactive pupils
Duration of CPR
Pre-hospital time
Organised ECG rhythm
Respiratory activity

Prolonged CPR - poor outcome (stop. after 20 mins if no response)

84
Q

What is a key focus of traumatic cardiac arrest management? What may be helpful to use in these cases?

A

Correct the reversible causes

Do chest compressions but unlikely to be successful without correction

FAST scan or CT may be useful in guiding treatment

Early tracheal intubation can be beneficial

85
Q

What can happen if positive pressure ventilation is used in low cardiac output conditions?

A

Further circulatory depression by impeding venous return

86
Q

How are tension pneumathoraces managed in traumatic cardiac arrest?

A

Bilateral thoracotomies
5th intercostal space mid axillary line

Can extend to clamshell thoracotomy if req

Needle decompression is a v temporary measure

87
Q

How is a cardiac tamponade managed?

A

Resuscitative clamshell thoracotomy

Needle aspiration unreliable - pericardium commonly full of clotted blood

88
Q

When should resuscitative thoracotomies be considered?

A

Penetrating torso trauma and <15min CPR

Blunt trauma and <10min prehospital CPR

No pulse after penetrating chest or cardiac injuries and signs of life or ECG activity

89
Q

What are the commonest causes of anaesthesia related cardiac arrest?

A

Airway management

90
Q

What are the most common rhythms seen in peri op cardiac arrest?

A

Asystole - 41%

VF - 35%

91
Q

What is important about the management of periop cardiac arrest?

A

Use fluid warmers and forced air warmers

PEA may not be immediately detected - use low end tidal CO2 to provoke pulse check

CPR is ideal in supine position but possible prone

Consider open cardiac compressions if heart easily accessed

Give pre-cordial thump if no immediate access to defib

Stop surgery in asystole or extreme Brady - likely excess vagal activity - atropine 0.5mg

If adrenaline, give dose in 50-100mcg increments instead of 1mg bolus. If no response then further 1mg boluses

92
Q

What is key to know about cardiac arrest following cardiac surgery?

A

Relatively common

Recognition of need to perform resteronomy early is key - tamponade or haemorrhage

External compressions may cause sternal disruption and cardiac damage

Use adrenaline v cautiously and titrate to effect IV upto 0.1mg

93
Q

When is emergency resternotomy indicated?

A

Adequate airway and ventilation
3 shock attempts in VF/pVT
Asystole/PEA

Do resternotomy without delay. Ideally within 5 mins of arrest

94
Q

Should you do external chest compressions in cardiac arrest following cardiac surgery?

A

Yes start immediately if no output

Verify effectiveness using arterial trace - systolic of >60 and diastolic >25. HR 100-120

If not reaching targets, resternotomy

95
Q

What is drowning and what are the “types”?

A

Respiratory impairment from submersion/immersion in liquid

Submersion - face underwater/covered by water

Immersion - head remain above water - e.g. life jacket

96
Q

What typically happens to patients who are immersed in water?

A

Become hypothermic

Airway remain patient

Water splashes can cause aspiration

97
Q

What happens in submersion?

A

Patient initially hold breath and swallow water

As pt. become hypoxic and hypercapnic, breath holding reflex and laryngospasm reflex lost. Patient aspirate water

Laryngospasm reflex prevent water entering lungs

Bradycardia due to hypoxia occur before sustaining cardiac arrest

98
Q

How should you correct hypoxaemia following submersion?

A

Ventilation only resus

99
Q

How do you attempt to rescue someone from the water?

A

Ideally throw rope or buoyant rescue aid

Assess risk and enter with flotation device

If submersion for <10 mins - likely good outcome. If >25 mins - likely poor outcome

Remove from water horizontally - spinal precautions rarely necessary

100
Q

Why remove patients horizontally from the water?

A

Hypovolaemia after prolonged immersion can cause cardiovascular collapse and arrest

101
Q

When are spinal precautions necessary in water rescue?

A 
Diving in shallow water
Signs of severe injury water side
Water skiing
Kite surfing
Watercraft racing

If pulseless and apnoeic - remove asap while limiting neck movement

102
Q

What initial rescue should you do for patients once retrieved from the water?

A

Check for response
Give 5 rescue breaths with supplemented oxygen
Start SPR as normal
If lots of foam - continue CPR until intubation
Turn victim to side and remove regurgitation material

103
Q

What modifications can be made to ALS after drowning?

A

Use PEEP and NG stomach decompress in drowning pt who hasn’t arrested or achieved ROSC

Check ECG and end tidal CO2 for signs of life. Consider echo (pulse not sufficient)

Give rapid IV fluid - pt. become hypovolaemic due to cessation of hydrostatic pressure from water

104
Q

What is important about post resus care after drowning?

A

Risk of developing ARDS - use standard protective ventilation stratefies

Consider ECMO for refractory cardiac arrest, hypoxaemia and submersion in ice cold water

Pneumonia common however prophylactic Abx only if sewage/grossly contaminated

Neurological outcome determined by hypoxia

105
Q

Define hypothermia

A

<35 degrees
Mild = 32-35
Mod = 28-32
Severe = <28

106
Q

What happens in each stage of hypothermia?

A

I Mild - shivering, conscious

II Mod - stop shivering, conscious,

III Severe - decreased consciousness, vitals present (28-24)

IV - unconscious, vitals not present <24

V - death due to irreversible hypothermia <13.7

107
Q

What may increase risk of hypothermia?

A

Things that decrease conscious level - drugs, alcohol, illness, exhaustion, neglect

Factors that impair thermoregulation - elderly and very young

108
Q

Where is a core body temperature taken from?

A

Lower third of oesophagus

109
Q

How much does hypothermia reduce oxygen demand?

A

6% reduction per 1 degree

110
Q

Why must you be careful diagnosing death in hypothermic?

A

Patients can have slow small volume irregular pulses and low BP but they may return once warm

Not dead until warm and dead

At 18 degrees, brain survive 10 times as long from circulatory arrest than at 37

Good survival has been reported in arrest and core temp of 13.7 degrees after immersion for 6.5 hours with CPR in adults

111
Q

How should CPR be modified in hypothermic patients?

A

<28 degrees 5 min CPR, 5 min break
<20 5 min CPR, 10 min break

Check for pulse for 1 minute - central artery and ECG

Consider using mechanical chest compression

Dont delay intubation

Hold adrenaline and amiodarone until >30 degrees. Then double dose interval (6-10 mins) until 35 degrees

112
Q

How are arrhythmia’s treated in hypothermia?

A

Sinus Brady –> AF –> VF –> asystole

Apart from VF, others revert spontaneously as temp increase. Cardiac pacing not indicated unless haemodynamic compromise persist after rewarming

Stop shocks after 3 until temp >28-30

113
Q

How are patients rewarmed after accidental hypothermia?

A

Remove from cold and take off wet clothes

stage II and worse - immobilise, handle carefully, oxygenate, dry and give clothes, heat packs

Stage I - mobilise as rewarm - exercise rewarm patient

Patients continue to cool after removal from cold environment - faster if stage II or worse

114
Q

Where should hypothermic patients be taken?

A

Stage I - nearest hospital

II - IV - Nearest hospital with ECMO facilities

V - Consider whether to withhold CPR, if not nearest hospital with ECMO

115
Q

What are the reasons to terminate CPR in a hypothermic patient?

A 
DNACPR
Obvious sign of irreversible death
Unsafe for rescuer
Avalanche burial for >60 min
Airway packed with snow
Asysole
116
Q

When are avalanche victims not likely to survive?

A

Buried for >60 mins and in cardiac arrest with obstructed airway on extraction

Buried and in cardiac arrest with K+ >8mmol/L

117
Q

When can extracorporeal life support rewarming be considered?

A

Temp <32
K+ <8mmol/L

Veno-arterial ECMO preferred as more rapidly available, less anticoagulation, provide prolonged cardioresp support after rewarming

118
Q

What other active rewarming techniques can be used?

A

Forced warm air
Warm infusions
Forced peritoneal lavage

119
Q

What are the stages of hyperthermia?

A

Heat stress
Heat exhaustion
Heat stroke –> multi-organ dysfunction and cardiac arrest

120
Q

What is heat stroke?

A

Core temp >40.6
Change in mental state
Varying levels of organ dysfunction

2 types:

  • exertional
  • non exertional - elderly in heat waves
121
Q

What can predispose someone to heat stroke?

A

Elderly:

  • underlying illness
  • medication use
  • declining thermoregulatory mechanisms
  • limited social support
Lack of acclimitisation
Dehydration
Alcohol
Obesity
CVS conditions
Skin disease
Hyperthyroidism
Phaeochromocytoma
122
Q

What drugs can predispose to hyperthermia?

A 
Anticholinergics
Diamorphine
Cocaine
Methamphetamine
Phenothiazines
Sympathomimetics
Ca2+ blockers
Beta blockers
123
Q

What are the features of heat stroke?

A 
Core Temp >40
Hot dry skin
Fatigue, headache, fainting, facial flush, D&V
CVS dysfunction - arrhythmia and hypotension
Resp dysfunction - ARDS
CNS dysfunction - seizures and coma
Liver and renal failure
Coagulopathy
Rhabdomyolysis
124
Q

What differentials do you have to consider for raised core temperature?

A 
Drug withdrawal syndromes
Neuroleptic malignant syndrome
Sepsis
CNS infection
Endocrine disorder - thyroid and phaeochromocytoma
125
Q

How is heat stroke treated?

A

Rapid cooling
Haemodynamic monitoring - fluid and electrolytes
Defibrillation as normal
Post resus care as normal

126
Q

How do you cool a patient in heat stroke?

A

Simple - cool drinks, take off clothes, fan, spray tepid water, ice packs over groin, axilla neck

Immerse in cold water - can cause vasoconstriction, preventing heat dissipation

Advanced - cold IV fluids, intravascular cooling catheters, ECMO

Diazepam for seizures

127
Q

What is used in treatment of malignant hyperthermia?

A

Dantrolene

128
Q

What factors influence severity of electrocution injury?

A 
AC/DC current
Voltage
Magnitude fo energy
Resistance to current flow
Pathway of current
Area and duration of contact
129
Q

What reduces skin resistance to electrocution?

A

Moisture

130
Q

What is most likely to be damaged in electrocution?

A

Conductive neuovascular bundles

131
Q

What does contact with AC current lead to?

A

Tetanic contract of skeletal muscle

132
Q

What can cause myocardial or respiratory failure in electrocution?

A

Resp arrest due to paralysis of respiratory muscles or resp depression

Current can precipitate VF if it crosses myocardium during vulnerable period.

Current can cause coronary artery spasm

Asystole ma be primary or secondary to asphyxia following resp arrest

133
Q

What current direction is more likely to be dangerous?

A

Current that transverse myocardium

Transthoracic pathway (hand to hand) more likely to be fatal than vertical (hand - foot) or straddle (foot - foot)

134
Q

In patients who survive an initial electric shock, what may happen?

A

Catecholamine release or autonomic stimulation:

  • tachycardia
  • hypertension
  • prolonged QT and transient t wave inversion
  • myocardial necrosis
  • CK release
135
Q

How are lightning strikes and electrical injuries treated?

A

Early intubation - airway management may be difficult if burns

Ventilatory support if muscle paralysis persist

Use standard defibrillation guidelines

Remove smouldering clothing and shoes to prevent thermal injury

IV fluids if tissue destruction - good urine output

Early surgery if req.

Check for compartment syndrome

136
Q

What arrhythmia is most likely to be seen in an electrocution?

A

AC - VF

DC - Asystole

137
Q

What determines long term prognosis for electrical injury?

A

Severe burns
Myocardial necrosis
Extent of CNS injury
Multiple system organ failure

Advanced Life Support (ALS) (8 decks)

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