Management of the patient in cardiac arrest

CLARIFICATION OF ALGORITHM

·    On arrival of the team with the defibrillator, application of the pads and hunt for a shockable rhythm are top priority.  Assign team members to take over CPR (give this away first), two to the airway/breathing, one to defibrillator, one to drugs, one to scribe if available. The team leader then analyses the heart rhythm, and if shockable should instruct the team member on the defibrillator to deliver a defibrillation shock.  CPR can be resumed while the defibrillator is charging when using a manual defibrillator, but the team should be cleared from the patient before pressing the button to deliver the shock.  CPR should be resumed immediately after defibrillation, there is no need to re-check either the rhythm or pulse until the next 2 minutes of CPR are completed

·    Shockable rhythms = ventricular fibrillation (VF) and pulseless ventricular tachycardia (pVT). 

Non-shockable rhythms = asystole and pulseless electrical activity (PEA).  If a non-shockable rhythm is present, check a pulse. If no pulse is present, resume CPR


When team arrive, follow the A-B-C-D of team management

-     Assign the team roles: one team member to CPR, 2 team members to respiratory management, one team member to the defibrillator, one to IV management, and additional team members should scribe, swop into CPR after 2 minutes, etc.

-     Brief the team: instruct the team to do 30 compressions to 2 breaths, repeat for 5 cycles, and to inform team leader when 5^th cycle is starting and finishing.  Let the team know that after 5 cycles / 2 minutes, CPR will stop, the person doing CPR should swop into a less strenuous job, with CPR to be taken over by a nominated person, and during the pause the team leader will analyse the cardiac rhythm...so called STOP, SWOP AND ANALYSE. Also give team brief overview of patient presentation / background to arrest

-    Check that all team members are performing well: that CPR is good quality with minimal interruptions, that oxygen is attached to bag-valve-mask and that patient is easy to ventilate, with chest rising and falling bilaterally

-     Draw up 1^st drug: this is epinephrine 1mg in all types of arrest. Give immediately intravenous access is available in non-shockable rhythms, give after 2^nd shock in shockable rhythms

What drugs are given in cardiac arrest, and when should they be given?

• Epinephrine 1mg is given immediately in asystole / PEA, and is then repeated every 3-5 minutes for the duration of the arrest.  No other drug is used in these rhythms
• Epinephrine 1mg is also the first drug given in the shockable rhythms, but is not given until the rhythm becomes refractory ie after the second shock.  It is again given every 3-5 minutes (every second cycle in practice) for the duration of the arrest
• In shockable rhythms only, either amiodarone or lignocaine can be given after the 3rd shock (300mg amiodarone in D5 IV push; lignocaine 1.0-1.5mg/kg IV push) and again after the 5th shock (150mg amiodarone in D5 IV push, lignocaine 0.5-0.75mg/kg IV push).  The drug sequence in shockable rhythms is therefore as follows:

An easy way to remember what needs to be done during an arrest is:

• Make sure CPR is ongoing at all times, but if a defibrillator arrives, prioritize hunting for a shockable rhythm and delivering shock.  If you have a second rescuer, CPR can be continued while you are organizing defibrillator
• As soon as the team arrive, do the A-B-C-D of team management. Organizing your team will probably take up most of the first two minutes of the arrest.  
• After the second analysis +/- shock, ensure the first drug is given, and consider reversible causes.  
• After every rhythm analysis, as soon as CPR resumes, consider giving the next drug in the algorithm sequence.

What are the reversible causes, and how do we manage them?
Reversible causes, also known as the Hs and Ts, should be considered during the second 2 minutes of the arrest algorithm, or earlier as you become more practiced at arrest management.  An easy way of remembering them is:

1. Stand at end of bed and watch the chest rise.  If it rises bilaterally,tension pneumothorax is unlikely.  Confirm that tension pneumothorax is not present by auscultating breath sounds and ascertaining whether the trachea is central.  Make sure that 100% oxygen is attached to the bag-valve-mask to reverse hypoxia, and good ventilation will reverse the respiratory component of acidosis.  Confirm that the patient is not profoundly acidotic with a venous blood gas (VBG)
2. "Fluids in, fluids out".  Hang a bag of normal saline and give in 250-500ml boluses to reverse any potential hypovolaemia.  More fluid may be indicated if the patient was hemodynamically compromised pre-arrest. "Fluids out" includes blood samples (VBG will confirm potassium levels, pH and lactate; point-of-care glucose can be done at the bedside) and urine sample (a catheter specimen may be dipped for toxins if there is any suspicion that the patient has taken pharmacological agents that may contribute to the cardiac arrest)
3. The 4 Ts: thrombus, tamponade and temperature and trauma - consider PE (ask for d-dimers on pre-arrest blood sample) or coronary thrombus (request troponin-I on pre-arrest blood sample; perform ECG if ROSC is achieved).  If tamponade is suspected on history or examination, organise a bedside echo / ultrasound.  Palpation of poor femoral pulses during CPR is an unreliable sign of either tamponade, tension pneumothorax or hypovolaemia, but may be done while waiting for ultrasound.  Tympanic temperature may reveal hypothermia, which is associated with irritable myocardium and arrest.  Rewarming is indicated in such cases. Manage trauma if present as per guidelines. 

FYI: the following management of Hs and Ts are not part of a basic ACLS course, but are useful to know.  Seek expert help unless you are proficient in the following techniques:

• Tension pneumothorax is managed in the first instance with needle decompression - a 14G cannula is inserted into the 2nd intercostal space just above the 3rd rib in the mid-clavicular line to decompress the chest, followed by a definitive chest drain. The alternative locations for placement of the needle in needle decompression are the 4th intercostal space in the anterior axillary line, or 4th intercostal space in the mid-axillary line.  Insertion in these cases should be just above the 5th rib to avoid puncturing the intercostal bundle.
• In acidosis, ventilatory correction is sufficient unless the acidosis is profound (<7.1 on arterial blood gas).  If profound acidosis is present, use of NaHCO3 may be considered  (seek expert help)
• Hyperkalaemia requires the use of calcium chloride to protect the myocardium; glucose-insulin infusion or sodium bicarbonate infusion to reduce plasma potassium can be considered, also removal of potassium from the body.  In hypokalaemia, potassium should be replaced carefully.
• Toxin overdose requires specialist management and possibly administration of antidote - liaise with local poison centre.
• Tamponade may require needle pericardiocentesis with cardiothoracic follow-through.

In cardiac arrest, when should you check a pulse?

1. If patient becomes responsive during resuscitation
2. If ETCO2 rises sharply to between 35-45mm Hg
3. If a rhythm changes: CHANGE OF RHYTHM: CHECK PULSE
4. If a potentially perfusing PEA rhythm is present at the "stop, swop and analyse" step

Candidates are often confused about pulse checks during arrest rhythms.  Broadly if a patient starts the arrest with ventricular fibrillation which is pulseless, if this rhythm persists at the 2-minute check, there is no need to check a pulse again.  The same applies to pulseless ventricular tachycardia, however with a change of rhythm to ventricular tachycardia it is reasonable to do a quick pulse check. Presence of a potentially perfusing rhythm other than pVT requires that the pulse be checked each time assessment is carried out.

In summary: when you stop, swop and analyse, you will see one of 4 situations on the monitor:

1. Ventricular fibrillation (VF): as the patient is already in established arrest, there is no chance of achieving return of spontaneous circulation (ROSC) with this rhythm.  Resume CPR while charging, clear to deliver shock, then continue CPR for 2 minutes until the next rhythm check.
   
2. Ventricular tachycardia (VT): if the patient was in pulseless ventricular tachycardia (pVT) at the onset of the arrest, the chances of a pulse returning when the same rhythm persists are slim. With persistent VT, it is correct to resume CPR while charging - defibrillate - continue CPR without checking a pulse. However, this often confuses candidates because technically it is possible to have a pulse with VT.  If in doubt, check a pulse for no more than 10 seconds; if no pulse present resume CPR while charging - defibrillate - continue CPR 
   
3. Asystole: "flatlining".  Once it has been established that there are no loose leads, and that the patient is pulseless, the treatment for this rhythm is: resume CPR, administer epinephrine 1mg every 3-5 minutes and consider reversible causes.  Increasing the gain on the monitor while CPR is ongoing and stopping briefly to re-analyse ensures that fine ventricular fibrillation is not being missed.  If asystole persists on further rhythm analysis,  further pulse checks are not indicated - this simply delays resumption of CPR.
   
4. Pulseless Electrical Activity (PEA): if a rhythm does not fit into any of the above categories, and the patient remains pulseless, the arrest is classified as PEA and is managed under the same algorithm as asystole.  Because PEA is associated with perfusing rhythms, pulse checks should be carried out to establish arrest at each rhythm analysis.  Pausing to define further what is on the monitor is not needed and delays return to CPR.  If it's not VF, pVT, or asystole and the patient is in cardiac arrest, manage as PEA
   

What about polymorphic ventricular tachycardia?
If your patient is in cardiac arrest, polymorphic ventricular tachycardia is managed in the same algorithm as VF and pVT (monomorphic).  The only difference in management is that MgSO4 1-2g IV may be considered as pharmacological therapy instead of amiodarone in Torsades de Pointes (ie polymorphic VT associated with a long QT interval)

Fast Rhythms_The Tachycardias

Fast rhythms >100 beats per minute: The Tachycardias

Tachycardias are in the first instance subdivided into those with wide QRS complexes (>0.12s or 3 small boxes on the ECG) and those with narrow QRS complexes.  For simplicity and safety, broad complex tachycardias are generally treated as ventricular in origin.

Monomorphic regular ventricular tachycardia with a broad-

complex QRS complex

     Normal Sinus Rhythm for comparison 

Sinus Tachycardia: 
  There’s fewer than 3 large boxes  between adjacent QRS complexes. QRS complexes are regular and narrow and there’s a normal P-wave before every QRS complex

                                                      Supraventricular tachycardia:

                                               no obvious p-waves, narrow QRS, regular

                                                                       Atrial flutter

    normal rate of ventricular response. Note narrow QRS and saw-toothed atrial flutter waves

Narrow complex tachycardia if regular should be differentiated into sinus tachycardia, supraventricular (atrial) tachycardia, or atrial flutter.  Junctional tachycardias may also fall into this group.

Tachycardias are further subdivided into regular and irregular.  Irregular broad-complex tachycardias with variable morphology on the monitor are treated as “Torsades de pointes”.  Irregularly irregular narrow complex tachycardias with no identifiable p-waves are treated as atrial fibrillation (a. fib).  In addition, atrial flutters are sometimes irregular.  Multifocal atrial tachycardias may also fall into this group.

Polymorphic irregular ventricular tachycardia, with broad-

complex QRS complexes all of which appear different.

           Atrial fibrillation: 
note irregularly irregular narrow - complex tachycardia, and absence of normal P-waves. There are fibrillatory f waves on the ECG isoelectric line.

Management of STABLE tachycardias:

If narrow complex regular tachycardias can be distinguished as sinus tachycardia, supraventricular tachycardia, or atrial flutter, treatment should be tailored to the specific rhythm.

If these rhythms cannot be distinguished on screen or on an ECG strip, empirical treatment using vagal manoeuvres and IV adenosine may slow the rhythm sufficiently to allow specific rhythm identification.

SINUS TACHYCARDIA: treatment is of the cause. 

SUPRAVENTRICULAR TACHYCARDIA: vagal manoeuvres (eg blowing into syringe followed by trendelenberg) should be tried initially.  Following ANY treatment or intervention, a full set of vital signs should be rechecked, starting with the pulse.  If vagal manoeuvres fail, the patient may be treated with adenosine 6mg by rapid IV injection followed by a 20ml saline flush.  Make sure the patient is not a brittle asthmatic or on drug therapy that may interfere with adenosine prior to treatment*.  If 6mg adenosine fails, 12mg may be tried.  The half-life of adenosine is approximately 10 seconds, so rapid administration is imperative.  Because of this short half-life, alternative drug therapy with either beta-blockers or calcium channel blockers may be considered if adenosine fails to abort the arrhythmia.  Request expert help before progressing beyond the adenosine steps.

ATRIAL FLUTTER: Considerations in the management of atrial flutter are the same as for management of atrial fibrillation. See below.

ATRIAL FIBRILLATION: This is one of the commonest arrhythmias seen by healthcare personnel, but management is often difficult.  Seek expert help if a patient presents with atrial fibrillation, because underlying pathologies, chronicity and left ventricular function will all impact on patient management.  As it is usually difficult to ascertain how long the patient has been in atrial fibrillation, initial recommended management is rate control with either a beta blocker (eg metoprolol 2.5-5mg by slow IV injection) or calcium channel blocker (eg diltiazem, verapamil), and commence anticoagulation.  If the patient becomes unstable, there may be no choice other than to perform synchronised cardioversion as a life-saving measure.  If time permits, a trans-oesophageal echo should be performed to rule out any thrombus in the left atrial appendage, and the patient should be covered with a heparin bolus.

SUMMARY:

·         If stable: rate control with beta blocker or calcium channel blocker

·         If unstable: synchronised cardioversion

Additional considerations with atrial fibrillation are left ventricular function (if LV function poor, consider treatment with digoxin, which is a positive inotrope) and length of time present (avoid synchronised cardioversion unless critically ill because of risk of embolization causing stroke.  Similarly, avoid chemical cardioversion with amiodarone if a. fib present >48hours). 

VENTRICULAR TACHYCARDIA – MONOMORPHIC:  A single dose of 6mg adenosine can be used to differentiate SVT with aberrancy from ventricular tachycardia in broad complex, regular, monomorphic tachycardias.  However, this may be dangerous in certain types of broad-complex tachycardia (eg very rapid atrial fibrillation with delta wave: Wolff-Parkinson-White syndrome), and establishing whether a very rapid ventricular tachycardia is regular or monomorphic may be difficult on ECG.  Broad-complex tachycardias may be treated safely as ventricular tachycardias.

Stable ventricular tachycardia may be treated with 150mg amiodarone in 5% dextrose, administered over 10-20 minutes.  As amiodarone has a vasodilatory effect and can drop the blood pressure markedly, the slower administration is safer.  Lignocaine, procainamide or sotolol are other drugs that may be considered as first-line therapy; procainamide and sotolol should be avoided with prolonged QT.  Polypharmacy should be avoided, so choose your drug and stick with it until expert help arrives.

VENTRICULAR TACHYCARDIA – POLYMORPHIC:  polymorphic VT is frequently associated with hypomagnesaemia, therefore serum chemistry should be checked and corrected.  MgSO4 1-2g by slow IV injection may be given instead of amiodarone.

Management of UNSTABLE tachycardias:

Management of unstable sinus tachycardia is of the cause.

Unstable monomorphic VT, SVT, atrial flutter and atrial fibrillation may all be treated with synchronised cardioversion.  In this procedure, a low-energy synchronised shock is delivered on the R wave in an attempt to return the patient to sinus rhythm.  Failure to synchronise may cause the shock to be delivered on the T wave, which may precipitate ventricular fibrillation and cardiac arrest.  Because the machine has to hunt for the R wave before the shock is delivered, there may be a delay between pressing the shock button and delivery of the shock.  For this reason, one needs to continue to press the shock button and maintain clearance until the shock is delivered.  This is a painful procedure, so if time and patient condition allows, an anaesthetist should be called, and the patient should be sedated, with appropriate respiratory management.

Narrow complex regular rhythms: cardioversion dose may start at 50J, and if unsuccessful the energy may be increased in 50J steps for subsequent cardioversions.  The rhythms treatable with 50J are SVT and atrial flutter

Broad complex regular rhythms require higher doses of energy to convert.  Cardioversion of monomorphic VT should commence at 100J.

Narrow complex irregular rhythm cardioversion requires higher doses of energy.  Doses for atrial fibrillation are 120-200J, depending on machine.

Broad complex irregular tachycardia (polymorphic VT) may not respond to synchronised cardioversion because the defibrillator may not be able to identify the r wave, on which synchronised cardioversion is usually delivered.  Therefore, an unsynchronised (defibrillation) shock may be  required to abort polymorphic VT

To perform synchronised cardioversion, the following steps should be performed:

1.  Call anaesthetist to administer sedation and manage airway if time permits, but this should not   delay cardioversion in a critically ill patient.  Call cardiology (ie SEEK EXPERT HELP)
2.  Place pads on patient’s chest
3.  Select joules appropriate to rhythm
4.  Press “Sync”
5.  Run a strip showing that Sync mode is working, and that markers co-incide with R waves
6.  Charge the machine. 
7.  Remove oxygen.
8.  Clear the patient.
9.  Deliver synchronised cardioversion.
10.  Take “Sync” mode off if it has not gone off automatically, and immediately check patient’s pulse 

Possible outcomes:

•        If pulseless with shockable rhythm: defibrillate immediately and call a code.
•        If pulseless with non-shockable rhythm: commence CPR and call a code
•        If pulse present: look at monitor to see if sinus rhythm present.  If cardiovertible            rhythm persists, check full vitals, and prepare to cardiovert at higher energy
•        If sinus rhythm present: check vitals, refer to cardiology for review.

Slow Rhythms_The Bradycardias

Slow rhythms <60 beats per minute: The Bradycardias

On a simple level, the bradycardia rhythms can be divided into:

·         Sinus bradycardia

·         Heart blocks

-          1^st degree: prolonged PR interval (>0.2s or 5 small squares on the ECG)

-          2^nd degree type 1 (Mobitz 1, Wenckebach phenomenon) where the PR interval prolongs with subsequent beats until there is a dropped beat (no QRS after P)

-          2^nd degree type 2 (Mobitz 2) where PR intervals are constant until there is a dropped beat (no QRS after P)

-          3^rd degree (Complete Heart Block, CHB) where there is no relationship between P waves and QRS complexes at all.

Sinus Bradycardia: regular rhythm, more than 5 large boxes between r waves, PR intervals <0.2s. There is a P-wave before every qrs complex, and a qrs after every P

1st degree Heart Block: regular rhythm, PR intervals >0.2s. There is a P-wave before 

every qrs complex, and a qrs after every P

2nd degree Heart Block type 1: The Wenckebach phenomenon.  PR intervals increase until there is a dropped beat.  There are therefore more P waves

than qrs complexes.

2nd degree Heart Block type 1: "Mobitz 2"

  PR intervals are constant until there is a dropped beat.  There are therefore more P waves than qrs complexes.

Third degree or Complete Heart Block.  There is no relationship between P waves and qrs complexes.

Management of STABLE AND UNSTABLE BRADycardias:

First of all, as with tachycardias, the questions we need to ask are:

• How is the patient? (stable or unstable)
• Is there an identifiable reason for the bradycardia?

SINUS BRADYCARDIA: treatment is of the cause in the first instance.  Causes of sinus bradycardia include:

• high vagal tone (eg in athlete)
• hypothermia
• hypothyroidism
• action of a therapeutic drug  (eg beta blockers,  calcium channel blockers, digoxin etc)
• Cushing's triad with raised intracranial pressure (bradycardia, high SBP, abnormal RR)
• problems in the heart's conducting system
• acute myocardial infarction
• electrolyte imbalance: eg Mg++, K+

Causes of bradycardia should be sought and rectified.  The reason we treat tachycardia is because the fast heart rate increases oxygen demand; the reason we treat bradycardia is because the slow heart rate makes the patient symptomatic or unstable.  If treatment is necessary, atropine 1mg can be given every 3-5 minutes up to a total atropine dose of 3mg.  If the patient fails to respond to atropine or becomes increasingly unstable, epinephrine (2-10mcg/min) or dopamine (5-20mcg/kg/min) infusions can be considered, or, if available, Transcutaneous Pacing (TCP).  TCP is a bridge to more definitive therapy (transvenous pacing), but is useful because it can be commenced quickly and can be controlled rapidly.  

HEART BLOCKS: Broadly speaking, provided there are no confounding complexes such as ectopic beats, the regular slow rhythms (ie rhythms with regular qrs complexes) are sinus bradycardia, 1st degree heart block, and 3rd degree heart block.  The slow rhythms with irregular qrs complexes are the 2nd degree heart blocks, due to dropped beats.  Note that Mobitz 2 may present as a regular rhythm if beats are dropped regularly with a 2:1 block, making it difficult to differentiate from 3rd degree heart block.  Mobitz 2 may progress to complete heart block, and the treatment considerations in both are similar. 

1ST DEGREE HEART BLOCK AND MOBITZ 1 (WENCKEBACH PHENOMENON): causes include high vagal tone, medications, electrolyte disturbances and myocardial problems.  Treatment considerations are as for sinus bradycardia.  These blocks tend to occur above or at the AV node, and therefore they can be expected to respond to atropine therapy.

MOBITZ 2 AND COMPLETE HEART BLOCK: These blocks are more likely to be associated with structural heart disease, such as myocardial infarction or congenital heart disease.  They may also be associated with electrolyte disturbances such as hyperkalaemia or with drug ingestion.  Atropine may have no effect in infranodal blocks.  Atropine should also be used with extreme caution in a patient who is infarcting, as it increases oxygen demand.  


SUMMARY

• the first line therapy that can be considered for all bradycardias is atropine 1mg +/- repeat every 3-5 minutes up to 3mg max.
• second line therapy should be considered rapidly in patients with higher degrees of block (Mobitz 2 and CHB), in patients who are infarcting, and in patients who fail to respond or deteriorate after 1st line therapy.  Note that many practitioners opt straight for pacing in patients with higher degrees of block or those having acute myocardial infarction.

TRANSCUTANEOUS PACING (TCP)

• Machine needs to read rhythm through the leads and deliver energy as needed through the pads, therefore patients should have pads and leads on from a single machine 
• Having selected an adequate heart rate and "Demand" mode on the pacer, the mAmp should be increased in steps until capture is achieved.  Capture is known to have occurred if all pacing spikes are followed by a qrs complex which differs in morphology from patient's intrinsically generated qrs complexes
• The patient should be checked to ensure that electrical capture is accompanied by mechanical output, by checking pulse (femoral is best), BP and full vital signs.
• The output should then be increased by one step to consolidate capture
• Sedation and/or pain relief will probably be required by the patient
• Transfer to cardiology for definitive care - TCP is a bridging treatment

Summary of Approach to Megacode

In a megacode evaluation, you need to demonstrate proficiency in assessment and management of

• the live patient: establish responsiveness / pulse, then assess whether patient is stable or unstable (see "The Live Patient" in this blog)
• the arrested patient
• the resuscitated patient

The priorities are:

• assess the patient clinically
• assess the rhythm
• apply the algorithm according to findings in 1 and 2

In the live patient, you need to establish the following:

1. stable or unstable? 

• responsive?
• short of breath? 
• hypoxic or showing evidence of LVF? 
• hypotensive?
• ischaemic chest pain?

      2. What rhythm is on the monitor?

• fast or slow?
• regular or irregular?
• narrow QRS or broad QRS (>0.12s)
• are normal p waves present?
• is there a p before every QRS and a QRS after every p?
• what is the PR interval like (normal length, always the same, etc)

Remember the aide memoire VOMIT SAMPLE.....

·       VITALS: BP, RR, Pulse, Temperature

·       OXYGEN: titrate to SpO₂ 94%

·       MONITOR: 3-lead ECG to see rhythm

·       IV: intravenous access; send bloods

·       TWELVE LEAD ECG and Targeted examination: CVS, lungs, oedema

·       SYMPTOMS: Chest pain? Shortness of breath? Palpitations? Etc.

·       ALLERGIES

·       MEDICATIONS

·       PAST HISTORY

·       LAST MEAL

·       EVENTS leading to presentation

      Apply the algorithm according to whether the patient has a stable or unstable tachycardia, or stable or unstable bradycardia.  In general, stable patients are treated with drugs, [unstable patients are treated with electricity (pacing for bradycardias, synchronised cardioversion for tachcardias) 

Arrested patient: General Principles

In the arrested patient consider whether the rhythm is shockable or non-shockable

Shock the shockables once defibrillator available then every 2 minutes while rhythm persists

Epinephrine is used in all arrest rhythms 

Amiodarone is only used with shockable rhythms

Initial management: ABCD of team management

Assign tasks to team

Brief the team

Check the team are performing well

Draw and give drugs

Ongoing management: consider the Hs and Ts

 Post-Resuscitation ABCDEFGH

• AIRWAY: open airway, consider intubation and EtCO2 monitoring
• Breathing: support respirations 1 every 6 sec, support oxygenation
• Circulation: pulse present - how is BP? If systolic BP remains below 90mmHg give IV fluids, consider pressor infusion
• Differentials: reconsider Hs and Ts, do post arrest ECG, portable CXR and bloods
• Environment: where does the patient have to go? PCI if ECG abnormal, HDU if intubated, monitored bed if not intubated
• Family, Foley, File: communicate with family, insert foley catheter for bladder emptying, monitoring perfusion, and obtaining urine specimen for toxins; check file for contributory past history and drug treatments
• Glucose, God, Gratitude, Gastric: check blood glucose, consider pastoral care, thank and debrief team, and insert NG tube if patient unconscious...useful for gastric decompression and for administration of certain drugs eg dual antiplatelet therapy before PCI
• Hypothermia: consider targeted temperature management post arrest if patient remains unresponsive. Cool to between 32 to 36 deg C