Below are my teaching notes from a recent Advanced Cardiac Life Support Course. I taught IO, death and dying, cardiac arrest management and bradycardia management for this class. I cover the mandatory content and mix in other evidence and experience based practices. A major reason I put this together is that there were some amazing experienced providers, advanced practice nurses and experts at resuscitation - so I wanted to come prepared. Much of this is borrowed and if so, I've tried to cite everything I can. Feel free to use/adapt and offer corrections. If you do, please cite us and let us know. I'd love to know how it is being used.

*Late edit after feedback - this content will likely not help you pass your course. This content is more for the experienced provider who performs resuscitation regularly as part of their work duties and is building on a very strong foundation of existing knowledge and skill.

Just a quick disclaimer. Advanced Cardiac Life Support (ACLS) is trademarked by the AHA/HSF in Canada. Effort was taken not to infringe on their copyrighted materials.

IO ACCESS

It is fast and dependable. It definitively out performs crash central venous access(1) and in our experience also out performs peripheral IVs in some cases.

Source: Teleflex EZ-IO

To choose needle size, insert the needle and keep your finger off the trigger. See how much needle is left when you hit the bone. It there’s 5mm or more (but not so much you’ll go through the other side of the bone), you’re good to go. If you bury the whole needle, just pull out and put on a longer needle and go again.

For causes of arrest that are associated with hypovolemia and need volume resuscitation the proximal humerus is the preferred site. The humerus is about 57mL/min (3.5L/hr) and the proximal tibia is about 31mL/min (1.8L/hr) in a non-manufacturer trial.(2) To get at the proximal humerus I like to put the hand of the arm i’m inserting into, under the patient’s glute or under the hardboard behind the small of their back. I find this helps me bring the humeral head into position.

The proximal tibia site is much less likely to get dislodged during cardiac arrest care. In a randomized trial of IV versus IO for out of hospital cardiac arrest patients the tibia was faster to insert and almost half as likely to become dislodged.(3) We rarely use the distal tibia and I can’t recommend it.

Don’t insert the IO into joints, don’t insert into fractures or failed IO sites. Don’t insert into sites with surgical scars as there may be orthopedic appliances. Osteogenesis imperfectica is a contraindication too - a super rare one.

After insertion with the EZ-IO apply dressing and attached primed extension. Flush briskly because you need to displace the contents of the medullary canal out the vasculature. After the flush it should get easier, though fluids will have to run by pressure bag or pump. In most cardiac arrests, it is acceptable to administer 1 to 2 liters of crystalloid, so be aware that if you are using a pneumatic pressure bag as soon as 50mL of crystalloids leaves the bag it is unpressurized. Pneumatic pressure bags need frequent re-pressurizing.

When trouble shooting displacement, you can use ultrasound or hook up a transducer to it.(4) If there’s any doubt, just drill the other side. If you absolutely need to, you can even insert 2 needles into one bone.(5)

COPING WITH DEATH

Caring for the cardiac arrest team is an important component of high quality cardiac arrest care that is often overlooked. It has been in the literature for almost 20 years.(6) Moderate-quality evidence suggests the offering of FPDR does not affect adult resuscitation outcomes and may improve family member psychological outcomes.(7)

The GRIEV_ING Mnemonic.(8)

G Gather; gather the family; ensure that all members are present. R Resources; call for support resources available to assist the family with their grief, i.e., chaplain services, ministers, family and friends. I Identify; identify yourself, identify the deceased or injured patient by name, and identify the state of knowledge of the family relative to the events of the day. E Educate; briefly educate the family as to the events that have occurred in the emergency department, educate them about the current state of their loved one V Verify; verify that their family member has died. Be clear! Use the words “dead” or “died.” _ Space; give the family personal space and time for an emotional moment; allow the family time to absorb the information. I Inquire; ask if there are any questions, and answer them all. N Nuts and bolts; inquire about organ donation, funeral services, and personal belongings. Offer the family opportunity to view the body. G Give; give them your card and access information. Offer to answer any questions that may arise later. Always return their call.

For the providers, there’s something called “the pause” first proposed by an emerg nurse in the States named Jonathan Bartels.(9) He suggests teams take 45 seconds of silence after the code is called. The suggested pause goes like this:

“Could we take a moment just to Pause and honour this person in the bed. This was someone who was alive and now has passed away. They were someone who loved and was loved. They were someone’s friend and family member. In our own way and in silence let us stand and take a moment to honour both this person in the bed and all the valiant efforts that were made on their behalf.”

45 seconds to a minute of silence.

“Thank you everyone.”

CORE ACLS CONTENT for VF/pVT/Asystole & PEA

Objectives:

1) Recognize cardiac arrest

2) Perform early management of cardiac arrest until termination of resusc or transfer of care

3) Evaluate Resusc during the arrest through cont. Ax of CPR quality, pt physiologic response and giving real-time feedback to the team

The cardiac arrest algorithm is the bread and butter of ACLS. It all starts with high quality CPR, giving oxygen and attaching the monitor/defibrillator. Once the monitor is attached you descend one of two pathways, either VF/pVT (shockable/defibrilatable) or Asystole/PEA (non-shockable/defibrilatable).

For VF/pVT the goal is to provide defibrillation as soon as possible for VF/pVT. After the first defibrillation, immediately resume high-quality CPR. During this 2-minute cycle of CPR initiate IV/IO access.

If you are a member of an experienced resuscitation team, multiple interventions may occur simultaneously. In reality, the most effective therapy for VF/pVT is defibrillation and high-quality CPR so this should be the focus of care. Do not worry about giving medications during the first cycle if it takes away from defibrillation or high-quality CPR in any way. However, if you’re the member of a large and experienced team, sure give epinephrine in the first cycle at the team leader’s discretion. If you don’t have an IV, consider an IO.

After another 2 minutes stop for a pulse and rhythm check. The team leader can position themselves in such a way that they can visualize the rhythm on the monitor and palpate femoral pulses. Again, if indicated, give another defibrillation. You can use the same dosage of joules, or escalate therapy at the team leader’s discretion.

After the second defibrillation, it is time to give epinephrine according to the guidelines. Epinephrine 1mg IV push is given every 3 to 5 minutes. In high functioning teams this is usually every other cycle of CPR. Now is also the time to consider an advanced airway with capnography. Again, depending on your team, don’t compromise the foundational care of high-quality CPR to put in an advanced airway.

After that 2-minute cycle of CPR it is the time for the third pulse/monitor check and if it is still pVT/VF, you defibrillate again and now administer amiodarone 300mg IV push. This medication doesn’t come in a prefilled syringe in our region, so a heads up to the nurse of medications is helpful. After amiodarone administration, it’s time to get after reversible causes. The H’s and T’s (more later).

If after these 3 cycles of CPR and 3 defibrillations you still don’t have return of spontaneous circulation (ROSC), you go back to the second cycle where you provide another 2 minutes of high-quality CPR and give epinephrine as required. A second dose of amiodarone of 150mg IV push can be given in 3 to 5 minutes after the first.

If you encounter a non-shockable rhythm anytime during a pulse/monitor rhythm check, or when you first apply the monitor/defibrillator you descend the Asystole PEA algorithm. In this algorithm, you also maintain high-quality CPR with minimal interruptions, but you only have epinephrine 1mg IV push to give. Try to give the epinephrine IV/IO as fast as it is feasible, because it is associated with increased ROSC (1).

There’s not much else to the algorithm. Keep up the high-quality CPR and give epinephrine 1mg IV push every 3 to 5 minutes. And search for and reverse potential causes, because that’s what will save lives. Identify your potential causes of arrest by addressing your H’s and T’s. In my shop this is achieved through history, physical, blood gas analysis and ultrasound.

It is not enough just to rattle off the H's and T's you must know how to identify them and what the subsequent treatment would be.

Source: Mackenzie Thompson at https://advancedmedicalcertification.com/how-to-memorize-the-hs-and-ts-of-acls/

EXPERIENCED PROVIDER CONSIDERATIONS

IO. IO is generally faster than IV for access/insertion time. It is definitely faster than the crash central venous catheter.(1) If it doesn’t look like an exceptionally easy IV, I would advocate for IO. The proximal tibia is my site of choice for any resuscitation that does not require volume resuscitation. It is also less likely to dislodge than the proximal humerus(10) and its location away from the head and chest makes it ideal for accessing and medication administration. My favourite approach is IV attempt on one side with phlebotomy and IO insertion on the other side.

Defib Pads. Defibrillation pads are often poorly placed(11), after the first defibrillation confirm correct pad placement. Don’t be afraid to correct their location.

Offload cognitively. If you’re a leader and have a high functioning team, cognitively off-load. Give the nurses or medics the responsibility of running the algorithm(12) and you get after identifying the reversible causes and the higher order tasks. Also, simulate for training purposes, in-situ and high fidelity because it improves team performance.(13)

Pulse checks. Pulse checks are junk. EtCO2 (if you haven’t filled the patient up sodium bicarbonate) and SpO2 (if you have perfusion) are better in my opinion. If you have an arterial line, even better. Research tells us that healthcare professional’s pulse check doesn’t beat a coin toss at determining if there’s a pulse present.(14) I would still perform a pulse check, while interpreting the rhythm on the monitor and looking at my Spo2 and arterial line waveform (or lack thereof) so I had all the information possible for decision making. Physiological monitoring during cardiac arrest is a real thing (ECG/SPO2/NIBP/ABP/EtCO2 etc.), though EtCO2 and diastolic BP are more validated.(15)

Peri-shock pause. At the very least you should be giving chest compressions while charging. If you’re a higher functioning team, you can pre-charge the defibrillator prior to the pulse rhythm check. This minimizes interruptions in chest compression even further.(16) And more interruption means less ROSC.(17) Twenty seconds prior to your rhythm check the person running the monitor can pre-charge. This allows the team lead to immediately defibrillate as soon as VF/pVT are recognized.

Dual Defib. Refractory VF/pVT and dual sequential defibrillation.(18) You may consider this if you have the right team and equipment.(19)

Indication: Use only in refractory or intractable ventricular fibrillation (VF) after multiple attempts (at least 3 to 5 attempts) at defibrillation and appropriate medications have been given.

Method: Apply TWO sets of defibrillator pads to the patient; one in traditional sternum/apex configuration and the other in anterior/posterior configuration. Some protocols suggest firing the defibrillators "sequentially" (less than 1 second apart), others recommend firing "as synchronously as possible" (simultaneously).

When to stop. Generally, run the arrest until you have reasonably identified and reversed potential causes. This is achieved with a point of care ultrasound probe and a venous blood gas combined with careful history and physical assessment in my setting. Often this is 40 minutes in my experience. If the resuscitation could have been called in the field using reasonable termination of resuscitation rules, that's appropriate soon after arrival. I am a fan of saying that the most important bit of knowledge in resuscitation is knowing who NOT to resuscitatie.

Even More H & T. The H’s and T’s are somewhat lacking - for instance, nonischemic cardiac disorders and intracranial haemorrhage occurred in 8.3% and 6.9% of PEA cases.(20)

Expanded H’s and T’s

Hypovolaemia – give fluid, blood products, stop bleeding, clamp vessels, give whatever the patient lost, use pressure to infuse if indicated, don't give fluid or fluid under pressure without a reason.

Hypoxia – intubation and ventilation (FiO2 1.0) - CO, cyanide?

Hypokalaemia – K+ replacement, give Ca++, consider the fastest K+ replacement... prearrest we max out around 10mmol/hr peripherall and 20mmol/hr centrally, intra-arrest you may have to push it a bit more

Hyperkalaemia – treat cause, Ca2+, insulin-dextrose, salbutamol, NaHCO3

Metabolic disorders – Mg2+ if low, Ca2+ if low, consider bicarbonate for acidaemia (e.g. with normal anion gap)

Hyperthermia – cool, ice in the body bag trick(21), dantrolene for malignant hyperthermia, stop seizures and battle the spiralling acidosis and metabolic derrangements

Hypothermia– warm them - duh, chest, bladder, peritoneum, IV fluids, bair hugger

Toxicity – stop absorption, lipid rescue (1.5mL/kg intralipid IV push then 0.25mL/kg gtt and MAX 8mL/kg), increase elimination, antidote to specific drug, med error or bystander info? peri-arrest? gastric lavage?

Tension pneumothorax – decompress (needle or finger thoracostomy prior to intercostal catheter), remember to avoid 2ICS and mid clavicular line in large folks(22)

Tamponade – pericardiocentesis, open chest

Thromboembolism – thrombolysis (proven or suspected pulmonary embolus), be prepared to give TNK/TPA early and run the arrest for a while(23)

PEA is so nebulous it is hardly even helpful for the experienced resuscitation leader. The Littman algorithm helps unpack this catch-all term. It is based on ECG waveform and bedside ultrasound findings and is helpful in guiding the treatment of PEA arrests:

One: Determine if the PEA is narrow (QRS duration <0.12) or wide (QRS duration ≥0.12)

Two: Narrow-complex PEA is generally caused by mechanical problems caused by right ventricular inflow or outflow obstruction.

Three: Wide-complex PEA is often due to metabolic problems, or ischemia and left ventricular failure (or the above causes with co-existent conduction abnormality)

Source: Littmann et al. A Simplified And Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity. Med Princ Pract 2014; 23: 1 – 6. PMID: 23949188

Note: As a skilled ACLS provider you don’t “shock”, you defibrillate or you synchronized cardiovert, try to avoid the non-specific term “shock” - it will also help us to recognize your knowledge and understanding.

BRADYCARDIA

Objectives:

1) Recognize bradyarrhythmias may result in cardiac arrest or complicate resusc outcomes

2) Perform early management of bradyarrhythmias that may result in cardiac arrest or complicate resusc outcomes

Know your equipment! The Philips MRX monitors at the RAH only demand pace and require all 5 leads to transcutaneous pace (TCP). The leading cause of failure to pace in our ED is definitely a lead detaching. Many EMS services used fixed modes and do not require limb leads. So, know your equipment in your setting.

Bradycardia begins at 50bpm and below. After you recognize the low heart rate you need to determine if it is stable or unstable. When determining stability, even more important than the numerical value of the blood pressure is the indicators of end-organ perfusion: skin, mentation/symptoms and urine output (that last one is not super relevant in this context though). In this course we won’t give you borderline blood pressures in your scenarios instead we’ll give you low blood pressures with pallor, diaphoresis, dizziness, reports of palpitations and light-headedness. The AHA suggests unstable bradycardias cause: hypotension, altered mental status, signs of shock, ischemic chest discomfort and acute heart failure.

When looking at conduction problems, you are best to look at whichever lead shows p waves most clearly. This is usually lead II or V1. The PR interval the time taken for the depolarization to spread from the SA node to the ventricular muscle. This should not be greater than 0.2s – i.e. 1 big square.

First degree Heart block

If the PR interval is greater than 0.2s, then we call it first degree block. All the waves will still be present, there will just be a larger than normal “gap” between the P wave and QRS complex.

First degree block is not in itself very important.

Second degree Heart block

This is where there is an intermittent absence of QRS complexes – and thus an indication that there is a blockage in conduction somewhere between the AV nodes and the ventricles.

Second degree type 1 (Wenckebach) – progressive lengthening of the PR interval followed by an absence of the QRS, then a shortened PR interval and normal QRS, and the cycle begins again. The cycle is variable in length, and the R-R interval shortens with the lengthening of the PR interval

Second degree type 2– this is where there is a regular rhythm for a while, and a constant PR interval, but every now and again there is an absent QRS.

Causes of second degree heart blocks

Acute – MI

Chronic – heart disease (CHD)

Weckenbach and Mobitz type 2 don’t require and specific treatment

just focus on stable versus unstable!

Third degree Heart block – complete heart block

This occurs when atrial contraction is normal, but no beats are conducted to the ventricles.

The ventricles are still excited by their own internal ‘ectopic pacemaker’ system! Thus, the definition of complete heart block is:

Causes

MI – it will occur acutely, and is often transient

If they have poor perfusion, you may give 0.5mg of atropine IV push every 3 to 5 minutes, just like the other meds we’ve mentioned. Atropine is a parasympatholytic medication (blocks the innervation of the vagus nerve). If atropine will significantly delay chronotropic medications or transcutaneous pacing, you may consider skipping it all together. Only works where the vagus nerve innervates.

You’ve got choices. The AHA puts TCP on the same level of evidence and strength of recommendation as dopamine and epinephrine infusion. There’s evidence to suggest that time from order to medication coming out of the intravenous cannula in the best possible lab situation will all your equipment already gathered is seven minutes.(24) In many settings TCP is faster and has less possibility of delay or error. In our scenarios, we’ll be emphasizing the use of TCP.

If you’re giving meds, then generally it’s:

Chronotropes

Dopamine 2-10 mcg/kg/min, (max 50 mcg/kg/min) - prefilled bag 400mg/250mL (1.6mg/mL)

Epinephrine 2-10 mcg/min (~0.03-0.2 mcg/kg/min, max 1 mcg/kg/min), the AHS parenteral manual does not include bradycardia as an indication for its use Standard concentration = 16mcg/mL, mix by putting 4mg/4mL 1:1000 epi in a 250mL minibag High concentration = 60mcg/mL, mix by putting 15mg/15mL 1:1000 in a 250mL minibag

Isoproterenol 2-10 mcg/min (RAH CCU occasional preference) - the parenteral manual states it is to be used when TCP and dopamine fail, but we sometimes see it first line. It also mentions its use in suppressing torsades de pointes - yet it doesn’t mention epi in bradycardia… WTF? Standard concentration is 4mcg/mL, mix 1mg in a 250mL minibag High concentration is 8mcg/mL, mix 2mg in a 250mL minibag



If TCP and meds are inefficient, consult and expert and prepare for Transvenous pacing.

This is such a fun algorithm because there are many treatment options.

References