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- FINALS > Emergency > Flashcards

Emergency Flashcards

1
Q

Anaphylaxis doses?

A

Adrenaline 0.5 mg 1:1000

Hydrocortisone 200mg IV
Chlorphenamine 10mg IV
Salbutamol 5mg neb

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2
Q

SIRS criteria?

A

HR >90
RR >20 or PaCO2 <4.3
Temp <36 or >38.3
WCC <4 or >12

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3
Q

Sepsis classification?

A

Sepsis = SIRS + known/suspected infection

Severe sepsis = sepsis + signs of hypoperfusion/organ failure

Septic shock = persistent hypotension despite adequate fluid resuscitation

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4
Q

Causes of cardiogenic shock?

A

Pump failure –> LV dysfunction, aortic dissection, dysrhythmia

Inadequate filling –> PE, pneumothorax, tamponade

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5
Q

What is Beck’s triad of cardiac tamponade?

A

Low BP
Raised JVP
Faint heart sounds

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6
Q

Causes of hypovolaemic shock?

A

Haemorrhage

Salt + water loss

3rd space loss

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7
Q

ABG result in vomiting and haemorrhage?

A

Vomiting = alkalosis

Haemorrhage = acidosis

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8
Q

Definitions of respiratory failure?

A

Type 1 = PaO2 <8 kPa, PaCO2 <6.5 kPa

Type 2 = PaO2 <8 kPa, PaCO2 >6.5 kPa

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9
Q

Causes of type 1 respiratory failure?

A

V/Q mismatch

Obstructed airways = asthma, COPD
Block in blood flow = PE
Pulmonary oedema, ARDS

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10
Q

Why is CO2 normal in type 1 RF?

A

Because areas that are perfused and ventilated can blow it off by increasing RR

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11
Q

Causes of T2RF?

A

Alveolar hypoventilation - O2 can’t get in and CO2 can’t get out

Reduced ventilatory effort, increased dead space, increased CO2 production

Severe asthma –> exhaustion
Acute epiglottitis
Respiratory muscle paralysis

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12
Q

Signs of hypoxia?

A

Restlessness, confusion –> coma

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13
Q

Signs of hypercapnia?

A 
Drowsiness
Flapping tremor
Warm peripheries
Headaches
Bounding pulses
Papilloedema
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14
Q

Oxygen therapy in T1RF?

A

Unrestricted (35%+)

Repeat gases after 20 mins to ensure correction of PaO2 and absence of rise of PaCO2

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15
Q

Oxygen therapy in T2RF?

A

Controlled (start at 24% and titrate)

Monitor PaCO2 closely by repeat gases - if it rises by more than 1 kPa, consider NIV

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16
Q

Contraindications to NIV?

A 
Inability to protect airway
Cardiac/respiratory arrest
Upper airway obstruction
Pneumothorax
Haemodynamic instability
Maxillofacial surgery
Basal skull fracture
Intractable vomiting
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17
Q

When is CPAP used?

A

Acute pulmonary oedema
Asthma
Obstructive sleep apnoea

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18
Q

When is BIPAP used?

A

COPD
Weaning
Asthma
Neuromuscular disease

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19
Q

PCM OD dose associated with hepatic necrosis?

A

250 mg/kg

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20
Q

Clinical features of PCM overdose after 24h?

A

RUQ pain +/- evidence of liver failure

PT, ALT, AST - raised

PT/INR is best marker of synthetic function

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21
Q

Clinical features of PCM overdose after 3-5 days?

A

Recovery may begin, or fulminant hepatic failure

Cogagulopathy
Hypoglycaemia
Encephalopathy
AKI (hepatorenal syndrome)

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22
Q

ABG in PCM overdose?

A

pH <7.3 despite fluid resuscitation predicts mortality

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23
Q

Management of PCM overdose? (levels)

A

<4 hrs - take levels and wait

4-8hrs - take levels and treat if over treatment line

8-15hrs - treat before levels come back, stop if under treatment line

> 15hrs/staggered - treat

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24
Q

Doses of parvolex/NAC?

A

150 mg/kg in 200ml over 1 hour

50 mg/kg in 500ml over 4 hours

100 mg/kg in 1000ml over 16 hours

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25
Q

When to discontinue NAC?

A

If plasma concentration later reported to be below treatment line and patient is asymptomatic with normal LFTs, creatinine and PT.

26
Q

Side effects of NAC?

A

20% have pseudoallergic (anaphylactoid) reaction

stop infusion and give chlorphenamine

27
Q

Pathophysiology of salicylate overdose?

A

Acid base disturbance

Uncoupling of oxidative phosphorylation

Disordered glucose metabolism

28
Q

Signs/symptoms of salicylate overdose?

A

N+V, abdominal pain, tinnitus

Deafness, hyperventilation, flushed skin, sweating, hyperthermia

29
Q

Complications of salicylate overdose?

A 
Aspiration
Pulmonary oedema
Cardiovascular instability
Hypo/hyperglycaemia
Hypokalaemia
Hypoprothrombinaemia
Thrombocytopenia
DIC
Renal failure
30
Q

Salicylate levels?

A

Mild - <500mg/L

Moderate - 500-750 mg/L

Severe - >750 mg/L

31
Q

ABG in salicylate overdose?

A 
Metabolic acidosis (lactate)
Respiratory alkalosis (hyperventilation)
32
Q

ECG in salicylate overdose?

A

Widened QRS
AV block
Ventricular dystrhythmias

33
Q

Bloods in salicylate overdose?

A

Glycaemic, Electrolytes, Bleeding, Renal

Hypo/hyerglycaeima
Hypokalaemia
Hypoprothrombinaemia
Thromboyctopenia
DIC
Renal failure
34
Q

Correcting acid-base, electrolyte, bleeding abnormalities in salicylate overdose?

A

Glucose infusion if hypoglycaemic

Correct electrolytes

Vitamin K if hypoprothrombinaemia

Sodium bicarb for severe acidosis

Dialysis in moderate-severe cases

35
Q

Pathophysiolog and dose of TCA overdose?

A

TCA = sodium-channel blocking agent –> seizures and ventricular dysrhythmias

10mg/kg potentially life threatening, 30mg/kg –> severe toxicity

Rapid deterioration within 1-2 hours of ingestion

36
Q

CNS, CVS and anticholinergic features of TCA overdose?

A

Sedation/coma/convulsions/delirium - FIRST

Sinus tachy + HTN –> hypotension
Broad complex tachydysrhythmia –> broad complex bradycardia (pre-arrest)

Agitation, restlessness, delirium, mydriasis, dry, warm flushed skin, urinary retention, tachycardia, ileus, myoclonic jerks

37
Q

ABG/ECG findings in TCA overdose?

A

Metabolic acidosis

Prolonged PR
Wide QRS/QTc
RAD of terminal QRS
Ventricular dyshythmia

38
Q

Management of TCA overdose?

A

Sodium bicarb IV - bolus every few minutes until BP improves and QRS narrows

SEIZURES
IV benzos, sodium bicarb, RSI/ventilation

HYPOTENSION
IV crystalloid bolus, vasopressors (ICU)

CNS DEPRESSION
Intubation - hyperventilate to pH 7.5-7.55

39
Q

Effects of iron overdose? (Local and systemic)

A

LOCAL (GI)
Corrosive injury to mucosa –> D+V, haematemesis, melena, fluid losses –> hypovolaemia

SYSTEMIC
Iron = cellular toxin, targets CVS and liver.
Secondary CNS effects
Metabolic acidosis due to hyperlactemeia and free proton production from hydration of free ferric ions
Coagulopathy

40
Q

Risk assessment of iron overdose?

A

<20 mg/kg = asymptomatic
20-60 mg/kg = GI symptoms only
60-120 mg/kg = potential for systemic toxicity
>120 mg/kg = potentially lethal

41
Q

Iron overdose presentation?

A

0-6 HOURS
vomiting, diarrhoea, haemetemesis, melena, abdominal pain. Significant fluid losses –> hypovolemic shock

6-12 HOURS
GI symptoms wane and the patient appears to be getting better. During this time iron shifts intracellularly from the circulation

12-48 HOURS
Cellular toxicity becomes manifest as vasodilative shock and third-spacing, high anion gap metabolic acidosis (HAGMA) and hepatorenal failure

2-5 DAYS
Acute hepatic failure, although mortality is rare

2-6 WEEKS
Chronic sequelae occur in survivors –– cirrhosis and gastrointestinal scarring and strictures

42
Q

Serum iron concentration levels in iron overdose?

A

Peak levels after 4-6 hours

Levels fall after 6 hours due to intracellular shift

90 micromol/L = systemic toxicity

43
Q

Blood gas in iron overdose?

A

HAGMA = high anion gap metabolic acidosis

Useful marker of systemic toxicity

44
Q

Managment of iron overdose?

A

ABCDE = priority –> restoration of circulating volume

Decontamination - whole bowel irrigation or surgical/endoscopic removal if lethal ingestion

45
Q

Antidote in iron overdose?

A

DESFERRIOXAMINE

Chelates free ferric and ferrous ions –> water soluble complexes that can be renally excreted

Cardiac monitoring mandatory when infusion running

46
Q

ECG findings in hypothermia?

A 
brady
J wave
1st degree heart block
Long QT
Arrhythmias
47
Q

Presentation of delirium?

A

New change in…

Cognition/concentration
Physical function
Social behaviour
Appetite, sleep, mood
Hallucinations
Falls
48
Q

Causes of delirium?

DELIRIUM

A

Drugs (withdrawal/toxicity, anticholinergics)/Dehydration

Electrolyte imbalance/Environmental factors

Level of pain

Infection/Inflammation (post surgery)

Respiratory failure (hypoxia, hypercapnia)

Impaction of faeces

Urine retention

Metabolic disorder (liver/renal failure, hypoglycaemia)/Myocardial infarction

49
Q

General measures for delirium?

A

Calming environment

Rationalise medications

Hydrate (oral best)

Monitor bowls/treat constipation

Frequently reassure/reorientate

Optimise sensory impairment (glasses, hearing aid)

Look for and treat infection

Don’t argue/confront, move bays, restrain or do unnecessary procedures

50
Q

Indications for sedation in delirium?

A

Carry out essential investigations
Prevent danger to self or others
Relieve patient distress

51
Q

Sedation agents in delirium?

A

Haloperidol 0.5mg PO, 1-2 hourly, max 5mg daily

Can add lorazepam - avoid due to hangover effect/dependence

52
Q

When should benzos be first line for sedation?

A

Prolonged QRS, DLB, Parkinson’s

Seizures, rec drug intoxication/withdrawal, alcohol withdrawal

53
Q

What is spinal shock?

A

Loss of sympathetic vascular tone –> dilation of arterioles/venous pooling –> low BP and low CO

Loss of sympathetic drive to heart (T1-T4)

54
Q

Causes of spinal shock?

A

Traumatic - transection of spinal cord at any level

Iatrogenic - final spinal anaesthesia

55
Q

Symptoms and signs of spinal shock?

A

Motor/sensory dysfunction below level of lesion (UMN lesion) + bladder/bowl dysfunction

Low BP, warm peripheries, may not be able to mount tachycardia if lesion above T1-T4
Focal neurology +/- up going plantars, loss of anal tone

56
Q

What are complications of shock?

A

PROLONGED HYPOTENSION –> HYPOPERFUSION

Brain - low CNS/coma
Kidneys - AKI/ATN
Liver - ischaemic hepatitis
Heart - myocardial ischaemia/MI

57
Q

Definition of AKI?

A

Rise in serum creatinine >26µmol/L within 48hrs or rise in serum creatinine 1.5 x baseline value within 1wk or urine output <0.5ml/kg/hr for 6hrs.

58
Q

AKI staging systems?

A

RIFLE
AKIN
KDIGO

59
Q

AKI Management? ABCCDD

A 
Assess (fluid balance)
Bloods (K+, urea, cr)
Catheter
Cannula (IV fluids)
Drugs (check chart)
Dialysis?
60
Q

Drugs to stop in AKI?

A

ACEi
Metformin
Diuretics
NSAIDs

61
Q

Indications for RRT in AKI?

A

Uraemic complications (enceph, pericarditis)
Refractory Pulmonary oedema
Refractory metabolic acidosis
Refractory hyperkalaemia

62
Q

HAGMA and NAGMA?

A

HAGMA = accumulation of organic acids/impaired H+ excretion (LKTR - lactate, toxins, ketones, renal)

NAGMA = loss of HCO3- from ECF (hyperchloraemia, acetazolamide/addison’s, GI losses)

- FINALS (24 decks)

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