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Resuscitation 2015 > Special Circumstances Cardiac Arrest - not hypothermia > Flashcards

Special Circumstances Cardiac Arrest - not hypothermia Flashcards

1
Q

Hypothermic patient without cardiac instability - action?

A

Rewarmed externally with minimally invasive techniques

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2
Q

Hypothermic patient with cardiac instability - action?

A

Transferred directly to ECLS (extracorporeal life support) centre

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3
Q

When is ECLS indicated in rewarming avalanche burial victims?

A
  • Duration of burial >60 minutes.
  • Core temperature at extrication is <30 degrees.
  • Serum potassium at hospital admission is < or equal to 8.
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4
Q

First line for acute asthma

A

inhaled beta 2 agonists eg salbutamol. Only IV if cannot inhale

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5
Q

Most common non-cardiac cause of cardiac arrest?

A

Asphyxia - ultimately hyperaemia causes arrest before hypercarbia.

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6
Q

At what oxygen saturations is consciousness lost at?

A

60% (arterial)

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7
Q

Common rhythms in asphyxia?

A

PEA/Asystole (VF very rare)

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8
Q

Most common electrolyte imbalance causing life-threatening arrhythmias?

A

Potassium disorders- hyperkalaemia is most common.

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9
Q

Who is at risk of electrolyte disturbances?

A

Renal failure, severe burns, cardiac failure and diabetes.

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10
Q

Normal extracellular potassium concentration?

A

3.5-5.0mmol/l

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11
Q

What happens to serum potassium when serum pH decreases?

A

In acidaemia - serum potassium increases -> from cellular to vascular space.

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12
Q

Causes of hyperkalaemia?

A
  • Impaired kidney excretion: AKI/CKD
    (CKD and diet)
  • Drugs: ACE-I, ARB, k-sparing diuretics, NSAIDs, beta blockers, trimethoprim
  • Increased K release from cells: tissue breakdown; rhabdomyolysis, tumour lusis, homeless
  • Metabolic acidosis - renal failure, DKA

Also - Pseudo-hyperkalaemia describes the finding of a raised serum (clotted blood) K+ value concurrently with a normal plasma (non-clotted blood) potassium value. The clotting process releases K+ from cells and platelets, which increases the serum K+ concentration by an average of 0.4 mmol/L. The most common cause of pseudo-hyperkalaemia is a prolonged transit time to the laboratory or poor storage conditions

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13
Q

By how much does the incidence of hyperkalaemia increases as GFR drops from 60ml/min to 20 ml/min?

A

2 -> 42%

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14
Q

Hyperkalaemia defintion

A

Above 5.5mmol/l

Severe: above 6.5mmol/l

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15
Q

Symptoms of hyperkalaemia?

A

Weakness -> flaccid paralysis.
Paresthesia.
Depressed deep tendon reflexes.

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16
Q

ECG changes in hyperkalaemia?

A 
First degree heart block. (PR >0.2)
Flattened/absent P waves.
Tall, tented T waves (larger than R in more than one lead)
ST depression
S and T wave merging (sine wave pattern)
Wide QRS (>0.12)
VT
Bradycardia
Arrest
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17
Q

What are 5 key treatment strategies for hyperkalaemia?

A
  • Cardiac protection.
  • Shifting K into cells.
  • Removing K from body.
  • Monitoring K/glucose.
  • Preventing recurrence
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18
Q

Mild hyperkalaemia treatment?

A

Consider cause/prevent recurrence.
Consider calcium resonium to remove from body (15g x4/day oral or 30g x2/day PR)
Monitor K/glucose

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19
Q

Moderate/severe hyperkalaemia with ECG changes treatment?

A

(Severe - get expert help as well)

  • IV calcium - 10 ml 10% calcium chloride IV or 30 ml 10% calcium gluconate IV
  • Insulin-glucose IV infusion (25g glucose with 10 units insulin over 15 mins)
  • 10-20mg salbutamol nebulised
  • ? dialysis/monitor glucose/K
  • Cause/prevent recurrence
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20
Q

Risk associated with treatment of hyperkalaemia?

A
  • Hypoglycaemia due to gluc/insulin infusion(1-3 hours of treatment)
  • Tissue necrosis (2nd to extravasation of Iv calcium salts)
  • Intestinal necrosis/obstruction 2nd to potassium exchange resins. Avoid prolonged and give laxative.
  • Rebound hyperkalaemia after drugs worn off.
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21
Q

Moderate hyperkalaemia without ECG changes - treatment?

A

Glucose/insulin

Dialysis?

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22
Q

Severe hyperkalaemia without ECG changes - treatment?

A

Expert help
Glucose/insulin
Salbutamol
Dialysis?

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23
Q

Indications for dialysis?

A 
Severe/life-threatening with or without ECG changes/arrythymias.
Resistance to medical tx
End stage renal disease
Oliguric AKI (<400ml/day urine output)
Marked tissue breakdown
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24
Q

Define hypokalaemia and severe.

A

Serum potassium <3.5,

severe if <2.5

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25
Q

Most common electrolyte disturbance seen in clinical practice?

A

Hypokalaemia (20% of hospital patients)

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26
Q

Causes of hypokalaemia?

A

GI loss - diarrhoea
Drugs - diuretics, laxatives, steroids.
Renal loss - renal tubular disorders, diabetes insipidus, dialysis.
Endocrine disorders - Cushing’s, hyperaldosteronism
Metabolic alkalosis
Magnesium depletion
Poor diet

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27
Q

Symptoms of hypokalaemia?

A 
Muscle weakness
Leg cramps
Constipation
Fatigue
Severe - rhabdomylosis, ascending paralysis and respiratory difficulties
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28
Q

ECG features of hypokalaemia

A 
U waves
T wave flattening
ST segment changes
Arrhythmias (esp if digoxin)
Arrest
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29
Q

Max recommended IV dose of potassium

A

20 mmol/hour

Can do more rapid if unstable arrhythmias.

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30
Q

Potassium deficiency often co-exists with?

A

Magnesium deficiency - important for K uptake/maintenance of intracellular K values.

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31
Q

Define accidental hypothermia

A

Temp drop below 35 degrees

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32
Q

How does hypercalcaemia present?

A

Confusion, weakness, abdominal pain, hypotension, arrhythmias and cardiac arrest

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33
Q

How does hypocalcaemia present?

A

Paresthesia, seizures, tetany, av-block and cardiac arrest

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34
Q

Normal values for calcium?

A

2.1-2.6 mmol/l

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35
Q

ECG changes for hypocalcaemia?

A

Prolonged QT, T wave inversion, heart block and arrest

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36
Q

ECG changes for hypercalcaemia?

A

Short QT interval, prolonged QRS, Flat T waves, AV block and rest

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37
Q

Causes of hypercalcaemia?

A

Primary/tertiary hyperparthyroidism, malignancy, sarcoidosis, drugs

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38
Q

Causes of hypocalcaemia?

A

Chronic renal failure, acute pancreatitis, CCB overdose, toxic shock syndrome, rhabdomyolysis, tumour lysis syndrome.

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39
Q

Normal magnesium levels?

A

0.6-1.1mmol/l

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40
Q

Symptoms of hypermagnesaemia?

A

Confusion, weakness, resp depression, AV block, arrest

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41
Q

ECG changes - hypermagnesaemia?

A

Prolonged PR and QT intervals, T wave peaking, AV block and arrest

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42
Q

Symptoms of hypomagnesaemia?

A

Tremor, ataxia, nystagmus, seizures, arthymias - torsades des pointes

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43
Q

ECG changes with hypomagnesaemia?

A

Prolonged PR/QT intervals, ST depression,, T wave inversion, flattened P waves, increased QRS inversion

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44
Q

Treatment of hypercalcaemia?

A 
IV fluid replace
Furosemide 1 mg/kg IV
Hydrocortisone 200-300mg IV
Pamidronate 30-90 mg IV
Underlying cause
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45
Q

Treatment of hypocalcaemia?

A

Calcium chloride 10% 10-40ml

Magnesium sulphate if necessary

46
Q

At what levels (biochem) would you consider treating hypermagnesaemia?

A

> 1.75 mmol/litre

47
Q

Treatment of hypermagnesaemia?

A

Calcium chloride 10% if necessary
Saline diuresis - saline with furosemide.
Haemodialysis.

48
Q

Treatment of severe/symptomatic hypomagnasaemia?

A

2g 50% magnesium sulphate IV over 5 minutes

49
Q

Treatment of hypomagnasaemia with torsades des pointes?

A

2g 50% magnesium sulphate IV over 1-2 minutes

50
Q

Treatment of hypomagnasaemia with seizure?

A

2g 50% magnesium sulphate IV over 10 minutes

51
Q

Progression of heat-related conditions?

A

heat stress -> heat stroke -> MODS -> arrest

52
Q

What drugs can precipitate malignant hyperthermia?

A

Halogenated anaesthetics.

Depolarizing muscle relaxants

53
Q

What differentiates heat exhaustion from heat stroke?

A

No change in mental status, core temp still below 40 degrees.

54
Q

Definition of heat stroke?

A

Hyperthermia accompanied by SIRS with a core temperature above 40 degrees, accompanied by mental state change and varying levels of organ dysfunction.

55
Q

Average fluid replacement in heat exhaustion?

A

1-2l crystalloid at 500ml/hour

56
Q

What are the two forms of heat exhaustion?

A

Classic Heat Stroke (non-exertional) e.g. elderly in heat waves
Exertional Heat Stroke - strenuous physical exercise in high ttemps/humidity (healthy young adults)

57
Q

Aim when cooling?

A

Rapidly to 39 degrees.

58
Q

Increased core temp - causes?

A

Drug withdrawal, drug toxicity, heat stroke, sepsis, neuroleptic malignant syndrome, thyroid storm, pheochromocytoma, CNS infection etc.

59
Q

Seizing due to heat stroke?

A

Diazepam may be useful

60
Q

What drug can be of use if malignant hyperthermia is caused by amphetamines?

A

Dantrolene.

61
Q

Anaphylaxis - why do people arrest?

A

Relative hypovolaemia

62
Q

Define anaphylaxis.

A

Severe, life-threatening, generalised/systemic hypersensitivity reaction

63
Q

Anaphylaxis criteria:

A

Any 1 of these 3:
1. Acute onset with skin/mucosal tissue involvement and at least one of:
- Resp compromise
- Reduced BP/symptoms of end-organ dysfunction
2. Two or more of following:
- Skin/mucosal tissue
- Resp compromise
- Reduced BP/associated symptoms
- Persistent GI symptoms
3. Reduced BP after exposure to known allergen
(Infants/kids cutoff vs adults?)

64
Q

For last anaphylaxis criteria, what is low systolic BP?

A

1 month - 1 year: <70mmHg
1 - 10 years: <70mmHg + (2x age)
11 years and above: <90mmHg or 30% decrease from their baseline.

65
Q

Anaphylaxis treatment - adrenaline dose?

A

Adult/child over 12 years: 500 mcg IM (0.5 mL of 1:1000)
Child 6-12: 300mcg
Child less than 6 years: 150 mcg

66
Q

Anaphylaxis treatment - chloramphenamine dose?

A

Adult/child over 12 years: 10mg
Child 6-12: 5mg
Child 6 months-6 years: 2.5mg
Child less than 6 years: 250 mcg/kg

67
Q

Anaphylaxis treatment - hydrocortisone dose?

A

Adult/child over 12 years: 200mg
Child 6-12: 100mg
Child 6 months-6 years: 50mg
Child less than 6 years: 25mg

68
Q

IV fluid challenge in anaphylaxis?

A

Adult: 500-1000mL
Child: 20mL/kg
NB; stop colloid, use crystalloid

69
Q

How does adrenaline help in anaphylaxis?

A

Alpha receptor agonist - reverses peripheral vasodilation and reduces oedema.
Beta receptor - reverses bronchospasm, increases myocardial contraction and suppresses histamine/leukotriene release - - on mast cells there are beta 2 adrenergic receptors. When activated inhibits their activation.

70
Q

Why IM adrenaline?

A

Greater safety margin, no IV access, easier to learn and easier to self-administer.

71
Q

Best site for Im injection?

A

Anterolateral aspect of middle third of thigh.

72
Q

What kind of anti-histamine?

A

H1 antihistamines - chloramphenamine (counter cutaneous symptoms, vasodilation and bronchospasm)

73
Q

Role of glucocorticoids in anaphylaxis?

A

More to prevent refractory/prolonged episodes. 2nd prevention.

74
Q

Other drugs for anaphylaxis?

A

?treat bronchospasm with salbutamol/ipatropium etc. If bet-blocker reaction ? glucagon

75
Q

What test confirms an anaphylaxis diagnosis?

A

Mast cell tryptase (from degranulation) - typically at least 30 mins or after

76
Q

TCA - survival factors?

A

PEARL, organised ECG and resp activity.

Also age, VF (v rare)

77
Q

TCA - withholding resus?

A

• no signs of life within the preceeding 15 min;
• massive trauma incompatible with survival (e.g. decapitation,
penetrating heart injury, loss of brain tissue).

We suggest termination of resuscitative efforts should be con- sidered if there is:
• no ROSC after reversible causes have been addressed; • no detectable ultrasonographic cardiac activity.

78
Q

In TCA, what happens simultaneously to starting ALS?

A

Address reversible causes (hypoxia, tension pneumothorax, tamponade and hypovolaemia):

  1. Control external catastrophic bleed
  2. Airway and maximise oxygenation.
  3. Bilateral chest decompression.
  4. Cardiac tamponade
  5. Surgery for haemorrhage control/aortic compression
  6. Transfusion/fluids.
79
Q

Damage control resuscitation principles?

A

Hypotensive resuscitation (permissive - maintain radial pulse until surgery/around 80-90mmHg for 1 hr) -> haemostatic resuscitation (early blood products: 1:1:1 - packed RBC: FFP: Platelets and TXA etc) -> damage control surgery

80
Q

Why can positive pressure ventilation be a problem in hypovolaemic patients?

A

Impedes venous return to the heart -> worsening hypotension. As a result - low tidal volumes and slow resp rates are better.

81
Q

Criteria for proceeding with resuscitative thoracotomy after hospital arrival?

A

Blunt trauma with less than 10 mins of prehsop CPR

Penetrating trauma with less than 15 mins prehosp CPS

82
Q

Successful RT: 4 Es rule?

A

Expertise, Equipment, Environment, Elapsed time (no longer than 10 mins)

83
Q

Why is needle aspiration of tamponade unreliable?

A

Pericardium often full of clotted blood.

84
Q

Signs of PE on ECG?

A

Right or left ventricular strain:

Inversion of T waves in leads V1-V4, QR pattern in V1, S1 Q3 T3, incomplete or complete RBBB.

85
Q

Most common rhythm in PE cause of cardiac arrest?

A

PEA

86
Q

Most likely underlying cause of arrest if patient is in VF?

A

Occluded coronary artery - MI

87
Q

Dermal decontamination?

A

Remove clothes, water irrigation (reactive alkali metals that can ignite).

88
Q

GI decontamination

A

Activated charcoal - if airway intact or protected. Most effective within 1 hr.

89
Q

What does activated charcoal not bind to?

A

Lithium, heavy metals and toxic alcohols

90
Q

Patient presents more than 2 hours after ingestion?

A

Whole bowel irrigation

91
Q

Enhances elimination techniques?

A

Multiple-dose activated charcoal, urinary alkalinisation and extracorporeal elimination.

92
Q

Dose of activated charcoal if doing MDAC?

A

50-100g in adults, 25-50g in children.

93
Q

How to do urinary alkalinisation? When is most useful?

A

IV sodium bicarbonate.

For salicylate intoxication (before dialysis levels), phenobarbitol/herbicide poisoning.

94
Q

Most common complication of urinary alkalinisation?

A

Hypokalaemia

95
Q

Benzodiazepine OD - presentation and treatment with mechanism.

A

LOC, resp depression, hypotension. Flumazenil - competitive anatgonist (only if no history of seizing)

96
Q

Opioid OD - presentation and treatment?

A

Pinpoint pupils, Reduced GCS and resp depression.

Naloxone - rapid reversal.

97
Q

Opioid acute withdrawal - presentation?

A

Sympathetic excess state - pulmonary oedema, ventricular arrhythmias and severe agitation.

98
Q

Naloxone dosing?

A

0.4-2mg - repeat every 2-3 mins.
Intranasal: 2mg.
Large overdose may require up to 10mg in total

99
Q

What do before naloxone administered?

A

Airway opening, oxygenation/ventilation.

100
Q

What arrthymia is common in TCA overdose and why?

A

VT - wide complex tachycardia due to anticholinergic and sodium channel blocking effects.

101
Q

TCA overdose - presentation?

A

Seizures, hypotension (exacerbated by alpha-1 receptor blockade), coma, arrthymias

102
Q

Anticholinergic effects?

A

Mydriasis, fever, dry skin, delirium, tachycardia and urinary retention.

103
Q

How to treat TCA-induced VT?

A

Sodium bicarbonate 1-2mmol/kg

104
Q

Cocaine overdose -what drugs are useful?

A

In patients with severe cardiovascular toxicity:

  • alpha blockers (phentolamine),
  • benzodiazepines (lorazepam, diazepam)
  • calcium channel blockers (verapamil)

Also - morphine and sub- lingual nitroglycerine may be used as needed to control hypertension, tachycardia, myocardial ischaemia and agitation.

105
Q

Additional treatment for local anaesthetic systemic toxicity?

A

IV 20% lipid emulsion

(Give an initial intravenous bolus injection of 20% lipid emulsion 1.5 mL kg−1 over 1 min followed by an infusion at 15 mL kg−1 h−1 . Give up to a max- imum of two repeat boluses at 5-min intervals and continue until the patient is stable or has received up to a maximum cumulative dose of 12 mL kg−1 of lipid emulsion.)

106
Q

Beta-blocker toxicity treatment?

A 
Glucagon (50-150mcg/kg)
high dose insulin/glucose
Lipid emulsions
Phosphodiesterase inhibitors
Calcium salts
107
Q

CCB OD tx?

A

Calcium chloride 10% (20ml) every 2-5 minutes in severe bradycardia/hypotension. This is not enough for stability.
High dose insulin and glucose etc.

108
Q

Digoxin OD tx?

A

(NB mortality high)
digoxin-Fab; specific antibody fragments: if haem unstable.
Give 2 bolus of 2 vials (38 mg/vial)

109
Q

What drugs can also push digoxin into lethal levels?

A

CCBs

Amiodarone

110
Q

Digoxin effect on heart?

A

Atrioventricular conduction abnormalities and ven- tricular hyperexcitability -> severe arrhthymias and arrest.

111
Q

Mechanism of cyanide toxicity?

A

Inactivation of cytochrome oxidase (at cytochrome a3) -> uncoupling mitochondrial phosphorylation and inhibiting cellular respiration.

112
Q

Options for cyanide scavenger therapy?

A

Hydroxocobalamin 100mg/kg IV
Nitrite -
Either of those followed by IV sodium thiosulfate.

Resuscitation 2015 (31 decks)

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