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PHM BSc - Resus Science > ERC - ALS > Flashcards

ERC - ALS Flashcards

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1
Q

What is a MET or RRT

A

medical emergency or rapid response team that responds to critically unwell patients in an attempt to reduce arrest cases

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2
Q

Syncope due to an arrhythmia is likely to present how

A

No prodrome

Can occur whilst supine or on exertion

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3
Q

What are the universal termination of resuscitation rules

A

Efforts to be terminated if no ROSC, no shocks administered, non EMS witnessed

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4
Q

You are in hospital and have a patient that is not breathing but you can feel a pulse, what do you do

A

Ventilate and check the circulation every 10 breaths to be sure there is still a pulse

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5
Q

Describe agonal breathing

A

Slow and laboured often with snoring and occasional gasps

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6
Q

Describe inspiratory time, volume and rate of ventilations given when performing in hospital CPR

A

1s per inspiration
Enough volume for normal chest rise (600-700ml)
10 breaths per minute

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7
Q

Once started, how much and how often is adrenaline given in an arrest

A

1mg (10ml 1:10,000) every 3-5 minutes (2 cycles)

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8
Q

When is adrenaline in cardiac arrest stopped

A

As soon as ROSC is suspected

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9
Q

Compare when adrenaline is started in VF/pVT and PEA/asystole

A

After the third shock for shockable

ASAP for non shockable

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10
Q

For what arrest rhythms is amiodarone given, at what dose and when

A

VF/pVT
300mg IV after 3rd shock
150mg IV after 5th shock

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11
Q

What is an acceptable alternative to amiodarone given to shockable rhythms in ALS

A

Lidocaine

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12
Q

What initial energy is used to shock someone in VF/pVT

A

At least 150J if used biphasic

120-150J is used pulsed biphasic

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13
Q

You don’t know which energy to use and there is no guidance on the defibrillator, what do you do

A

Use the highest energy possible

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14
Q

To escalate or not to escalate? (Defibrillation energy)

A

Escalate for failed shocks and refibrillation

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15
Q

You have shocked a patient, do you now pulse check? Why?

A

NO
Compressions won’t do any harm ie they won’t cause VF again
A pulse is unlikely to be palpable so soon after
Not starting compressions could further damage the myocardium

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16
Q

How soon after a peripheral injection does adrenaline exert it’s maximum benefit on coronary perfusion pressure

A

70 seconds

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17
Q

What is the role of compressions when there is a shockable rhythm

A

They increase oxygen delivery to the myocardium
Increase the amplitude and frequency of VF waveform
Increase chance of a shock working

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18
Q

What signs would indicate ROSC

A

Purposeful movements
Normal breathing and coughing
Raised ETCO2

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19
Q

You witness a patient go into VF/pVT on the monitor, in terms of CPR and shocks what do you do

A

3 shock strategy - give 3 successive shocks with a very quick rhythm check between each
Commence CPR after 3rd shock

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20
Q

A patient has had a 3 shock strategy and there is no ROSC, at what point do you give adrenaline

A

You treat the 3 shocks as the first. So give adrenaline after a further 2 shocks

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21
Q

A patient has had a 3 shock strategy and there is no ROSC, at what point do you give amiodarone

A

Give amiodarone after the 3rd shock regardless of whether or not they are stacked

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22
Q

You witness a patient go into VF/pVT on the monitor but there is no defib, what do you do?

A

Precordial thump

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23
Q

How would you perform a precordial thump

A

Take the ulnar edge of a clenched fist to the lower half of the sternum from a height of 2cm and retract first immediately

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24
Q

What is the relationship of CPR interruptions and coronary perfusion pressure

A

Less interruptions = high coronary perfusion pressure

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25
Q

State the advantages and disadvantages of using central access in ALS

A

+ve: quicker effect

-ve: pause compressions for insertion of a central line, increased risk of ADRs

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26
Q

Which IO location most closely resembles IV in terms of adrenaline pharmacokinetics on delivery

A

Sternum

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27
Q

Define PEA

A

Cardiac arrest in the presence of an electrical rhythm (aside from ventricular tachyarhthmias) that would normally give a palpable pulse

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28
Q

What is pseudo PEA

A

There is an element of myocardial contraction but it is too weak to produce any detectable pulse or BP

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29
Q

You think you see a very fine VF but it could be asystole - shock or CPR?

A

Continue with CPR, don’t defibrillate

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30
Q

Severe haemorrhage often leads to which rhythm

A

PEA

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31
Q

Preferred echo view (according to ERC) in cardiac arrest

A

Sub-xiphoid

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32
Q

Describe the limitations of the femoral and carotid pulse in an arrest

A

Femoral - could be venous (no valves between IVC and retrograde flow can seem like a pulse)
Carotid - doesn’t indicate adequate myocardial or cerebral perfusion

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33
Q

What is invasive arterial pressure monitoring used for in an arrest

A

Can detect even a very low BP signifying ROSC

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34
Q

What is ETCO2

A

The partial pressure of CO2 at the end of an exhaled breath

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35
Q

What does the ETCO2 value rely on

A

Pulmonary blood flow (which in turn relies on a CO)

Ventilation minute volume

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36
Q

What are the benefits of using ETCO2 in an arrest

A

Ensures tube placement
Avoids hyperventilation
Monitors compression quality
Identifies ROSC (preventing adrenaline being given to a ROSC patient)

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37
Q

You’ve been performing CPR for 20 minutes, what ETCO2 value indicates a poor prognosis

A

<1.33KPa (10mmHg)

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38
Q

Aim of defibrillation is

A

Restore spontaneous sychronised electrical activity

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39
Q

In which patients is ECPR likely to improve survival

A

Reversible cause
No comorbidities
Witnessed arrest with immediate high quality CPR
eCPR within 1hr

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40
Q

You are about to shock a patient and the O2 mask is 99cm away, is this ok?

A

Nope! All sources of O2 eg masks and nasal cannulae at least 1m away

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41
Q

Describe acceptable electrode pad positioning for VF

A

Sterno apical - R of sternum under clavicle and L mid axillary line
Bi-axillary - R and L lateral chest walls
Anterioposterior - L precordium and inferior to L scapula
L mid axillary line and R upper back

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42
Q

Describe electrode pad placement in atrial arrhythmias

A

Sterno apical - R of sternum below clavicle and L mid axillary
Anteroposterior - L precordium and inferior to L scapula

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43
Q

What energy should be used for shocking atrial arrhythmias

A

120-150J

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44
Q

Why might a high energy be needed to shock an asthmatic patient

A

Auto PEEP increased impedance

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45
Q

When timing shocks with ventilation, when should you shock and why

A

End of expiration as impedance is minimal

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46
Q

Define refibrillation

A

Recurrence of VF during a documented arrest in which VF has already been terminated
The patient remains with the same providers

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47
Q

Define refractory VF

A

Fibrillation that persists after one or more shocks

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48
Q

You become aware that a patient you are about to shock has an ICD/pacemaker. Where should the electrodes be placed?

A

8cm away from device or antero-lateral or anterio-posterior

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49
Q

What does synchronisation mean in terms of electrical cardioversion

A

Shock is synchronised with the R wave

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50
Q

What could happen if a shock isn’t synchronised to the R wave

A

If given during T wave (relative refractory period) then VF may occur

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51
Q

Which rhythms require shock synchronisation and which don’t

A

Synchronised: atrial and ventricular tachyarrhythmias
Unsynchronised: VF or pVT

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52
Q

State the initial energy given for AF, flutter, SVT and VT

A

Flutter and SVT: 70-120J biphasic

Fibrillation and VT: 120-150J biphasic

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53
Q

Where is an ICD placed

A

Under the pectoral muscle below the left clavicle

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54
Q

What does an ICD do

A

On detecting a shockable rhythm it will deploy 40J of energy via a wire in the RV no more than 8 times

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55
Q

How can you stop an ICD

A

Place a magnet over it

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56
Q

Describe see-saw breathing

A

Paradoxical movement of the chest and abdomen in a patient making respiratory effort against an obstructed airway

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57
Q

What are the anatomical landmarks used to size an OPA

A

Incisors to angle of jaw

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58
Q

An NPA size corresponds to what

A

It’s internal diameter

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59
Q

If suction is to be used for airway clearance what device is suitable

A

Wide bore rigid sucker (Yankaver)

60
Q

What factors increase the likelihood of gastric inflation during ventilation

A

Higher airway pressures (excessive flow and volume)
Malalignment of the head and neck obstructing the airway
Incompetent oesophageal sphincter

61
Q

What does gastric inflation during ventilation increase the risk of

A

Regurgitation and pulmonary aspiration

62
Q

For continuous compression technique what is the ventilation rate

A

10 breaths/minute

63
Q

Describe the benefits of intubation over SGAs

A

Less likely to dislodge
Reduced risk of aspiration
Can do continuous compressions
Effective ventilation can be achieved in cases of poor lung compliance

64
Q

Describe the downsides of tracheal intubation

A

Misplaced tube may go unrecognised
Compressions stop whilst the tube is placed
Higher failure rate

65
Q

What forms the primary assessment of tracheal tube placement

A

Listening for bilateral breath sounds in the axilla
Absence of breath sounds in the epigastum
Bilateral chest rise

66
Q

What methods can be used for the secondary assessment of ET tube placement

A

Exhaled CO2

Oesophageal detection device

67
Q

Describe the oesophageal detection device and the results if it is in the trachea or oesophagus

A

It creates a suction force at the end of the tube
Trachea - air easily aspirated as cartilagenous rings keep it open
Oesophagus - collapses meaning no air can be aspirated

68
Q

Exhaled CO2 after 6 ventilations confirms what

A

The tube is either in the carina OR the main bronchus

69
Q

What are the different methods ETCO2 is detected

A

Colorimetric devices
Waveform capnography
Non waveform electronic digital ETCO2

70
Q

Why might a colorimetric device be of no use in cardiac arrest

A

Pulmonary blood flow so low that theres insufficient exhaled CO2 to detect

71
Q

Describe the colour changes of an ETCO2 colorimetric device and what % this relates to

A 
Purple  = ETCO2 <0.5%
Tan = ETCO2 0.5-2%
Yellow = ETCO2 >2%
72
Q

Which ETCO2 colorimetric colour responds to correct tube placement

A

Purple -> yellow

73
Q

Adrenalines actions on a1 receptors leads to what

A

Receptors are found in vascular smooth muscle and activation leads to vasoconstriction
This increases aortic diastolic pressure
This increases coronary and cerebral perfusion pressure

74
Q

Adrenalines actions on B1 receptors. What are the benefits and cons of this in arrest

A

Increased chonotropy and inotropy which increases coronary and cerebral flow BUT increased myocardial oxygen consumption
+ Impaired cerebral microcirculation
+ ectopic ventricular arrhythmias
+ pulmonary AV shunting leading to hypoxaemia

75
Q

Adrenaline given post ROSC leads to what

A

Tachycardia
Myocardial ischaemia
VT and VF

76
Q

What is the mechanism of action of amiodarone and its effects

A

It is a non-competitive inhibitor of adrenergic receptors: Negative inotropic action and peripheral vasodilation
Class 3 antiarrhythmic: Leads to prolonged refractory period (QT interval) of the atrial and ventricular myocardium therefore slowing AV conduction

77
Q

What dose of amiodarone is given in cardiac arrest

A

300mg diluted in 5% glucose to a volume of 20ml

78
Q

What are some adverse effects of amiodarone

A

Bradycardia
Polymorphic VT
Hypotension

79
Q

You give amiodorone peripherally, what is at risk of happening?

A

thrombophlebitis

80
Q

What class of drug is Lidocaine and which channel does it therefore block

A

1b - sodium channels

81
Q

How does lidocaine help in VF/pVT

A

increases myocyte refractory period
reduces ventricular automacity
prevents ventricular ectopics (via working as a local anaesthetic)

82
Q

Dose of lidocaine in arrest

A

1-1.5mg/kg (often around 100mg)

83
Q

how would someone with lidocaine toxicity present

A

parasthesia, twitching, convulsion

84
Q

What are some risk factors for digoxin toxicity

A

hypomagnesaemia or hypokalaemia

85
Q

If you are giving Mg in an arrest patient, what dose would you give

A

2g (4ml of 50%)

86
Q

In which situations would you give calcium in a cardiac arrest

A

hyperkalaemia
hypocalcaemia
CCB toxicity

87
Q

What dose of calcium do you give in a cardiac arrest

A

10ml of 10% calcium chloride

88
Q

In which situations is sodium bicarbonate given in an arrest

A

TCA toxicity

life threatening hyperkalaemia

89
Q

giving sodium bicarbonate in an arrest leads to what

A

production of CO2 = intracellular acidosis (CO2 can freely diffuse across membrane)
increase sodium load (and therefore volume) to already compromised circulation = pulmonary oedema and congestive HF
left shift of oxygen dissociation curve so less O2 delivery to tissues
negative inotropic effect
corrects the acidosis induced vasodilation so reduce cerebral blood flow

90
Q

If sodium bicarbonate is given in an arrest what dose

A

50mmol IV (50ml of 8.4%)

91
Q

Describe the 2 types of mechanical CPR device

A

LUCAS: piston and suction cup that provides CPR at 100bpm to a deapth of 4-5cm
Autopulse: load distributing band

92
Q

Describe an ACD device

A

suction cup lifts the chest wall up during decompression creating a negative intrathoracic pressure to increase venous return to the heart and therefore CO

93
Q

Describe and ITD and how it improves CPR

A

impedance threshold device: one way valve that limits air flow into the chest during decompression. This lowers intrathoracic pressure therefore increasing venous return to the heart and increasing CO

94
Q

Describe how to perform a carotid sinus massage

A

check for bruits

at the level of the cricoid apply pressure in a circular motion for 5seconds

95
Q

What is the mechanism behind carotid sinus massage

A

stimulate baroreceptors so increases vagal tone. This leads to slowing of AV conduction

96
Q

describe the valsalval manoeuvre

A

blow into a 20ml syringe hard enough to push the plunger back

97
Q

What are the actions of class 1 antiarrhythmics and via which channel do they work

A

Na channel block = slow conduction velocity through atrial and ventricular myocytes. 1c is the strongest
K channel block = prolong refractory period so longer AP. 1a is the strongest

98
Q

class 1a antiarrhythmics block K channels therefore leading to which ECG change

A

QT prolongation which can lead to TdP

99
Q

When would you consider using a class 1c antiarrhythmic (and which one) in a tachycardia

A

flecainide is used as rhythm control for irregular narrow complex tachy that has been present for <48 hours

100
Q

MOA of class 2 antiarrhythmics

A

B blockers
inhibit adenylate cyclase = reduced cAMP = reduced intracellular calcium = harder to reach threshold for depolarisation = reduced upstroke of the pacemaker AP.

101
Q

class 2 antiarrhythmics result on conduction velocity and AVN repolarisation

A

slow conduction velocity

prolong AVN repolarisation

102
Q

When would B-blockers be used in treating tachyarrhythmias

A

rate control in irregular narrow complex tachycardia
rate control in regular narrow complex tachycardia following unsuccessful vagal manoeuvre and adenoside (as it’s probably atrial flutter)

103
Q

ADR’s of B-blockers

A

bradycardia, hypotension, AV conduction delay

104
Q

Class 3 antiarrhythmic: channel and effects

A

K channel blocker

prolongs repolarisation and therefore the AP duration

105
Q

example of class 3 antiarrhythmics

A

amiodorone

sotalol

106
Q

When would class 3 antiarrhythmics be used in tachyarrhythmia

A

unstable tachyarrhythmia following 3 unsuccessful shocks
stable, regular, broad complex tachyarrhythmia inc. VT
Heart failure patient with an irregular narrow complex tachyarrhythmia

107
Q

ADR of amiodarone

A

hypotension and bradycardia

108
Q

Dose of amiodorone given in an unstable tachyarrhythmia after 3 unsuccesful shocks

A

300mg IV over 10-20 minutes then

900mg IV over 24 hours

109
Q

class 4 antiarrhythmics: channel and MOA

A

calcium channel blockers
slower conduction velocity (decrease slope of AP in pacemaker cells)
prolong repolarisation in AVN
This terminates re-entrant arrhythmias to control ventricular response rate
prolonged PR

110
Q

When is a class 4 antiarrhythmic indicated in tachyarrhythmias

A

stable regular narrow complex tachycardia not controlled by vagal manoeuvre or adenosine (could be flutter)
rate control in irregular narrow complex tachycardia

111
Q

What adverse effects can CCBs have on the heart

A

reduced contractility and CO

112
Q

What is a class 5 antiarrhythmic and how does it work

A

Adenosine
inhibit adenylate cyclase = reduced cAMP = reduced Ca.
It also increases K entry
This combined leads to hyperpolarization and a transient AVN block

113
Q

When is adenosine used and what is its dose

A

regular narrow complex tachycardia
6mg IV bolus
12mg IV bolus if this doesn’t work
12mg IV bolus again if above haven’t worked

114
Q

Why is adenosine bad in WPW

A

preventing normal conduction through AVN could promote the accessory pathway therefore worsening the situation

115
Q

When would Mg be used in tachyarrhythmias

A

polymorphic VT
TdP
tachycardia associated with hypomagnesaemia

116
Q

What dose of Mg is given in polymorphic VT

A

2g over 10 minutes

can repeat once more only

117
Q

Digoxin MOA

A

inhibits the NaKATPase = increased intracellular Na = reduced work of NaCa exchanger = increased intracellular Ca = increased contractility

118
Q

When is digoxin used in a tachyarrhythmia

A

Heart failure patient with irregular narrow complex tachycardia

119
Q

a patient is unstable with a bradycardia, what do you do

A

0.5mg IV Atropine

repeat to a maximum TD of 3mg

120
Q

a bardycardic patient has not responded to the maximum dose of atropine, what can you try

A

isoprenaline 5 micrograms
adrenaline 2-10 micrograms
transcutaneous pacing

121
Q

transcutaneous pacing is not available, what can you do in the mean time

A

fist pacing - closed fist over left lower sternal edge to pace heart at 50-70bpm

122
Q

the bradyarrhythmia is due to BB or CCB overdose, what drug do you give

A

Glucagon

123
Q

the bradycardia is due to an inferior MI or spinal cord injury, what drug do you give

A

theophylline

124
Q

bradycardic stable patients can be observed unless they have what

A

recent history of asystole
Mobitz type 2 or complete heart block
ventricular pause >3 seconds

125
Q

name some causes of bradycardia

A

cardiac: MI, sick sinus syndrome
non cardiac: hypothermia, hypoglycaemia, hypothyroid, RICP
drugs: digoxin, BB, CCB

126
Q

length of QRS defining it as narrow or broad

A

greater than or less than 0.12s (3 small squares)

127
Q

Which drugs should be avoided in WPW

A

adenosine, digoxin and CCB

128
Q

How is a irregular broad complex tachycardia managed

A

Often polymorphic VT eg TdP - treat with Mg 2g over 10 minutes

129
Q

How is regular broad complex tachycardia managed

A

Amiodarone 300mg over 20-60 minutes

then 900mg over 24 hours

130
Q

State some examples of irregular narrow complex tachycardias

A

AF

atrial flutter with variable AV block

131
Q

State some examples of regular narrow complex tachycardias

A

Sinus tachycardia
atrial flutter with constant AV block (often 2:1)
PSVT eg AVNRT or AVRT

132
Q

How is a irregular narrow complex tachycardia managed

A

rate control with a Bblocker or Diltiazem
if >48 hours then anticoagulate
If <48 hours then rhythm control with Flecainide (class 1C)

133
Q

In heart failure patients what changes to the management of irregular narrow complex tachycardia

A

give digoxin or amiodarone

134
Q

How is a regular narrow complex tachycardia managed

A

vagal manoeuvre
Adenosine 6mg IV bolus
2 further 12mg bolus’ can be given
Seek help and potentially rate control with Bblocker

135
Q

You’ve been doing CPR for 20 minutes: what ETCO2 value signifies a poor prognosis?

A

<1.3KPa (10mmHg)

136
Q

A patient has an arrest from a shockable rhythm during cardiac catheterisation, how do you manage them

A

3 stacked shocks

CPR using a mechanical device (high quality + reduced radiation exposure to CPR providers)

137
Q

Airway and ventilation options for in hospital arrest management

A

pocket mask
2 person technique of bag-mask ventilation
SGA with self inflating bag

138
Q

What does RSVP handover tool stand for

A

reason
story
vital signs
plan

139
Q

What is the peri-shock pause

A

pauses in chest compressions before and after a defib shock

140
Q

What is the role of adrenaline in cardiac arrest

A

to increase myocardial blood flow and improve the chance of successful defibrillation

141
Q

In ALS, when should a pulse check take place

A

only when an organised rhythm (regular or narrow complexes) is observed at the rhythm check

142
Q

following administration of drugs peripherally in an arrest, what needs to happen

A

flush of 20ml

elevate the limb for 10-20 seconds

143
Q

what is cerebral oximetry

A

uses near-infrared spectroscopy to measure regional cerebral oxygen saturations. Could potentially help in prognostication

144
Q

in an arrest how can you best estimate tissue pH

A

central venous blood samples (arterial gas may be misleading)

145
Q

why should dextrose not be used as a fluid in an arrest

A

redistributed away from the intravascular space rapidly and causes hyperglycaemia which worsens neurological outcome

146
Q

in an arrhythmia, what things suggest the patient is unstable

A

shock
syncope
heart failure (pulmonary oedema)
ischaemia (angina pain)

PHM BSc - Resus Science (29 decks)

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