ALS book

Question 1

What are the two biggest single causes of death in the UK?

Answer 1

1. Dementia
2. Ischaemic heart disease

Question 2

The average survival to discharge from in-hospital cardiac arrest was slightly less than 24%.

The average survival to discharge from out of hospital cardiac arrest is around 10%

Around half of cardiac arrest are witnessed by either a bystander or ambulance staff. How common are the four different presenting rhythms for out of hospital cardiac arrest?

Answer 2

OUT OF HOSPITAL CARDIAC ARREST

Shockable (ventricular fibrillation and pulseless ventricular tachycardia) account for a quarter of cases
Non shockable the remainder of cases - asystole in about 50% and pulseless electrical activity in about 25%

In hospital is difficult to accurately assess due to other factors eg people have DNA CPRs

Question 3

Defibrillation within 3-5 min of collapse can produce survival rates as high as 50-70%. Each minute of delay to debrillation reduces the probability of survival to hospital discharge by 10-12%.

When should you start CPR?
When do you attempt defibrillation?
Which drugs are given in both shockable and non-shockable rhythms?

Answer 3

Start CPR if unresponsive and not breathing normally in a 30 compression to 2 rescue breaths format

Attempt defibrillation if shockable (VF / pulseless VT) - shock as soon as you know this is the rhythm and repeat rhythm check +/- shock every 2 minutes
Shockable - give adrenaline every 3-5 mins (initial dose after 3 rd shock and then at every other shock), give amiodarone after 3 shocks

Non-shockable - give adrenaline every 3-5 mins

Question 4

Whagt is the usual current for a shock in a patient?

How long should the puase in chest compressions to confirm the rhythm last?

Answer 4

120-150Joules (in reality shock can range anywehere between 120 and 360 Joules) for first shock and the same or higher for consecutive shocks

Pause in the chest compression - should aim for less than 5 seconds

Question 5

As stated, give adrenaline every 3-5 mins or every rhythm check/shock
What is the dose of adrenaline given in adults?

Would you give a second dose of amiodarone in shockable rhythms? If so, what dose?

Answer 5

1mg IV adrenaline given every 3-5 minutes in both shockable/non-shockable

Amiodraone - given 300mg IV after 3 shock attempts, consider a further 150mg IV after 5 shocks if remaining in pulseless VT/VF

Question 6

How does adrenaline work to help in cardiac arrrest?

How does amiodarone work to help in cardiac arrrest?

Answer 6

Adrenaline - increased myocardial force of contraction (positive inotrope) and heart rate (positive chronotrope) occur as a result of β1 receptor stimulation. Systemic vascular resistance is increased overall because the stimulation of α1 receptors results in peripheral vasoconstriction, which counters the vasodilation due to β2 receptor activation

Amiodarone - blocks potassium currents that cause repolarization of the heart muscle during the third phase of the cardiac action potential. As a result amiodarone increases the duration of the action potential as well as the effective refractory period for cardiac cells (myocytes).

Question 7

What are the four Hs and four Ts that are reversible causes of cardiac arrest?

Answer 7

Hypoxia
Hypovalaemia
Hypo-hyperkalaemia / metabolic acidosis
Hypo/hyperthermia

Thrombosis - coronary or pulmonary
Tension pneumothorax
Tamponade - cardiac - need a focussed cardiac ultrasound to exclude held in sub-xiphotic space (also helps detect aortic dissections and pneumothorax)
Toxins

Question 8

Whats do you do once you achieve ROSC?

Answer 8

Aim for SpO2 of 94-98% and normal PaCO2
12-lead ECG
Identify and treat cause
Targeted temperature management

Question 9

What is the frequency of monitoring for different NEWS scores:

• 0
• 1-4
• 3 in single parameter
• 5or6 (urgent response threshold)
• 7or more (emergency response threshold)

Answer 9

• 0 - minimum 12 hourly monitoring
• 1-4 - minmum 4-6 hourly monitoring (registered nurse must be informed, can decide if it requirres increased monitoring / escalation)
• 3 in a single parameter - minmum 1 hourly - (medical team to be informed and should review, can decide on escalation)
• 5or6 - medical team to be informed and can decide on escalation
• 7or more - medical team to be informed, at least specialist registrar level , consider HDU or ICU

Question 10

Medical emergenecy team criteria discuss different reasons to call.

WHat are they? (can split into the different parts of the ABCDE)

Answer 10

• Airway - threatened
• Breathing - all resp arrests, resp rate <5/min or >36/min
• Carciulation - all cardiac arrests, 40>HR<140 or SBP <90
• Disability/neurology - sudden decrease in level of consciousness, decrease in GCS of >2 ppoints, repeated/prolonged seizures
• Exposure - any patient causing concern who does not fit above criteria

Question 11

Use the ABCDE approach to assess and treat the deteriorating or critically ill patient. Do a complete initial assessment and re-assess regularly. Call for appropriate help early and use all members of the team.

How long should the initial look, listen and feel take?

Answer 11

The initial look listen and feel should take no longer than 10 seconds in a patient who is unresponsive and will often indicate if the patient is critically ill

You can feel for a pulse to check if it is solely a repsiratory arrest -

Question 12

What does surgical emphysema or cepitus in the chest wall suggest until proven otherwise?

Answer 12

A pneumothorax (obviously can also get it with Boerhaave’s)

Question 13

What coould suggest hypovalaemia on quick assessment of the unwell patient?

How do you measure capillary refill time?
What does prolonged CRT suggest? What can affect it?

Answer 13

Hands/digits - are they blue/pink/pale/mottled. Are they cool or warm.

CRT - apply cutaneous pressure for 5s with enough pressure to cause blanching - press on sternum for central CRT or on a finger tip at hear level for peripheral |CRT

Normal is <2 seconds.
Proloned suggest poor perfusion. Cold surroundings, poor light and old age can prolong CRT

Question 14

What are the KDIGO stages of acute kidney injury? (describe bopth serum creatinine and urine output)

Ooliguira is a sign of low cardiac output

Answer 14

Question 15

If there are symptoms and signs of cardiac failure - dyspnoea, increased heart rate, raised JVP, a third heart sound and pulmonary crackles on auscultation, how should you change your fluid management of the acutely unwell patient?

Answer 15

Decrease fluid infusion rate or stop the fluid altogether - seek alternative means of improving tissue perfusion eg inotropes or vasopressors

Question 16

During the acute phase of STEMI, there is a substantial risk of ventricular tachycardia , ventricular fibrillation and sudden death.

Do not wait for confirmation of elevated troponin to make initialy diagnosis if ECG and symptoms are suggestive.

What is the inital treatment if suspecting a STEMI in GGC?

Answer 16

Morphine IV 10mg +Metoclopramide IV 10mg Oxygen if O2 <94%, GTN spray 2 puffs sublingual, Aspirin 300mg oral, Tricagrelor 180mg oral

+/- fondaprinux 2.5mg SC (or heparin IV 5000units)

Question 17

What are the two cardiac specific tropnonins? What is the other troponin?

Answer 17

• There is Troponin C - calcium binding site (pulls troponin tropmyosin complex apart exposing actin filaments for actin-myosin cross bridge linking) - identical in heart and skeletal muscle
• TROPNIN I (inhibits actin-myosin interactions) and
• TROPONIN T (facilitates contraction) are the cardiac specific troponin isoforms

Question 18

What on an echo could indiccate the likelihood of an ACS?

Answer 18

Echo - left ventircular systolic function is directly related to prognosis. IN patient with acute chest pain - regional wall motion abnormalities increases the likelihood of ACS - but are not diagnostic

Question 19

Adenosine-diphosphate (ADP) receptor antagonists (aka P2Y12 receptor antagonists) are drugs which prevent the aggregation (‘clumping’) of platelets and consequently reduce the formation of blood clots.

They include clopidogrel, prasgruel and ticagrelor

If considering PPCI for STEMI, one of the above should be given in addition to 300mg aspirin. What are the doses of the above drugs?

Answer 19

Clopidogrel - should be 600mg
Prasgruel 60mg (if not >75 years or <60kg, history of bleeding or stroke)
Ticagrelor 180mg

Question 20

For patients presenting with STEMI, within 12 h of symptoms onset, mechanical (eg PCI) or pharmacological (thrombolysis) reperfusion must be achieved without delay

What is the preferred method revasuclarisation and when can it be carried out? What is the alternative?

Answer 20

Preferred method revascularisation is primary PCI with angiographic identification
* Should be offered to all patients who present within 12 hours of symptoms onset and who can be transferred to a primary PCI centre within 120 minutes of STEMI diagnosis
* If patient presents within 12 hours and cannot be transferred to a primary PCI centre within 120 minutes of diagnosis, they should recieve thrombolysis

Question 21

In patients who cannot make the PCI, and are given thrombolysis instead, when shold you re-record a 12-lead ECG to check for resolution of ST segment elevation?
What do you do if they havent resovled?

Answer 21

Re-check ECG in 60-90 minutes
If successful, still transfer to CCU if not alreay
If unsuccessful, transfer immediately to cardiac cath lab for coronary angiography + PCI - rescue PCI

Question 22

What is the rhythym that is seen commonly and transiently after reperfusion of a previously occluded coronary artery?

Answer 22

This is an accelrated idioventricular rhythm - usually transient, no haemodynamic compromise caused and require no treatment

Question 23

In some people, cardiac arrest in VF or pVT may be the presenting feature of ACS. If return of ROSC is achieved, record a 12 lead ECG as soon as possible. If this shows evidence of STEMI, emergency re-perfusion may be needed.

• If a ventricular arrythmia occurs within 24-48 hours of a confirmed ACS, would an implanatable cardioverter-defibrillator be indicated?
• If a sustained ventricular arrythmia occurs more than 24-48 hours of a confirmed ACS, would an implanatable cardioverter-defibrillator be indicated?

Answer 23

• Within 24-48 hours of ACS - ICD is not indicated for a ventircular arrythmia unless the patient has peristently severely impaired LV function for at least 4 weeks post ACS
• Sustained ventricular arrythmia occuring more than 24-48 hours after an ACS - ICD is usually recommended unless the arrythmia was associated with signifcant myocardial sichaemia which can be reverse without vascularisation

if the ventricular arrythmia occurs without evidence of severe ischaemia, refer to heart rhythm specialist as they will be at risk of recurrent ventricular arrythmia and need be assessed for insertion of ICD priore to discharge

Question 24

If AV block occurs in the context of an inferior acute myocardial infection, there is often transient dysfunction of conducting system and excessive vagal activity. How would symptomatic bradycardia be treated?

Answer 24

Treat with atropine
If resistant to atropine, can try temporary cardiac pacing (permanent not usually needed)

Question 25

What should be given for symptomatic management of heart failure complication AMI or other ACS?

Answer 25

Give a loop diuretic eg furosmide and/or GTN spray for immediate symptomatic relief then continue maintenance loop diuretic. Give the other secondary prevention drugs (Statin, aspirin, beta blocker, ace +/- secondary anti-thrombotic) If LVSD <40%, aldosterone receptor antagonist

Question 26

If an in-hospital cardiac arrest takes place. How soon should defibrillation be attempted if indicated?

Answer 26

Attempt defirbillation within 3 minutes

Question 27

Where is the best location for CPR? How deep are compressions and at what rate? What rate are rescue breaths given once tracheal intubation has been succeeded?

Answer 27

Middle of lower half of the sternum Depth of 5-6cm Rate of 100-120 compressions /min (30compressions to 2 rescue breaths) Rescue breaths given at 10 breaths per minute once the trachea has been intubated

Question 28

If the patient has a monitored and witnessed cardiac arrest in the cath lab, CCU or cirticcal area area or whilst monitored after cardiac surgery and a manual defibrillator is rapidly available, you can give stacked shocks if in a shockable rhythm. How many shocks is this? Do you do CPR between shocks? What do you do after these shocks if still in arrest? What do these three shocks count as in the ALS algorithm?

Answer 28

* If a monitored and witness cardiac arrest with a manual defibrillator available, you can give three quick successive (stacked shocks). Rapdily check for a rhythm change and if appropriate pulse or other signs of ROSC after each attempt * Do not do CPR between attempts * If still in arrest, start CPR for 2 minutes as per ALS algorithm * The three shocks are considere as giving the first shock in the ALS algorithm

Question 29

When would you give adrenaline / amiodarone after stacked shocks?

Answer 29

Three stacked shocks counts as first initial shock in ALS algorithm - give adrenaline after 3rd shock in ALS algorithm Amiodraone is given after three shock attempts irrespective of when they are given during the cardiac arrest - ie give amioraone during the 2 min of CPR after the three stacked-shock attemps

Question 30

If the three stacked shocks have been given in the post cardiac srgery setting, what should then be prepared for as you conitnue CPR?

Answer 30

Emergency resternotomy should be prepated for

Question 31

When would you ever consider a precordial thump? Very low success rates and therefore routine use is not recommended

Answer 31

A precordial thump rarely works and must not delay calling for help or accessing a defibrillator. Consider only when it can be used without delay whilst awaiting the arrival of a defibrillator in a monitored VF/pVT arrest Use ulnar edge of tightly clenched fist to delvier sharp impact to lower have of the sternum from approx height of 20cm then retract fist immediately - creats impulse like stimulus

Question 32

Whcih is more important for contributing to improved survival after cardiac arrest Prompt and effective bystander CPR, uninterrupted high quality chest compressions and early defib for VF/pVT or drugs and advanced airways?

Answer 32

Prompt and effective bystander CPR, uninterrupted high quality chest compressions and early defib for VF/pVT are the most important

Question 33

Where on the body are the defib pads placed?

Answer 33

One below the right clavicle and the other in the V6 position, midaxillary line on the left side

Question 34

After the intiial check for signs of life prior to initial defibrillation, when should you next manually check for signs life? (if signs of ROSC, start post-resuscitation care)

Answer 34

After giving the 3rd shock in shockable rhythm continue immediately CPR for 2 mins before next pulse check Check for a pulse in non-shockable rhythm if changes on the ECG show a rhythm compatible with life or if symptoms of ROSC

Question 35

Describe fully what you would do in shockable rhythm?

Answer 35

ALS Algorithm shockable * Once defib ready, immeidately give shock then immediate CPR for 2 mins before re-checking * If remaining in VF/pVT, continue shocks every 2 minutes * After 3rd shock, give 1mg IV adrenaline (1:10,000) and amiodarone 300mg IV * Give further 1mg IV adrenaline every 3-5 minutes (alternate cycles) * A further 150mg of IV amiodarone may be given after a total of 5 defibrillation attempts

Question 36

What is an alternative to amiodarone for shockable rhythms?

Answer 36

* Lidocaine 100 mg IV (IO) may be used as an alternative if amiodarone is not available or a local decision has been made to use lidocaine instead of amiodarone. * An additional bolus of lidocaine 50 mg can also be given after five defibrillation attempts.

Question 37

Describe fully what you would do in non-schockable rhythm?

Answer 37

* Give 1mg IV adrenaline (1:10,000 = 1g in 10,000ml, = 1000mg in 10,000ml = 1mg in 10ml) as soon as IV access achieved * Re-check the rhythm every 2 minutes - if electrical activity compatible with a pulse, check for pulse and/or signs of life. If neither conitnue CPR and reheck rhythm every 2 minutes again * Give further 1mg IV adrenaline every 3-5 minutes (alternate cycles)

Question 38

What must drugs injected peripherally be followed with?

Answer 38

Must be followed with at least 20ml of fluid and elevation fo the extemrity for 10-20seconds to facilitate delivery to the central circulation - can hang up a 500ml bag of saline during arrest to provide this

Question 39

Even if the defibrillation attempt is successful in restoring a perfusing rhythm, it is very rare for a pulse to be palpapble immediately after defib, how long can it take?

Answer 39

Return of a palpable pulse may be longer than 2 min in as many as 25% of successful shocks * Delay in trying to palpate a pulse with further compromise the myocardium if a perfusing rhythm has not beenr estored * If a perfusing rhythm has been restored, giving chest compressions does not increase chance of VF re-occuring

Question 40

Important in shock-refractory VF/pVT to check position and contact of defib pads. How long is it usually considered worthwhile continuing resuscitation for?

Answer 40

Usually as long as the patient remains in identifiable Vf/pVT. Generally accepted asystole for more than 20 minutes in the absence of a reversible cause constitutes grounds for stopping Can consider changing pad position in refractory VF/pVT from anterior-lateral to anterior-posterior

Question 41

If a rhythm that is compatible with life shows, try to palpate for central pulse and look for other evidence of ROSC. What is other evidence of ROSC? What is the normal end tidal CO2 range?

Answer 41

ROSC - sudden increase in end-tidal CO2 (normal range is 4.3-5.5 - normal is 4.8) Evidence of cardiac output Any invasive monitring rquipment When the normal end tidal CO2 is seen or when a patient starts displaying signs of life, chest compressions should be paused and patient should be reassessed.

Question 42

If during CPR, the underlying rhythm on the monitor displays VF, should you attempt defib at this stage?

Answer 42

If the monitor displays VF int he middle of a CPR 2 min cycle, continue CPR until the 2 minute rhythm check period

Question 43

Continue 30:2 chest compressions until the airway is secured. What is the ideal method of securing the airway? What can be used in the absence of personal skilled in this method?

Answer 43

Ideal method is using a cuffed endotracheal tube In the absence of this, a bag mask or preferably, a supraglotttic ariway (SGA) eg i-gel is used. Can now attempt to devler continuous chest compressions, uninterrupted during ventilation - 10 breaths / min

Question 44

Waveform capnography during PCR has an important role. Which airway tube does it work most reliably with and who can it be used with ? WHat is its role?

Answer 44

Works most reliably in patients with a tracheal tube - can be sued wtih supraglottic airway device or bag mask Role- ensures travheal tube placement in trachea, monitoring ventilation during CPR, quality of chest compressions, idnetifying rosc, prongosis (lower end-tidal volume has increasied mortality)

Question 45

What is the normal end-tidal CO2? How would you help clarif that the tracheal tube is situated correctly?

Answer 45

Normal - 4.3-5.5 (normal is 4.8kPa) Observation and auscultation to ensure both lungs are ventiliating and eg tube hasnt passed into a bronchus

Question 46

If rapid IV access if difficult or imporrible, consider IO route. WHat are the three main sites for access? WHat are contraindications?

Answer 46

Sites - proximal humerus, proximal tibia and distal tibia Contraindication - truma, infection or a prosthesis at target site, recent IO access within prev 48 hours in same limp incl failed attmept - failure to identify landmarks

Question 47

Again, state the 4Hs and 4Ts

Answer 47

Hypoxia Hypovalaemia - may not be obvious eg GI bleeding or ruptured AAA Hypo/hyperkalaemia, hypoglycamiea, metabolic disorder Hypo/hyperthermia Thrombosis - conroary or pulmonary Tensions pneumothorax Tamponade Toxins

Question 48

If a fibrinolytic drug is given during CPR for a suspected PE, how long should you consider preforming CPR for before stopping?

Answer 48

Consider CPR for 60-90 minutes

Question 49

How long should you observe the patient after stopping CPR before confirming death?

Answer 49

Minimum of 5 minutes

Question 50

What is the commonest site of airway obstruction? What is the comonest in trauma?

Answer 50

Commonest site of airway obstruction is the soft palate and epiglottis rather than the tongue The commonest cause of airway obstruction in trauma is the loss of pharyngeal tone with posterior tongue displacement

Question 51

Complete airway obstructin - often see paradoxical chest and abdo movements - known as see-saw breathing In partial airway obstruction, air entry is diminsihed and usually nosy Where do the following noises heard suggest the obstruction is occurrign: * Inspiratory stridor * Expiratory wheeze * Gurgling * Snoring

Answer 51

* Inspiratory stridor - laryngeal level or above * Expiratory wheeze - lower airways which tend to collapse and obstruct during expiration * Gurgling - presence of liquid or semisolid foreign material in upper airways * Snoring - arises when pharynx is partially occluded by the gonue or palate

Question 52

What are signs of severe airway obstruction and what should you do?

Answer 52

Pt unable to speak, can only respond by nodding, unable to breathe, breathing sounds wheezy, attempts at coughing are silent, may be unconscious Give 5 back blows - between scapula with heel of hand Give 5 abdominal thrusts Continue to alternate if no success If becomes unconscious, call arrest team and start CPR

Question 53

How would you attempt to remove a foreign body in a chocking unconscious patient?

Answer 53

If back blows/abdo thrusts failed, start CPR ONce a trained pro arrives, use laryngoscopy + Magill's forceps

Question 54

There are basic airway manoevures as well as airway technique for herlping to increase oxygenation. Artificial ventilation is started as soon as possible in patients whom spontenous ventilation is inadequate or asbent. If a self-inflation bag (non rebreather, resevoir bag) is attached directly to high fllow oxygen as well as a reservoir system, what is the percentage of inspired oxygen?

Answer 54

Approx 85%

Question 55

In comparison with bag-mask ventilation, use of SGAs (supraglottic airways) may enable more effective ventilation and reduce the risk of gastric inflation (reduces risk of regurgitation and pulmonary aspiratiomn) Try to maintain chest compressions throighout. If it is necessary to stop, how long should this pause take? What size will suit most adults? What should you do before inserting the igel?

Answer 55

If it is necessary tos top to insert the i-gel, limit the pause to compression to max 5s Size 4 will suit most adults Before inserting - lubricate the front, back and sides

Question 56

What position should the patient be for igel insertion?

Answer 56

Sniffing the mornig air position - neck flexed and head extended

Question 57

How do you know how deep to insert the i-gel?

Answer 57

Should feel a defintive resistance on insertion - at this point the tip of the airway should be loacted at uppe roseophageal opening and cuff should be klocated against the larynx - the incisors should be resting on the integral bite-block - where a horizontal line is present as a guide

Question 58

What does expert consensus define the skill threshold for tracheal tube insertion? How do you confirm placement of tracheal tube?

Answer 58

95% success rates with up to two intubation attempts Confirm placement with both clinical assessment (observation/auscutation of lungs, auscultate over epigastric area also - should not hear breath sounds) and waveform capnography - studies show this is both 100% sensitive and 100% specific for correctly placed cuffed endotracheal tube

Question 59

What does failure to detect any exhaled CO2 by the waveform capnography suggest?

Answer 59

This would suggest the tube is in the oesophagus - No trace - Wrong Place

Question 60

If a person's ECG displays VF requiring immediate defib and they are conscious or have a pulse, is it VFib?

Answer 60

No the rhythm must be artefact

Question 61

Which rhthm displays capture and fusion beats? How do these occur?

Answer 61

This would be monomorphic VT Atrial activity may continue independently of ventricular activity leading to caputr and fusion beats Capture beat- single normal looking QRS without interrupting the arrythmia Fusion beat - wave of depolarisation from AV node occurs at the same time as a wave of depolarisation travelling up from ventricle causing a hybdrid QRS

Question 62

Rhythms that can mimic VF include polymorphic VT and AFib with abberancy * Atrial fibrillation in the presence of either bundle branch block or pre-excitation (accessory pathway) will result in an irregular wide complex tachycardia It is important to identify polymorphic VT. How are these patients treated? What is this rhythm also known as?

Answer 62

Poolymorphic VT eg Torsades de Pointes Treated with IV magnesium 2g over 10 minutes May also require potassium as many patients are hypokalaemia and/or hypomagnaesamic

Question 63

Peri-arrest arrythmias are defined according to heart rate - bradyarrythmia, tachyarrythmia or arrythmia with a normal heart rate. What is bradyarrythmia defined as? When can it be considered physiological? What is the emergency treatment?

Answer 63

Bradyarrythmia is defined as resting heart rate of <60 / min Can be physiological in athletes or during sleep If associated with life threatneing signs - atropine 500mcg IV and /or cardiac pacing

Question 64

Peri-arrest arrythmias include bradyarrythmia, tachyarryhmia, Aflutter/Afib, Heart block Describe the different types of heart block

Answer 64

* 1st degree heart block - PR interval consistently >0.2 seconds * Mobitz type I AV block (aka second degree aka Wenckebach) - progressive prolongation of PR interval until a p-wave occurs without a resulting QRS complex * Mobitz type 2 AV block - constant PR interval (often prolonged) but some p-waves are not followed by QRS complexes - can occur randomly without any consistent pattern * Third degree AV block (aka complete heart block) - no relationship between p-waves and QRS complexes - atrial and ventircular depolarisation arising from separate pacemakers

Question 65

* 1st degree heart block - PR interval consistently >0.2 seconds * Mobitz type I AV block (aka second degree aka Wenckebach) - progressive prolongation of PR interval until a p-wave occurs without a resulting QRS complex * Mobitz type 2 AV block - constant PR interval (often prolonged) but some p-waves are not followed by QRS complexes - can occur randomly without any consistent pattern * Third degree AV block (aka complete heart block) - no relationship between p-waves and QRS complexes - atrial and ventircular depolarisation arising from separate pacemakers Which require treamtnet? Which are at danger of progressing to complete heartblock>

Answer 65

1st degree - rarely causes any symptoms and rarely requires treatment Mobitz type 1- need for treatment determined by effect of the bradyarrythmia Mobitz type 2 - always pathological, requires treatment and at risk of progression to complete heart block and asystole Complete heart block - may require immediate treatment

Question 66

What is an agonal rhythm?

Answer 66

Agonal rhythm occurs in dying patients. Slow irregular wide ventricular complexes - doesnt usually generate a palpable pulse - usually seen in latter stages of unsuccessful resuscitation attempts

Question 67

Narrow complex tachycardias arise above the bundle of HIS - termed supraventircular. Where can broad complex tachycardias originate?

Answer 67

A tachyardia arising in the ventricle or A supraventricular tachycardia conducted abberantly (right or left bundle branch block) to the ventricles

Question 68

What is the safest approach for treating all broad complex tachycardias as?

Answer 68

Treat all broad complex tachycardias as ventricular tachycardia unless there is good evidence to suggest it is supraventricular in origin

Question 69

Why is a QTc >0.5 seconds worrying? What is the target QTc in men and women?

Answer 69

QTc>0.5seconds indicates a high risk of cardiac arrest and sudden death. Prolongation predisposes to ventricular arrythmia, in particular TdP and VF QTc men <0.44, QTc women <0.46

Question 70

How far away should the defib electrodes be placed away from an implnatable medical device?

Answer 70

At least 10-15cm away from the device

Question 71

What is successful defibrillation defined as?

Answer 71

Successfull defibrillation is defined as the absecne of VF/pVT at 5s after shock delivery Remember to keep immediate CPR post-shock delivery until the post-shock circulation is established (the duration of asystole before ROSC can be longer than 2 min in as many as 25% of successful shocks)

Question 72

In an oxygen-enriched atmosphere, sparking from poorly applied defibrillator paddles can cause a fire and significant burns to the patient. The use of the self-adhesive electrodes if far less likely to cause sparks than manual paddles. What is good practice for safe use of oxgen during defibrillation When it comes to oxygen mask/nasal cannulae? When it comes to ventilation bag connected to a tracheal tube or supraglottic away?

Answer 72

Oxygen mask/nasal cannulae - remove and take at least 1m away from patient Leave the ventilation bag connected to tracheal tube or supraglottic airway device - no increase in O2 occurs in the zone of defib as this is a sealed circuti Alternatively, can disconnect the ventilation bag from the tube/SGA device and remove it at least 1m from the patients chest during def

Question 73

What is the difference between synchronous and asynchronous chest compressions? Which is preferred?

Answer 73

During cardiopulmonary resuscitation (CPR), the need to interrupt chest compressions to provide synchronous ventilations prevents blood flow continuity, reducing the possibility to ensure high-quality CPR bundles of care and, thus, having a potentially negative impact on perfusion and patient outcome. a strategy of continuous compressions with “asynchronous” ventilations during CPR in patients with an advanced airway, that is, breaths interposed every six seconds without interruption in CPR—OR 10 breaths/minute without stopping CPR - this can hopefully prevent the negative effects of stopping for synchronous ventilation

Question 74

In the community, automated external defibrillation (AEDs) are used to carry out defibrillation Are AEDs or mannual defib preferred in hospital and why?

Answer 74

In hospitals, where there is rapid access to manual defibs and trained staff are present, use a manual defib- they enable the operator to diagnose the ryhthm and deliver a shock rapidly without having to wait for rhythm anyalysis and this minimises the interruption in chest compressions

Question 75

Is defibrillation in cardiac arrest asynchronous or synchronous? When would you use the other?

Answer 75

Defibrillation in cardiac arrest uses asynchronous cardioverison Defibrillation or unsynchronized cardioversion is indicated in any patient with pulseless VT/VF or unstable polymorphic VT, where synchronized cardioversion is not possible. Synchronized cardioversion is utilized for the treatment of persistent unstable tachyarrhythmia (atrial or ventricular) in patients without loss of pulse

Question 76

Why is synchronised cardioverson important in atrial/ventricular cardioverson? WHat is the shock syncrhonised with? Can it be carried out when the patient is conscious?

Answer 76

It is important to carry out synchronous cardioversion with the R wave of the ECG - by avoiding the relative refractory period in this way, the risk of inducing VF is minmised Conscious patients must be anaesthetised or sedated prior to attmepting synchronise cardioversion

Question 77

What is the difference between absolute refractory period and relative refractory period?

Answer 77

During the absolute refractory period, a second stimulus (no matter how strong) will not excite the neuron. During the relative refractory period, a stronger than normal stimulus is needed to elicit neuronal excitation. Therefore cardioversion in the RRP could cause Vfib - hence avoided by syncing with R waves Most manual defibs incorporate a switch that enables the shock to be triggered by the R wave on the electrocardiogram- the operator should anticipate the slight delay between pressing the buttons and the discharge of the hshock when the next r wave occurs

Question 78

If the patient has an implanted electronic device, choose the position for the defibrillator electrode placement carefully. Usually cardiac pacemakers and Implantable cardioverter-defibrilators are implanted in the pectoral region, more commonly on the left side rather than the right side An implantable ICD gives no warning when delivering a shock WHat dose will be discharge from an ICD when detecting a shockable rhythm?

Answer 78

ICD will discharge approximately 40J (approximately 80J for subcutaneous devices) through an internal pacing wire embedded in the right ventricle - will often fire up to 8 shocks

Question 79

How can you disable an ICD? Will deactivation of this disable the ability to act as a pacemaker if it has this function?

Answer 79

A ring magnet placed over the ICD will disable the defibrillation function. Decativation of the ICD in thi way does not disable to the ability of the device to act as a pacemaker if it has this function

Question 80

Any cardiac tissue that has the ability of generating an electrical signal without any external stimulus is capable of initiating a heartbeat and behaving as a 'pacemaker'. This is known as automaticity. The fastest 'pacemaker' will generate the cardiac rhythm and slower natural pacemakers will only take over if the faster ones slow down or stop working. What is the intrinsic rate of the cells at the SA node, AV node (junctional region) and Distal His-Purkinje fibres?

Answer 80

SA node - 60-70 / min AV node - 40-50 /min DIstal purkinje fibres (ventircular in orgiign) - 0-30/min

Question 81

Broad complex CHB requires pacing and the occurence of long ventricular pauses makes this urgent How long are ventricular pauses that makes this urgent?

Answer 81

Ventiruclar pauses >3 seconds

Question 82

In the peri-arrest setting, pacemakers are use when heart rate is too slow/unreliable and not respondinng to treatmment algorithm for bradycardia In the setting of cardiac arrest, what makes tje heart more likely to respond to pacing stimulus?

Answer 82

The presence of P-waves

Question 83

If pacing stimulus induces an immediate QRS complex this is referred to as a capture - check to make sure the acitivty seenon ECG is accompanied by mechanical activity that produces a pulse WHat are the methods of pacing?

Answer 83

Non invasive- * Percussion pacing - fist pacing * Transcutaneous pacing Invasive * Temproary transvenous pacing (internal temporary transvenous / externlaised permanaenet transvenous, endocardial systems or surgical epicardial systems) * Permanant pacing - using an implanted pacemaker

Question 84

Percussion pacing is a precordial thump. When can you consider trying this? If it does not result in regular pulse promptly regardless of generating QRS complexes, what should be started?

Answer 84

Conssider trying percussion pacing when the bradycardia is so profound that is causes clinical cardiac arrest If this fails to generate QRS complex, start CPR immediately

Question 85

Advantages of transcutaneous pacing - can be established very quickly, widely aviialbly, easy to perform and minimum training, can be initiating by healthcare providers while waiting for expert help to estblish transvenous pacing What is its disadvantage?

Answer 85

Transcutaneous pacing - doesnt provide reliable ventricular stimulation and causes a lot of discomfort in a conscious patient

Question 86

How would you set up transcutaneous pacing?

Answer 86

Apply electrode pads in conentrial anterior-lateral position on chest (one over right pectoral muscle below right clavicle and one overlying V6 electrode position in left mid-axillary line) Select an approrpiate pacing rate on the machine - usually between 60-90 bpm for most adults Should see a pacing spike on the ECG

Question 87

How would you be able to tell if the trancutaneous pacing is working?

Answer 87

With each increase in the ouput of the pacing, the muscle of the chest wall will contract and a pacing spike will appear on ECG Increase the current until the spike is immediatedly followed by a QRS complex - if the QRS complex is followed by a T wave, this shows capture capture and indicated depolarisation of a ventricle If the QRS complex is not followed by a twave, this is likely artefact

Question 88

What current does capture typically occur with? What may make transcutaneous pacing more challenging?

Answer 88

50-100mA typically will allow for capture Transcutaneous pacing made more challneging in patients with hyperkalaemia and who are moving

Question 89

Non-invasive pacing can be delivered by an ALS provider and is the immediate treatment for svere bradyarrythmia that is a potential risk to a patient who does not respond to initial drug treatment Is this a temporary or pemanent solution?

Answer 89

Non-invasive pacing (can attempt percussion if arrest, if bradyarrythmia not responding to drug treatment, try transvenous pacing) Non invasive pacing is a temporary , emergency measure to be used briefly until either stable and effective spontaneous rhythm returns or a competent person establishes transvenous pacing

Question 90

When a person dies with an active ICD in place, what should you arrange for?

Answer 90

Arrange for deactiveation - usually done by a cardiac physiologist ICD must be deactivated prior to its removal from the body or performance of an autopsy Any implantated electronic devices (including pacemakers, ICD, evenet (loop) recorders and neurostimulators) must be removed prior to cremation

Question 91

Arrythmias can occur without causing cardiac arrest - many are a common complication of myocardial infarction as well as in people with other cardiac abnroamities. Some require no treatment. Arrythmias that occur after initial resuscitation indicate that the condition is still unstable Arrythmias can be classified broadly as - tachyarrythmias, bradyarythmias and arrythmias with normal heart rate What is the normal assessment that should taken in all patients with an arrythmia?

Answer 91

ABCDE Obviously if arrested, CPR

Question 92

Important to document in patients with arrythmia or suspected arrythmia - condition of patient (ie presence or absence of adverse features), heart rate, nature of arrythmia What are the different adverse features (aka life threatening feature) to watch out for which may indicated need for immediate treatment?

Answer 92

Adverse features * Shock - hypotension (SBP <90), pallor, sweating, cold extremities, confusion or imparired consciousness * Syncope * Severe heart failure - pulmonary oedema and /or raised JVP * Myocardial ischaemia - typical ischaemic chest pain Can consider extremes of heart rate as a possible life threatening feature also

Question 93

WHat are the extremes of heart rate that can be considered as life threatening feature?

Answer 93

Extreme tachycardia - eg >150min. Extreme bradycardia - eg <40/min

Question 94

Most drugs act more slowly and less reliably than electrical treatments, so electrical treatments are usually preferred treatment for an unstable patient with life-threatening features TACHYARRYTHMIA What is the initial management if a tachyarrythmia showing life threatneing features? WHat if this does not work?

Answer 94

Synchronised DC shock up to 3 attempts (sedation or anaesthesia if conscious) If unsuccessful - give amiodoraone 300mg IV over 10-20min and attempt further synchronised cardioversion

Question 95

What setting (Joules) should be given in an arrest? What setting should be given in broad-complex tachycardia with life threatening features? What setting should be tried if the rhythm is AF with life threatening features? What setting should be tried if the rhythm is a regular narrow complex tachycardia with life threatening features?

Answer 95

Arrest - start with 120-150Joules and increase in increments Broad complex tachycardia with life threatening featurex- 120-150J and increase in increments AF with life threatening features - start at max defibrillator output Regular narrow complex tachycardia with life threatening features - often terminated by lower-energy shocks - 70-120Joules

Question 96

The loading dose of 300mg IV amiodarone over 10-20 min can be followed by an infusion What is the dose of this infusion over 24 hours?

Answer 96

Can give an amiodarone infusion of 900mg over 24 hours - given into alarge vein (preferably via central venous catheter)

Question 97

REGULAR BROAD COMPLEX TACHARRYTHMIA If the person has no life threatening features, consider firstly whether or not any treatment is necessary. In a tachyarrythmia, what is the QRS decision for treating as supra ventricular or ventricular? What are the treatment options for regular broad QRS? WHat if first line treamtent is ineffective?

Answer 97

QRS < 0.12 - narrow complex QRS >/= 0.12 = broad complex Regular broad complex - if VT or uncertain - amiodarone 300mg IV over 10-60 minutes - if successful give amiodarone 900mg over 24 hours (if previous certain diagnosis of SVT with abberancy - treat as narrow complex) If amiodarone is ineffetive, synchronised DC shock up to 3 attempts (sedation or anaesthesia if conscious)

Question 98

IRREGULAR BROAD COMPLEX TACHYARYTHMIA What are the treatment options for irregular broad QRS?

Answer 98

If AF with abberancy, treat as irregular narrow complex If polymoprhic VT (eg Torsades de Pointes) - give IV magnesium 2g over 10minutes, correct any electrolyte abnromalities especially hypokalaemia

Question 99

REGULAR NARROW COMPLEX TACHYARRYTHMIA What are the treatment options for regular narrow QRS in the absence of life threatening features? WHat if first line treamtent is ineffective? What should be carried out during each attempted treatment?

Answer 99

Initially trial vagal manoevures - carotid massage, valsalva maneouvure - will terminate up to a quarter of episodes of paroxysmal SVT If this fails - give adneosine, 6mg rapid boolus followed by 12mg followed by 18mg each time followed with a flush - warn patient of potential unwell feeling and chest discomfort Record a 12-lead ECG during the manoeuvures/treatment - can help to look for atrial activity eg reveal an atrial flutter

Question 100

If the vagal maneovures and adenosine fail to terminate th tachycarruthmia or adenosie is contraindicated Name when adenosine may be contraindicated? What alternative medications can be tried?

Answer 100

Contrainidcated in eg asthma, COPD, decompensated heart failure; long QT syndrome; second- or third-degree AV block and sick sinus syndrome (unless pacemaker fitted); severe hypotension Consider giving - verapamil - 2.5-5mg IV over 2 mins or a beta-blocker eg metoprolol 2.5-15mg given IV in 2.5mg bolus doses

Question 101

What is the treatment of rapid narrow complex-tachycardia with no pulse and unconscioius?

Answer 101

This would be pulseless electrical activity - start CPR

Question 102

If adenosine has failed to terminate the regular narrow complex tachycardia and verapamil or beta blocker have failed, what should be done?

Answer 102

Cnsider synchronised DC shock up to 3 attempts (rememebr 70-120 Joules for narrow complex)

Question 103

IRREGULAR NARROW COMPLEX TACHYCARDIA If no life threatneing features of tachyarrythmia, what is offered for rate control? When would you consider cardioversion?

Answer 103

Rate control of AF - trial beta blocker - dilitiazem if contraindication * Can given digoxin instead if heart failure Consider cardioversion (electrical or chemical) if within first 48 hours (anticoagulate before) If in AF >48 hours, will need 3 weeks of anti-coagulation prior to cardioversion (electrical or chemical Magnesium 2g 50% IV over 10minutes often given for rate control but the data supporitng this is limited

Question 104

In general, patients who have been in AF for longer than 48 h should not be treated by cardioversion (electrical or chemical) until they have been fully anticoagulated for at least 3 weeks, or unless transoesophageal echocardiography has detected no evidence of atrial thrombus. If the clincla situation dictates that cardioversion is needed more urgently in AFib (ie life threatening features), how should this be treated?

Answer 104

If cardioversion is needed more urgently, give: * EITHER regular low-molecular-weight heparin in therapeutic dose * OR an IV bolus of unfractionated heparin followed by a continuous infusion to maintain the activated partial thromboplastin time (APTT) at 1.5-2.0 times the control value Give maximum defibrillator output Joules for AFib * Continue heparin therapy and commence oral anticoagulation after successful cardioversion. * * Seek expert advice on the duration of anticoagulation, which should be a minimum of 4 weeks, but substantially longer treatment is required in many cases.

Question 105

For patients with atrial flutter or atrial fibrillation, how should the pads be situated for cardioversion?

Answer 105

For patients who are in atrial fibrillation or atrial flutter, use anteroposterior self-adhesive pad positions when it is practical to do so.

Question 106

BRADYARRYTHMIA if the patient has evidence of life threatening signs (eg shock, syncope, severe heart failure of myocardial ischaemia) What is first line treatment and what is carried out if unsatisfactory response?

Answer 106

Atropine - 500micrograms IV If unsatisfactory response - can contuinue 500micrograms IV every 3-5 minutes to max of 3mg

Question 107

If bradycardia with adverse signs, despite atropine, what can be cosndieered? What if this is not available?

Answer 107

If not respoinsive to atropine - should arrange pacing, transcutaneous pacing until transvenous pacing can be arranged If no pacing available, consider second line drugs incl isoprenaline at 5micrograms/min IV or adrenaline 2-10micrograms /min IV

Question 108

If the bradycardiac patient is not at risk of life threatening features, what are the choices?

Answer 108

If at risk of asystole - ie recent asystole, mobitz II block, complete heart block with broad QRS or ventricular pause>3 seconds, give atropine If not at risk of asystole - then observe

Question 109

What should be used if the overdose is secondary to beta blocker or calciumm gluconate overdose?

Answer 109

IV glucagon

Question 110

If there is a delay in waiting for transcutaneous pacing in a patient with the presence of life threatneing extreme bradycardia, percusssion pacing can be an option How is this achieved and at what rate?

Answer 110

Percussion pacing - repeated rhythmic thumps from 20cm in the air to lower half of sternum at a rate of 50-70 / min

Question 111

Life threatening electrolyte disorders What changes to ECG can hyperkalamia cause? How may a patient present?

Answer 111

Hyperkalaemia - tall tented T waves, prolonged PR interval (first degree heart block), absent/flat pwaves, widened QRS, ventricular tachy, bradycardia, asystole Patients can present - arrest, paraesthesia, flaccid paralysis, muscle weakness

Question 112

What is the treatment of hyperkalaemia?

Answer 112

If mild - calcium resonium 15g TDS IF ECG changes or severe >6.5 - * Protect the heart - 10ml 10% calcium gluconate over 10 mins (the ALS guidleines stated for calcium gluconate, 30ml, 10% over 15 minutes or can use calciuum chloride 10ml, 10% over 2-5 minutes) (can repeat after5 minutes if ECG changes persist) * Shift potassium into the cells - 8 units actrapid (ALS says 10 units) in 200ml 10% glucose or 100ml 20% glucose over 30 minute (ALS says 10units actrapid in 25g glucose IV by rapid injection) and can trial 5-10mg nebulised salbutamol

Question 113

How is the cardiopulmonary resusscitation steps modified when in the presence of severe hyperkaleamia?

Answer 113

* CPR is the first priority in any patient in cardiac arrest and follow the algorithm - if found to be hyperkalaemic as the cause give 10 mL 10% calcium chloride IV by rapid bolus injection to antagonise the toxic effects of hyperkalaemia at the myocardial cell membrane * sodium bicarbonate: 50 mmol IV by rapid injection (if severe acidosis or renal failure) * glucose/insulin: 10 units short-acting insulin and 25 g glucose IV by rapid injection * consider haemodialysis: this may be an option for cardiac arrest induced by hyperkalaemia which is resistant to medical treatment. * Several dialysis modes have been used safely and effectively in cardiac arrest, but this may only be available in specialist centres that offer acute renal replacement therapy in critically ill patients. Although salbutamol can be useful for patients with hyperkalaemia who still have a pulse, nebulisers cannot be easily administered during cardiac arrest.

Question 114

WHat is hypokalaemia? What is severe hypokaelamia?

Answer 114

Hypokaelamia - potassium < 3.5 Severe hypokalaemia - K < 2.5 - usually requires IV supplementation

Question 115

What are signs of hypokalaemia?? What are ECG changes? What are the treatments?

Answer 115

Signs include fatigue, muscle weakness, leg cramps, constipations ECG features - t wave flattening, pathological U waves, arrythmias, cardiac arrest Can give 20 or 40mmol KCl in 500ml saline or glucose 5% - dont usually exceed 10mmol/hour (rates above 20mmol/hour can be irritant to vessels)

Question 116

Many patients who are deficient in potassium (as well as calcium and sodium) are also deficient in magnesium as magnesium is also importatn for potassium uptake and the maintenance of intracellularpotassium values - particularly in the myocardium What is the treatment of a severe eg <0.3 or symptomatic hypomagnesaemia?

Answer 116

-give 2g 50% magnesium sulfate if severe or symptomatic

Question 117

SEPSIS WHat is the qSOFA scoring for sepsis?

Answer 117

qSOFA score - respiratory rate (RR) ≥ 22 breaths per minute, altered mentation (Glasgow Coma Scale [GCS] < 15), and systolic blood pressure (SBP) < 100 mmHg. A score of>/=2 indicates a 10% mortality risk in hospital patient

Question 118

Timely achievement of the 'hour 1' care bundle following recognition of sepsis should be sufficient to prevent organ dysfunction. What isthe sepsis 6 and what is appropriate fluid resuscitation?

Answer 118

Blood cultures, monitor Urine output hourly measurmenets, fluids, IV Abx within first hour, Lactate measurment, oxygen FLuids resuscitation - give initial 500ml bolus - max of 30ml/kg in patients with hypotensuon, serum lactate >2mmol/l or other signs of circulatory dysfunction

Question 119

Septic shock is defined as sepsis plus sign of at least one acute organ dysfunction Septic shock can also be defined based on the lactate levels and MAP How does NICE define sepsis based on these?

Answer 119

Septic shock can be defined as sepsis with * persisting hypotension despite fluid correction and inotropes (requiring vasopressors to maintain a mean arterial pressure [MAP] of 65 mmHg or more) * and hyperlactataemia with a serum lactate level of greater than 2 mmol/L (if lactate level \>4, mortality rate of 38%) (Septic shock can also be defined as sepsis with a suspected calculated mortality of over 50%)

Question 120

What are the differnet signs in sepsis following initial appropriate fluid resusc that are worrying?

Answer 120

Hypotensions, oliguira, acute confusion, lactate >2mmol/l

Question 121

Patients recieving long term haemodialysis are a high-risk group for OOH cardiac arrest - occurring up to 20 times more frequently than in the general population Risks factors in dialysis include electrolyte disturbances, fluid volume shifts and medical comorbidities How can risks of cardiac arrests be minnimised in dialysis patients?

Answer 121

Adherence to dietary and fluid restrictions and that dialysis prescriptions are carefully managed

Question 122

Resuscitation in people with dialysis should follow the standard ALS algortihm with a few modifications WHat are the modifications (this is for discussing cardiac arrest in the dialysis unit)?

Answer 122

* Assigned a trained dialysis nurse to operate the haemodialysis machine * Stop dialysis and return the patients blood volume * Disconnect from the dialysis machine - unless defib prrof in accordance with the International Electrochemical Standards * Leave dislayiss access open to use for drug administration * Dialysis may be rquired in the early post resuscitation phase * Provude prompt management of hyperkalaemia * Avoid excessive potassium and voluume shifts during dialysis

Question 123

In patients with cardiac arrest that is suspected to be secondary to toxins, you should be prepared to continue resuscitation forr a prolonged period, particulary in young patients. Why is this? What may be of assistance to help with the CPR if happening for a prolonged period?

Answer 123

Toxins may be metabolised or excreted during extended resuscitation measures Consider extracorporeal life support

Question 124

There are a few specific therapies for poisons that are useful immediately. The emphasis is on intensive supportive therapy using ABCDE approach, with correction of hypoxia, hypotensions, acid/base and electrolyte disorders . Therapies includ decontamination, limiting absorption or the use of specific antidotes. Is gastric lavage recommended for GI decontamination?

Answer 124

Gastric lavage for GI decontamination is not recommended

Question 125

What are the signs of opioid poisoning? What can be given to rapidly reverse these effects and what dose?

Answer 125

Signs - resp depression, pinpoint pupils, coma followed by resp arrest Naloxone can be given- IV/IM/SC/Intranasal can be used - if struggling with IV eg IV drug user, consider a different route Can start with 400microgramsIV naloxone, if no response, trial 800micrograms after 1 minutes

Question 126

If there are large opioid overdose, what can the total naloxone given be titrated to? When should you stop with the naloxone doses?

Answer 126

If large opioid doses are given, may require naloxone titrate up toa total of 10mg Give naloxone until the patient is breathing adequatly and has protected airway refllexes - continue need for ongoing infusion if resp rate is not maintained and long acting opioids have been ingested

Question 127

What are potential acute withdrawal signs from opioids?

Answer 127

Acute withdrawal can produce sympathetic excess - cause complications eg pulmonary oedema, ventricular arrythmia and severe agitation

Question 128

Overdose of benzos can cause loss of consciousness, resp depression and hypotension (pupils generally smaller) (very similar symptoms to opioids) What is the antidote for benzo overdose? Why is it usually not given?

Answer 128

Can trial flumazenil (comepetitive antagonist of GABA - where benzos would normally exhibit their effect) (rememebr - GABA and glycine and inhibitory neurotransmitters, glutamate is excitatory) * The specific antidote flumazenil is a potent benzodiazepine antagonist but will precipitate withdrawal symptoms in individuals who are benzodiazepine dependent and reduce the seizure threshold in those patients who have a seizure disorder or who have taken another pro-convulsant drug in overdose such as tricyclic antidepressants. * It also has a half-life which is much shorter than most benzodiazepines resulting in resedation a while after it has been given. For these reasons flumazenil is not indicated for the treatment of benzodiazepine overdose.

Question 129

Tricyclcics can also cause hypotensions, seizures, coma and life threatneing arrythmias What is the specific antidoes? What are the symptoms of tricyclic overdose (remember anticholingergic)

Answer 129

Sodium bicarbonate Hypotensiosn - exacerbated by alpha 1 receptor blockade Seziures coma Agitatation, Blurred vision, Confusion/constipation, Dry mouth, sedation/stasis of urine

Question 130

WHat is the antidote for local anaesthetic toxicity? Name the first sign you may see?

Answer 130

IV Intralipid emulsion 20% First sign - circumoral numbness, tongue paresthesia, and dizziness

Question 131

Stimulants eg cocaine and amphetamine cause sympathetic overstimulation - agitation, sympomatic tahcycardia, hypertensive crisis, myocardial ischamia with angina What is the antidote here?

Answer 131

Small doses of IV benzos are effective first line GTN can reverse cocaine induced coronary vasoconstriction

Question 132

ASTHMA Most patients who die of asthma have a combination of chronically severe asthma and one or more adverse psychological factors . What are different features of severe asthma?

Answer 132

Requiring hospitilsation or emergency care for asthma in past year Requiring three or more classes of asthma medication INcrease use and dependence of beta 2 agonists History of near fatal asthma requiring intuubation and mechanical ventilation]

Question 133

Cardiac arrest in a patient with asthma is often a terminal event after a period of hypoxaemia. Cardiac arrest in patients with asthma has been linked to several different methods Try and name 2 (there are 4)

Answer 133

* Linked to severe bronchosopasm and mucous pluggin leading to asphyxia * Cardiac arrythmias caused by hypoxia * Dynamic hyperinflation (autopositive end-expiratory pressure (auto-PEEP)) - can occur in mechanically ventilated patients with asthma. Caused by air trapping and breath stacking, gradual build up of pressure occurs and reduces venous return and BP * Tension pneumothorax- occasionally bilateral

Question 134

What are life threatening features of asthma?

Answer 134

A CHEST * Arrhythmia/ Altered conscious level * Cyanosis, PaCO2 - usually low in acute asthma due to hyperventilation * Hypotension, Hypoxia (PaO2< 8kPa (normal is 10.5 to 13.5kPa), SpO2 < 92%) * Exhaustion * Silent chest * Threatening PEF < 33% best or predicted (in those >5yrs old)

Question 135

What is the emergency management of a severe or worse asthma exacerbation?

Answer 135

* Oxygen * Salbutamol 5mg nebs - can repeat every 15-30mins * Hydrocortisone 10mg IV 6hourly or pred 40mg orally * Ipratroptium 500micgrams nebs * Theophylline - aminophylline * Magnesium - 2g IV single dose (8mmol) over 20 minutes * Escalation to Anaesthetics - consider aminophylline - discuss with senior

Question 136

Why may ventilation be difficult in cardiorespiratory arrest associated with asthma and therefore what should you try to do early?

Answer 136

Cardiorespiratory arrest may be difficult due to increased airway resistance Intubate the trachea early as there is significant risk of gastric inflation and hypoventilation of the lungs when attempoting to ventilate a severe asthmatic without a tracheal tube

Question 137

Overall prognosis of anaphylaxis is good with a case fatality ratio of less than 1% reported Anaphylaxis and risk of death is increased in those with pre-existing asthma especially if asthma is poorly controlled, severe or adrenaline is dealyed How longdoes it take for fatal food reactions, insect stings and IV medications to cause death?

Answer 137

Fatal food reaction - resp arrestt ypically after 30 mins Insect sings - collapse from shock after 10-15 mins Deaths caused by IV medications occur commonly within 5 minutes

Question 138

Anaphylasix has three didfferent criteria What are they?

Answer 138

Sudden onset and rapid progression of symptoms Life threatening airway and/or Breathing and/or Circulation SKin and/or mucosal changes (flushing, urticaria, angiodema) Exposure to known allegern for patient supports the diagnosis

Question 139

Are skin or mucosal changes alone a sign of anphylaxis? Outside the likely criteria, what are other symptoms?

Answer 139

Skin or mucosal changes alone are not a sign of anaphylaxis Can also have associated vomiting, abdo pain, incontinence (more common when exposure is non-oral route ie sting) Remember IV trigger more rapid than sting which is more rapid than oral

Question 140

What are the ariway and breathing problems that may be experienced?

Answer 140

Airway - swelling of throat/tongue/pharyngeal/laryngeal oedema Hoarse voice (new), stridor Breathin - SOB, wheeze, exhaustion, cyanosis - usually late, resp arrest

Question 141

What are circulatory symptoms of anaphylaxis?

Answer 141

Hypotensions (due to Histamine receptor mediated artriole dilation), decreased/LOC, myocardial ischameia, cardiac arrest

Question 142

What are potential mimics of anaphylaxis?

Answer 142

Septic shock - low BP and skin changes eg petechial or purpuric rash, ACE inhibitor angioedema, faint, panic attach

Question 143

Anaphylaxis must use ABCDE for sick patient What must the patient not do?

Answer 143

Death can occur within minutes if a patient stands, walks or sits up suddenly Patients must NOT walk or stand during acute reactions Lying flat with or without leg elevation is helpful for patients with low BP, and a patient may prefer to sit up to make breathing easie and STOP any suspected cause eg IV infusion

Question 144

After carrying out ABCDE, calling for help (resusc team or ambulance), remove trigger, lie patient flat, if pregnant lie on left side What should then be given? Include dose in adults?

Answer 144

Give adrenaline 500micograms = 0.5ml IM into anterolateral aspect of middle third of the thigh (1in 1000 = 1g in 1000ml =1mg in1ml)

Question 145

What is the dose of adrenaline in other age groups?

Answer 145

Adults and children over 12 = 500micrograms (0.5ml) Children aged 6-12 = 300micograms (0.3ml = epipen dose) Children 6 months to 6 years = 150micrograms (0.15ml) Children < 6 months = 100-150 micograms (0.1-.015ml)

Question 146

AFter giving adrenaline what should you do? What can you also give if and when repeating dose?

Answer 146

Make sure airway is established, give high flow oxygen and apply monitoring Give a repeated IM adrenaline dose after 5 minutes And give IV fluid bolus - hartmanns or saline (can be 500-1000ml in an adult, child 10ml/kg)

Question 147

How does adrenaline work?

Answer 147

Alpha agonist - reverse peripheral vasodilation and reduces oedema Beta agonist - dilated the bronchial ariways and increases force of myocrdial contraction, suppreses histamine and leukotriene release

Question 148

What happens if features of anaphylaxis persist despite 2 doses of IM adrenaline?

Answer 148

Follow refractory anaphylaxis algorithm and start adrenaline infusion with expert support if no improvemen in respiratory or cardiovascular sumptoms despite 2 appropriate doses of IM adrenaline Give 1mg of 1in1000 (1ml) in 100ml of saline 0.9% - start at 0.5-1ml/kg/hour

Question 149

Anaphylaxis can cause cardiorespiratory arrest, why is it important to attempt for airway intubation early?

Answer 149

Airway obstruction can occur rapidly - early tracheal intubation with anaethetist is import. As obstruction progression, SGA devices are less and less liekly to be successful and attempts at tracheal intubation may exacerbate layngeal oedema

Question 150

Nebulised adrenaline may be effective as an adjunct to treat upper airways obstruction caused by laryngeal oedema Should this be given as an alternative to IM 500micrograms of adrenaline? What is the recommended dose of nebulised adrenaline?

Answer 150

Give as an adjunct only after treatment with IM adrenaline - not as an alternative Recommmended doses are 5ml of 1mg/ml (1in 1000)

Question 151

Investigation of anaphylaxis includes usual for a medical emegrency, 12 lead ECG, chest xray, urea and electroyltes, ABG Specific test to help confirm a diagnosis is measurement of what? When should these measurmeents take place?

Answer 151

Measurement of mast cell tryptase * Minimum of one smaple within 2 hours but no later than 4 hours from symptoms onset * Ideally - three time samples - one as soon as feasible, second sample at 1-2 hour but no later than 4 hours, thirs sample at 24 hours Yellow tube serum or plasma satisfactory in most labs - time of onsert of analphyalctic reaction is from when symptoms were first noticed

Question 152

What dose of adrenalie should be used for cardiac arrest associated with anaphylaxis?

Answer 152

Use the standard 1mg dose of IV or IO adrenaline for cardiac arrest associated with anphylaxis

Question 153

A maternal cardiac arrest is a cardiac arrest that occurs in any stage in prenancy and up to 6 weeks after delivery Effective resuscitation of the mother is often the best way to optimise faetal outcome What are the common causes associated with maternal cardiac deaths?

Answer 153

Maternaldeaths most commonly asssociated with Cardiac disease - congenital and acquired PE EPilespy and stroke Sepsis Mental health conditions Bleeding Malignancy Hypertensive disorders of pregnancy

Question 154

Many cardiovascular problems associated with pregnancy are caused by compression of the IVC and aorta by a gravid uterus. How should a distressed or compromised pregnnay patient be treated (ie before cardiac arrest to prevent this) - ie what steps?

Answer 154

Place in left lateral position- if not possible manually displace the uterus to the left (eases pressure of IVC and aorta) Give high flow oxygen guided by pulse oximetry Give fluid bolus if hypotensive or evidence of hypovalaemia Immediately re-evaluate need for nay drugs being givenand seek expert help - obstetric, anaethetic and neonatal specialists

Question 155

Normally patients lie flat during chest compressions if arrested What is the optimum angle to recieve chest compressions if pregnant (past the 20 week mark usualyl for uterus to compresss on IVC/aorta?

Answer 155

Add left lateral tilit if feasabile aiming for between 15-30 degress - the angle of tilt needs to permit high quality chest compressions - if tilit not possible, maintain left uteirne displacement and maintain chest compression

Question 156

Start preparing for emergency C-section in arrest. Featus will need to be delivered if initial resucitation efforts fail Rememebr to intubate early to reduce risk of pulmonary aspiration of gastric contents in pregnancy Remember 4Hs and 4Ts What are harmorrhagic causes of arrest in pregnancy?

Answer 156

Ectopic pregnancy, placental abruption (off uterine wall), placental praevia (over internal os), placental accreta/increta/percreta (abnromal placentation), uterine rupture

Question 157

Women may need fluid resusc and massive hameorrhage protocol actviate in pregnancy if haemorrhagic If women are on magnesium sulfate for eclampsia, they can overdose. What should be given to treat agnesium toxicity?

Answer 157

Rspiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression

Question 158

When initial resucitation attempts fail, delivery of the foetus may improve the chances of successful resuscitation of both mother and foetus. What weeks gestation is best survival rate for infants and how soon after arrest is this best acheieved in?

Answer 158

Infants over 25-25 weeks delivered within 5 minutes of mothers arrest have the best survival rate - procedure should be done at the site of the arrest as moving the mother signficantly impairs CPR attempts

Question 159

Delivery relieves IVC compression and my imrpvoe the likelihood of resuscsitatng mother by permitting increase in venous return durig the cpr attmept When shoudl you consider emergency C-section * < 20 weeks? * 20-23 weeks? * < 24 weeks?

Answer 159

< 20 weeks gestatio - urgent c-section not needed as gravid uterus of this size unlikely to be palpable above umbilicus/compromised IVC and foetal viability not an issue 20-23 weeks - emergency delivery of foetus to permit successful resusc of mother, survivial of infant at this stage unlikely > 24 weeks - intiiate emergency delivery to help save both mother and infant

Question 160

Post resuscittion care should follow standard guidelines - targeeteed temperature management and consider ICD implant Foetal heart monitoring very improtant also TRAUMATIC CARDIORESPIRATOY ARREST What is it known as when actual or near cardiac arrest is caused by a blunt impact blow to the chest wlal over th eheat? WHow does it cause arrest?

Answer 160

Known as commotio cordis Mostly during sports (most commonly baseball), recreationala ctivities and in teen males Cuases arrest by causing VF/pVT usually

Question 161

In traumatic cardiac arrest damage control resuscitation combines permissive hypotension with damage control surgery Are chest compressions or control of the harmorrhage the main priority here? How long should you conitnue attempting |CPR?

Answer 161

Chest compression in arrest caused by hypovalameia, tamponade or tension pneumothorax are unlikely to be as effective as in normovalameic In these situations, chest compressions have a lower priority than the correction of these reversible causes and should be delayed Continue CPR up to 20 minutes if all reversible causes have been excluded and no detectable activty on focussed cardiac ultraosun

Question 162

In patients who have exsanguinating and uncontrollable infra-diaphragmatic torse haemorrhage, what can be done?

Answer 162

Immediate aortic occlusion - can be done by resusictate thoractoomy and cross clamping of descending aorta or intravascular occlusion device

Question 163

In traumatic cardiac arrest with penetrating trauma to chest or epigastrstrium, how would ou treat cardiac tamponade?

Answer 163

Immediate resuscitative thoracotmy with a clamshell incision and opening of pericardium to relieve tampoonade in pts who less than 15 min have elapses since loss of vital signs Needle aspiration of tamponade with or without US guidance is unreliable because pericardium is commonly full of clotted blood

Question 164

In peri-operative cardiac arrest is deemed a high risk possibilty, defib pads should be attached before induction of anaesthesia and adequate venous access and resusc drugs at the ready. Asystole and VF will be detected immeidately but PEA may not be. WHat is a good sign to indicate pulseless electricl acitivty?

Answer 164

Loss of pulse oximeter signal and very low end-tidal CO2 calues

Question 165

If peri-operative cardiac arrest occurs, and adrenaline is required according to ALS, how should it be given?

Answer 165

Give in 50-100mcg IV dose incremeents rather than 1mg IV bolus

Question 166

DROWNING Defined as a process resulting in primary respriatory impairment from submersion/immersion in a liquid medium. Asphyxia and cardiac orrest occurs within minutes of submersion. Pathophysiology - following subermsion - intially breath hold reflex and freuqnely swallos water. As breath holding conitnues, hypoxia and hypercapnia devlop (temporoary laryngospsasm may prevent entrance of water) What is the key consequence of hypoxia prior to sustainign cardiac arrest?

Answer 166

Bradycardia as a consequenece of hypoxia occurs before sustaining cardiac arrest

Question 167

Should bystanders enter water to help save a person?

Answer 167

They should attempt rescue without entry if psosoible - safer to enter with two rescuers than alone

Question 168

Which submerssion durations are associated with good outcomes and low chance of good outcomes?

Answer 168

Good outcomes of less than 5-10 min duration Poor outcomes if more than 25 min submersion

Question 169

The drowning person rescued from water within a few minutes of submersion is likely to exhibit abnromal (agonal)breathing, not to be confused with normal breathing. How should CPR take place?

Answer 169

Intially give 5 intiial ventilations - supplemtned with O2 if available If not responding, place them on a hard surfac before sustaining CPR at 30:2 Most drowning people suffer arrest secondary to hypoxia and compression only CPR should be avoided

Question 170

Massive amounts of foam caused by mixing air whith water and surfactant can sometimes come out of the mouth of people. Does this mean you should stop CPR?

Answer 170

If this osccurs, continue resuce breaths/ventilation until an ALS provider arrives and is able to intubate the trachea

Question 171

Palpation of the pulse paritcularly in the wet and cold drowining patient is not a reliable indicator of cardiac output, how should this be confirmed?

Answer 171

Check the ECG, end-tidal CO2 and consider echocardiography to confirm presence of cardiac output

Question 172

HYPOTHERMIA What is the core body temperature that classifies as hypothermia The Swiss staging criteria classifies it based on clinical signs as well as temp What ar ethe tmep stages?

Answer 172

Mild hypothermia - 32-35 degreees Moderate hypotheramia 28-32 degrees Severe hypothermia - 24-28 degrees Cardiac arrest or low flow state - < 24 degrees Death due to irreversible hypothermia - < 11.8 degrees

Question 173

What are the clinical signs at the different stages of the Swiss cstaging for hypothermia - this helps rescuers at the scene to describe people? Mild hypothermia - 32-35 degreees Moderate hypotheramia 28-32 degrees Severe hypothermia - 24-28 degrees Cardiac arrest or low flow state - < 24 degrees Death due to irreversible hypothermia - < 11.8 degrees

Answer 173

Mild hypothermia - 32-35 degreees - conscious, shivering Moderate hypotheramia 28-32 degrees - impaired consciousness without shivering Severe hypothermia - 24-28 degrees - unconscious, vital signs present Cardiac arrest or low flow state - < 24 degrees, no or minmal vital signs Death due to irreversible hypothermia - < 11.8 degrees

Question 174

Commonly used tympanic thermometers based on infrared tachnique do not seal the ear canal are are not designed for low core body temp readings WHat should be used to measure core temp in hypothermia?

Answer 174

A low reading therometer is needed Core temp in lower 3rd of oesophagus correlates well with heart tempt Can only be perfored in patients with an advanced airway

Question 175

In a hypothermic patient, beware of diagnosis death as it can produce a very slow, small-volume, irregular pulse and unrecordable BP In hypothermic patient, no signs of life alone is unreliable for declaring death If continous CPR cannot be delivered, intermittent CPR can be attempted during rescue. How long should this be given and what is the max stopping break>

Answer 175

Patients with core temp < 28 degrees, give 5 min CPR alternating with periods

Question 176

How long should you check for signs of life in the hypothermic patient? Why can hypothermia make for difficult CPR?

Answer 176

Check for isgns of life for up to 1 minute in hypotehrmic patient Hypothermia can cause chest walll stiffness, making ventilations and chest compressions difficult. Consider use of mechanical chest compression devices

Question 177

Hypothermia heart may be unresponsive to cardiactive drugs, attempted electrical pacing and defibrillation At what temp can drugs be given in arrest? What should the intervales between drug doses be? When can normal drug protocols be given?

Answer 177

Withhold adrenaline and other CPR drugs until patient has been warme to core tmep>/= 30 degrees Once 30d egrees rached, double normal drug doses ie adrenaline every 6-10 minutes during CPR Start using standard drug protocols after reaching 35 degrees core temp

Question 178

HYPERTHEMIA Conitnuum of heat-related illness from milder illness (heat syncope, exhaustion) to severe ilnness (heat stroke) How does heat syncope, exhuastion present? How does heat stroke persent?

Answer 178

Heat syncope/exuhastion - intense thirst, weakness, syncope, dizzieness Heat stroke - symptoms similar to septic shock

Question 179

How is heat stroke treated? Should dluids be given?

Answer 179

Transfer to cool environment and lie flat Immediately cool to less than 39 degrees - rapid cooling of 0.2-0.35 degrees / min is achievable Give IV fluids - isootnic eg saline or hartmans. Hypertonic fluids eg 3% NaCl if Na

Question 180

What causes malignant hyperthermia? What sis it characterised by>

Answer 180

Caused by life-threatnenign genetic sensitivty of skeletal muscle to voltailse anaesthetic agents and depolarising NMJ blcoking drugs Characterised by muscle rigidity and hyperreflexia

Question 181

What is given to treat malignant hyperthermia?

Answer 181

Stop triggering agenets immeidately Give oxgen Starta ctive cooling and give dantorlene (prevents calcium release from sarcoplasmic reticulum)

Question 182

POST-RESUSCITATION CARE ROSC is an improtant step in the continuum of resuscitation howver the next goal is to return the patient to a state of normal cerebral function and to establish and maintain a stable cardiac rhythm and normal haemodynamic function. Post cardiac arrest syndrome compromised of brain injury/myocardial dysfunction, sysemic ischaemia/reperfusion resonse and persistent precipitating pathology How does post cardiac arrest brain injury mainfest?

Answer 182

Coma, seziures, myoclonus, varying degrees of neurocognitive dysfunction and brain death Seizures occur in about one-third of patients who remain comatose after ROSC.

Question 183

Signfiicant myocardial dysfunction is common but typically starts to recover 2-3 days, althoguh full recovery may take longer Adult post-rescuitation care involves careful ABCDE What BP should be aimed for? If this cannot be maintained, what should be given? What temp should be aimed for?

Answer 183

Aim for Systolic Bp >100, if unable to maintain then consider vasopressor / inotrope to maintain Aim for temp constant between 32-36

Question 184

During circulation part of ABCDE, record a 12 lead ECG as soon as possible IF STEMI or new LBBB in opatient with typical history, what shoud be considdered?

Answer 184

Coronary angiography +/- PCI within 120 minutes If not feasible, consider fibrinolytic therapy Due tot he fact that absence of ST elevation does not completely exclude the presence of recent coronary occlusion, all patients suspected of having coronary artery disease as the cause of their arrest should be discussed with an interventional cardiologist for consideration fo coronary angiography +/- PCI

Question 185

If cardiac cause for arrrest isnt likely, what should be considered?

Answer 185

Consider CT brain and / or CTPA

Question 186

Where should a patient be admission post cardiac arrest? What temp is aimed to be maintained at?

Answer 186

Admit to ICU - can consider doing this prior to eearly coronary angiography in patients with a medium probabality of ischaemic cause of cardiac arrest. If low probabality initial ICU management may be preferred Aim for temp constant between 32-36 for >/=24 hours and prevent fever for at least 72 hours - sedate for at least 24 hours and during the period of targert temp management Maintain normoxia and normocapnia - protective ventilation Echo/normoglycaemia/diagnose/treat seizures

Question 187

What is given as secondary preventuon to prevent further arrest?

Answer 187

ICD, screen for inherited disorders RIsk factor management

Question 188

Severalphysiological variables may be abnormal immeidately after a cardiac arrest and urgent buichemical and cardiological investigations should be taken WHat do these include?

Answer 188

Biochemiesty - FBC, UE&S - incl magnesium and calcium, Glucose, serial troponins 12 lead ECG Chest radiograph - assesses tracheal tube position as well as lungs ABGs Echo CT scan - intracranial bleed or eg PE

Question 189

When deciding to tranfer the patient to CCU or ICU, make sure to doa full reassessment immediatley before the patient is transferred WHat should accompany the patient and transfer team?

Answer 189

Portable suction apparatus Oxygen supply Defibrillator / monitor

Question 190

Post resuscitation myocardial dysfunction causes haemodynamic instaiblity which manifests as hypotension, low cardiac output and arrythmias. Perform early echo in all patients to detect and quantify degree of myocardial dysfunction. What is usually the most effective treatment given in myocardial dysfunction is present?

Answer 190

Noradrenaline with or without dobutamine ANd IV fluids

Question 191

Aim for a mean arterial blood pressure that achieves a urine output of ≥ 0.5 mL kg-1 h-1 and normal or decreasing plasma lactate values, taking into consideration the patient's normal blood pressure, the cause of the arrest and the severity of any myocardial dysfunction. If treatment with fluid resuscitation and vasoactive drugs is insufficient to support the circulation, what should you consider?

Answer 191

Consider insertion of an intra-aortic balloon pump.

Question 192

Good glucose control is important. Aim for between 4mmol/L and 10mmol/l Target temperature management involves induction, maintenance and rewarming Whata re methods or inducing, maintaining and re-warming?

Answer 192

Inducing TTM - can give 30ml/kg saline or hartmanns, simple ice packs or wet towels, cooling blankets, extracorporeal circuluation Maintaing - external or internal cooling devises are used Rewarming - aim for about 0.25-0.5 degrees per hour

Question 193

Initial cooling is facilitated by neuromuscular bblockeade and sedation, what can be given for this?

Answer 193

Magnesium sulphate - a naturally occcuring NMDA receptor antagnosit - reduces shivering threshold slightly

Question 194

Prognositication is not reliable until after 72 hour from cardiac arrest What can be measuremeed biochemically to help prognose?

Answer 194

Neuron-specific enolase (NSE) - an acidic protease unique to neurons and neuroendocrine cells High serum levels of neuron-specific enolase (NSE) and S-100B protein are known to be associated with ischemic brain injury and poor outcome after cardiac arrest. Therapeutic hypothermia has been shown to improve neurological outcome after cardiac arrest.

Question 195

A structured approach to providing key informatio handover for pre-jospital to hospital care used the mnemonic ATMIST State what each letter stands for

Answer 195

Medical * Age * Time of onset * Medical complaint / history * Ix - brief explnaation of fidngins * vital Signs * Treatment including ETA Trauma * Age * Time of incident * Mechanism of injury * Injuries (top to toe) * vital SIgns * Treatment including ETA

Question 196

How long should you continue to attempt to provide resuscitiation pre-jospital before transporting to hospital?

Answer 196

If PEA/Asystole - attmpt for 20 mins and if all reversible causes have been identified and corrected, consider stopping If in VF/pVT - take to cardiac arrrest centr with ongoing CPR If failure to achieve ROSC within 20 min but aiming to continue resuscitation, aim to leave the scene as soon as possible and conitnue CPR en route

Question 197

Interestingly, atmospheric pressure is close to 100kPa. Therefore its easy to estimate thr partial pressure of each gas in the atmosphere - since oxygen is 21% of the mixture, its partial pressure is close to 21kPa. This is important because increasing the partial pressure of O2 can help a damaged lung take in more of the gas due to a bigger concentration graient Room air contains 21% O2 so normally poeople breathe in about 21kPa. Normal PaO2 is about 10-13kPa because air is humidified then mixess with expired CO2 int he alveoli both of which dilute tohe oxygen a little. - as a rule of thumb the PaO2 should be about 10 less than the inspured concentration of O2 in a healthy lung. Ie if breathing 40% oxygen, the PaO2 should rise to about 30kPa. If a patients base excess is greater than +2, what would this indicate? If less than -2, what would this indicate?

Answer 197

Base excess greater than +2 indicates metabolic alkalsis Base ecess more negative than -2 indicates a metabolic acidosis