ERC - ALS Flashcards
What is a MET or RRT
medical emergency or rapid response team that responds to critically unwell patients in an attempt to reduce arrest cases
Syncope due to an arrhythmia is likely to present how
No prodrome
Can occur whilst supine or on exertion
What are the universal termination of resuscitation rules
Efforts to be terminated if no ROSC, no shocks administered, non EMS witnessed
You are in hospital and have a patient that is not breathing but you can feel a pulse, what do you do
Ventilate and check the circulation every 10 breaths to be sure there is still a pulse
Describe agonal breathing
Slow and laboured often with snoring and occasional gasps
Describe inspiratory time, volume and rate of ventilations given when performing in hospital CPR
1s per inspiration
Enough volume for normal chest rise (600-700ml)
10 breaths per minute
Once started, how much and how often is adrenaline given in an arrest
1mg (10ml 1:10,000) every 3-5 minutes (2 cycles)
When is adrenaline in cardiac arrest stopped
As soon as ROSC is suspected
Compare when adrenaline is started in VF/pVT and PEA/asystole
After the third shock for shockable
ASAP for non shockable
For what arrest rhythms is amiodarone given, at what dose and when
VF/pVT
300mg IV after 3rd shock
150mg IV after 5th shock
What is an acceptable alternative to amiodarone given to shockable rhythms in ALS
Lidocaine
What initial energy is used to shock someone in VF/pVT
At least 150J if used biphasic
120-150J is used pulsed biphasic
You don’t know which energy to use and there is no guidance on the defibrillator, what do you do
Use the highest energy possible
To escalate or not to escalate? (Defibrillation energy)
Escalate for failed shocks and refibrillation
You have shocked a patient, do you now pulse check? Why?
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
How soon after a peripheral injection does adrenaline exert it’s maximum benefit on coronary perfusion pressure
70 seconds
What is the role of compressions when there is a shockable rhythm
They increase oxygen delivery to the myocardium
Increase the amplitude and frequency of VF waveform
Increase chance of a shock working
What signs would indicate ROSC
Purposeful movements
Normal breathing and coughing
Raised ETCO2
You witness a patient go into VF/pVT on the monitor, in terms of CPR and shocks what do you do
3 shock strategy - give 3 successive shocks with a very quick rhythm check between each
Commence CPR after 3rd shock
A patient has had a 3 shock strategy and there is no ROSC, at what point do you give adrenaline
You treat the 3 shocks as the first. So give adrenaline after a further 2 shocks
A patient has had a 3 shock strategy and there is no ROSC, at what point do you give amiodarone
Give amiodarone after the 3rd shock regardless of whether or not they are stacked
You witness a patient go into VF/pVT on the monitor but there is no defib, what do you do?
Precordial thump
How would you perform a precordial thump
Take the ulnar edge of a clenched fist to the lower half of the sternum from a height of 2cm and retract first immediately
What is the relationship of CPR interruptions and coronary perfusion pressure
Less interruptions = high coronary perfusion pressure
State the advantages and disadvantages of using central access in ALS
+ve: quicker effect
-ve: pause compressions for insertion of a central line, increased risk of ADRs
Which IO location most closely resembles IV in terms of adrenaline pharmacokinetics on delivery
Sternum
Define PEA
Cardiac arrest in the presence of an electrical rhythm (aside from ventricular tachyarhthmias) that would normally give a palpable pulse
What is pseudo PEA
There is an element of myocardial contraction but it is too weak to produce any detectable pulse or BP
You think you see a very fine VF but it could be asystole - shock or CPR?
Continue with CPR, don’t defibrillate
Severe haemorrhage often leads to which rhythm
PEA
Preferred echo view (according to ERC) in cardiac arrest
Sub-xiphoid
Describe the limitations of the femoral and carotid pulse in an arrest
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
What is invasive arterial pressure monitoring used for in an arrest
Can detect even a very low BP signifying ROSC
What is ETCO2
The partial pressure of CO2 at the end of an exhaled breath
What does the ETCO2 value rely on
Pulmonary blood flow (which in turn relies on a CO)
Ventilation minute volume
What are the benefits of using ETCO2 in an arrest
Ensures tube placement
Avoids hyperventilation
Monitors compression quality
Identifies ROSC (preventing adrenaline being given to a ROSC patient)
You’ve been performing CPR for 20 minutes, what ETCO2 value indicates a poor prognosis
<1.33KPa (10mmHg)
Aim of defibrillation is
Restore spontaneous sychronised electrical activity
In which patients is ECPR likely to improve survival
Reversible cause
No comorbidities
Witnessed arrest with immediate high quality CPR
eCPR within 1hr
You are about to shock a patient and the O2 mask is 99cm away, is this ok?
Nope! All sources of O2 eg masks and nasal cannulae at least 1m away
Describe acceptable electrode pad positioning for VF
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
Describe electrode pad placement in atrial arrhythmias
Sterno apical - R of sternum below clavicle and L mid axillary
Anteroposterior - L precordium and inferior to L scapula
What energy should be used for shocking atrial arrhythmias
120-150J
Why might a high energy be needed to shock an asthmatic patient
Auto PEEP increased impedance
When timing shocks with ventilation, when should you shock and why
End of expiration as impedance is minimal
Define refibrillation
Recurrence of VF during a documented arrest in which VF has already been terminated
The patient remains with the same providers
Define refractory VF
Fibrillation that persists after one or more shocks
You become aware that a patient you are about to shock has an ICD/pacemaker. Where should the electrodes be placed?
8cm away from device or antero-lateral or anterio-posterior
What does synchronisation mean in terms of electrical cardioversion
Shock is synchronised with the R wave
What could happen if a shock isn’t synchronised to the R wave
If given during T wave (relative refractory period) then VF may occur
Which rhythms require shock synchronisation and which don’t
Synchronised: atrial and ventricular tachyarrhythmias
Unsynchronised: VF or pVT
State the initial energy given for AF, flutter, SVT and VT
Flutter and SVT: 70-120J biphasic
Fibrillation and VT: 120-150J biphasic
Where is an ICD placed
Under the pectoral muscle below the left clavicle
What does an ICD do
On detecting a shockable rhythm it will deploy 40J of energy via a wire in the RV no more than 8 times
How can you stop an ICD
Place a magnet over it
Describe see-saw breathing
Paradoxical movement of the chest and abdomen in a patient making respiratory effort against an obstructed airway
What are the anatomical landmarks used to size an OPA
Incisors to angle of jaw
An NPA size corresponds to what
It’s internal diameter
If suction is to be used for airway clearance what device is suitable
Wide bore rigid sucker (Yankaver)
What factors increase the likelihood of gastric inflation during ventilation
Higher airway pressures (excessive flow and volume)
Malalignment of the head and neck obstructing the airway
Incompetent oesophageal sphincter
What does gastric inflation during ventilation increase the risk of
Regurgitation and pulmonary aspiration
For continuous compression technique what is the ventilation rate
10 breaths/minute
Describe the benefits of intubation over SGAs
Less likely to dislodge
Reduced risk of aspiration
Can do continuous compressions
Effective ventilation can be achieved in cases of poor lung compliance
Describe the downsides of tracheal intubation
Misplaced tube may go unrecognised
Compressions stop whilst the tube is placed
Higher failure rate
What forms the primary assessment of tracheal tube placement
Listening for bilateral breath sounds in the axilla
Absence of breath sounds in the epigastum
Bilateral chest rise
What methods can be used for the secondary assessment of ET tube placement
Exhaled CO2
Oesophageal detection device
Describe the oesophageal detection device and the results if it is in the trachea or oesophagus
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
Exhaled CO2 after 6 ventilations confirms what
The tube is either in the carina OR the main bronchus
What are the different methods ETCO2 is detected
Colorimetric devices
Waveform capnography
Non waveform electronic digital ETCO2
Why might a colorimetric device be of no use in cardiac arrest
Pulmonary blood flow so low that theres insufficient exhaled CO2 to detect
Describe the colour changes of an ETCO2 colorimetric device and what % this relates to
Purple = ETCO2 <0.5% Tan = ETCO2 0.5-2% Yellow = ETCO2 >2%
Which ETCO2 colorimetric colour responds to correct tube placement
Purple -> yellow
Adrenalines actions on a1 receptors leads to what
Receptors are found in vascular smooth muscle and activation leads to vasoconstriction
This increases aortic diastolic pressure
This increases coronary and cerebral perfusion pressure
Adrenalines actions on B1 receptors. What are the benefits and cons of this in arrest
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
Adrenaline given post ROSC leads to what
Tachycardia
Myocardial ischaemia
VT and VF
What is the mechanism of action of amiodarone and its effects
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
What dose of amiodarone is given in cardiac arrest
300mg diluted in 5% glucose to a volume of 20ml
What are some adverse effects of amiodarone
Bradycardia
Polymorphic VT
Hypotension
You give amiodorone peripherally, what is at risk of happening?
thrombophlebitis
What class of drug is Lidocaine and which channel does it therefore block
1b - sodium channels
How does lidocaine help in VF/pVT
increases myocyte refractory period
reduces ventricular automacity
prevents ventricular ectopics (via working as a local anaesthetic)
Dose of lidocaine in arrest
1-1.5mg/kg (often around 100mg)
how would someone with lidocaine toxicity present
parasthesia, twitching, convulsion
What are some risk factors for digoxin toxicity
hypomagnesaemia or hypokalaemia
If you are giving Mg in an arrest patient, what dose would you give
2g (4ml of 50%)
In which situations would you give calcium in a cardiac arrest
hyperkalaemia
hypocalcaemia
CCB toxicity
What dose of calcium do you give in a cardiac arrest
10ml of 10% calcium chloride
In which situations is sodium bicarbonate given in an arrest
TCA toxicity
life threatening hyperkalaemia
giving sodium bicarbonate in an arrest leads to what
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
If sodium bicarbonate is given in an arrest what dose
50mmol IV (50ml of 8.4%)
Describe the 2 types of mechanical CPR device
LUCAS: piston and suction cup that provides CPR at 100bpm to a deapth of 4-5cm
Autopulse: load distributing band
Describe an ACD device
suction cup lifts the chest wall up during decompression creating a negative intrathoracic pressure to increase venous return to the heart and therefore CO
Describe and ITD and how it improves CPR
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
Describe how to perform a carotid sinus massage
check for bruits
at the level of the cricoid apply pressure in a circular motion for 5seconds
What is the mechanism behind carotid sinus massage
stimulate baroreceptors so increases vagal tone. This leads to slowing of AV conduction
describe the valsalval manoeuvre
blow into a 20ml syringe hard enough to push the plunger back
What are the actions of class 1 antiarrhythmics and via which channel do they work
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
class 1a antiarrhythmics block K channels therefore leading to which ECG change
QT prolongation which can lead to TdP
When would you consider using a class 1c antiarrhythmic (and which one) in a tachycardia
flecainide is used as rhythm control for irregular narrow complex tachy that has been present for <48 hours
MOA of class 2 antiarrhythmics
B blockers
inhibit adenylate cyclase = reduced cAMP = reduced intracellular calcium = harder to reach threshold for depolarisation = reduced upstroke of the pacemaker AP.
class 2 antiarrhythmics result on conduction velocity and AVN repolarisation
slow conduction velocity
prolong AVN repolarisation
When would B-blockers be used in treating tachyarrhythmias
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)
ADR’s of B-blockers
bradycardia, hypotension, AV conduction delay
Class 3 antiarrhythmic: channel and effects
K channel blocker
prolongs repolarisation and therefore the AP duration
example of class 3 antiarrhythmics
amiodorone
sotalol
When would class 3 antiarrhythmics be used in tachyarrhythmia
unstable tachyarrhythmia following 3 unsuccessful shocks
stable, regular, broad complex tachyarrhythmia inc. VT
Heart failure patient with an irregular narrow complex tachyarrhythmia
ADR of amiodarone
hypotension and bradycardia
Dose of amiodorone given in an unstable tachyarrhythmia after 3 unsuccesful shocks
300mg IV over 10-20 minutes then
900mg IV over 24 hours
class 4 antiarrhythmics: channel and MOA
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
When is a class 4 antiarrhythmic indicated in tachyarrhythmias
stable regular narrow complex tachycardia not controlled by vagal manoeuvre or adenosine (could be flutter)
rate control in irregular narrow complex tachycardia
What adverse effects can CCBs have on the heart
reduced contractility and CO
What is a class 5 antiarrhythmic and how does it work
Adenosine
inhibit adenylate cyclase = reduced cAMP = reduced Ca.
It also increases K entry
This combined leads to hyperpolarization and a transient AVN block
When is adenosine used and what is its dose
regular narrow complex tachycardia
6mg IV bolus
12mg IV bolus if this doesn’t work
12mg IV bolus again if above haven’t worked
Why is adenosine bad in WPW
preventing normal conduction through AVN could promote the accessory pathway therefore worsening the situation
When would Mg be used in tachyarrhythmias
polymorphic VT
TdP
tachycardia associated with hypomagnesaemia
What dose of Mg is given in polymorphic VT
2g over 10 minutes
can repeat once more only
Digoxin MOA
inhibits the NaKATPase = increased intracellular Na = reduced work of NaCa exchanger = increased intracellular Ca = increased contractility
When is digoxin used in a tachyarrhythmia
Heart failure patient with irregular narrow complex tachycardia
a patient is unstable with a bradycardia, what do you do
0.5mg IV Atropine
repeat to a maximum TD of 3mg
a bardycardic patient has not responded to the maximum dose of atropine, what can you try
isoprenaline 5 micrograms
adrenaline 2-10 micrograms
transcutaneous pacing
transcutaneous pacing is not available, what can you do in the mean time
fist pacing - closed fist over left lower sternal edge to pace heart at 50-70bpm
the bradyarrhythmia is due to BB or CCB overdose, what drug do you give
Glucagon
the bradycardia is due to an inferior MI or spinal cord injury, what drug do you give
theophylline
bradycardic stable patients can be observed unless they have what
recent history of asystole
Mobitz type 2 or complete heart block
ventricular pause >3 seconds
name some causes of bradycardia
cardiac: MI, sick sinus syndrome
non cardiac: hypothermia, hypoglycaemia, hypothyroid, RICP
drugs: digoxin, BB, CCB
length of QRS defining it as narrow or broad
greater than or less than 0.12s (3 small squares)
Which drugs should be avoided in WPW
adenosine, digoxin and CCB
How is a irregular broad complex tachycardia managed
Often polymorphic VT eg TdP - treat with Mg 2g over 10 minutes
How is regular broad complex tachycardia managed
Amiodarone 300mg over 20-60 minutes
then 900mg over 24 hours
State some examples of irregular narrow complex tachycardias
AF
atrial flutter with variable AV block
State some examples of regular narrow complex tachycardias
Sinus tachycardia
atrial flutter with constant AV block (often 2:1)
PSVT eg AVNRT or AVRT
How is a irregular narrow complex tachycardia managed
rate control with a Bblocker or Diltiazem
if >48 hours then anticoagulate
If <48 hours then rhythm control with Flecainide (class 1C)
In heart failure patients what changes to the management of irregular narrow complex tachycardia
give digoxin or amiodarone
How is a regular narrow complex tachycardia managed
vagal manoeuvre
Adenosine 6mg IV bolus
2 further 12mg bolus’ can be given
Seek help and potentially rate control with Bblocker
You’ve been doing CPR for 20 minutes: what ETCO2 value signifies a poor prognosis?
<1.3KPa (10mmHg)
A patient has an arrest from a shockable rhythm during cardiac catheterisation, how do you manage them
3 stacked shocks
CPR using a mechanical device (high quality + reduced radiation exposure to CPR providers)
Airway and ventilation options for in hospital arrest management
pocket mask
2 person technique of bag-mask ventilation
SGA with self inflating bag
What does RSVP handover tool stand for
reason
story
vital signs
plan
What is the peri-shock pause
pauses in chest compressions before and after a defib shock
What is the role of adrenaline in cardiac arrest
to increase myocardial blood flow and improve the chance of successful defibrillation
In ALS, when should a pulse check take place
only when an organised rhythm (regular or narrow complexes) is observed at the rhythm check
following administration of drugs peripherally in an arrest, what needs to happen
flush of 20ml
elevate the limb for 10-20 seconds
what is cerebral oximetry
uses near-infrared spectroscopy to measure regional cerebral oxygen saturations. Could potentially help in prognostication
in an arrest how can you best estimate tissue pH
central venous blood samples (arterial gas may be misleading)
why should dextrose not be used as a fluid in an arrest
redistributed away from the intravascular space rapidly and causes hyperglycaemia which worsens neurological outcome
in an arrhythmia, what things suggest the patient is unstable
shock
syncope
heart failure (pulmonary oedema)
ischaemia (angina pain)
