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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

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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5
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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6
Q

What do you do for each stage of hyperkalaemia?

A

Mild: 5.5-5.9

  • Address cause
  • Calcium resonium (bind to calcium)

Mod: 6.0-6.4

  • Insulin dextrose infusion
  • Address cause
  • Calcium resonium

Severe: 6.5+

  • Expert help
  • Calcium gluconate
  • Insulin dextrose infusion
  • Address cause
  • Salbutamol nebulisers back to back
  • Calcium resonium
  • Remove K+ - dialysis

To give calcium gluconatecalcium chloride if ECG changes.
Repeat ECGs

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7
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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8
Q

How is hypokalaemia defined?

A

<3.5mmol/L

Severe = <2.5mmol/L

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9
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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10
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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11
Q

What ECG features are seen in hypokalaemia?

A 
U waves
Small t waves
Tall P waves
ST segment changes
Arrhythmia's
Cardiac arrest
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12
Q

How should K+ be replaced?

A

Gradually
Max 10mmol/L per hour on normal ward
Ma 20mmol/L per hour in HDU/ICU

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

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13
Q

What can cause hypercalcaemia? (>2.6mmol/l)

A

Primary/tertiary hyperparathyroid
Malignancy
Sarcoid
Drugs

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14
Q

How does hypercalcaemia present?

A 
Confusion
Weakness
Abdo pain
Hypotension
Arrhythmia
Cardiac arrest
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15
Q

What ECG changes are seen in hypercalcaemia?

A 
Short QT
Wide QRS
Flat t waves
AV block
Cardiac arrest
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16
Q

How is hypercalcaemia treated?

A 
Fluid replacement
Furosemide - 1mg/kg
Hydrocortisone 200-300mg
Pamidronate 30-90mg/ bisphosphonates
Treat underlying cause
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17
Q

What can cause hypocalcaemia? (<2.1mmol/l)

A 
Chronic renal failure
Pancreatitis
Calcium channel blocker OD
Toxic shock syndrome
Rhabdomyolysis
TLS
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18
Q

How does hypocalcaemia present?

A 
Paraesthesia
Tetany
Seizures
AV block
Cardiac arrest
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19
Q

What ECG changes are seen for hypocalcaemia?

A

Prolonged QT
T wave inversion
Heart block
Cardiac arrest

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20
Q

What can cause hypermagnasaemia? (>1.1mmol/l)

A

Renal failure

Iatrogenic

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21
Q

How does hypermagnasaemia present?

A 
Confusion
Weakness
Resp. depression
AV block
Cardiac arrest
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22
Q

What ECG changes are seen for hypermagnasaemia?

A

Prolong PR and QT
T wave peak
AV block
Cardiac arrest

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23
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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24
Q

What can cause hypomagnasaemia? (<0.6mmol/l)

A 
GI loss
Polyuria
Starvation
Alcohol
Malabsorption
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25
Q

How does hypomagnasaemia present?

A 
Tremor
Ataxia
Nystagmus
Seizures
Arrhythmia - torsades 
Cardiac arrest
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26
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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27
Q

How is hypomagnasaemia managed?

A

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

  • mild = oral replacement (0.5-0.8)
  • severe = over 15 mins
  • torsades = over 1/2 mins
  • Seizure = over 10 mins
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28
Q

How to manage sepsis

A

Sepsis 6 -
02, Blood cultures, lactate, Abx, fluids, urine output

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29
Q

What specific treatments are available for poisoning?

A

Skin exposure - remove clothes

Activated charcoal - <1hr and intact airway

Whole bowel irrigation using polyethylene glycol

Sodium Bicarb IV - salicylate poisoning and amitriptyline

Haemodialysis

Specific antidotes

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30
Q

What is the specific antidote for paracetamol?

A

N-acetylcysteine

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31
Q

What is the specific antidote for organophosphate poisoning?

A

High dose atropine

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32
Q

What is the antidote for cyanides poisoning?

A

Sodium nitrite
Hydroxocobalamin
Amyl nitrite

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33
Q

What is the antidote for digoxin poisoning?

A

Digibind - digoxin specific Fab antibodies

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34
Q

What is the antidote for benzodiazepines?

A

Flumazenil if no risk of seizure

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35
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

Can give naloxone infusion

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36
Q

What does opioid poisoning cause?

A

Resp depression
Pinpoint pupils
Coma following resp. arrest

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37
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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38
Q

What can a benzodiazepine OD cause?

A

Loss of consciousness
Respiratory depression
Hypotension

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39
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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40
Q

Is flumazenil used in comatose patients?

A

No

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41
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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42
Q

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

A

Wide QRS
Right axis deviation

Usually noted with prolonged QT

Consider sodium bicarb

43
Q

When can you get local anaesthetic toxicity?

A

Regional anaesthesia - enters artery or vein

44
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

45
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
46
Q

What can cocaine toxicity cause?

A

Sympathetic overstimulation:

  • agitation
  • symptomatic tachycardia
  • hyperthermia
  • hypertensive crisis
  • myocardial ischaemia with angina
47
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

48
Q

How is drug induced severe bradycardia managed?

A

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

2-4mg IV repeated doses

49
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

50
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
51
Q

What signs indicate acute severe asthma?

A
  • PEFR 33-50%
  • RR >25
  • HR >110
  • Inability to complete sentence in 1 breath
52
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

53
Q

What indicates asthma mat be near fatal?

A

Raised PaCO2 and/or mechanical ventilation with raised inflation pressures

54
Q

What may absence of wheezing in asthma indicate?

A

Critical airway obstruction

Increased wheezing may indicate + response to therapy

55
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

56
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)

57
Q

What can beta agonist and steroid therapy in asthma cause?

A

Hypokalaemia

58
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

59
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

60
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 - abdo pain as blood and fluid redirected away from gut

61
Q

How is anaphylaxis managed in an adult?

A 
Remove trigger
Lie down + legs up
IV Fluid challenge 500-1000ml
IV chlorphenamine 10mg
IV hydrocortisone 200mg
IM Adrenaline 0.5mg (0.5ml of 1:1000) - anterolateral middle thigh - repeat at 5min mark if no response with fluid bolus
62
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

63
Q

How can anaphylaxis be investigated?

A

Mast cell tryptase - 3 timed samples:

  • ASAP after resus
  • 1-2hr after start of symptoms
  • 24hr after
64
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

65
Q

How is pre-eclampsia treated?

A

Magnesium sulphate - prevent eclampsia in labour

66
Q

How are amniotic fluid emboli managed?

A

Supportive

Correct coagulopathies

67
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
68
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

69
Q

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

A

Further circulatory depression by impeding venous return

70
Q

How are tension pneumathoraces managed in traumatic cardiac arrest?

A

Needle decompression - 2nd intercostal space midclavicular line

71
Q

How is a cardiac tamponade managed?

A

Resuscitative clamshell thoracotomy

Needle aspiration unreliable - pericardium commonly full of clotted blood

72
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

73
Q

What are the commonest causes of anaesthesia related cardiac arrest?

A

Airway management

74
Q

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

A

Asystole - 41%

VF - 35%

75
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

76
Q

What typically happens to patients who are immersed in water?

A

Become hypothermic

Airway remain patient

Water splashes can cause aspiration

77
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

78
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

79
Q

Why remove patients horizontally from the water?

A

Hypovolaemia after prolonged immersion can cause cardiovascular collapse and arrest

80
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 CPR as normal
If lots of foam - continue CPR until intubation
Turn victim to side and remove regurgitation material

81
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

82
Q

Define hypothermia

A

<35 degrees

83
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

84
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

85
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

86
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

87
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

88
Q

What other active rewarming techniques can be used?

A

Forced warm air
Warm infusions
Forced peritoneal lavage

89
Q

What are the stages of hyperthermia?

A

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

90
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
91
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
92
Q

What drugs can predispose to hyperthermia?

A 
Anticholinergics
Diamorphine
Cocaine
Methamphetamine
Phenothiazines
Sympathomimetics
Ca2+ blockers
Beta blockers
93
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
94
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
95
Q

How is heat stroke treated?

A

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

96
Q

What is used in treatment of malignant hyperthermia?

A

Dantrolene

97
Q

What reduces skin resistance to electrocution?

A

Moisture

98
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

99
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
100
Q

What determines long term prognosis for electrical injury?

A

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

101
Q

What level of potassium definetely causes ECG changes

A

6.7mmol l

102
Q

What other electrolyte to check with hypokalaemia

A

Mg

103
Q

What is refractory anaemia

A

No improvement of cardiovascular or respiratory symptoms despite 2 doses of adrenaline

Give - IV 500ml bolus and adreanlaine infusion

Advanced Life Support (ALS) (9 decks)

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