ALS Flashcards
What proportion of OHCAs have which rhythm?
Shockable (VF / pVT) - 25%
Asystole - 50%
PEA 25%
What proportion of OHCAs on which CPR is attempted is ROSC achieved ?
How many of these survive to go home from hospita?
30%
10%
What is the survival to discharge rate for IHCA?
24%
The chain of survival for successful outcome of cardiac arrest
Early recognition and call for help
Early CPR
Early defibrillation
Post-resuscitation care
Reversible causes of cardiac arrest
Hypoxia
Hypovolaemia
Hypo/hyperkalaemia / metabolic
Hypo/hyperthermia
Thrombosis (coronary or pulmonary)
Tension PTX
Tamponade
Toxins
Chain of Prevention of IHCA
Education - A-E and stabilisation
Monitoring - vital signs and accurate documentation
Recognition
Call for help
Response
Causes of airway obstruction
CNS depression
Blood
Vomit
FB
direct trauma to face/throat
Epiglottitis
Pharyngeal swelling (e.g. infection, oedema)
Laryngospasm
Bronchospasm
Bronchial Secretions
Blocked tracheostomy
Complete airway obstruction
Silent
Rapidly leads to cardiac arrest
Partial airway obstruction
Breathing efforts will be noisy
may cause cerebral/pulmonary oedema, exhaustion, secondary apnoea, hypoxic brain injury and eventually cardiac arrest
Airway - management
- suction if needed
- turn patient on their side if possible
- assume actual/impending airway obstruction in anyone with reduced GCS
- airway manoeuvres
- OP / NP / SG airway
- intubation
- tracheostomy
Respiratory arrest
= apnoea
will rapidly cause cardiac arrest if breathing is insufficient to oxygenate blood adequately
Possible causes of respiratory arrest
- reduced respiratory drive (e.g. CNS depression)
- reduced respiratory effort (e.g. high C-spine injury, GBS, restrictive chest wall deformities)
- Lung disorders (e.g. COPD, ARDS, PE, asthma, lung contusion, PTX, pulmonary oedema)
Innervation of the diaphragm
C 3,4,5 keep the diaphragm alive
spontaneous breathing cannot occur with cervical cord injury above this level
Breathing - management
- oxygen
- manage presenting problem (e.g. needle decompression for PTX)
- ?NIV
- consider sedation & intubation
What is the commonest cause of sudden cardiac death?
An arrhythmia caused by either ischaemia or MI
Causes of VF
- ACS
- hypertensive heart disease
- valve disease
- drugs (e.g. antiarrhythmics, TCAs, digoxin)
- inherited cardiac diseases (e.g. long QT)
- acidosis
- electrolyte abnormalities (eg. K, Mg, Ca)
- hypothermia
- electrocution
Primary heart problems
- arrhythmia
- HF
- cardiac tamponade
- cardiac rupture
- myocarditis
- hypertrophic cardiomyopathy
Secondary heart problems
when the heart is affected by changes elsewhere in the body
e.g. apnoea, tension PTX, hypovolaemia, septic shock
What features indicate a high probability of arrhythmic syncope?
- syncope in supine position
- syncope during/after exercise (although after can be vasovagal)
- syncope with no/brief prodromal symptoms
- repeated episodes of unexplained syncope
- syncope in individuals with a FHx of sudden death or inherited heart condition
Circulation - treatment
2 large bore cannulae if possible
Treat the underlying cause of circulation failure (e.g. IV fluids for hypovolaemia, correct electrolyte abnormalities)
consideration of vasoactive drugs and advanced CV monitoring/echo
“see-saw” respirations
= paradoxical chest and abdomen movements
seen in airway obstruction
A to E - AIRWAY
Look for signs of airway obstruction
Remove obstruction
O2 at high concentration
A to E - BREATHING
Look, listen, feel - ?signs of respiratory distress
RR
O2 Sats
Depth/pattern of breathing
Equal chest expansion ?
Any chest deformity?
Tracheal deviation?
Surgical emphysema?
Auscultate and percuss chest
Specific Tx depends on cause
If depth/rate of breathing inadquate - bag-valve mask ventilation
A to E - CIRCULATION
Colour of digits / limb temperature
?any external or concealed haemorrhage
CRT
BP
HR
Auscultate heart
12-lead ECG
Bloods, cannula, VBG
Tx depends on cause but aim to replace fluids, haemorrhage control, restore tissue perfusion
A to E - DISABILITY
Examine pupils (size, equality, reaction to light)
Rapid initial assessment of ACVPU (formal GCS if possible)
BLOOD GLUCOSE
Check drug chart
A to E - EXPOSURE
Full clinical history
Fully expose patient and examine - rashes, abdo, etc
Temperature
Review notes and charts
Unstable angina
- crescendo angina
- recurrent/unpredictable episodes of angina-like pain without specific provocation by exercise
- unprovoked/prolonged episode of CP raising suspicion of MI but without ECG changes/lab evidence of MI
NORMAL TROPONINS
Crescendo angina
Angina on exertion, occurring with increasing frequency over a few days, provoked by progressively less exertion
ECG changes in unstable angina
- normal ECG
- acute MI changes (usually ST depression)
- non-specific abnormalities (eg. TWI)
Higher risk NSTE ACS
- ST depression
- dynamic ECG changes
- unstable rhythm
- unstable haemodynamics
- DM
- high GRACE score
management of STEMI
PCI if available within 120 minutes of onset of CP
If PCI not possible - fibrinolytic therapy considered as alternative
DO NOT wait for trops to come back in pts with STEMI
Anterior / anteroseptal MI
V1-V4
Lesion in LAD artery
Anterolateral MI
V1-V6 and I and aVL
Which distribution of MI has the worst prognosis
= Anterior
more likely to cause impairment of LV function
Lateral MI
V5-V6, I and aVL
lesion in circumflex artery or diagonal branch of LAD artery
Inferior MI
Leads II, III and aVF
usually lesion in RCA
Less commonly lesion in circumflex artery
Posterior MI
when there is reciprocal ST-depression on anterior leads this could reflect ST-elevation posteriorly
most commonly RCA occlusion
Suspicion can be confirmed by placing V8-V10 posteriorly (posterior leads)
Immediate Tx for ACS
300mg Aspirin asap
sublingual GTN (unless hypotensive)
O2 to maintain sats in target range
Analgesia - titrated IV morphine with anti-emetic
Absolute contraindications to fibrinolytic therapy
Previous haemorrhagic stroke
Ischaemic stroke in past 6 months
CNS damage/neoplasm
Recent (3/52) major surgery/head injury/major trauma
Active internal bleeding or GI bleed in last 1 month
Known/suspected aortic dissection
Known bleeding disorder
Relative contraindications to fibrinolytic therapy
Refractory HTN (SBP >180mmHg)
TIA in last 6 months
DOACs
Pregnancy or <1 week post-partum
Traumatic CPR
Non-compressible vascular puncture
Active PUD
Advances liver disease
Infective endocartitis
Previous allergic reaction to fibrinolytic drug
cardiogenic shock
= hypotension, poor peripheral perfusion often accompanied by drowsiness/confusion and oliguria
if develops in a patient after a STEMI consider acute complications such as myocardial rupture, papillary muscle rupture, VSD
SCD - Long QT Syndrome
Inherited (autosomal dominant) ion channel disorder
Predispose to torsade de pointes VT and VF
SCD - Acquired QT interval prolongation
caused by IHD/drug therapy/myocarditis
Predispose to torsade de pointes VT and VF
SCD - Brugada syndrome
inherited (autosomal dominant) ion channel disorder
More common in SE asians
SCD - Short QT syndrome
Rare
Inherited (autosomal dominant) ion channel disorder
Predispose to torsade de pointes VT and VF
SCD - Catecholaminergic Polymorphic VT
Rare
Inherited (autosomal dominant) ion channel disorder
Predisposes to torsade de pointes VT and VF, especially on exercise
SCD - Arrythmogenic Right Ventricular Cardiomyopathy (ARVC)
Inherited (autosomal dominant)
Predisposes to VT and VF
SCD - Hypertrophic Cardiomyopathy
Inherited (autosomal dominant)
Several genotypes
SCD risk is due to VT/VF
Risk varies with genotype and individual factors
SCD - WPW Syndrome
Mostly sporadic, infrequent familial incidence
Risk is due to rapid transmission of AF to the ventricles, triggering VT/VF
SCD - High-grade AV block
Caused by conducting stem fibrosis, calcified AS, myocardial diseases, cardiac surgery, drug therapy, occasionally congenital
Predisposes to ventricular standstill (asystole)
SCD - Aortic Stenosis
Caused by congenital bicuspid valve (becomes severe age 50-70) or degenerative changes
Many develop HF, risk of SCD due to VT/VF
SCD - Dilated Cardiomyopathy
Multiple causes, familial in minority of cases
Many develop HF, risk of SCD due to VT/VF
SCD - IHD due to coronary atheroma
partly genetic, partly acquired
SCD risk mainly due to VT/VF either due to acute ischaemia or chronic scarring
SCD - anomalous coronary artery anatomy
congenital
rare cause of SCD, often on exercise, risk varies with pattern of anomaly
SCD - adult congenital heart disease
often remain at risk of cardiac arrest even when they have had corrective surgery as a child
What are early signs on observations preceding onset of cardiac arrest?
Hypoxia
Hypotension
what is the target time for starting defibrillation in a cardiac arrest?
3 minutes
Collapsed Patient in-hospital
- check for safety
- check for patient response
- no response, no signs of life, no pulse –> CPR algorithm
- response / signs of life –> urgent assessment +/- MET call
Signs to not be confused as signs of life in arrest/pre-arrest
Agonal breathing (occasional, irregular gasps)
Arm movements during CPR
Seizure-like movements - can occur right at the start of arrest
Collapsed patient - no signs of life
Call for help & crash trolley
Check airway +/- manoeuvres
Check for breathing
Check for pulse
Commence 30:2 CPR
Correct chest compressions
Depth of 5-6cm
Rate of 100-120 compressions/min
Allow chest to recoil completely after each compression
Approx. same amount of time for compression and relaxation
Minimise hands-off time
If there are enough team members, swap every 2 mins
good ventilation of patient
use what ever equipment is available immediately
aim for inspiratory time of about 1 sec
give enough volume to produce visible rise of chest wall
add supplementary oxygen as soon as possible
avoid rapid/forceful breaths
If intubated (+/i iGel) - ventilate and compressions simultaneously and uninterrupted
Waveform Capnography
= continuous real-time end-tidal CO2
Uses:
- confirming correct intubation
- monitoring ventilation rate
- used to monitor quality of CPR
- used as indicator of ROSC
- prognostic indicator
Benefits of using a manual defib
ALS provider can immediately recognise rhythm and shock if needed
This can reduce hands-off time to less than 5 seconds
If the patient is not breathing, but has a pulse
= respiratory arrest
Diagnosis can only be made if confident in assessing pulse and signs of life (e.g. perfusion/normal CRT)
Ventilate patient’s lungs
Check for pulse every 1 minute
All pts with respiratory arrest will develop cardiac arrest if it is not treated rapidly and effectively
Monitored and witnessed cardiac arrest (e.g. CCU / cath lab / crit care)
If shockable rhythm, can deliver 3 rapid successive shocks
Check for any rhythm change/other signs of ROSC after each shock
Start 30:2 CPR if no ROSC after 3rd shock (these 3 are considered the 1st shock in the ALS algorithm)
Precordial Thump
rarely works
Only to be used whilst awaiting defibrillator in a monitored VF/pVT arrest
ulnar edge of tight fist - sharp impact of lower half of sternum from about 20cm, then retract immediately
Energy setting for shocks (manual)
First shock 120-150 J
Same or higher for subsequent shocks
Using the defib
- rhythm check - confirm shockable rhythm
- resume compressions
- STAND CLEAR (only person on the chest should be touching)
- charge to appropriate energy
- everyone to STAND CLEAR
- when clear, deliver shock
- immediately restart CPR for next 2 minutes
Drugs in shockable rhythm
After the 3rd shock (whilst 2 mins CPR ongoing)
- Adrenaline 1mg IV
- Amiodarone 300mg IV
Then further adrenaline IV after alternate shocks (roughly every 3-5 mins)
If shockable rhythm persists/recurs - a further dose of 150mg amiodarone can be given after a total of 5 defibrillation attempts
why is it key to reduce interruptions on chest compressions
longer interruptions in chest compressions reduce the chance of a shock achieving ROSC
Lidocaine vs amiodarone in arrest
Lidocaine 1mg/kg can be used as an alternative if amiodarone unavailable - but DO NOT give lidocaine if amiodarone already given.
What might show evidence of ROSC
presence of carotid pulse
sudden increase in end-tidal CO2
evidence of Cardiac Output on invasive monitoring equipment
When to check for pulse in an arrest
only when there is a rhythm that could be compatible with a pulse
PEA
= cardiac arrest in the presence of electrical activity that would normally be associated with a palpable pulse
these Pts often have some mechanical myocardial contractions but these are too weak to produce a detectable pulse/BP
Survival of non-shockable rhythms
Survival of PEA or asystole is unlikely unless a reversible cause can be found and treated quickly and effectively
Asystole
= the absence of electrical activity on ECG trace
Important to check trace for evidence of P waves as then ventricular standstill may be treated effectively by cardiac pacing
Attempts to pace true asystole are unlikely to be successful
PEA / asystole - treatment
Start CPR 30:2
Adrenaline 1mg IV as soon as access achieved
Continue CPR 30:2 until airway secured (then continous compressions and ventilation)
Recheck rhythm after 2 mins
- If pulse/signs of life - commence post-resuscitation care
- if no pulse/signs of life - recommence CPR
Further adrenaline every 3-5 mins
If at any point VF/pVT on rhythm check, switch to shockable algorithm
Intubation during arrest
- only carried out by someone competent to intubate
- no evidence that intubation is any better than bag-valve or SGA during an arrest
- avoid interruptions on compressions (max 5 sec while tube going through vocal cords)
- intubation may be avoided until ROSC achieved
Normal PaCO2
4.7-6.0 kPa
End-tidal CO2
What is the normal range?
= the partial pressure of CO2 at the end of an exhaled breath
4.3-5.5 kPa (i.e. lower than arterial)
End-tital CO2 in CPR
During CPR, end-tidal CO2 is low (reflecting the low CO generated by compressions)
How does waveform capnography confirm effective CPR
the more effective the compressions, the greater the end-tidal CO2
Identifying ROSC with waveform capnography
an increase in end-tidal CO2 during CPR may indicate ROSC
Waveform capnography as prognostic factor
Low end-tidal CO2 values during CPR are associated with lower ROSC rates and increased mortality
Higher values associated with better ROSC rates and survival
End-tidal CO2 should be part of a multifactorial approach to prognostication (do not use alone)
What airway is needed to measure waveform capnography
Intubation
SGA with good seal
Rate of ventilation during CPR when continuous ventilation possible
10 per min
Vascular access in arrest
If pt has CVC - use this
Otherwise attempt to gain peripheral access
- drugs will need to be followed by a flush of 20mL fluid and elevation of extremity (for 10-20s) to allow adequate delivery to central circulation
If IV access difficult, consider IO
IO access sites
Proximal humerus
Proximal Tibia
Distal Tibia
Contraindications to IO access
Trauma
Infection
Prosthesis at target site
Recent IO access (last 48h) in the same limb
Failure to identify anatomical landmarks
Complications associated with IO access
- extravasation into soft tissues around insertion site
- dislodgement of needle
- compartment syndrome (due to extravasation)
- fracture or chipping of bone during insertion
- pain related to drugs/fluid
- fat emboli
- infection/Osteomyelitis
Four Hs - Hypoxia
Ensure adequate:
- ventilation with 100% O2 during CPR
- chest rise
- bilateral breath sounds
Four Hs - hypovolaemia
PEA caused by hypovolaemia is usually due to severe haemorrhage
Restore IV volume rapidly with fluid/blood (effective compressions require an adequate circulating volume)
Urgent interventions to stop haemorrhage
Four Hs - Hyper/hypokalaemia, hypoglycaemia, hypocalcaemia, other metabolic disorders
identified on biochemical tests or suggested by Pt’s PMHx
IV CaCl is indicated in the presence of hyperkalaemia, hypocalcaemia and CCB overdose
Four Hs - hypothermia/hyperthermia
Suspect hypothermia in any drowning incident
Four Ts - thrombosis
Coronary thrombosis is a common cause
- if ACS is suspected as cause it may be feasible to perform PCI during ongoing CPR but this requires mechanical compressions
Massive PE
- consider fibrinolytic therapy immediately if suspected
- if given, CPR needed for 60-90 mins after this
Four Ts - tension PTX
clinical Dx or focussed US of chest
Decompress rapidly by thoracostomy or needle thoracocentesis and then insert a chest drain
Four Ts - tamponade
difficult to diagnose in arrest (typical signs difficult to see)
Focused cardiac ultrasound can diagnose pericardial effusion
Have strong suspicion in an arrest after penetrating chest trauma or after cardiac surgery
Four Ts - toxins
If no specific history, may be difficult to detect but may be revealed later by lab tests
Where available, appropriate antidotes should be used but a lot of treatment is supportive
Extracorporeal CPR
Requires vascular access and a circuit with a pump and oxygenator
Can buy time until restoration of adequate spontaneous circulation in select patients who have a reversible cause, there is little comorbidity, and arrest was witnessed/has had immediate high-quality CPR
Duration of CPR attempt
If attempts at achieving ROSC are unsuccessful the team leader should discuss stopping CPR with the team
Consider the circumstances and perceived prospect of a successful outcome
If it was considered appropriate to start CPR, it is usually considered worthwhile continuing whilst the patient remains in a shockable rhythm or there are potentially reversible causes that can be treated
Asystole >20mins in absence of reversible causes, generally constitutes reasonable grounds for stopping
Diagnosing death after unsuccessful CPR
After stopping CPR observe the patient for 5 mins before confirming death
- absence of central pulse on palpation
- absence of heart sounds on auscultation
One or more can supplement the above:
- asystole on continuous ECG display
- absence of pulsatile flow on direct intra-arterial pressure monitoring
- absence of contractile activity using echo
After 5 mins of continued arrest, check pupil responses, corneal response, and motor response to supra-orbital pressure.
Time of death is recorded as the time at which these criteria are fulfilled
What’s the most common site of airway obstruction in the unconscious patient?
the pharynx (soft palate / epiglottis rather than tongue)
Sounds associated with airway obstruction
Inspiratory Stridor - laryngeal level or above
Expiratory Wheeze - lower airways
Gurgling - liquid foreign material in upper airways
Snoring - pharynx partially occluded by tongue/palate
Mild choking
= effective cough
Able to answer “yes” to the question are you choking?
Able to speak, cough, breathe.
Mx => encourage coughing
Severe choking
= ineffective cough
unable to speak, unable to breathe, attempts at coughing are silent, may lose consciousness
Mx if conscious => 5 back blows, 5 abdominal thrusts
Mx if unconscious => start CPR
Basic techniques for opening the airway
Head tilt & chin lift
Jaw thrust
How to perform head tilt, chin lift
one hand on pt’s forehead and tilt head back
fingertips of other hand under point of pt’s chin
gently lift to stretch anterior neck structures
How to perform jaw thrust
identify angle of mandible
with the index and other fingers placed behind the mandible, apply steady upwards and forwards pressure to lift the mandible
With the thumbs, slightly open the mouth by downward displacement of the chin
estimating size of OP/Guedel airway
checking length between pt’s incisors and the angle of the jaw
if in doubt, a bigger airway will be more beneficial than a smaller airway
Insertion of OP/guedel airway
only attempt in unconscious patients (vomiting or laryngospasm may occur if gossopharyngeal/laryngeal reflexes are present)
- open pt’s mouth
- remove any foreign material if present
- insert airway upside down into oral cavity until you reach junction between hard/soft palate
- rotate it 180 degrees
- advance airway until it lies within the pharynx
remove airway if pt gags or strains
NP airway
better tolerated than OP airway in Pts who are not deeply unconscious
Size 6-7mm usually suitable for adults
Can cause bleeding in up to 30% of uses
If tube is too long it can stimulate laryngeal / glossopharyngeal reflexes
When not to use NP airway
in a patient with suspected basal skull #
(rare chance of inadvertently inserting into cranial vault through the fracture)
Suction
Wide-bore rigid sucker (yankauer) to remove liquid (blood, saliva, gastric contents) from the upper airway
=> use cautiously if gag reflex intact
Fine-bore flexible suction catheters may be needed in pts with limited mouth opening (can also be passed through OP/NP airways)
Insertion of i-Gel airway
- try to continue compressions throughout insertion (if necessary to stop, limit pause to 5 sec)
- select appropriate size
- lubricate the back, sides and front with a thin layer of lube
- position so that the cuff outlet is facing the chin of the patient
- ensure patient is ‘sniffing the morning air’
- insert in direction towards the hard palate, glide device downwards and backwards with continuous but gentle push until a definitive resistance is felt
Limitations of i-Gel airway
- there is risk of significant leak around the cuff in presence of high airway resistance (e.g. COPD, pulmonary oedema) - may cause gastric inflation
- uninterrupted chest compressions are likely to cause some gas leak, can revert to 30:2 if needed
- theoretical risk of aspiration of stomach contents but rarely seen in clinical practice
- may cause coughing, straining or laryngeal spasm (but not in an arrest)
Laryngeal mask airway
= wide-bore tube with elliptical inflated cuff designed to seal around laryngeal opening
Types of Supraglottic airways
i-Gel
Laryngeal Mask Airway
” no trace = wrong place”
exhaled CO2 will be detectable by waveform capnography even during cardiac arrest, failure to detect any CO2 indicate that the tube is in the oesophagus
Cricothyroidotomy
most often needed in patients with extensive facial trauma or severe laryngeal obstruction (eg. anaphylaxis/foreign material)
=> surgical airway below the level of obstruction
should only be performed by those trained in the technique
Conventional defibrillator pad positions
Beneath right clavicle
Left mid-axillary line
Alternative pad positions
e.g. if permanent pacemaker, chest wall trauma
Anterior/posterior - left precordium and on the back behind the heart
Lateral/posterior - left mid-axillary line, on the bakc behind the heart
Bi-axillary - both lateral chest walls
pre-excited AF
occurs in the presence of an accessory pathway in WPW syndrome
produces an irregular broad complex tachycardia which might be mistaken for polymorphic VT
Correct Tx is immediate defibrillation
left untreated, this can leat to VT/VF causing cardiac arrest
VT with pulse
management follows broad-complex tachycardia algorithm
what is a capture beat
when atrial beats are conducted to the ventricles during VT
produces a single normal-looking QRS complex during monomorphic VT
what is a fusion beat
can be seen in VT
a wave of depolarisation travelling down from the AV node occurs simultaneously with a wave of depolarisation travelling from the ventricular focus producing the arrhythmia
results in a hybrid QRS complex
SVT in bundle branch block
in the presence of BBB, SVT will cause a broad-complex tachycardia
however the safest approach is to regard all broad-complex tachycardias as VT unless proven otherwise
Torsade de Pointes
= polymorphic VT
the axis of electrical activity changes in a rotational way, so that the overall pattern of the ECG rhythm strip is sinusoidal
What should be avoided in patients with TdP
drugs that prolong QT interval (e.g. amiodarone)
What is bradycardia
<60 bpm
may be physiological in fit people/during sleep
may be an expected result of Tx (e.g. beta blockers)
Pathological bradycardia may be caused by malfunction of the SA node or partial/complete failure of AV node.
Emergency Tx of bradycardia
Atropine and/or cardiac pacing
the need for treatment depends on haemodynamic effect and risk of developing asystole, rather than the precise ECG classification
1st degree AV block
fixed PR interval >0.20s
rarely requires Tx
2nd degree Mobitz 1 heart block
PR interval shows progressive prolongation, until a P wave occurs without a QRS complex
Also called Wenckeback heart block
Does not usually require immediate Tx
2nd degree Mobitz 2 heart block
A constant prolonged PR interval, with some P waves not followed by QRS complex
Occurs randomly without a consistent pattern
Increased risk of progression to AV block and asystole
Complete heart block (3rd degree)
no correlation between P waves and QRS
Likely to stop abruptly, resulting in asystole
Escape rhythm
If the SA node fails, cardiac depolarisation may be initiated from a subsidary ‘pacemaker’ elsewhere
the resulting escape rhythm will be slower than normal
Agonal rhythm
occurs in dying patients
Commonly seen in later stages of unsuccessful resuscitation attempts
Slow, irregular, wide ventricular complexes
Often become progressively broader before progressing to asystole
Does not generate a palpable pulse
mechanism of defibrillation
= the passage of an electrical current of sufficient magnitude across the myocardium to depolarise a critical mass of cardiac muscle simultaneously
the aim is to enable the natural pacemaker tissue to resume control
Factors affecting defibrillation success
Thoracic Impedence:
- ensure good skin contact (removal of drug patches, shave chest)
Electrode position
What is considered successful defibrillation?
= the absence of VF/pVT at 5s after shock delivery
although, the ultimate goal is ROSC
Synchronised cardioversion
used for atrial or ventricular tachyarrhythmias (not pVT or VF)
the shock must be synchronised with the R wave to reduce the risk of inducing VF
Defibrillation near a pacemaker ICD
to minimise risk, place the defibrillator electrodes >8cm away from the pacemaker or ICD
if necessary use anterior/posterior or bi-axillary position
you may need to deactivate the ICD with a magnet
Internal defibrillation
= internal paddles applied directly to the ventricles
requires considerably less energy (10-20 J) - do not exceed 50 J
Intrinsic rates of cardiac conducting system
SA node - 60-70bpm
AV node - 40-50 bpm (narrow QRS)
Distal to Bundle of His - 0-30 bpm (broad QRD)
Broad-complex complete heart block
when the HB occurs lower in the conducting system than bundle of His
The escape rhythm is unreliable and may fail transiently (leading to syncope) or fail completely (leading to ventricular standstill / cardiac arrest)
THIS WILL NEED PACING
Stokes-Adams Attack
= a sudden, brief loss of consciousness from a large drop in cardiac output
methods of pacing
NON-INVASIVE
percussion (fist) pacing
transcutaneous pacing
INVASIVE
temporary transvenous pacing
permanent pacing
Percussion Pacing
may produce an adequate cardiac output with less trauma to the patient than CPR
more likely to be successful when ventricular standstill is accompanied by P wave activity
- with side of closed fist deliver repeated, firm thumps to precordium, just lateral to left sternal edge
- raise hand to about 20cm above the chest before each thump
- monitor ECG to assess if QRD is achieved by each thump
- if initial thumps don’t work, try slightly harder
- if this still fails, move the point of contact around the precordium until a point is found that produces ventricular stimulation
If does not produce a regular pulse promptly, start CPR immediately
advantages vs disadvantages of transcutaneous pacing
- can be established quickly, widely available, easy to perform
- causes discomfort in a conscious patient, not as reliable so only short-term solution
How to perform transcutaneous pacing
- remove chest hair if needed and ensure skin is dry
- Apply pads in conventional position (A-P if needed)
- select appropriate pacing rate (usually 60-90)
- set energy output to lowest setting and gradually increase until a pacing ‘spike’ appears on ECG followed by a QRS immediately and check a T wave follows
- having achieved electrical capture, ensure there is a palpable pulse
WARN PATIENTS THERE WILL BE DISCOMFORT
what can cause a temporary transvenous pacing system to fail?
1 - HIGH THRESHOLD
2 - CONNECTION FAILURE
3 - LEAD DISPLACEMENT
Where should defib pads be placed if the pt has an ICD or pacemaker?
> 8cm from device
ICDs
implanted device to terminate life-threatening tachyarrythmia
- delivers a shock when it detects VF or fast VT
- most can also function as demand pacemakers in the event of bradycardia
- some devices will deliver biventricular pacing for heart failure
life-threatening features of arrhythmia
Shock
Syncope
Heart Failure
MI
Extremes of heart rate
Extreme tachycardia
when HR increases, diastole is shortened to a greater degree than systole
if rate >150 this can reduce cardiac output dramatically (due to inability to fill correctly due to short diastole)
Extreme bradycardia
HR <40 often tolerated poorly
especially when people have severe heart disease and cannot compensate for bradycardia by increasing SV
Treatment for extreme arrythmias
depending on the presence or absence of life-threatening features
- no treatment needed
- simple clinical intervention (e.g. vagal manoeuvres / percussion pacing)
- pharmacological
- electrical (cardioversion for tachy, pacing for brady)
Adult tachycardia management guidelines
if life-threatening features –> up to 3x synchronised DC shocks, if unsuccessful then amiodarone 300mg IV over 10-20 mins
If no features, then depends if QRS narrow/broad
NARROW:
- irregular - Tx as AF
- regular vagal manoeuvres, then adenosine
BROAD:
- if VT –> amiodarone 300mg IV over 10-60mins
Adenosine in tachycardia
for narrow complex tachycardia after vagal manoeuvres failed
Give adenosine (if no pre-excitation) 6mg rapid IV bolus
If unsuccessful, give 12mg
If unsuccessful, give 18mg
Needs continuous ECG monitoring
If still ineffective, verapamil/beta-blocker
synchronised cardioversion
either under conscious sedation or GA
set defib to deliver a synchronised shock (it will coincide with the R wave)
Press the shock button and keep pressed until after the shock has occured (might eb a slight delay)
Why do you use specifically a synchronised shock when doing cardioversion
an unsynchronised shock could coincide with a T wave and cause VF
Post-cardiac arrest brain injury
= cause of death in 68% of patients who have an OHCA and have survived to ITU
usually manifests as coma, seizures, myoclonus, varying degrees of neurological dysfunction and brain death.
Worsened by: mpaired autoregulation, hyper/hypocapnia, hypoxia/hyperoxia, hypo/hyperglycaemia, pyrexia and seizures. Thus treatment is aimed at preventing these.
Post-cardiac arrest myocardial dysfunction
‘myocardial stunning’
may result in a temporary but significantly reduced LV ejection fraction and therefore cardiac output.
It typically recovers after 72h.
Systemic ischaemia-reperfusion response
whole body ischaemia/reperfusion that occurs after resuscitation from cardiac arrest activates immunological and coagulation pathways that cause multiple organ failure and increase the risk of infection.
Post-cardiac arrest syndrome
Often complicates the post-resuscitation phase. This comprises of:
Post-cardiac arrest brain injury.
Post-cardiac arrest myocardial dysfunction.
Systemic ischaemia/reperfusion response.
Persistence of precipitating pathology.
ROSC - persistence of precipitating pathology
Any persisting pathology relating to the cause of the cardiac arrest, such as a myocardial infarction or a pulmonary embolism, will also need treatment.
ROSC - temperatures
fevers are common post-arrest
continuously monitor core temperature in a ROSC pt
treat any pyrexia with cooling and antipyrexials
Rate control in AF
First-line usually beta-blocker
Can use diltiazem if BB contraindicated
Digoxin may be used in patients with heart failure.
Amiodarone may be used to assist with rate control but is most useful in maintaining rhythm control.
Rhythm control in AF
If AF is <48 hours
PHARMACOLOGICAL
- Flecanide (seek expert help)
- Amiodarone (300 mg over 20-60 min followed by 900 mg over 24 h) may be used but is less often effective than drugs like flecainide and takes longer to work.
ELECTRICAL
Contraindications to using Flecanide
Do not use flecainide in the presence of heart failure, known left ventricular impairment, ischaemic heart disease, or a prolonged QT interval.
AF >48 hours
If the pt has been in AF for >48 hours, do not attempt cardioversion until they have been fully anticoagulated for at least 3 weeks, or unless transoesophageal echocardiography has detected no evidence of atrial thrombus.
Appropriate energy settings for cardioversion
For a broad-complex tachycardia, start with a 120-150 J biphasic shock and increase in increments if this fails to a maximum of three attempts.
For atrial fibrillation, start at the maximum defibrillator output.
Atrial flutter and regular narrow-complex tachycardia will often be terminated by lower-energy shocks: start with 70-120 J biphasic.
What is the best pad placement for electrical cardioverion
Anterior-posterior placement
Failure of electrical cardioversion in tachycardia
If cardioversion is unsuccessful at terminating the arrhythmia after delivery of three shocks of increasing energy:
Give the patient amiodarone 300mg IV over 10-20 min.
Attempt further synchronised cardioversion.
The loading dose of amiodarone may be followed by an infusion of 900mg over 24h, given into a large vein (preferably via a central venous cannula).
Treatment of sinus tachycardia
Sinus tachycardia is not an arrhythmia.
It is a common physiological response to stimuli such as exercise or anxiety.
Do not attempt to treat sinus tachycardia with cardioversion or anti-arrhythmic drugs as treatment is directed at the underlying cause.
Use of atropine in bradycardia
Used when there is evidence of life-threatening signs in bradycardia
Dose = 500mcg IV
Repeat to a maximum of 3mg
Other drugs to use:
- Isoprenaline
- Adrenaline
- aminophylline
- glucagon (in BB/CCB overdose)
PACING
What increases the risk if asystole in bradycardia?
recent asystole
mobitz II AV block
complete heart block with broad QRS
ventricular pause > 3 s.
Causes of broad-complex tachycardia
either ventricular in origin
or supraventricular with BBB
Safest approach is to manage as VT if in doubt
Irregular broad-compplex tachycardia
most likely to be AF with BBB
will need careful examination of 12-lead ECG
can be polymorphic VT (but this is unlikely to present without adverse features)
narrow-complex tachycardias
REGULAR:
- sinus tachy
- SVT
- atrial flutter with regular AV conduction (i.e. 2:1)
IRREGULAR
- most likely AF
- atrial flutter with variable conduction
Management of SVT
If life-threatening features –> synchronised shock
If no adverse features:
- Vagal manoeuvres (record an ECG during each manoeuvre ? identify any flutter waves)
- Adenosine 6mg -> 12mg -> 18mg (rapid IV boluses)
Exception to non-shockable branch of ALS algorithm
rapid narrow complex tachy with no pulse
technically this is PEA and CPR should be started
however, the most appropriate Tx is synchronised shock
Contraindications to atropine
patient with cardiac transplant (heart is denervated and will not respond)
Patient with bradycardia and no life-threatening features
If NO life threatening features and NO high risk of progression to asystole then do not initiate immediate treatment
Monitor and re-assess
Seek expert help
Main causes of hyperkalaemia
- renal failure
- drugs (e.g. ACEi, ARB, NSAIDs, BBs, trimethoprim)
- tissue breakdown
- metabolic acidosis
- endocrine disorders
- diet
- spurious (e.g. haemolysed sample)
ECG changes in hyperkalaemia
1st degree AV block
flattened/absent P waves
tall, peaked T-waves
ST-depression
sine-wave pattern
widened QRS
VT
bradycardia
Cardiac arrest
tall, tented T-waves
T waves larger than R wave in more than one lead
Treatment of hyperkalaemia
- cardiac protection (calcium gluconate)
- shift potassium into cells
- insulin (+ glucose)
- salbutamol - remove potassium from body
- Lokelma
- dialysis - monitor serum K and glucose
- prevention of recurrence
Modifications of CPR associated with hyperkalaemia
- confirm hyperkalaemia on VBG
- protect heart with CALCIUM CHLORIDE 10%
- shift potassium into cells
- give sodium bicarb
- consider dialysis and need for mechanical chest compressions for prolonged CPR during this
Giving sodium bicarb in hyperkalaemia
50mmol IV by rapid injection
(50mL of 8.4% solution)
try to give separately to CaCl as can cause a precipitate
Risk of SCD in hypokalaemia
Hypokalaemia itself increases the risk of SCD
this risk is increased further in patients with pre-existing heart disease and in those on digoxin Tx
Main causes of hypokalaemia
GI loss
drugs
renal losses
endocrine disorders
metabolic alkalosis
Mg depletion
poor dietary intake
ECG features of hypokalaemia
U-waves
T-wave flattening
ST-segment changes
arrhythmias (especially if on digoxin)
Cardiac arrest
ECG changes in Hypercalcaemia
short QT interval
Prolonged QRS
Flat T-waves
AV block
Cardiac arrest
ECG changes in Hypocalcaemia
prolonged QT
TWI
Heart block
Cardiac arrest
Emergency Tx of hypercalcaemia
fluid replacement IV
Furosemide 1mg/kg IV
Hydrocortisone
Pamidronate
Tx underlying cause
Emergency Tx of hypocalcaemia
Calcium chloride 10% 10-40mL IV
1-2g 50% Mg sulphate (4-8mmol) IV if necessary
ECG changes in Hypermagnesaemia
prolonged PR and QT
T-wave peaking
AV block
Cardiac arrest
Emergency Tx of hypermagnesaemia
consider when Mg >1.75
Calcium chloride10% 5-10mL IV, repeated if necessary
Ventilatory support if necessary in resp. depression
Saline diuresis (saline & furosemide)
Haemodialysis
ECG changes in hypomagnesaemia
Prolonged PR and QT
ST-depression
TWI
flattened P waves
broad QRS
TdP VT
Emergency Tx of hypomagnesaemia
Magnesium sulfate IV 2g 50%
over different lengths of time depending on presentation
What is the risk of OHCA in dialysis patients?
Up to 20x more risk than general population
Resuscitation during dialysis
mostly the same but also:
- dialysis nurse present for HD macine
- stop dialysis
- fluid bolus
- prompt management of any hyperkalaemia
- avoid excessive potassium and volume shifts during dialysis
Sepsis 6
Bloods and cultures
Urine output (catheter, hourly)
Fluid resuscitation
ABX (broad-spectrum)
Lactate
Oxygen, if needed
Modifications to CPR in event of toxins suspected
PPE and avoid mouth-to-mouth
treat life-threatening tachyarrythmias with cardioversion
try to identify toxins (relatives, friends, ambulance crews)
measure temperature
standard CPR if arrest occurs
be prepared to continue CPR for a long time, particularly in young patients, while the poisin is excreted (consider ECLS)
Specific antidotes - opiate poisoning
Naloxone
400mcg IV (800mcg IM/SC)
titrate up to a maximum dose of 10mg
duration of action = 45-70 mins
give until pt is breathing adequately and then consider need for ?ongoing infusion
caution in pts with opiate dependence
Specific antidotes - benzodiazepine poisoning
Flumazenil
(a competitive antagonist of benzos)
caution in pts with benzo dependence
Specific antidotes - TCA poisoning
Consider sodium bicarb for treatment of TCA-induced ventricular conduction abnormalities
Local anaesthetic toxicity
typically when a bolus of LA enters a blood vessel by mistake
= severe agitation, LOC +/- tonic-clonic convulsions, sinus brady, conduction blocks, asystole, VT
follow standard resuscitation measures
may benefit from 20% lipid emulsion in addition to standard ALS
Stimulant toxicity
e.g. cocaine and amphetamines
agitation, tachycardia, hypertensive crisis, hyperthermia, MI
Tx with small doses of benzodiazepaines first-line
Managing acute severe asthma
- O2 to maintain sats
- salbutamol nebs
- ipratropium nebs
- steroids
- IV Magnesium 8mmol IV over 20 mins
- following senior advice, consider aminophylline in severe/near fatal asthma only
- fluid and electrolyte replacement as needed
- ICU input
arrest associated with asthma
follow standard ALS protocols
ventilation will be difficult due to increased airway resistance, so intubate early
try to avoid dynamic hyperinflation of lungs (gas trapping)
always consider bilateral tension PTX in asthma
What is anaphylaxis
= systemic hypersensitivity reaction, usually rapid in onset and may cause death
suspect if sudden illness develops after exposure to a trigger, with rapidly progressing skin changes and life-threatening airway and/or breathing and/or circulation problems
Anaphylaxis - life-threatening problems
AIRWAY
- airway swelling
- hoarse voice
- stridor
BREATHING
- SOB
- sheeze
- tiring
- cyanosis
- resp arrest
CIRCULATION
- pale, clammy
- tachycardia
- hypotension
- reduced consciousness
- myocardial ischaemia
- cardiac arrest
Anaphylaxis - skin changes
can affect the skin, the mucosa, or both
- erythema
- urticaria
- angioedema (deeper tissues - eyelids, lips, mouth, throat)
Skin changes without breathing/circulation problems does not signify anaphylaxis
Anaphylaxis - Mx
LIE PATIENT FLAT
(can sit up if breathing difficulties but DO NOT STAND)
Remove trigger
O2 to maintain sats
ADRENALINE IM - 0.5mg for adults
IV fluid bolus
Repeat dose after 5 mins if no response
If no response –> REFRACTORY ANAPHYLAXIS GUIDELINES
Injecting adrenaline in anaphylaxis
IM is best and quickest option
0.5mg in adults
anterolateral aspect of middle third of thigh
How to confirm an event was anaphylaxis
mast cell tryptase (will be markedly increased in anaphylaxis)
Maternal cardiac arrest
= a cardiac arrest at any stage of pregnancy up to 6 weeks after delivery
modifications:
- obtain expert help including obstetrician, paeds, anaesthetist
- if risk of IVC compression, aim to establish IV/IO access above the diaphragm
- left uterine displacement
- prepare for emergency C-section
Prevention of cardiac arrest in pregnancy
- place distressed/compromised person in left lateral position
- high flow O2 to maintain sats
- fluid bolus if needed
- expert obstetric and anaesthetic help
Peri-mortem C-section
Best done within 5 mins of maternal arrest
Not done <20 weeks gestation (no risk of IVC compression)
20-23 weeks - initiate emergency delivery to permit successful resuscitation of mother
gestation >24 weeks - initiate to help save the life of both mother and fetus
Causes of cardiac arrest in trauma patients
TBI
hypovolaemia from massive blood loss
hypoxia from respiratory arrest or airway obstruction
direct injury to vital organs/major vessels
tension PTX
cardiac tamponade
commotio cordis
= near cardiac arrest caused by blunt impact to chest wall which causes pVT/VF
Tension PTX - Mx
immediate decompression of chest cavity
NEEDLE DECOMPRESSION
- 2nd intercostal space
- 4th/5th intercostal space mid-axillary line
- chest drain asap
OPEN THORACOSTOMY (preferred if trained clinician available)
- inciscion in chest wall (5th ICS mid-axillary line) followed by dissection into pleural space
- insert chest drain following ROSC
CLAMSHELL THORACOTOMY
- may be required in traumatic cardiac arrest
Cardiac arrest following submersion in water
correction of hypoxaemia by ventilation only is critical and may lead to ROSC
Water resuce
- attempt to rescue the drowning person without entering the water yourself
- open airway and check for signs of life (agonal breathing is common)
- give 5 initial ventilations (with O2 if available)
- if not responded to initial ventilations, commence CPR 30:2 (avoid compression only as likely to be hypoxia driven)
Mild hypothermia
core temp 32-35 degrees
moderate hypothermia
core temp 28-32 degrees
severe hypothermia
core temp <28 degrees
modifications of CPR in hypothermia
- heart may be unresponsive to drugs until warmed - without meds until core temp >30
- once 30*C reached, double usual length of intervals between drugs
- as normothermia is approached, use standard drug protocols
Rewarming after hypothermia
removal from cold environment
remove wet clothes
conscious people should mobilise
full body insulation
heated IV fluids
Malignant hyperthermia
= rare disorder of skeletal muscle calcium homeostasis characterised by muscle contracture and life-threatening hypermetabolic crisis following exposure tof genetically predisposed individuals to halogenating anaesthetics and depolarising muscle relaxants
Forms of heat stroke
- NON-EXERTIONAL - during high environmental temperatures
- EXERTIONAL - during strenuous physical exercise in high environmental temperatures and/or high humidity
Treatment of hyperthermia/heat-stroke
transfer to cool environment, lie flat
cool to <39 (ideally lower)
cold water immersion / full body conductive cooling systems
cold fluids
correct electrolyte abnormalities
Mx of malignant hyperthermia
stop triggering agents
give O2
correct acidosis and electrolytes
start active cooling
DANTROLENE
Base Excess
= a measure of the amount of excess acid or base that is in the blood as a result of a metabolic derangement.
A base excess that is:
- more negative than -2 mmol L-1 (negative base excess) and pH less than 7.35 indicates a metabolic acidosis.
- greater than +2 mmol L-1 (base excess) and pH greater than 7.45 indicates a metabolic alkalosis.
