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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
  1. Serum K+ increase as it moves from cells to serum
  2. H+/K+ pump
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2
Q

How is hyperkalaemia defined and what classifies as severe?

A

K+>5.5 mmol/L

Severe >6.5 mmol/L

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3
Q

What can cause hyperkalaemia?

A
  1. Renal failure
  2. Acidosis
  3. DKA
  4. Drugs - Spironolactone, ACEi, amiloride, ARB, NSAID’s, B blockers, trimethoprim
  5. Endocrine - Addison’s disease
  6. 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
  1. Absent/small p waves
  2. Prolonged PR
  3. Wide QRS
  4. Can see ST segment depression
  5. S and T merging
  6. Tall tented T waves
  7. VT
  8. Bradycardia
  9. Cardiac arrest
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6
Q

How is hyperkalaemia treated?

A
  1. STOP DRUGS/K+ fluids
  2. IV Calcium chloride - 10ml/10% over 2-5 mins
  3. Insulin/Dextrose - 10 units in 250ml of 10% 15-30min
  4. Sodium bicarbonate - 50mmol IV bolus - severe acidosis or renal failure
  5. Salbutamol nebulised 10-20mg
  6. Dialysis
  7. 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
1. Address cause
2. Calcium resonium or sodium polystyrene sulfonate

Mod: 6.0-6.4
1. Insulin dextrose
2. As above

Severe: 6.5+
1. Expert help
2. Calcium chloride
3. Shifting agents
4. Remove K+ - dialysis

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8
Q

What are the main risks associated with hyperkalaemia treatment?

A
  1. Hypoglycaemia - monitor BM
  2. Tissue necrosis - secondary to extravasation of intravenous calcium salts - Ensure secure vascular access
  3. Intestinal necrosis and obstruction - K+ exchange resin - avoid prolonged use and give laxative
  4. 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
  1. Sudden cardiac death most common cause
  2. Usually ventricular arrhythmia
  3. Stop ultrafiltration, give fluid and return pt blood volume
  4. Disconnect dialysis machine
  5. Use dialysis access for drugs
  6. Early defib
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10
Q

How is hypokalaemia defined?

A
  1. < 3.5mmol/L
  2. Severe = < 2.5mmol/L
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11
Q

What can cause hypokalaemia?

A
  1. GI losses
  2. Alkalosis
  3. Drugs - loop diuretics, thiazides, laxatives, steroids
  4. Renal losses
  5. Cushings/hyperaldosteronism
  6. Mg depletion
  7. Poor intake
  8. Overtreated High K+
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12
Q

How can you recognise hypokalaemia?

A
  1. R/O in all arrhythmia/cardiac arrest
  2. Seen at end of haemodialysis or in peritoneal dialysis
  3. Symptoms: Fatigue / Weakness / Leg cramps / Constipation
  4. If severe: Rhabdomyolysis / Ascending paralysis / Resp difficulties
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13
Q

What ECG features are seen in hypokalaemia?

A
  1. ST segment changes
  2. Small T waves
  3. U waves
  4. Arrhythmia
  5. Cardiac arrest
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14
Q

How should K+ be replaced?

A
  1. Gradually
  2. Max 20mmol/L per hour
  3. 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
  1. Primary/tertiary hyperparathyroidism
  2. Malignancy
  3. Sarcoid
  4. Drugs
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16
Q

How does hypercalcaemia present?

A
  1. Abdo pain
  2. Hypotension
  3. Weakness
  4. Confusion
  5. Arrhythmia
  6. Cardiac arrest
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17
Q

What ECG changes are seen in hypercalcaemia?

A
  1. Short QT
  2. Wide QRS
  3. Flat T waves
  4. AV block
  5. Cardiac arrest
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18
Q

How is hypercalcaemia treated?

A
  1. Fluid replacement
  2. Furosemide - 1mg/kg
  3. Hydrocortisone 200-300mg
  4. Pamidronate 30-90mg
  5. Rx underlying cause
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19
Q

What can cause hypocalcaemia?

A
  1. Chronic renal failure
  2. Pancreatitis
  3. CCB OD
  4. Toxic shock syndrome
  5. Rhabdomyolysis
  6. TLS
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20
Q

How does hypocalcaemia present?

A
  1. Paraesthesia
  2. Tetany
  3. Seizures
  4. AV block
  5. Cardiac arrest
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21
Q

What ECG changes are seen for hypocalcaemia?

A
  1. Prolonged QT
  2. T wave inversion
  3. Heart block
  4. Cardiac arrest
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22
Q

What can cause hypermagnasaemia?

A
  1. Renal failure
  2. Iatrogenic
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23
Q

How does hypermagnasaemia present?

A
  1. Confusion
  2. Weakness
  3. Resp. depression
  4. AV block
  5. Cardiac arrest
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24
Q

What ECG changes are seen for hypermagnasaemia?

A
  1. Prolong PR
  2. Prolonged QT
  3. T wave peak
  4. AV block
  5. Cardiac arrest
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25
Q

How is hypermagnasaemia managed?

A
  1. Calcium chloride 10ml 10%
  2. Saline diuresis - furosemide 1mg/kg + 0.9% saline
  3. Ventilatory support if req.
  4. Haemodialysis
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26
Q

What can cause hypomagnasaemia?

A
  1. GI loss
  2. Malabsorption
  3. Starvation
  4. Alcohol
  5. Polyuria
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27
Q

How does hypomagnasaemia present?

A
  1. Tremor
  2. Ataxia
  3. Nystagmus
  4. Seizures
  5. Arrhythmia - torsades
  6. Cardiac arrest
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28
Q

How does hypomagnasaemia present on ECG?

A
  1. Flat p waves
  2. Prolong PR and QT
  3. Wide QRS
  4. ST depression
  5. T wave inversion
  6. Can get polymorphic VT - torsades
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29
Q

How is hypomagnasaemia managed?

A
  1. 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
  1. Lactate > 4mmol/L
  2. Hypotension unresponsive to fluid resus

50% mortality

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31
Q

What are the common causes for mortality in poisoning?

A
  1. Airway obstruction and respiratory arrest secondary to decreased conscious level - early tracheal intubation
  2. 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
  1. Avoid mouth to mouth breathing in presence of cyanide, hyrogen sulphide, corrosives and organophosphates
  2. Check for hypo/hyperthermia
  3. Focus on correcting hypoxia, hypotension, acid/base and electrolytes
  4. Be prepared for long resus time and consider ECLS
  5. Seek expert advise and consult TOXBASE
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33
Q

What specific treatments are available for poisoning?

A
  1. Removal of clothes - skin exposure
  2. Gastric lavage and laxatives NOT used
  3. Activated charcoal - < 1hr and intact airway
  4. Whole bowel irrigation using polyethylene glycol
  5. Sodium Bicarb IV
  6. Haemodialysis
  7. Specific antidotes

Activated Charcoal (QuiT CPD) - carbamazepine, dapsone, phenobarbital, quinine and theophylline

Polyethylene glycol - sustained release/enteric coated drugs, oral iron poisoning, removal of ingested packets illicit drugs

Soda Bic - salicylate poisoning

Haemodialysis - Drugs with LMW, low protein binding, small VoD, high H2O solubility

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34
Q

What is the specific antidote for paracetamol?

A

1.N-acetylcysteine

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35
Q

What is the specific antidote for organophosphate poisoning?

A
  1. High dose atropine
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36
Q

What is the antidote for cyanide poisoning?

A
  1. Hydroxocobalamin
  2. 50% mortality thiosulphate
  3. Sodium nitrite
  4. Amyl nitrite
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37
Q

What is the antidote for digoxin poisoning?

A
  1. Digibind - digoxin specific Fab antibodies
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38
Q

What is the antidote for benzodiazepines?

A
  1. Flumazenil if no risk of seizure
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39
Q

What is the antidote for opioid poisoning?

A
  1. Naloxone 400mcg IV, 800mcg IM, 800mcg SC or 2mg Intranasal
    2.Non IV may be quicker - save time getting access
  2. 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
  1. Pinpoint pupils
  2. Resp depression
  3. Resp. arrest - Coma
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41
Q

What happens if opioids are withdrawn acutely in poisoning?

A

State of sympathetic excess leading to complications:
1. Severe agitation
2. Pulmonary oedema
3. Ventricular arrhythmia

Use naloxone cautiously in patients with dependence

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42
Q

What can a benzodiazepine OD cause?

A
  1. LOC
  2. Resp depression
  3. 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
  1. Withdrawal syndrome
  2. Seizure
  3. Hypotension
  4. Arrhythmia
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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
  1. Anti-cholinergic effects - mydriasis, fever, dry skin, delirium, tachycardia, ileus, retention
  2. Life-threatening arrhythmia - commonly shockable
  3. Hypotension
  4. Seizure
  5. Coma
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46
Q

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

A
  1. Wide QRS
  2. Right axis deviation

Rx - Consider sodium bicarb

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47
Q

When can you get local anaesthetic toxicity?

A
  1. Regional anaesthesia - enters artery or vein
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48
Q

What issues can you get with local anaesthetic toxicity?

A
  1. Severe agitation
  2. LOC
  3. With or without tonic-clonic convulsions
  4. Sinus Bradycardia/ Conduction blocks/Asystole/VT
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49
Q

How can local anaesthetic toxicity be treated?

A
  1. Resus measures
  2. IV 20% lipid emulsion
  3. Initial 1.5mL/kg bolus in 1 min
  4. Give up to 3 boluses at 5 min intervals
  5. Followed by 15mL/kg/hr infusion
  6. Max 12mL/kg emulsion
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50
Q

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

A
  1. Exclude Pancreatitis - daily amylase or lipase assays for 2 days
  2. Safe. transfer to clinical area
  3. Report cases to National Patient Safety Agency
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51
Q

What can cocaine toxicity cause?

A

Sympathetic overstimulation:
1. Agitation
2. Hyperthermia
3. Symptomatic tachycardia
4. Hypertensive crisis
5. Myocardial ischaemia with angina

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52
Q

What can be done to treat cocaine toxicity?

A
  1. Small dose IV benzo (midazolam, diazepam, lorazepam)
  2. GTN and phentolamine - reverse coronary vasoconstriction
  3. Can consider beta blockers and anti-arrhythmics - best unclear
  4. If arrest - use normal adreanline dose
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53
Q

How is drug induced severe bradycardia managed?

A
  1. Atropine - organophosphate, carbamate, nerve agent poisoning or acetylcholinesterase inhibitors
  2. 2-4 mg 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
  1. Can use Isoprenaline at high dose if refractory bradycardia due to beta blockers
  2. Inotropes
  3. Vasopressors
  4. Calcium
  5. Glucagon
  6. Phosphodiesterase inhibitors
  7. High dose insulin-dextrose-potassium infusions
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55
Q

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

A
  1. Prev Hx of intubation and mechanical ventilation
  2. Hospitalisation/emergency care in last year
  3. Low or no use of inhaled ICS
  4. Increased use/dependence on SABA
  5. Anxiety, depression and/or poor compliance
  6. Food allergy
56
Q

What can cause cardiorespiratory arrest in asthmatic patients?

A
  1. Severe bronchospasm and mucous plugging - asphyxia
  2. Hypoxia - cardiac arrhythmia
  3. Dynamic hyperinflation in mechanically ventilated - reduced venous return and BP
  4. Tension pneumothorax

Arrhythmia - Can also be due to drugs or electrolyte abnormalities

57
Q

What signs indicate acute severe asthma?

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

What signs indicate life-threatening asthma?

A
  1. Altered conscious level
  2. Exhaustion
  3. Arrhythmia
  4. Hypotension
  5. Cyanosis
  6. Silent chest
  7. Poor resp effort
  8. PEFR < 33
  9. SpO2 < 92%
  10. PaO2 < 8kPa
  11. ‘Normal’ PaCO2 - 4.6-6
59
Q

What indicates asthma may be near fatal?

A
  1. Raised PaCO2
  2. And/or mechanical ventilation with raised inflation pressures
60
Q

What may absence of wheezing in asthma indicate?

A
  1. Critical airway obstruction

Increased wheezing may indicate + response to therapy

61
Q

What can happen to SpO2 in SABA therapy of asthma?

A
  1. May initially decrease
  2. Beta agonists cause bronchodilation and vasodilation
  3. D/t - increased intra pulmonary shunting
62
Q

How can acute asthma attacks be managed?

A
  1. High flow O2 - sats of 94-98%
  2. Salbutamol 5mg neb - repeat every 15-30 mins or cont. 5-10mg/hr
  3. Add neb ipratropium bromide 500mcg 4-6hr
  4. Prednisolone 40-50mg PO or hydrocortisone 100mg IV
  5. Can give IV Magnesium sulphate 2g (8mmol) over 20 mins
  6. 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
  1. Hypokalaemia - correct
64
Q

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

A
  1. Reducing peak flow
  2. Reduced consciousness
  3. Persisting/worsening hypoxaemia
  4. Worsening resp. acidosis
  5. Worsening agitation & confusion - fighting against O2 mask
  6. Worsening exhaustion
  7. Cardioresp. arrest

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

65
Q

How is ALS modified in acute asthma?

A
  1. Intubate early - high risk of GI inflation and hypoventilation if ventilate without tracheal tube
  2. RR 10 breaths
  3. Normal tidal volume
  4. If dynamic hyperinflation - compress chest wall + disconnect tracheal tube
  5. Be aware of tension pneumothorax
  6. 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
  1. Skin and mucosal changes alone not a sign
  2. Skin and mucosal changes can be subtle/absent
  3. Can be GI symptoms
68
Q

How is anaphylaxis managed in an adult?

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

How is anaphylaxis managed in children?

A

Fluids:
1. Crystalloid 20ml/kg

Child 6-12:
1. IM adrenaline 0.3mg
2. IV chlorphenamine 5mg
3. IV hydrocortisone 100mg

Child 6 month to 6 yo:
1. IM adrenaline 0.15mg
2. IV chlorphenamine 2.5mg
3. IV hydrocortisone 50mg

Child < 6 months:
1. IM adrenaline 0.15mg
2. IV chlorphenamine - 250mcg/kg
3. IV hydrocortisone 25mg

70
Q

When can IV adrenaline be used in anaphylaxis?

A
  1. Only by specialists
  2. May be used if repeated IM doses

Max 50mcg in adults
1mcg/kg in children
Can cause hypertension, tachycardia, ischaemia, arrhythmia if spontaneous circulation

71
Q

How can anaphylaxis be investigated?

A

Mast cell tryptase - 3 timed samples:
1. ASAP after resus
2. 1-2hr after start of symptoms
3. 24hr after

72
Q

What can cause cardiac arrest in pregnancy?

A
  1. Haemorrhage
  2. Ectopic
  3. Cardiac disease
  4. Hypertensive disease - eclampsia/pre-eclampsia
  5. PE
  6. Amniotic fluid embolus
  7. Sepsis
  8. Psychiatric disorders
73
Q

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

A
  1. Left lateral position/manually displace uterus - relieve pressure on IVC
  2. High flow O2
  3. Fluid bolus
74
Q

How is cardiac arrest management modified in pregnancy?

A
  1. Summon help immediately
  2. Start CPR - hand may be slightly higher
  3. Establish IV access above diaphragm
  4. Manually displace uterus/left lateral tilt 15-30 degrees
  5. Prep for C/S
  6. Early tracheal intubation
  7. May need alternative pad positions for defibrillation
75
Q

How is haemorrhage in pregnancy managed in cardiac arrest?

A
  1. Fluid Resus
  2. Tranexamic acid and correct coagulopathies
  3. Rx uterine atony - Oxytocin, ergometrine, prostaglandins and uterine massage
  4. Uterine compression sutures, packs or intrauterine balloon devices
  5. Surgical control - aortic cross clamp/compression and hysterectomy.

Placenta percreta may req. intra-pelvic surgery

76
Q

How is pre-eclampsia treated?

A
  1. Magnesium sulphate - prevent eclampsia in labour
77
Q

How are amniotic fluid emboli managed?

A
  1. Supportive
  2. Correct coagulopathies
78
Q

Should fibrinolysis be given in PE in pregnancy?

A
  1. Must be carefully considered
  2. Yes If - Dx suspected and maternal cardiac output CANNOT be restored
79
Q

When is peri-mortem C-section considered?

A
  1. < 20 wks - not considered
  2. 20-23 wks - Initiate emergency delivery to permit successful resus of mother not for survival of infant
  3. > 24 wks - initiate for both mother and infant
80
Q

What is important in post resus care for pregnant patients?

A
  1. Targeted temperature management
  2. Fetal heart monitoring
  3. ICD’s can be used
81
Q

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

A
  1. Severe TBI
  2. Hypovolaemia
  3. Hypoxia
  4. Tension pneumothorax
  5. Cardiac tamponade
  6. Direct injury to vital organs
82
Q

What is commotio cordis?

A
  1. Actual or near arrest caused by blunt impact to chest wall over the heart
  2. If coincide with T wave - can lead to VF
83
Q

What factors are associated with survival from traumatic cardiac arrest?

A
  1. Pre-hospital time
  2. Duration of CPR < 20 min
  3. Presence of reactive pupils
  4. Organised ECG rhythm
  5. 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
  1. Correct the reversible causes
  2. Do chest compressions but unlikely to be successful without correction
  3. FAST scan or CT may be useful in guiding treatment
  4. Early tracheal intubation can be beneficial
85
Q

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

A
  1. Further circulatory depression
  2. By impeding venous return
86
Q

How are tension pneumathoraces managed in traumatic cardiac arrest?

A

Bilateral thoracotomies:

  1. 5th ICS, MAL
  2. Can extend to clamshell thoracotomy if req
  3. Needle decompression is a v temporary measure
87
Q

How is a cardiac tamponade managed?

A
  1. Resuscitative clamshell thoracotomy
  2. Needle aspiration unreliable - pericardium commonly full of clotted blood
88
Q

When should resuscitative thoracotomies be considered?

A
  1. Penetrating torso trauma and < 15min CPR
  2. Blunt trauma and < 10min prehospital CPR
  3. 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
  1. Airway management
90
Q

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

A
  1. Asystole - 41%

VF - 35%

91
Q

What is important about the management of periop cardiac arrest?

A
  1. Use fluid warmers and forced air warmers
  2. PEA may not be immediately detected - use low end tidal CO2 to provoke pulse check
  3. CPR is ideal in supine position but possible prone
  4. Consider open cardiac compressions if heart easily accessed
  5. Give pre-cordial thump if no immediate access to defib
  6. Stop surgery in asystole or extreme Brady - likely excess vagal activity - Atropine 0.5mg
  7. If adrenaline - give dose in 50-100mcg increments instead of 1mg bolus. No response - further 1mg boluses
92
Q

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

A
  1. Relatively common
  2. Recognition of need to perform re-steronomy early is key - tamponade or haemorrhage
  3. External compressions may cause sternal disruption and cardiac damage
  4. Use Adrenaline cautiously and titrate to effect IV upto 0.1mg
93
Q

When is emergency resternotomy indicated?

A
  1. Adequate airway and ventilation
  2. 3 shock attempts in VF/pVT
  3. 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
  1. Yes - start immediately if no output
  2. Check effectiveness using arterial trace - systolic of >60 and diastolic >25; HR 100-120
  3. If not reaching targets - resternotomy
95
Q

What is drowning and what are the “types”?

A
  1. Respiratory impairment from submersion/immersion in liquid
  2. Submersion - face underwater/covered by water
  3. Immersion - head remain above water - e.g. life jacket
96
Q

What typically happens to patients who are immersed in water?

A
  1. Become hypothermic
  2. Airway remain patient
  3. Water splashes can cause aspiration
97
Q

What happens in submersion?

A
  1. Patient initially hold breath and swallow water
  2. As pt. become hypoxic and hypercapnic
  3. Breath holding reflex and laryngospasm reflex lost
  4. Patient aspirate water
  5. Hypoxia - Bradycardia - cardiac arrest

Laryngospasm reflex prevent water entering lungs

98
Q

How should you correct hypoxaemia following submersion?

A
  1. Ventilation only resus
99
Q

How do you attempt to rescue someone from the water?

A
  1. Ideally throw rope or buoyant rescue aid
  2. Assess risk and enter with flotation device
  3. If submersion for < 10 mins - likely good outcome
  4. If > 25 mins - likely poor outcome
  5. Remove from water horizontally - spinal precautions rarely necessary
100
Q

Why remove patients horizontally from the water?

A
  1. Hypovolaemia after prolonged immersion
  2. Can cause CV collapse and arrest
101
Q

When are spinal precautions necessary in water rescue?

A
  1. Diving in shallow water
  2. Signs of severe injury water side
  3. Water skiing
  4. Kite surfing
  5. 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
  1. Check for response
  2. Give 5 rescue breaths with supplemented oxygen
  3. Start CPR as normal
  4. If lots of foam - continue CPR until intubation
  5. Turn victim to side and remove regurgitation material
103
Q

What modifications can be made to ALS after drowning?

A
  1. Use PEEP and NG stomach decompress in drowning pt who hasn’t arrested or achieved ROSC
  2. Check ECG and end tidal CO2 for signs of life
  3. Consider echo (pulse not sufficient)
  4. 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
  1. Risk of developing ARDS - use standard protective ventilation stratefies
  2. Pneumonia common however prophylactic Abx only if sewage/grossly contaminated
  3. Neurological outcome determined by hypoxia
  4. Consider ECMO for refractory cardiac arrest, hypoxaemia and submersion in ice cold water
105
Q

Define hypothermia

A
  1. < 35 degrees
  2. Mild = 32-35
  3. Mod = 28-32
  4. Severe = < 28
106
Q

What happens in each stage of hypothermia?

A
  1. Mild - shivering, conscious
  2. Mod - stop shivering, conscious
  3. Severe - decreased consciousness, vitals present (28-24)
  4. Unconscious - vitals not present < 24
  5. Death - due to irreversible hypothermia < 13.7
107
Q

What may increase risk of hypothermia?

A
  1. Things that decrease conscious level - drugs, alcohol, illness, exhaustion, neglect
  2. Factors that impair thermoregulation - elderly and very young
108
Q

Where is a core body temperature taken from?

A
  1. Lower third of oesophagus
109
Q

How much does hypothermia reduce oxygen demand?

A
  1. 6% reduction per 1 degree
110
Q

Why must you be careful diagnosing death in hypothermic?

A
  1. Patients can have slow small volume irregular pulses and low BP but they may return once warm
  2. Not dead until warm and dead
  3. 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
  1. < 28 - 5 min CPR, 5 min break
  2. < 20 - 5 min CPR, 10 min break
  3. Check for pulse for 1 minute - central artery and ECG
  4. Consider using mechanical chest compression
  5. Early intubation
  6. Hold adrenaline and amiodarone until >30 degrees
  7. Then double dose interval (6-10 mins) until 35 degrees
112
Q

How are arrhythmia’s treated in hypothermia?

A
  1. Apart from VF, others revert spontaneously as temp increase
  2. Cardiac pacing not indicated unless haemodynamic compromise persist after rewarming
  3. Stop shocks after 3 attempts until temp >28-30

Sinus Brady –> AF –> VF –> asystole

113
Q

How are patients rewarmed after accidental hypothermia?

A
  1. Remove from cold
  2. Take off wet clothes
  3. Stage II and worse - immobilise, handle carefully, oxygenate, dry and give clothes, heat packs
  4. 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
  1. Stage I - nearest hospital
  2. II - IV - Nearest hospital with ECMO facilities
  3. V - Consider whether to withhold CPR, if not nearest hospital with ECMO
115
Q

What are the reasons to terminate (or not attempt) CPR in a hypothermic patient?

A
  1. DNACPR
  2. Obvious sign of irreversible death
  3. Unsafe for rescuer
  4. Avalanche burial for >60 min
  5. Airway packed with snow
  6. Asysole
116
Q

When are avalanche victims not likely to survive?

A
  1. Buried for > 60 mins + cardiac arrest + obstructed airway on extraction
  2. Buried + cardiac arrest + K+ >8mmol/L
117
Q

When can extracorporeal life support rewarming be considered?

A
  1. Temp < 32
  2. 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
  1. Forced warm air
  2. Warm infusions
  3. Forced peritoneal lavage
119
Q

What are the stages of hyperthermia?

A
  1. Heat stress
  2. Heat exhaustion
  3. Heat stroke –> multi-organ dysfunction and cardiac arrest
120
Q

What is heat stroke + types?

A
  1. Core temp >40.6
  2. Change in mental state
  3. Varying levels of organ dysfunction

2 types:
1. Exertional
2. Non exertional - elderly in heat waves

121
Q

What can predispose someone to heat stroke?

A

Elderly:
1. Underlying illness
2. Medication use
3. Declining thermoregulatory mechanisms
4. Limited social support

General:
1. Lack of acclimitisation
2. Dehydration
3. Alcohol
4. Obesity
5. CVS conditions
6. Skin disease
7. Hyperthyroidism
8. Phaeochromocytoma

122
Q

What drugs can predispose to hyperthermia?

ABCCD - MPS

A
  1. Anticholinergics
  2. Beta blockers
  3. Ca2+ blockers
  4. Cocaine
  5. Diamoprhine
  6. Methamphetamine
  7. Phenothiazines
  8. Sympathomimetics
123
Q

What are the features of heat stroke?

A
  1. Core Temp >40
  2. Hot dry skin
  3. Fatigue, headache, fainting, facial flush, D&V
  4. CVS dysfunction - arrhythmia and hypotension
  5. Resp dysfunction - ARDS
  6. CNS dysfunction - seizures and coma
  7. Metabolic dysfunction - Liver and renal failure
  8. Haematological dysfunction - Coagulopathy
  9. Skeletal mm. dysfunction - Rhabdomyolysis
124
Q

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

A
  1. Drug withdrawal syndromes
  2. Neuroleptic malignant syndrome
  3. Sepsis
  4. CNS infection
  5. Endocrine disorder - thyroid and phaeochromocytoma
125
Q

How is heat stroke treated?

A
  1. Rapid cooling
  2. Haemodynamic monitoring - fluid and electrolytes
  3. Defibrillation as normal
  4. Post resus care as normal
126
Q

How do you cool a patient in heat stroke?

A
  1. Simple - cool drinks, take off clothes, fan, spray tepid water, ice packs over groin, axilla neck
  2. Advanced - cold IV fluids, intravascular cooling catheters, ECMO

Immerse in cold water - can cause vasoconstriction, preventing heat dissipation
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
  1. Type of current - AC/DC
  2. Voltage
  3. Magnitude of energy
  4. Resistance to current flow
  5. Pathway of current
  6. 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
  1. Conductive neuovascular bundles
131
Q

What does contact with AC current lead to?

A
  1. Tetanic contract of skeletal muscle
132
Q

What can cause myocardial or respiratory failure in electrocution?

A
  1. Resp arrest due to paralysis of respiratory muscles or resp depression
  2. Asystole may be primary or secondary to asphyxia following resp arrest
  3. Current can precipitate VF if it crosses myocardium during vulnerable period.
  4. Current can cause coronary artery spasm
133
Q

What current direction is more likely to be dangerous?

A
  1. Current that transverse myocardium
  2. 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:
1. Tachycardia
2. Hypertension
3. Prolonged QT and transient t wave inversion
4. Myocardial necrosis
5. CK release

135
Q

How are lightning strikes and electrical injuries treated?

A
  1. Early intubation - airway management may be difficult if burns
  2. Ventilatory support if muscle paralysis persist
  3. Use standard defibrillation guidelines
  4. IV fluids if tissue destruction - good urine output
  5. Remove smouldering clothing and shoes to prevent thermal injury
  6. Check for compartment syndrome
  7. Early surgery if req.
136
Q

What arrhythmia is most likely to be seen in an electrocution - AC & DC?

A
  1. AC - VF
  2. DC - Asystole
137
Q

What determines long term prognosis for electrical injury?

A
  1. Severe burns
  2. Myocardial necrosis
  3. Extent of CNS injury
  4. Multiple system organ failure

Advanced Life Support (ALS) (13 decks)

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