ACC revision Flashcards
1
Q
how to treat an airway obstruction (in RRAPID)
A
give 15L oxygen NRBM
2
Q
what does stridor at rest infer
A
reduction of airway diameter of >50%
3
Q
how is hypotension defined in the ED
A
SBP <90mmHg, MAP <60mmHg OR decrease in greater than 40mmHg of 30% from patient’s baseline MAP or combination
4
Q
4 ways hypoxia is classified
A
- hypoxic hypoxia (reduced O2 supply)
- anaemic hypoxia (reduced Hb function = less O2 delivered)
- stagnant hypoxia (blood and O2 can’t get to tissues)
- histotoxic hypoxia (alcohol, drugs, poisons)
5
Q
how is hypovolaemic shock treated
A
fluids +/- blood (usually over a litre of warmed crystalloids then switch to blood products)
6
Q
what is cariogenic shock
A
tissue hypo perfusion due to damage/insufficiency of the heart
7
Q
most common cause of cardiogenic shock
A
MI
8
Q
confusion assessment method (CAM) of diagnosing delirium
A
- onset and fluctuating course - change from baseline
- inattention - easily distracted
- disorganised thinking - rambling/irrelevant conversations/illogical flow of ideas
- altered level of consciousness
9
Q
antidote for benzodiazepine toxicity
A
flumanezil
10
Q
antidote for hyperkalaemia
A
dextrose + insulin
11
Q
antidote for LA toxicity
A
20% lipid emulsion
12
Q
antidote for bradycardias
A
atropine
13
Q
2 shockable rhythms
A
V fib pulseless VT (no cardiac output)
14
Q
what does pulseless electrical activity look like
A
fairly normal ECG but there is NO pulse
15
Q
which medications to ask specifically about in a pre-op assessment
A
anticoagulants
antiplatelets
insulin
anticonvulsants
drug allergies and OTC
16
Q
questions to ask in a pre-op assessment if someone has rheumatoid arthritis
A
Joints:
- TMJ: problems with jaw
- crico-arythenoid joints: glottic arthritis (problems with throat?)
CVS:
- asymptomatic pericardial effusion
RS:
- pulmonary nodules/fibrosis
anaemia, renal impairment, peripheral neuropathy
17
Q
tests to do for diabetics pre-op
A
BM, urine glucose and ketones
ECG
electrolytes
first on the list
18
Q
characteristics of pre-oxygenation for RSI
A
- 3 minutes pre-oxygenation
- 5 full vital capacity breaths over 30 seconds
- EtO2 concentration >90
this is to replace forced respiratory capacity with oxygen
19
Q
causes of bradycardia
A
- normal (athletes)
- MI, myotonic dystrophy, sick sinus syndrome
- endocarditis
- hypothyroid, hypo/hyperkalaemia
- Cushing’s response (to trauma)
- drugs
- anorexia nervosa
20
Q
location of MI most likely to cause bradycardia
A
inferior MI
21
Q
drugs which can cause bradycardia
A
- beta blockers
- CCBs
- digoxin
- clonidine
- opiates
- amiodarone
22
Q
what is Cushing’s reflex
A
physiological response to increased ICP:
- bradycardia
- widened pulse pressure (increased SBP, decreased DBP)
- irregular respirations
23
Q
4 main signs of reduced end-organ perfusion/ haemodynamic instability (from bradycardia?)
A
- shock
- syncope
- MI
- heart failure
24
Q
treatment of bradycardia if there are adverse features of HD instability
A
atropine 500mcg - if doesn’t work:
- atropine 500mcg IV repeat up to 3mg OR
- isoprenaline 5mcg/min IV
- adrenaline 2-10mcg/min IV etc.
25
when might glucagon be used for bradycardia
if it is due to beta blockers or CCBs
26
how does atropine work
blocks effects of vagus nerve = increases HR (prevents parasympathetic input)
27
drugs used during RSI
- Thiopentone: 4-5mg/kg with onset of 15-30 seconds, lasting 4-8 minutes
- Propofol: 1.5-2.5mg/kg, onset in 30 seconds, duration 2-6 minutes
- Rocuronium: 1mg/kg, DOA: 6 minutes OR Suzemethonium: 1-1.5mg/kg, DOA 6 minutes
28
3 steps in the technique for RSI
1. Cricoid pressure: 10-30N
2. Apnoeic ventilation
3. Confirm tube positioning- Co2
29
safe dose of lignocaine with vs without adrenaline
```
without = 3mg/kg
with = 7mg/kg
```
30
characteristics for pre-oxygenation for RSI
- 3 minutes pre-oxygenation
- 5 full viral capacity breaths over 30 seconds
- EtO2 concentration >90
this is to replace forced expiratory capacity with oxygen
31
normal AV node delay
120m/s
32
why does Cushing's reflex cause bradycardia
inappropriate stimulation of baroreceptors during cerebral artery dilation
33
specific treatment of bradycardia if there are adverse features of HD instability (shock, MI, syncope, HF)
atropine 500mcg
34
what is 1st degree heart block
consistent prolonged PR interval (>120m/s)
35
3 causes of 1st degree heart block
- normal physiology (athletes)
- inferior MI
- electrolyte disturbances
36
when does 1st degree heart block become a problem and how is it managed
haemodynamically unstable - give atropine 500mcg IV or TC pacing
37
causes of 2nd degree heart block Mobitz type 1 (Wenckeback) - increasingly prolonged PR interval followed by dropped QRS
- drugs: CCBs, BBs, amiodarone, digoxin
- inferior MI
- electrolyte disturbances
38
main pathological cause of 2nd degree heart block type 2
Purkinje fibre dysfunction - often due to anterior/septal MI, fibrosis (surgery), SLE, systemic sclerosis
39
how is mobitz type 2 treated
permanent pacemaker - much more likely to be clinically problematic (haemodynamically unstable)
40
how to treat complete heart block
- TC pacing followed by pacemaker
| - atropine if broad QRS
41
what is a broad complex tachycardia vs narrow complex
tachycardia >100bpm with broad QRS >120m/s (2 small squares)
narrow complex = <120m/s
42
treatment for broad complex tachycardia if there are adverse features of shock (including VT)
synchronised DC shock
43
treatment for broad complex tachycardia if there are NO adverse features of shock (including VT)
amiodarone 300mcg IV over 1 hour (900mg IV over 24 hours)
44
treatment for narrow complex tachycardia if there are adverse features of shock
synchronised DC shock
45
treatment for narrow complex tachycardia if there are NO adverse features of shock
1. vasovagal manoeuvres
2. IV adenosine (6mg IV bolus) - further 2 x 12mg if no effect
3. if still no effect - consider high dose BBs (verapamil) and call for cardiologist
46
most common cause of VT (type of broad complex tachycardia)
ischaemic heart disease
47
what drugs can lead to VT
- macrolides
- fluoroquinolones
- digoxin
48
what must first be done if VT is recognised
check pulse - can be an arrest rhythm so must check
49
main causes of V fib
- CAD
- Previous MI: scar tissue
- Myocarditis
- Cardiomyopathy
- Congenital heart disease
- WPW
- Long QTc syndrome
50
management of V fib
- ABCDE
- synchronised DC shock
- 1mg IV adrenaline + amiodarone 300mg IV then 900mg over 24 hours
- more amiodarone
- lignocaine 1mg/kg
51
what is the seldinger technique
general way lines are inserted into arteries or veins - needle goes in, then guide wire through needle
then catheter is fed around the guide wire
52
arterial line waveforms - what does the maximum height show and the minimum height show
```
maximum = SBP
minimum = DBP
```
53
what does the upstroke of the curve in arterial line waveforms show
cardiac contractility
54
what does the area under the curve in arterial line waveforms show
cardiac output
55
typical abnormal findings of arterial line waveform in cariogenic failure
- reduced gradient of upstroke
- reduced peak height
- altered position of dichrotic notch
56
most common site of central venous line
internal jugular vein
57
what is the Trendelenburg position
entire bed is tilted with head of bed LOWER than foot of bed
facilitates venous return - used when inserting central venous lines
58
how long is the central venous line
16cm long - MUST be inserted under US guidance
59
how is the positioning of a central venous line confirmed before use
must have CXR to confirm positioning and to check for any pneumothorax
60
normal central venous pressure
5-10mmHg
61
indications of central venous lines
- TPN
- monitoring of central venous pressure
- resuscitation with blood/fluids
- delivery of irritant drugs: vasopressors, amiodarone
62
complications of central venous catheter insertion
- failure
- accidental injury/cannulation of artery
- arrhythmias - guidewire irritation of heart
- pneumothorax
- air embolism
63
what does aldosterone do
Na+ and Cl- reabsorption = water follows to be reabsorbed (osmosis)
also excretion of K+ into urine
64
describe RAAS system
1. drop in BP = detected by juxtaglomerular apparatus = renin secretion
2. renin converted to angiotensin I by angiotensinogen from liver
3. angiotensin I converted to angiotensin II by ACE in the lungs
65
effects of angiotensin II on BP
- increased sympathetic activity
- adrenal gland secretion of aldosterone = Cl- and Na+ and water reabsorption
- arteriole vasoconstriction
- pituitary release of ADH = H20 reabsorption
66
AEIOU indications for renal replacement therapy
```
A = acidosis
E = electrolyte disturbances - resistant hyperkalaemia
I = ingestion of toxins (alcohol, lithium, theophylline, barbiturates, valproate)
O = overload of fluid
U = uraemia symptoms (encephalopathy, pericarditis)
```
67
anticoagulant complications of RRT
- hypocalcaemia
- bleeding
- thrombocytopenia
68
circuit related complications of RRT
-Air embolism
-Clotting of circuit
-DIC
-Anaemia
-Thrombocytopaenia
-Hypothermia
-Hypotension
-Electrolyte disturbance
Dialysis Disequilibrium Syndrome (DDS)
69
3 things you should ask before carrying out an ABG
- do you take any anticoagulants
- do you experience Raynaud's
- have you ever had any LN or axillary clearance in this arm
70
what do base excess values mean
below -2 = metabolic acidosis
above +2 = metabolic alkalosis
71
2 things which can cause respiratory alkalosis
- hyperventilation
| - T1RF
72
what effect can acidosis have on the heart
negative chronotrophic effect = BRADYCARDIA
73
what anaesthetic should be used in non-emergency blood gases
lidocaine 0.5-1ml SC 1% via orange 25G needle
74
what is diaphragmatic/ respiratory splinting
when a patient breathes in v shallowly in an attempt to avoid inspiratory pain
75
What percentage of oxygen is delivered at:
a) . 1 Litre
b) . 2 Litre
c) . 3 Litre
d) . 4 litre
e) . 5 litres
a) . 1 litre = 24%
b) . 2 litres = 28%
c) . 3 Litres = 32%
d) . 4 Litres = 36%
e) . 5 litres = 40%
76
What percentage of oxygen is delivered at:
a) . 6L
b) . 7L
c) . 8L
d) . 9L
e) . 10L
a) . 6L = 44%
b) . 7L = 48%
c) . 8L= 52%
d) . 9L= 56%
e) . 10L = 60%
77
what must be done before a NRBM is used
finger over the valve in the mask to allow it to inflate the bag
78
which concentrations of O2 are often given to patients with chronic lung disease
24-28%
79
What percentage/litre of O2 does each venturi valve deliver?
a) . Blue
b) . White
c) . Yellow
d) . Red
e) . Green
a) . Blue = 2/L- 24%
b) . White = 4/L - 28%
c) . Yellow = 8/L - 35%
d) . Red = 10/L - 40%
e) . Green = 15/L - 60%
80
how many litres of O2 does a bag-valve mask deliver
15L flow rate (+ positive pressure)
81
how many litres of O2 can a CPAP machine or ventilator deliver
1-15L O2
ventilator = 1-15L via invasive positive pressure
82
most important cause of pulmonary oedema
cardiac
83
scale used to assess severity of COPD
MRC dyspnoea scale
84
what is the MRC dyspnoea scale
```
1 = breathless with strenuous exercise
2 = SOB when hurrying on a level or walking up slight hill
3 = walks slower than people of same age due to SOB
4 = stops for breath after walking 100 years (90m)
5 = too breathless to leave the house or breathless when dressing/undressing
```
85
what should be done for COPD exacerbation if there is no change with bronchodilator + O2
NIV
86
4 contraindications for NIV
- untrained pneumothorax
- facial burns
- fixed upper airway obstruction
- at least 2 weeks after oesophagectomy
87
1st line tool for recognising delirium
SQiD - single question to identify delirium
'is this person more confused than normal'
88
what is used after SQiD if the answer is yes (for delirium)
AMT4 (abbreviated mental test 4):
- age
- DOB
- location
- year
89
what medications can cause delirium
- STEROIDS
- Benzodiazepines (sedatives)
- Analgesia- opiates can cause constipation
- Cimetidine (H2 antagonist)
- Anticholinergics
- Digoxin
- Muscle relaxants
90
when would epithelial cells be found in a urine sample
when it has touched the skin - invalidated
91
normal levels of WBCs in MSU
normal = <40
elevated = pyuria/infection or inflammation??
92
what can RBCs in the urine indicate
infection
trauma
malignancy
renal stones
93
3 cancers associated with cannonball lung mets
prostate
renal cell
sarcoma
94
how many seconds is one small square on ECG
0.04 seconds (one large square = 0.2 seconds because is 5 small squares)
95
how long is normal PR interval
3-5 small squares (0.12-0.2 seconds)
96
how long is a normal QRS
<0.12 seconds (<3 small squares)
97
where do the limb leads on ECG go
RIDE
YOUR
GREEN
BICYCLE
R: R- upper left arm
Y: Left- upper left arm
Green: Left lower limb
B: Right lower limb
98
3 most common causes of right axis deviation
increased RV workload:
- right ventricular hypertrophy
- PE
- COPD
99
most common causes of left axis deviation
conduction defects
100
in which leads do you look for RBBB and LBBB
```
RBBB = leads V1 and V2
LBBB = leads V1 and V6
```
101
how can DKA lead to hyperkalaemia
hyperglycaemia = hypertonia = shift of K+ out of cells into blood
102
top 3 causes of DKA
- INFECTION
- poor diabetic control and use of insulin
- unknown diagnosis - 1st presentation of T1DM
103
2 other conditions which can cause DKA
stroke
| steroids
104
type of shock in DKA
hypovolaemia - severe dehydration
severe dehydration = hyponatraemia
105
rate of insulin needed for DKA
FIXED rate IV insulin 0.1 units/kg/hour
106
what should be done for DKA if blood glucose falls below 15
infusion of 10% dextrose along with insulin
107
what dose of fluids to use in DKA
- 500ml bolus over 10-15 mins if not hypotensive
| - 1L over 1 hour if hypotensive
108
when would K+ be infused with saline in DKA
when it falls below 5.5
this happens because glucose uptake into cells is co-transported with potassium = hypokalaemia
109
4 main metabolic treatment targets in DKA
1. Reduction of blood ketones by 0.5mmol/L/hour
2. Increase of venous bicarb by 3.0mmol/L/hour
3. Reduction of cap glucose by 3.0ml/hour
4. Maintain K+ between 4-5.5mmol/L
110
risk of fluid resuscitation in children and young adults with DKA
cerebral oedema
111
how can AKI present
- Can be ASYMPTOMATIC
- N&V, diarrhoea
- Dehydration: reduced skin turgour, dry mucous membranes
- Fatigue
- Oliguria/anuria
- Can have signs of uraemia later on: anorexia & nausea, encephalopathy, asterixis, pericarditis, platelet dysfunction
112
DIAMOND HAL - nephrotoxic drugs
```
diuretics
iodine contrast/IV contrast
ACEi/ARB
metformin
opioids
NSAIDs
digoxin
```
heparin
aminoglycosides (gentamicin)
lithium
113
STOP treatment for AKI
1. SEPSIS: complete sepsis 6 if suspected (BUFALO)
2. Toxins: avoid or stop any nephrotoxins the patient is on
3. Optimise BP: give crystalloid fluids if the patient is hypotensive
4. Volume assessment:
5. Prevent harm: treat complications such as hyperkalaemia, identify cause, review medications, fluid balance
Also review medication doses in medications excreted by kidneys
114
when would RRT be considered in AKI
- Intractable hyperkalaemia
- pH <7.1
- Intractable pulmonary oedema
- Uraemic pericarditis
- Encephalopathy
115
complications of AKI
- Hyperkalaemia
- Electrolyte imabalances: Hyperphosphataemia, hyponatraemia, hypermagnesia
- Metabolic acidosis
- Volume overlode: peripheral and pulmonary oedema
- Uraemia
- CKD
116
how long does an induction agent take to start working
1-2 brain-arm circulations i.e. 10-20 seconds
117
4 main induction agents
propofol (most common)
thiopentone (barbiturate)
ketamine
etomidate
118
2 benefits of propofol
- excellent airway suppression reflexes
| - decreases incidence of PON+V
119
3 unwanted effects of propofol
- drop in HR and BP
- pain on injection
- involuntary movements
120
dose of propofol
1.5-2.5 mg/kg
121
3 benefits of thiopentone
- faster than propofol
- used mainly for RSI
- antiepileptic properties - protects brain
122
3 unwanted effects of thiopentone
- Drops HR BUT rise in BP
- Rash/bronchospasm
- Vasospasm can cause thrombosis and gangrene distally if injected intra-arterial
123
what is contraindicated in thiopentone
porphyria
124
dose of thiopentone
4-5mg/kg
125
3 features of ketamine
- slow onset 90 seconds
- bronchodilation
- rise in HR and BP = good for when circulation is compromised
126
dose of ketamine
1-1.5mg/kg
127
3 benefits of etomidate
- rapid onset
- haemodynamic stability
- lowest incidence of hypersensitivity
useful for patients with limited cardiac reserve (elderly, heart failure etc)
128
4 unwanted effects of etomidate
- Pain on injection
- Spontaneous movements
- Adreno-corticol suppression for 72 hours
- High incidence of PONV
129
why can etomidate lead to high mortality
Critically ill patients such as in septic shock need adrenocorticoids to deal with the stress
130
best induction agent for patient needing burns dressing on ward
ketamine
131
best induction agent for a patient having an LMA
propofol (good airway suppression for LMA)
132
2 main options for maintenance anaesthesia
- propofol infusion
| - inhalation agents (started AFTER induction)
133
4 main maintenance inhalation anaesthetics
isoflurane
desflurane
sevoflurane
enflurane
134
definition of MAC
Concentration of vapour that prevent reaction to a standard surgical stimulus
- In 50% of subjects (50% pain free, 100% amnesia)
135
what percentage of ... is 1 MAC:
- NO
- sevoflurane
- isoflurane
- desflurane
- enflurane
- NO = 104%
- sevoflurane = 2%
- isoflurane = 1.15%
- desflurane = 6%
- enflurane = 1.6%
136
best maintenance for a child with no IV access
sevoflurane - sweet smelling, inhalation induction
137
best maintenance for a long 8 hour finger reimplantation
desflurane - low lipid solubility, rapid onset and offset, LONG OPERATIONS
138
best maintenance for organ retrieval
isoflurane - least effect on organ blood so can be used for organ donation
139
3 main short acting opiates in order of strength
for suppressing response to laryngoscopy and airway insertion
remifentanil - alfentanil - fentanyl
140
2 main long acting opioids
for intra and post-op analgesia
```
morphine
oxycodone (can use in renal failure)
```
141
when are analgesics administered in surgery
before amnesic - 1-5 minutes for onset and peak is slower than amnesic agents
142
2 advantages of tramadol
- can be used for both nociceptive and neuropathic pain
| - can be used with morphine
143
2 side effects of tramadol
- N+V
| - confusion
144
2 IV NSAIDs
- ketorolac
| - parecoxib
145
how do depolarising muscle relaxants work
act similarly to Ach - binds to nicotinic receptors on post-synaptic membrane
slowly broken down by acetylcholinesterase
146
how do non-depolarising muscle relaxants work
block nicotinic receptors - so Ach can't get to receptors
147
main depolarising muscle relaxant
suxamethonium (used for RSI - 1-1.5mg/kg)
148
5 side effects of suxamethonium
- muscle pain
- fasciculations
- hyperkalaemia (muscle breakdown)
- malignant hyperthermia
- rise in ICP, IOP and gastric pressure
149
short acting non-depolarising muscle relaxant
mivacurium
150
3 intermediate acting non-depolarising muscle relaxants
vecuronium
rocuronium
atracurium
151
long acting non-depolarising muscle relaxant
pancuronium
152
2 muscle relaxant reversal agents
neostigmine
| glycopyrrolate
153
what can cause intraoperative hypertension and how is it treated
inadequate anaesthesia
increase anaesthesia +/- analgesic OR increase amnesia
154
3 most common vasoactive drugs
ephedrine
phenylephrine
metaraminol
155
3 main vasoactive drugs used in severe hypotension/ICU
adrenaline
noradrenaline
dobutamine
156
best vasoactive drug for low BP and low HR
ephedrine
157
best vasoactive drugs for low BP and high HR
metaraminol
| phenylephrine
158
5 main antiemetics used in PONV
1. 5HT3 blockers: Ondansetron
2. Anti-histamine: Cyclizine
3. Steroids: Dexamethasone
4. Phenothiazine: Prochlorperazine (Stemetil)
5. Anti-dopamidergic: Metoclopramide
159
usual order of use of antiemetics in PONV
1. ondansetron
2. dexamethasone
3. cyclizine
4. prochlorperazine
160
features of neostigmine and why isn't it used on its own
- Anti-cholinesterase
- Prevents breakdown of ACh
- Muscarinic effects of ACh leads to PROFOUND BRADYCARDIA
SO much be combined with Glycopyrrolate
161
3 downsides of neostigmine
- N+V
- inability to reverse profound block
- slow onset to peak: 7-11 minutes
162
another reversal agent is
sugammadex
163
how does sugammadex work
It has a hydrophobic core (the donut hole part) and a hydrophilic exterior. The rocuronium (or other NMB) gets stuck in the hole and this keeps it away from the Ach receptor. It forms a 1:1 complex with the NMB and is eliminated in the kidneys in this form.
Water-soluble complex 1:1 with steroidal muscle relaxants
NO effect on nicotinic/muscarinic receptors
164
which muscle relaxants is sugammadex compatible with
Rocuronium > Vecuronium >Pancuronium
165
order of general anaesthesia with LMA
1. Oxygenation
2. Opioids: Fentanyl/Alfentanyl
3. Induction agent: Propofol
4. Inhalation agent: sevo/isoflurane
5. Bag mask ventilation
6. LMA insertion
if patient is then intubated, give muscle relaxant and then intubate
166
how does paracetamol toxicity occur
In overdose the Glutathione is all used up due to high levels of NAPQI so NAPQI is not all safely mopped up by Glutathione causing liver toxicity - patients tend to be asymptomatic for 24 hours
167
questions to ask when asking about paracetamol overdose
- WHEN did they take the paracetamol?
- Staggered or single overdose?
- How much did they take?
- Did they take any other drugs or alcohol?
- Do they have any medical conditions- liver disease/poor nutrition
- Are they taking any other medications?
168
ATOM FC injuries which could compromise ventilation
Airway obstruction
Tension pneumothorax
Open chest wound
Massive haemothorax
Flail chest
Cardiac tamponade
169
what does HEP B assess (in circulation)
Hands: temp, sweating, colour, CRT
End organ perfusion: consciousness urine output
Pulse: rate, quality, regularity
BP - hypotension is a late sign
170
how is a secondary brain injury prevented
- Opitimise oxygenation
- Maintain cerebral perfusion with BP >90mmHg
- Avoid hypoglycaemia
- Avoid pyrexia
- Definitive imaging and treatment
171
what radiological investigation should be done within 30 mins of arrival at a MTC
full trauma CT
172
what is positive predictive value
probability that a pt w/ a positive test truly has the disease.
The more specific a test, the higher its PPV
prevalence dependent: the higher the disease prevalence, the higher the PPV of the test for that disease
173
what happens to the negative predictive value as the prevalence of the disease increases
NPV decreases
| number of negative tests who do NOT have the condition
174
5 causes of PE
1. MAIN CAUSE: DVT which breaks off and travels to pulmonary vasculature
2. Air emboli
3. Fat emboli from large fractures (trauma)
4. Talc due to IV drug use
5. Amniotic fluid
175
what is a provoked PE
PE which occurs within 3 months of a TRANSIENT risk factor:
- Surgery
- Trauma/major immobility/surgery
- Pregnancy/puerperium
- Hormonal contraception
NB: one without RFs or which are NOT transient e.g. thrombophilia = unprovoked PE
176
what must be done before wither a CTPA or V/Q for PE
plain CXR to check for other pathology
177
criteria for massive PE (= thrombolysis)
- Hypotension 90/60 for >15 mins
OR
- Cardiac arrest
178
criteria for sub-massive PE
- Hypoxia/increased O2 demand
- Cardiac echo/ECG shows right heart strain
- +ve cardiac markers: troponin
179
how is a sub-massive PE managed
RISK STRATIFICATION (VERY important)
- using PESI score/modified PESI score
- If the score is <85 then is low risk, higher should be admitted
If lower: anticoagulate [DOAC] and send home
180
1st line anticoagulants for PE
DOACs - lower bleeding risk
181
when should LMWH be used for PE instead of DOACs
- pregnant
- already on warfarin
- clots present around metal work e.g. heart valves, stents
182
how long should anticoagulants be used in provoked vs non-provoked PE
provoked = min. 3 months
unprovoked = beyond 3 months (risk of another PE)
183
what investigations to carry out after an unprovoked PE
Should have limited investigations into whether there is any underlying malignancy:
- FBC
- U&E's
- Calcium/PSA
- Clotting factors and LFT's (liver mets)
- Consider a breast/prostate/testicular examination
- Systems review
ONLY do further investigations if clinical suspicion of cancer after all these tests
184
PERC criteria - PE rule out criteria (if 0 don't even do D-dimer!)
PERC: PE-rule out criteria:
- Age <50 years
- HR <100bpm
- O2 sats >94% on air
- NO unilateral leg swelling
- No haemoptysis
- No surgery/trauma in last 4 weeks
- No Hx of VTE
- No oestrogen use
if can't rule out PE = do Well's score
185
which Well's score is high and would bypass D dimer going straight to CTPA
4+
186
4 examples of ester LAs
prilocaine
cocaine
benzocaine
tetracaine
187
why are ester LAs not commonly used
high rates of hypersensitivity reactions
188
5 examples of amide LAs
```
lidocaine (lignocaine)
bupivacaine
prilocaine
levobupicaine
ropivacaine
```
189
max safe dose of lidocaine with and without adrenaline
```
without = 3mg/kg
with = 7mg/kg
```
190
max safe dose of prilocaine
6mg/kg
191
how to work out concentration of 0.25% bupivacaine
0.25 x 10 = 2.5mg/ml
192
what are the 3 ligaments of the spinal cord which are passed through when doing a spinal anaesthetic
- supraspinous ligament
- interspinous ligament
- ligamentum flavum
193
describe a spinal block
1. Patient sat sitting hunched forward- line between the 2 iliac crests is L2/3
2. Skin infiltrated with 1% lidocaine
3. 25g spinal needle into L3/4 space
4. Free flow of CSF from the spinal needle indicates in correct place
5. Attach marcain syringe (bupivacaine + glucose) and retract syringe slightly to see swirls of CSF in synringe
6. Inject LA
7. Lie patient down immediately and monitor Bp closely
194
why is marcaine (bupivacaine + glucose) used in a spinal anaesthetic
heavier molecule = sinks to bottom of spinal cord = no sympathetic block of whole body
NB: blocking sympathetic chains = BP reduction with spinal anaesthesia
195
describe an epidural catheter anaesthetic
Indwelling catheter into the epidural space: LA +/- opioid
- Longer, slower onset= 15-20 minutes
1. Hooked needle inserted into potential epidural space and NaCl injected to create a space
2. spinal catheter in: should feel loss of resistance
3. Inject 3ml and see if patient feels any systemic signs suggesting accidently into CSF
4. If not then continue to inject through catheter- fluid should be sucked up by needle due to negative pressure
196
how does ephedrine work
indirect general agonist; releases stored catecholamines (used for nasal decongestion, urinary incontinence, hypotension)
Direct and indirect action on Alpha & Beta receptors:
- Indirect action: agonist releasing stored catecholamines
Alpha: Vasoconstriction on V receptors
Beta: Increase HR (beta = beats)
197
how do metaraminol and phenylephrine work
Metaraminol has direct and indirect effects on Alpha receptors causing vasoconstriction
Phenylephrine just has direct action on Alpha receptors causing vasoconstriction
198
which organism tends to cause pneumonia AFTER influenza infection
staph aureus (gram +ve cocci)
199
organisms causing severe CAP
- gram +ve cocci = strep pneumoniae, staph aureus
- gram -ves = H. influenzae
- atypical = legionella, mycoplasma
200
how is CURB score 0-1 pneumonia treated
doxycycline/amoxicillin
201
how is CURB score 2 pneumonia treated
co-amoxiclav +/- clarithromycin OR still doxycycline
202
how is CURB score 3-5 pneumonia treated
co-amoxiclav + clarithromycin
levofloxacin if allergic???
203
specific antibiotic used for strep pneumonia
IV benzylpenicillin
204
specific antibiotic used for s. aureus pneumonia
flucloxacillin
205
main causes of HAP
same causes as CAP plus gram negatives - E. coli, pseudomonas
206
antibiotics suitable for non-severe HAP
co-trimoxazole
207
antibiotics suitable for severe HAP
linezolid + ciprofloxacin
208
how is MRSA treated and when is a patient deemed MRSA free
Nasal mupirocin plus chlorahexidine body washes for 5 days
- Once decolonised- send repeat MRSA swabs
- 3 consecutive negative screens, each 48 hours apart is MRSA free
209
what is a parapneumonic effusion
exudative pleural effusions that occur adjacent to a bacterial pneumonia and result from migration of excess interstitial lung fluid across the visceral pleura; although inflammatory cells are present, parapneumonic infections are STERILE
typically these are small and uncomplicated and resolve with resolution of the pnuemonia
if bacteria from the pneumonia invade the pleural space a complicated parapneumonic effusion or empyema will result***
210
4 features of a simple parapneumonic effusion
- Non-infective: no gram stain/culture positives
- LDH <1000
- pH >7.2
- Glucose >2.2
211
how are simple parapneumonic effusions managed
antibiotics alone
| sometimes chest drain for symptom relief
212
4 features of complication parapneumonic effusion
- Infected effusion - positive gram stain/culture
- LDH >1000
- pH <7.2
- Glucose <2.2 (bacteria eat it up)
213
what is present in empyema
frank pus - don't need to check pH
214
when might a yeast empyema occur
after oesophageal rupture/anastomotic leak from GI tract
215
1st line antibiotics for empyema /parapneumonic effusion
IV co-amoxiclav OR IV levofloxacin/ metronidazole if penicillin allergic
also need to do aspiration +/- chest drain insertion, could also do fibrinolysis
216
minimum insertion length of an NG tube
55cm
217
what does procalcitonin indicate
bacterial infection
218
what is often raised in a GI bleed
urea: digested blood
219
what antibiotics can cause muscle breakdown when someone is also taking a statin
macrolides: clarithromycin, clindamycin, erithromycin
220
normal JVP is
less than 4cm
221
common post-op airway problems
- Decreased muscle tone due to certain drugs
- Secretions
- Sleep apnoea- body habitus larger
- Laryngospasm
222
some causes of hypoxia
1. Alveolar hypoventilation
2. V/Q mismatch- PE, Atelectasis, bronchopneumonia, aspiration pneumothorax, pulmonary oedema
3. Circulatory problems:
- Increased oxygen demand: sepsis
- Low cardiac output states: hypotension
223
signs of LA toxicity
- tongue and Perioral tingling/numbness
- tinnitus
- light-headedness
- speech slurring
- confusion
- restlessness
- muscle twitching
- diplopia
- convulsions
excitatory due to inhibition of inhibitory neurone via GABA receptors
224
safe dose of prilocaine (ester) with adrenaline
8mg/kg (6 without)
225
colours of vessels, bones and soft tissues in USS
- vessels and fluid = black (anechoic - don't reflect the sound waves)
- bones = white (hyper echoic - reflect all the sound waves back to probe)
- soft tissues = grey (isoechoic - reflect some US waves)
226
what do nerves look like on USS
honeycomb appearance - hypoechoic/hyperechoic
227
features of high frequency transducers
- 7-18MHz
- High resolution but LOW DEPTH
- Superficial vessels, muscles
228
features of low frequency transducers
- 2-6 MHz
- Penetrate deeper but lower resolution
- Cardiac, abdominal and obstetric uses
229
what is gain in USS
the amount the amplifier increases the incoming signal - especially the brightness of the image
230
colour of Doppler when signal is moving away and towards probe
signal from fluid moving AWAY from probe = lower frequency = blue
signal from fluid moving TOWARDS probe = higher frequency = red
231
what is acoustic shadowing
The reduced echo intensity behind a highly attenuating or reflecting object such as a stone creating a shadow
Structure behind an object which reflects all the US waves looks black
232
what is acoustic enhancement
Increased echo intensity behind a minimally attenuating object such as a cyst or blood vessel
Sounds waves going through fluid structure such as vessel- less are absorbed so tissues after fluid can look white (hyperechoic) but they shouldn't
233
4 ultrasound views of the heart
- parasternal long
- parasternal short
- apical (4 chamber view)
- suprasternal
234
where to put ultrasound probe for parasternal view
left of sternum in 3/4th intercostal space
235
where to put ultrasound probe for apical view
under left nipple
236
preferred areas of guided peripheral vascular access
- cephalic vein
- basilic vein
- brachial vein
237
most common site of arterial cannulation
radial
can also do brachial, femoral or dorsals pedis
238
what are vasopressors
Drugs which work on alpha 1 receptors to cause vasoconstriction and therefore increase BP
239
what are inotropes
Drugs which increase myocardial contractility and HR
however this can lead to myocardial ischaemia due to increasing myocardial O2 demand
240
3 examples of inotropes
adrenaline
dopamine
dobutamine
241
4 examples of vasopressors
phenylephrine
metaraminol
adrenaline
noradrenaline
242
side effect of vasopressors
increased after load = more stress on heart
hypertensive episodes = reduced blood flow to end organs
243
role of B1 and B2 receptors
B1 = increase HR and cardiac contractility
B2 = vasodilation
244
how does phenylephrine work
Works purely on alpha-1 receptors to cause vasoconstriction with no effect on heart
Good for when low BP and body has already compensated with tachycardia
245
how does ephedrine work
Direct and indirect action on beta and alpha receptors due to release of stored catecholamines
Therefore increases HR and vasoconstriction
Good to use when Low BP and Low HR
246
how does noradrenaline work
stimulates A1 and B1/2 receptors to cause vasoconstriction AND increased CO due to B1 action
247
how does dopamine work
higher B1 affinity = increases HR and contractility
mild A1 vasoconstriction effect
248
how does adrenaline work
strong B1 affinity and mild A1/B2 affinity = increases HR and contractility a lot
249
how does dobutamine work
very high B1 affinity = increases HR and contractility
can initially have some hypotension due to B2 affinity
250
what does paradoxical breathing indicate
complete airway obstruction
251
2 main cautions for penicillins
- renal impairment (dose reduction)
| - using with methotrexate - reduces renal excretion = increases risk of toxicity
252
what happens if you take allopurinol with penicillin
can increase likelihood of rash
253
side effects of cephalosporins
- GI upset: D&V
- Antibiotic associated colitis
- Hypersensitivity, especially if patient has penicillin allergy
- Neurological toxicity in high doses/renal impairment
- Agitation
- Arthritis
- Confusion & fatigue
- Pruiritis
- Transient hepatitis + jaundice
- Increases INR and bleeding by inhibiting vitamin K dependent clotting factors (1972)
254
2 interactions of cephalosporins
1. Warfarin: enhances anticoagulant effect by killing normal gut flora which make Vitamin K
2. Aminoglycosides: increases nephrotoxicity
