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ALS > 12. Resuscitation in special circumstances > Flashcards

12. Resuscitation in special circumstances Flashcards

1
Q

while serum pH decreases (acidaemia), serum potassium DECREASES/ INCREASES - why?

A

increases - because potassium shifts from the cellular to the vascular space - a process that is reversed when serum pH increases

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2
Q

severe hyperkalaemia is defined as serum concentration >____mmol/L

A

6.5

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3
Q

main causes of hyperkalaemia?

A

renal failure
drugs (ACEI, ARB)
tissue breakdown (rhabdomyalysis, tumour lysis)
metabolic acidosis (renal failure, DKA)
endocrine disorders (addison’s)
diet (advanced CKD)
spurious (clotted blood)

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4
Q

name the progressive ECG changes seen with hyperkalaemia?

A

first degree heart block
flattened of absent p wave
tall tented T waves
ST depression
S and T wave merging (since wave pattern)
QRS widening
VT
bradycardia
cardiac arrest

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5
Q

T/F: calcium gluconate lower potassium by 1mmol/ minute

A

false - it protects the heart by reducing risk of VF/pVT but doesn’t lower serum potassium

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6
Q

treatment of severe hyperkalaemia with ECG changes

A

1) protect the myocardiumL 30ml 10% calcium gluconate over 15 minutes
2) shifting agents (glucose/ insulin and salbutamol)
3) remove potassium from the body: consider dialysis, sodium zirconium and/or patiromer

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7
Q

insulin/ glucose in hyperkalaemia

A

8units Actrapid in 100ml IV glucose 20% vial over 30 minutes

(follow up with 10% glucose infusion at 50ml/hr for 5 hours if pre-treatment BM <7)

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8
Q

treatment of severe hyperkalaemia during cardiac arrest?

A

confirm using blood gas if available
10ml 10% calcium gluconate rapid bolus injection if available
give glucose/ insulin by rapid injection (10 units short acting insulin in 25g glucose)
give sodium bicarbonate (50mmol IV) if severe acidosis/ renal failure
consider dialysis

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9
Q

what is the most common electrolyte disorder in clinical practice

A

hypokalaemia

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10
Q

main causes of hypokalaemia?

A

GI loss
Drugs (diuretics, laxatives, steroids)
Renal losses (renal tubular disorders, DI, dialsis)
Endocrine disorders (cushing’s, hyperaldosteronism)
Metabolic alkalosis
Magnesium depletion
Poor dietary intake

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11
Q

table 12.1 on pg 149

A

to do

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12
Q

symptoms of hypokalaemia

A

nerves and muscles are mainly affected > fatigue, weakness, leg cramps, constipation.

in severe cases (<2.5) - rhabdomyolsis, ascending paralysis and respiratory difficulties

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13
Q

ECG features of hypokalaemia?

A

U waves
T wave flattening arrhythmias (esp if pt on digoxin)

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14
Q

max rate for IV potassium replacement?

A

20mmol/ hr
(can be faster if periarrest)

continuous ECG monitoring essential

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15
Q

consider replacing what other electrolyte in hypokalaemia

A

magnesium

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16
Q

modifications to the ALS algorithm for a patient in the dialysis unit?

A

assign a trained dialysis nurse to operate the HD machine

stop dialysis and return the pts blood volume with a fluid bolus

disconnect from the dialysis machine (unless dialysis proof)

leave dialysis access open to use for drug administration

prompt management of hyperkalaemia

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17
Q

score for identifying sepsis?

A

Sequential Organ Failure Assessment (SOFA)

score >/= 2 reflection 10% mortality

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18
Q

septic shock has a ___% mortality

A

40

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19
Q

septic shock = sepsis requiring vasopressors to maintain MAP > ____ and a lactate > ___mmol/L

A

65
2

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20
Q

sepsis 6 bundle?

A

take: blood culture, urine output, serum lactate
give: IV antibiotics, fluids, high flow oxygen

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21
Q

in sepsis, give fluid boluses to a max of ___ml/kg

A

30

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22
Q

what to do in sepsis if MAP remains <65 despite repeated fluid challenges?

A

escalate to consider vasopressor therapy

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23
Q

T/F: drug induced hypotension usually responds well to IV fluids

A

true

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24
Q

hypertensive emergencies may be managed with what drugs?

A

benzos
vasodilators
alpha antagonists

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25
Q

in suspected poisoning, retain samples of blood and urine for analysis

A

ok

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26
Q

Poisoning: immediate management
1) when skin has been exposure to poison, do what
2) T/F: routine use of gastric lavage for GI decontamination is recommended
3) T/F: use of activated charcoal improves outcomes
4) Whole bowel irrigation can reduce drug absorption using enteral administration of what? When is it considered
5) laxatives and emetics are useful agents in poisoning
6) what is a useful treatment in pts with mod-severe salicylate poisoning who don’t require haemodialysis
7) haemodialysis is good for what sort of drugs?

A

1) remove clothing
2) false - not routinely recommended
3) false - no clear evidence for this. Consider a single dose in pts who have ingested a potentially toxic amount of poison known to be adsorbed by activated charcoal up to 1 hr previously (only if intact/ protected airway).
4) polyethylene glycol solution. Sustained release or enteric-coated drugs, oral iron poisoning, removal of ingested packets of illicit drugs
5) false - no role
6) urine akalinisation by giving IV sodium bicarbonate
7) low molecular weight, low protein binding, small volume of distribution and high water solubility

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27
Q

Opioid poisoning
1) presentation
2) routes and doses of the antidote?
3) large opioid overdoses require titration to a total of ___mg naloxone
4) duration of action of naloxone?
5) consider what is the RR is not maintained and long-acting opioid preparations have been ingested?

A

1) respiratory depression, pinpoint pupils, coma, respiratory arrest
2) naloxone: 400mcg IV/ 800mcg IM or sc, 2mg IN
3) 10
4) 45-70 mins (but respiratory depression may persist for 4-5 hrs post overdose, so clinical effects of naloxone may be outlasted in significant overdose)
5) naloxone infusion

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28
Q

acute withdrawal from opioids produces what response?

A

state of sympathetic excess and can cause complications including pulmonary oedema, ventricular arrhythmia, severe agitation

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29
Q

Benzo overdose
1) presentation
2) reversal agent
3) only use when there is no history or risk of _____

A

1) LOC, resp depression, hypotension
2) flumazenil (competitive antagonist)
3) seizures

NB: reversal with flumazenil can cause significant toxicity (seizure, arrhythmia, hypotension, withdrawal) in benzo dependent patients/ if co-ingestion of pro-convulsant meds has occurred e.g. TCAs. Do not routinely use in the comatose patient

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30
Q

Tricyclic acid poisoning
1) examples of TCAs
2) presentation
3) can cause what arrhythmia?
4) treatment for tricyclic-induced ventricular conduction abnormalities

A

1) amitriptyline, desipramine, imipramine, nortriptyline, doxepin
2) hypotension, seizures, coma, arrhythmia, dilated pupils, fever, dry skin, delirium, tachycardia, ileus, urinary retention
3) VT
4) sodium bicarbonate

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31
Q

Local anaesthesia toxicity
1) presentation
2) management in pts with CVS collapse/ cardiac arrest

A

1) severe agitation, LOC, tonic-clonic seizure, bradycardia, conduction block, asystole, ventricular tachyarrhythmia
2) IV lipid emulsion: 1.5ml/kg 20% lipid emulsion

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32
Q

Stimulant overdose (cocaine/ amphetamine)
1) presentation?
2) effective 1st line treatment?
3) what can be used to reverse cocaine induced coronary vasoconstriction

A

1) sympathetic overstimulation - agitation, symptomatic tachycardia, hypertensive crisis, hyperthermia, myocardial ischaemia with angina
2) small doses IV benzos
3) GTN and phentolamine (nitrate 2nd line)

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33
Q

give ____ for bradycardia caused by acetylcholinesterase-inhibiting substance

A

atropine - large (2-5mg) and repeated doses may be required to achieve a clinical effect

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34
Q

_____ may be useful at high doses in refractory bradycardia induced beat receptor blockade

A

isoprenaline

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35
Q

what pts can be said to have severe asthma?

A

history of near-fatal asthma requiring intubation, mechanical ventilation

hospitalisation or emergency care for asthma in past year

requiring 3 or more class of asthma meds

increasing use and dependent on beta-2-agonists

adverse behavioural or psychological factors e.g. non-adherence, psychiatric illness/ self-harm, alcohol and drug dependent, learning difficulties

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36
Q

management of asthma attack?

A

‘O SHIT MA’

oxygen target 94-98%

salbutamol 5mg via oxygen driven nebuliser (repeat every 15-30 mins or continuous)

steroids (pred 40mg orally or hydrocortisone 100mg IV)

ipratropium 500mcg 4-6 hourly

consider aminophylline following senior advice (loading dose 5mg/ kg over 20 mins followed by infusion of 500-700mcg/ kg/hr)

single dose IV magnesium sulfate 2g over 20 mins

anaesthetist: intensive care specialist should assess pts who fail to respond to initial treatment, or who develop signs of life-threatening asthma

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37
Q

what if a nebuliser is not immediately available in an asthma attack?

A

can give beta-2 agonist temporarily by repeating activations of a metred dose inhaler via a large volume spacer device

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38
Q

when should IV salbutamol be given in an asthma attack?

A

only when inhaled therapy is not possible e.g. pt receiving bag-mask ventilation (monitor lactate if used for evidence toxicity)

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39
Q

near-fatal asthma features?

A

raised PaCO2 and/ or mechanical ventilation with raised inflation pressures

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40
Q

life-threatening asthma features?

A

any one of:
Clinical signs
- altered LOC
- exhaustion
- arrhythmia
- hypotension
- cyanosis
- silent chest
- poor expiratory effect
Measurements
- PEF <33% best or predicted
- SpO2 <92%
- Pao2 < 8kPa
- ‘normal PaCO2 (4.6-6)

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41
Q

acute severe asthma features?

A
  • PEF 33-50% best or predicted
  • RR >/= 25
  • heart rate >/= 110
  • inability to complete sentences in one breath
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42
Q

in asthma attacks be aware beta agonists and steroids may induce ____kalaemia

A

hypokalaemia - monitor and correct

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43
Q

when to consider tracheal intubation in asthma attack?

A

despite optimised drug therapy
- reduced peak flow
- reducing LOC
- persisting/ worsening hypoxaemia
- worsening respiratory acidosis
- severe agitation, confusion and fighting against the oxygen mask (clinical signs of hypoxaemia)
- progressive exhaustion, feeble respiration
- respiratory or cardiac arrest

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44
Q

T/F: elevation of PaCO2 in an asthma attack is an indication for the need for tracheal intubation

A

false - not on its own

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45
Q

what to do if dynamic hyperinflation of the lungs is suspected during CPR?

A

compression of the chest wall and/ or period of apnoea

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46
Q

what additional cause of hypoxia should always be considered in asthma?

A

bilateral pneumothoraces

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47
Q

GI symptoms in anaphylaxis are more common when the route of exposure is ORAL/ NON-ORAL

A

non-oral e.g. a sting

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48
Q

T/F: skin or mucosal changes alone are not a sign of anaphylaxis

A

true - without airway/ breathing or circulation problems this does not indicate anaphylaxis

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49
Q

treatment of anaphylaxis?

A

do not allow pt to walk/ stand up

place in recovery position if breathing normally and unconscious (left lateral in pregnancy)

remove the trigger (IV agent/ sting)

monitor and give oxygen

fluid boluses

0.5ml of 1:1000 IM adrenaline (0.5mg) in anterolateral middle third of thigh (repeat after 5 mins in no response)

consider early tracheal intubation

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50
Q

if features of anaphylaxis persist despite 2 doses of IM adrenaline, what treatment can be started?

A

refractory anaphylaxis algorithm > start an adrenaline infusion with expert support and appropriate monitoring

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51
Q

what can be a useful adjunct to treat upper airway obstruction caused by laryngeal oedema in anaphylaxis

A

5ml of 1:1000 nebulised adrenaline
(but only after giving IM adrenaline, not as an alternative)

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52
Q

T/F: antihistamines are not recommended for the treatment of anaphylaxis

A

true - no benefit in treating life threatening symptoms

can help the cutaneous symptoms only after the pt is stable - give non-sedating oral agent like cetirizine

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53
Q

T/F: corticosteroids may be used in preference to adrenaline in anaphylaxis where an acute asthma exacerbation may have contribute

A

false - adrenaline always first line

oral steroids may be indicated once pt stability if asthma exacerbation contributed to the severity

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54
Q

blood test to help confirm a diagnosis of anaphylaxis?

A

mast cell tryptase

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55
Q

timing for mast cell tryptase sampling in anaphylaxis?

A

at minimum: one sample within 2 hr of symptom onset

ideally: three samples- one as soon as feasible after resuscitation, second sample at 1-2 hrs following onset of symptoms, third sample at 24hr (for baseline levels)

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56
Q

dose and rate of IV adrenaline infusion in refractory anaphylaxis?

A

1ml/kg/hr of 1mg adrenaline in 100ml saline

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57
Q

what should all pts presenting with first time anaphylaxis receive prior to discharge

A

a hug

jk

  • info about anaphylaxis (recognition, allergen avoidance, use of epipen, call 999)
  • provide an epipen
  • referral to allergy services to identify allergen
  • info about pt support groups
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58
Q

what is a maternal cadiac arrest defined as?

A

any time in pregnancy + up to 5 weeks after delivery

59
Q

T/F: effective resuscitation of the mother is often the best way to optimise foetal outcome

A

true

60
Q

causes of cardiac arrest in pregnancy?

A

cardiac disease
PE
epilepsy/ stroke
sepsis
mental health conditions
bleeding
malignancy
hypertensive disorders

61
Q

positioning of a distressed/ compromised pregnant women?

A

place in left lateral position/ manually displace the uterus to the left if lateral position not possible

62
Q

modification to ALS algoritm in pregnancy?

A

involve obs and gynae early

over the head CPR may be needed if morbidly obese

ideally gain IV/ IO access above the level of the diaphragm due to potential for IVC compression

manually displace the uterus to the left to minimise IVC compression (aim for full table tilt of 15-30 degrees only if feasible)

start prepping for emergency c section

consider early intubation (increased risk aspiration in pregnancy)

63
Q

specific reversible causes of collapse/ cardiac arrest to consider in pregnancy?

A

haemorrhage
drugs
cardiovascular disease
pre-eclampsia/ eclampsia
amniotic fluid embolism
PE

64
Q

causes of haemorrhage in pregnancy?

A

ectopic
placental abruption/ praevia/ increta/ percreta
uterine rupture

65
Q

management of maternal haemorrhage

A

maternal massive haemorrhage protocol

  • fluid resus (consider rapid transfusion and cell salvage)
  • tranexamic acid and correct coagulopathy
  • oxytocin, ergometrine, prostaglandins and uterine massage to correct uterine atony
  • uterine compression sutures/ packs/ balloon devices
  • IV radiology
  • surgery
66
Q

treatment of magnesium toxicity in a pregnant lady whose been overdosed for treatment of eclampsia

A

calcium

67
Q

treatment of ST elevation MI in pregnancy?

A

PCI
consider fibrinolysis if urgent PCI unavailable

68
Q

what is eclampsia

A

the development of convulsion and/ or unexplained coma during pregnancy or postpartum in pts with signs and symptoms of pre-eclapmsia

69
Q

how does amniotic fluid embolism present?

A

usually around the time of delivery: sudden cardiovascular collapse, breathlessness, cyanosis, arrhythmias, hypotension, haemorrhage ass with DIC

70
Q

treatment of amniotic fluid embolism?

A

supportive: ABCDE, correct coagulopathy

71
Q

treatment of PE causing cardiopulmonary collapse in pregnancy?

A

consider use of fibrinolytic therapy

72
Q

in the supine position, the gravid uterus begins to compromise blood flow to the ICVC and abdominal aorta at approx ___ weeks gestation

A

20

73
Q

T/F: when initial resuscitation attempts fail, delivery of the foetus may improve the chances of successful resuscitation of both the mother and foetus

A

true - best when resuscitative hysterotomy is attempted within 5 mins after the mother’s cardiac arrest

74
Q

peri-mortem c-section (resuscitative hysterotomy) is not worth doing before what gestation?

A

<20 weeks/ or if the uterus is not palpable above the level of the umbilicus

because a gravid uterus of this size is unlikely to compromise maternal cardiac output and foetal viability (at 20-23 weeks, delivery immediately to improve maternal outcomes but unlikely the foetus will survive)

75
Q

what gestation does foetal viability begin at?

A

24 weeks

76
Q

T/F: traumatic cardiac arrest has a very high mortality

A

true - but when ROSC is achieved, neurological outcomes are better

77
Q

causes of cardiac arrest in trauma patient?

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
cardiac tamponade

78
Q

what are the prevalent initial heart rhythms in traumatic cardiac arrest?

A

PEA and asystole

79
Q

what is commotio cordis

A

actual or near cardiac arrest caused by a blunt impact to the chest wall over the heart (can cause VF/ pVT)

80
Q

what is permissive hypotension

A

administering only enough fluid to achieve a radial pulse - may be used until surgical haemostasis is achieved

81
Q

the duration of hypotensive resuscitation should not exceed _____ min

A

60

82
Q

what additional treatment can be useful in traumatic cardiac arrest?

A

1g IV tranexamic acid over 10 mins
followed by 1g IV over 8hr

(may increase mortality if started >4hrs post injury)

83
Q

T/F: do not delay transfer to hospital in a traumatic cardiac arrest in order to carry out spinal immobilisation

A

true

84
Q

factors associated with survival in traumatic cardiac arrest?

A

presence of reactive pupils, organised ECG rhythm, respiratory activity

85
Q

T/F: in cardiac arrest caused by hypovolaemia, cardiac tamponade or tension pneumothorax, chest compressions are unlikely to be as successful as early correction of the reversible cause

A

true - so chest compressions have a lower priority than e.g. thoracotomy or controlling haemorrhage

86
Q

in traumatic cardiac arrest, prolonged CPR has a poor outcome -if no response to 20 mins ALS, exluding all reversible causes, and there’s no detectable cardiac activity on ultrasound then can stop

A

ok

87
Q

uncontrolled haemorrhage is a common cause of traumatic cardiac arrest, so early haemorrhage control and restoration of circulating volume is essential

how to achieve this?
1) for compressible external haemorrhage
2) for non-compressible haemorrhage
3) for exsanguinating and uncontrollable infradiaphragmatic torso haemorrhage

A

1) compressible external haemorrhage - elevation, direct pressure, tourniquets

2) non-compressible haemorrhage - splints including pelvic bindings and, where necessary, blood products, IVF and TXA while transferring to surgical/ radiological control

3) immediate aortic occlusion through resuscitative thoracotomy and cross-clamping/ intravascular occlusion of the descending aorta

88
Q

neurogenic shock arising after a spinal cord injury can exacerbate hypovolaemia - indicators of this?

treatment?

A

warm, vasodilated peripheries
loss of reflexes below the injury segment
severe hypotension with low HR

vasopressors may be needed in addition to fluids

89
Q

T/F: positive pressure ventilation is indicated in low cardiac output conditions

A

false - can cause further circulatory depression and even cardiac arrest by impeding venous return to the heart

(monitor waveform capnography and set the lower minute volume consistent with normocapnia to minimise rise in transpulmonary pressure)

90
Q

during CPR use ___% oxygen

A

100

91
Q

management of cardiac tamponade in cardiac arrest

A

in traumatic cardiac arrest following penetrating chest trauma to the chest/ epigastrium immediate resuscitative thoracotomy with clamshell incision and opening of the pericardium (needle aspiration unreliable as often its clotted blood)

92
Q

indications for resuscitative thoracotomy

A

pts with penetrating chest trauma in whom less than 15 mins have elapsed since loss of vital signs

93
Q

how does tension pneumothorax cause cardiac arrest

A

entry and trapping of air in the pleural cavity causes mediastinal shift thereby obstructing venous return

94
Q

causes of tension pneumothorax

A

trauma
asthma
other resp illness
clinical procedures e.g. central venous line insertion

95
Q

clinical signs of tension pneumothorax

A

resp distress/ hypoxia prior to cardiac arrest
haemodynamic compromise prior to cardiac arrest
absence breath sounds on auscultation
chest crepitations/ subcut ephysema
tracheal deviation
jugular venous distention

(NB: can present atypical/ bilateral in cardiac arrest)

96
Q

treatment of tension pneumothorax

A
  • needle decompression (most rapid, 2nd IC space just above 3rd rib or the 4th/5th IC space mid-axillary line. Preferably with a long, non-kinking needle)
  • open thoracostomy (incision in 5th IC space mid-axillary line followed by dissection into the pleural space)
  • clamshell thoracotomy (may be required in traumatic cardiac arrest)
97
Q

where appropriately trained clinicians are available, what should be the initial strategy for chest decompression in tension pneumothorax?

A

open thoracostomy

98
Q

what should be sited following ROSC in a tension pneumothorax arrest

A

chest drain

99
Q

T/F: overall survival from perioperative cardiac arrest is low compared to other settings

A

false - HIGH

100
Q

causes of perioperative cardiac arrest?

A

hypovolaemia (bleeding)
cardiac problems
anaesthesia related problems

101
Q

what is the rhythm associated with the best chance of survival to hospital discharge following perioperative arrest?

A

Asystole (unlike other circumstances)

102
Q

T/F: CPR is possible in the prone position

A

true - although optimal when supine

103
Q

if there is asystole or extreme bradycardia during any surgery liely to be causing excessive vagal activity, what is the treatment of this?

A

give 0.5mg IV atropine and start CPR

104
Q

T/F: in perioperative cardiac arrest, adrenaline should always be given as a 1mg bolus

A

false - give in increments (50-100mcg) rather than a 1mg bolus

105
Q

in the treatment of cardiac arrest associated with anaphylaxis, titrate IV adrenaline using ___ boluses

if repeated adrenaline doses are needed, start what?

A

50mcg (1/2 ml of the pre-filled syringe)
an IV adrenaline infusion

106
Q

key to successful resuscitation in cardiac arrest following cardiac surgery?

A

recognising the need for emergency re-sternotomy early - esp in tamponade or haemorrhage where external chest compressions may be ineffective

107
Q

in arrest post cardiac surgery, in VF or asystole, attempt ___ ___ or emergency ___ ___ at maximum amplitude

A

external defibrillation
temporary pacing

108
Q

in arrest post cardiac surgery, start external compressions in pts with no output

verify effectiveness by looking at the arterial trace: aim SBP >60 and DBP >25 at a rate of 100-120bppm

inability to achieve these targets indicates the need for what procedure?

A

emergency resternotomy
(because ineffective chest compressions may indicate cardiac tamponade and/ or hypovolaemia)

109
Q

if cardiac arrest post cardiac surgery is thought to be caused by pacing failure, check the pacing box output and pacing wire integrity - do what if connection broken?

A

in asystole, can pause compressions briefly to connect wires and re-establish pacing (DDD mode at 100/ min max amplitude)

110
Q

treatment of a witnessed and monitored VF/pVT cardiac arrest?

A

up to three quick successive (stacked) defibrillation attempts

(if post cardiac surgery, 3 failed shocks should trigger emergency resternotomy)

111
Q

if resternotomy has been performed in a pt with cardiac arrest post-cardiac surgery, how to perform defibrillation?

A

with internal paddles at 20J

112
Q

drowning is a process resulting in primary respiratory impairment from submersion/ immersion in a liquid medium

difference between the two?

A

submersion: the face is underwater/ covered in water: asphyxia and cardiac arrest occur within a matter of minutes

immersion: the head remains above water, often supported by a life jacket, often with an open airway but eventually becoming hypothermic

113
Q

pathophysiology of drowning?

A

person initially breath holds by reflex, often swallowing water

> hypoxia and hypercapnia develop

> reflex laryngospasm may temporarily prevent the entrance of water into the lungs but eventually the person aspirates water

> bradycardia as a consequence of hypoxia occurs before cardiac arrest (therefore ventilation only resuscitation is critical and leads to ROSC in some cases)

114
Q

how to rescue someone from water?

A

avoid going into the water if possible
go in pairs if necessary
remove the person promptly, spinal precautions rarely needed
keep the person in a horizontal position during and after retrieval

115
Q

submersion durations of less than ___ mins are associated with a very high chance of a good outcome

A

5-10
(more than 25 min very low chance of good outcome)

116
Q

initial resuscitation once retrieved from water?

A

5 initial ventilations, supplemented with O2 if available

if no response, place on firm surface and start chest compression. 30:2 ratio (avoid compression only CPR as most will have sustained arrest secondary to hypoxia)

117
Q

what to do when resuscitating someone submerged in water if
1) massive amounts of foam caused by mixing of air with water and surfactant come out of the mouth
2) regurgitation of stomach contents and swallowed water occurs preventing ventilation

A

1) continue rescue breaths/ ventilation until someone’s able to intubate
2) turn the person on their side and suction the regurgitated material

118
Q

T/F: tracheal intubation is preferred to SGA insertion in drowning arrest

A

true - because pulmonary compliance is reduced and high inflation pressure may limit the use of SGAs

119
Q

can defib pads be applied to a drowned person’s chest?

A

yes- just dry the chest first

120
Q

T/F: after prolonged immersion, most people will have become HYPO/HYPER-volaemic

A

hypovolaemia - as the hydrostatic pressure of water on the body is removed

give rapid IV fluid

121
Q

definition of hypothermia?

A

core body temperature below 35 degrees

122
Q

describe the 4 stages of hypothermia

A

stage I: mild (conscious, shivering, core temp 32-35)
stage II: moderate (impaired LOC without shivering, core temp 28-32)
stage III: severe (unconscious, vital signs present, core temp 24-28)
stage IV: cardiac arrest or low flow state (no/ min vital signs core temp <24)
stage V: death due to irreversible hypothermia (core temp <11.8)

123
Q

what instrument is needed to measure the core temperature in hypothermia?

A

low reading thermometer

124
Q

the core temp in the lower third of the ____ correlates well with heart temperature

A

oesophagus

but measurement can only be performed in pts with an advanced airway

125
Q

what thermometers are not appropriate for use in hypothermia

A

commonly used tympanic thermometers that are based on infrared techniques - they don’t seal the ear canal and are not designed for low temp readings

also bladder and rectal temperatures lag behind core temps and are not recommended

use a consistent core temp measurement site throughout resus and warming measures

126
Q

cooling of the human body decreases cellular oxygen consumption by about ___% per 1 degree decrease in core temp

A

6

127
Q

intermittent CPR can be of benefit in cardiac arrest caused by what if continuous CPR cannot be achieved

A

hypothermia

5 mins CPR followed by <5mins without if temp less than 28

5 mins CPR followed by <10mins without if temp less than 20

128
Q

modifications to ALS in hypothermic pt
1) check for signs of life for up to __ __: palpate a central artery, assess the cardiac rhythm, use capnography/ ECHO/ ultrasound with doppler - if any doubt re adequate CO start CPR asap
2) can cause stiffness of chest wall so consider use of …
3) aim for SGA airway/ tracheal intubation
4) confirm hypothermia with what device once CPR started
5) the hypothermic heart may be unresponsive to cardioactive drugs&raquo_space; therefore what changes are necessary

A

1) 1 minute
2) mechanical compression devices
3) tracheal intubation - pros of adequate oxygenation and protection from aspiration outweigh minimal risk of triggering VF by doing intubation
4) low reading thermometer
5) withhold adrenaline and other CPR drugs until core temp >/= 30. At this point, double the durations between drug doses compared to normothermia (ie adrenaline every 6-10 mins). Standard protocol >35

129
Q

if VF is detected in a hypothermic pt, do what?

A

defibrillate as usual
if persist after 3 shocks delay further attempts until core temp >30

CPR and rewarming may have to be continued for several hours to facilitate successful defibrillation

130
Q

in hospital prognostication of successful rewarming in a hypothermic cardiac arrest should be based on what scoring systems?

A

HOPE or ICE

131
Q

general principles of managing a hypothermic patient?

A
  • remove wet clothes/ dry the pt
  • mobilise if conscious to help rewarm
132
Q

what is ‘rescue death’ in a hypothermic pt?

A

pts will continue cooling after removal from the cold environment, which can lead to life-threatening decreases in core temp triggering a cardiac arrest

133
Q

methods for rewarming pre-hospital
1) passive
2) active external
3) active internal

A

1) if still able to shiver (mild) use wool blankets, aluminium foil, cap and warm environment
2) stages II-IV, apply chemical heat packs to the trunk
3) not feasible pre-hospital

134
Q

in pre-arrest hypothermic patients in hospital, use what methods to reward?

A

forced warm air
warm IV infusions

135
Q

in deteriorating hypothermic pts, or those in hypothermic arrest, how should rewarming be achieved in hospital?

A

with ECLS, preferably ECMO

136
Q

definition of hyperthemia

A

when the body’s ability to thermoregulate fails and core temp exceeds that normally maintained by homeostatic mechanisms

body temp rises above normothermia (36.5-37.5)

137
Q

what is the continuum of heat related conditions?

A

heat stress > heat exhaustion > heat stroke > multiorgan dysfunction and sometimes cardiac arrest

138
Q

what is malignant hyperthermia

A

a rare, life threatening genetic sensitivity of skeletal muscles to volatile anaesthetics and depolarising NM blocking drugs occurring during or after anaesthesia

139
Q

mortality from heat stroke is up to ___%

A

33

140
Q

the key risk factors ass with heat stroke?

A

impaired ability to sweat

elderly increase risk- illness, med use, declining thermoregulatory mechanisms, limited social support

141
Q

triad of symptoms in heat stroke?

A

severe hyperthermia (core temp >40)
neurological symptoms (confusion/ seizure/ coma)
exposure to high environmental temps or recent strenuous physical exertion

142
Q

treatment of heat stroke?

A

transfer to cool environment and lay flat
immediately start cooling to <39 and transferring to hospital
best rapid cooling methods are cold water immersion or fully body conductive cooling systems
isotonic or hypertonic fluids (hypertonic when sodium <130)

143
Q

T/F: rapid cooling of a hyperthermic pt is safe

A

true

144
Q

management of malignant hyperthermia

A

stop triggering agents immediately
give O2
correct acidosis and electrolyte imbalances
start active cooling
give dantrolene

ALS (15 decks)

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