Acute Care Flashcards
What are the causes of airway obstruction
central nervous system depression
swelling - infection or anaphylaxis
foreign body
bronchospasm
What can cause central nervous system depression
head injury intracerebral bleed hypercapnia hypoglycaemia alcohol opioids general anaesthetic
What can cause respiratory arrest
decreased respiratory drive (due to CNS depression)
decreased resp effort
lung disorders
What is the treatment for ACS
IV morphine + antiemetic
15L oxygen via non-rebreathe mask if sats <94%
sublingual glyceryl nitrate (unless hypotensive)
Aspirin 300mg crushed/chewed
How is A assessed
speak to patient
listen to breathing sounds
look at breathing pattern
How is airway obstruction treated
15L oxygen via non-rebreathe mask
airway manoeuvres
suction
Guedel/nasopharyngeal
How is B assessed
resp rate o2 sats pattern of breathing chest deformity trachea chest expansion percussion breath sounds - ?rattle, wheeze, stridor auscultate
How is C assessed
hands - ?cool, warm, pale, pink, mottled CRT peripheral and central pulses HR BP - wide PP = arterial vasodilation, narrow PP = arterial vasoconstriction auscultate ECG
How is D assessed
AVPU
check drug chart for drugs that cause reduced consciousness
pupils
blood glucose
Which cardiac arrest rhythms are shockable?
VF
pulseless VT
Which cardiac arrest rhythms are non-shockable?
asystole
PEA
describe the treatment of shockable cardiac arrest
CPR
secure airway
break CPR every 2 mins to assess rhythm
give shock 150J first
repeat
after third shock give 300mg amiodarone IV and adrenaline 1mg IV
continue CPR and checks every 2mins
repeat 1mg adrenaline IV at alternate shocks
can give 150mg amiodarone IV after five shocks
describe the treatment of non-shockable cardiac arrest
CPR
adrenaline 1mg IV STAT
check rhythm every 2 mins
give 1mg adrenaline IV every other cycle
State the reversible causes of cardiac arrest
Hypoxia
Hyperkalaemia, hypokalaemia, hypoglycaemia
Hypovolaemia
Hypothermia
Thrombosis - MI/PE
Tension pneumothorax
Tamponade
Toxins
State the steps in management of bradycardia
if signs of adverse features, give atropine 500mcg IV
if unsuccessful, arrange senior help and transvenous pacing
if no adverse features, assess for risk of asystole
if risk of asystole, ger senior help and arrange transvenous pacing
What are the adverse features in tachy/bradycardia
shock
heart failure
syncope
MI
What are the steps in management of broad complex tachycardia
are there adverse features present?
no
- correct electrolyte abnormalities
- if most likely monomorphic VT give amiodarone 300mg IV over 20 mins
- if polymorphic VT give 2g magnesium sulfate IV over 10mins
yes - call for senior help, sedate and cardiovert. give 300mg amiodarone IV over 20 mins
900mg amiodarone IV via central line over 24h
What is the difference between monomorphic and polymorphic VT
mono - caused by structural abnormalities. not likely to convert into VF
poly - caused by electrolyte abnormalities, likely to convert into VF
What are the steps in management of narrow complex tachycardia
vagal maneouvres
IV adenosine 6mg, 12mg, 12mg
adverse features?
yes
- sedation and cardioversion
- amiodarone 300mg IV over 20 mins then 900mg amiodarone IV via central line over 24h
no - beta blocker eg. IV metoprolol, amiodarone 300mg IV over 1h or digoxin
How is GCS calculated?
Eye Opening Spontaneous 4 To sound 3 To pressure 2 None 1
Verbal Response Orientated 5 Confused 4 Words 3 Sounds 2 None 1
Motor Response Obeys commands 6 Localise to pain 5 Withdraws from pain 4 Flexor response 3 (decorticate) Extensor response 2 (decerebrate) None 1
What are the common causes of reduced GCS
metabolic: drugs sepsis hypoglycaemia/hyperglycaemia respiratory acidosis hypoxia hypothermia addisonian crisis hepatic or uraemic encephalopathy
neurological: trauma meningitis/encephalitis tumour stroke, SAH epilepsy
What are the key signs and symptoms of anaphylaxis
Onset within minutes Airway and breathing Dyspnoea, respiratory distress, wheeze, stridor Cyanosis Circulation Tachycardia, hypotension Skin Urticaria, angioedema
Describe the pathophysiology of anaphylaxis
Sensitisation phase:
Immune system encounters allergen and makes immunoglobulin E (IgE) against it
No clinical features occur
Effector phase:
Allergen cross-links IgE on surface of mast cells
widespread degranulation and release of histamine
mediates inflammatory bronchospasm, vasodilatation, increased capillary permeability, and tissue oedema
What dose of adrenaline do you give to an adult in anaphylaxis
0.5mg (0.5 ml of 1:1,000) IM