A  75 year old male experienced a syncopal episode. The event was witnessed by family members who contacted 9-1-1. On arrival of EMS personnel the patient appears acutely ill. He is pale, diaphoretic and cool to touch. He states that he is feeling lightheaded and weak.

Medical History

• Hypertension
• Hyperlipidemia
• Gout
• Bilateral knee replacement
• Left bundle branch block

The family reports the patient is seeing a cardiologist and is scheduled for pacemaker implantation in 3 weeks due to previous episodes of symptomatic bradycardia.

Medications

• Zocor (Simvastatin)
• Lopressor (Metoprolol)
• Aloprim (Allopurinol)
• Multi-vitamins

Vital Signs

• RR: 20
• HR: 20
• BP: 80/48 mm Hg
• SpO2: 93% on room air
• Capillary blood glucose: 118 mg/dL

Breath sounds are clear bilaterally.

The patient is placed on O2 via nasal cannula at 2 LPM with ETCO2 of 16 mmHg.

Cardiac monitoring is established and the following 12 lead ECG is obtained.

When considering bradycardia management, 3 initial questions should be answered:

• Is the patient bradycardic?
• Is the patient symptomatic?
• Is the patient symptomatic from the bradycardia?

If all of these have been answered with a YES, determine the patient’s hemodynamic status.

Signs of hemodynamically instability:

• Altered mental status
• Hypotension
• Ischemic chest pain
• Signs of hypoperfusion
• Acute pulmonary edema

Based on these criteria this patient is clearly unstable.

Defibrillation pads are placed as a precaution, IV access is obtained, and 250 ml of normal saline is administered en route to the Emergency Department which is 4 minutes away from the scene.

Upon arrival blood samples are obtained and the following 12 lead ECG is obtained.

The patient’s level of consciousness deteriorates and he responds only to painful stimuli.

0.5 mg atropine is administered rapid IV push followed by 10 ml saline flush.

After 1 minute transcutaneous pacing is initiated with no electrical capture up to 90 mA. Transcutaneous pacing is discontinued by the arriving cardiologist who requests vasopressors.

Prior to vasopressors being administered a change is noted on the cardiac monitor and another 12 lead ECG is obtained.

The patient now reports he is feeling better. His skin color improves and his blood pressure normalizes.

The patient was taken to cardiac cath lab for angiography and a permanent pacemaker. The procedure was successful and he was placed in the cardiac step-down unit for further observation.

Discussion

Atropine is an anticholinergic drug – also known as a parasympatholytic – which means that it counteracts increased vagal tone by binding to cardiac muscarinic receptors, which can improve sinus, atrial, and AV-nodal conduction. However, it is not believed to have a direct affect on rhythms of ventricular origin.

The 2010 AHA ECC Guidelines caution:

“Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with TCP…”

There is a caveat regarding TCP:

“TCP is, at best, a temporizing measure. TCP is painful in conscious patients, and, whether effective or not (achieving inconsistent capture), the patient should be prepared for transvenous pacing and expert consultation should be obtained. It is reasonable for healthcare providers to initiate TCP in unstable patients who do not respond to atropine. Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated.”

In this case transcutaneous pacing was not successful but the milliamperes were not increased beyond 90 milliamperes. On the plus side, the clinicians who were caring for this patient realized that they had not achieved capture, which is not always the case!

Fortunately, the patient spontaneously converted into a perfusing rhythm. The atropine may have contributed to the termination of this 3rd degree AV block, it may have been related to sympathetic stimulation from attempted transcutaneous pacing, or it could be a coincidence. These types of scenarios are susceptible to the “post hoc ergo propter hoc” fallacy (after this, therefore because of this).

A common error when treating patients with bradycardia is a rush to drug or electrical therapy prior to identifying reversible causes. Remember, Hs and Ts aren’t just for asystole and PEA!

Most importantly, hypoxemia should be rapidly identified and treated, but other conditions like hyperkalemia can also cause bradycardia. There is little to lose and much to gain from giving a patient calcium gluconate or calcium chloride prior to pacing. The quote Stephen Smith, M.D.: “The treatment [of hyperkalemia with calcium] is benign and cheap. How many life-threatening diseases can you treat benignly and cheaply?”

The definitive care for this patient was a permanent pacemaker.

Further reading: ACLS Bradycardia Algorithm

References

Neumar R, Otto C, Link M et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18_suppl_3):S729-S767. doi:10.1161/circulationaha.110.970988.

Abrich V, Le R, Friedman P, et al. Aggressive Management of Bradycardia is Associated With Improved Clinical Outcomes and Shorter Length of Stay: A Comparison of Two Academic Centers. Circulation. 2016;134:A20838

EMCrit Podcast 42: A phD in EKG with Steve Smith. EMCrit Podcast. 2011. Available at: https://emcrit.org/emcrit/phd-in-ekg/. Accessed November 26, 2017.

 

It’s 06:30 when EMS is called to an inner-city apartment for an 18-year-old male having a seizure. After gaining entry into the building, Paramedics and First Responders trudge up two flights of stairs and down a narrow, dimly lit hallway, until they find an open door into a dark two-bedroom apartment.  There are three people in the living room, all about 18-years-old, and one of them is lying awkwardly on the floor, propped up against the side of the couch. There is evidence of extensive alcohol and drug consumption littering the scene.

It proves difficult to obtain a complete patient history, since bystanders on scene are still somewhat inebriated, and they remain apprehensive about cooperating with emergency responders. However, the story gathered is as follows.

The three of them were up all night partying, drinking, and ingesting multiple illicit substances. It is reported that the patient was witnessed to have ingested copious amounts of cocaine, “DXM” (Dextromethorphan, or ‘cough syrup’), marijuana, nicotine, and alcohol. Precise amounts are vague, and it’s possible that there may have been even more ingestions that were not reported. The party ended, and they all went to sleep, until one of the party-goers found the patient seizing on the floor at about 06:30 this morning. It’s unknown how long the patient was down prior to being found.

The patient’s medical history is unknown, though it is believed that he is generally a “pretty healthy guy”.

The patient is unresponsive to any stimuli, has a weak and agonal respiratory effort, and a faint and slow carotid pulse. His general appearance is poor, with significant pallor and central cyanosis noted, though he is hot to the touch.

Crews began administering high-quality 2-person BVM ventilation, utilizing a jaw thrust while inserting an OPA, and positioning the patient with padding behind the head to support a proper ear-to-sternal-notch alignment. Intravenous access, fluid resuscitation, reoxygenation, and basic cardiac monitoring is being maintained while extrication from the apartment is coordinated.

His initial vital signs are as follows:

HR – 60/min, and increasing to 100/min once oxygenation and ventilation is administered
RR – 6/minute and ineffective
SpO₂ – Initially <50%, improving to 83% with oxygenation and ventilation
NIBP – 66/34 [44]
Pupils – 6mm bilaterally, extremely sluggish
BGL – 5.0 mmol/L (90 mg/dl)
Temp – 38.5 Celsius (101.3 F)

The following rhythm is observed on the monitor. Shortly later, the patient has a generalized seizure which lasts approximately 5 minutes.

Due to access limitations, the stretcher could not be brought inside to the patient, and so the team of paramedics, police officers and firefighters worked together to move the patient to the ambulance via a device not unlike a large tarp with handles. Once in the ambulance, passive cooling is initiated, and a supraglottic airway is placed. His blood pressure has improved to 87/44 [59], his SpO2 remains in the mid-80’s, and his initial ETCO₂ is 86mmHg. The following 12-lead is acquired:

Paramedics identified this arrhythmia to most-likely be a complication of the cocaine toxicity, and treatment was aimed at hyperventilation and administration of intravenous sodium bicarbonate (NaHCO₃) to correct the acidosis.

The following 12-lead was recorded following the administration of one amp of 50mEq of NaHCO₃ with ongoing attempts at hyperventilation.

The patient’s SpO₂ improved to 100%, his blood pressure remained 85/35 [55], and despite being ventilated at a rate of 30/minute his ETCO₂ remained 86mmHg. Another 50mEq of NaHCO₃ is administered, and the following 12-lead is acquired:

Conclusion

The crew arrived at the hospital shortly after the second amp of NaHCO₃ was given. The ED staff continued administering subsequent doses of NaHCO₃ , a peripheral vasopressor (norepinephrine) was initiated, and he was intubated and placed on a ventilator. Initial arterial blood gases revealed a pH of <6.8, pCO2 of >100mmHg, and a lactate of >20mmol/L. He was sent for a CT-head, which revealed no obvious findings of hemorrhage or anoxic brain injury.

He was admitted to ICU, and his repeat ABG thirty minutes later revealed an improved pH of 7.28 and pCO2 of 48mmHg. Unfortunately, no further follow-up was made available to the author.

Discussion

The critically ill toxicology patient can present many unique challenges to prehospital and ED professionals alike. Obstacles often present themselves simultaneously, including airway compromise, cardiac dysrhythmias, and hemodynamic collapse. In an unconscious patient, this is further complicated by unknown co-ingestions, quantities, and comorbidities.

This patient’s presentation can likely be explained by the complex interaction between each of the substances that were ingested. Cocaine mixed with alcohol forms cocaethylene when metabolized by the liver; a substance that’s significantly more cardiotoxic, and possesses a half-life 3-5 times that of cocaine alone. Amongst it’s multiple mechanisms, it acts as a Class Ic sodium-channel blocker, which is represented on the ECG as a progressive widening of the QRS complexes, and the development of an extreme rightward axis in the frontal plane. These channel-toxic effects are amplified by increases in heart rate and decreases in pH – two elements that are found in spades for this young man.

The deleterious effects of the cocaethylene, combined with the ingestion of significant amounts of dextromethorphan; an antitussive and a NMDA-receptor antagonist;  would likely result in euphoria, tachycardia, hypertension, dissociation, a decreasing level of consciousness, and potentially severe serotonin syndrome. Hyperthermia, tachycardia, and a disrupted respiratory drive would lead to hypercapnia, worsening acidosis, and a decreased seizure threshold. Left unchecked, this would predictably spiral into a self-perpetuating loop, inevitably resulting in profound shock and hemodynamic collapse.

Treating a patient like this with intravenous sodium bicarbonate (NaHCO₃) provides a multi-pronged attack. Following administration, there’s an rapid dissociation of NaHCO₃ into Na + HCO₃. The extra sodium acts to “overload” the sodium-channels blocked, while the bicarbonate acts as a buffer and binds with free hydrogen (H+) ions to form Carbonic Acid (H₂CO₃), which then dissociates into water and carbon dioxide, expressed as HCO₃ + H → H₂CO₃ → H₂O + CO₂. This allows for respiratory correction of the acidosis, and the subsequent alkalinization of the blood helps to reduce the channel-toxic effects of the cocaine.  It should be noted, however, that this requires an increased rate of ventilation to ensure adequate elimination of the rising CO₂ levels that will follow.

In a case as advanced as this one, where severe decompensated shock has developed, stabilization becomes a delicate and complex hurdle. Since our initial treatments are aimed at alkalinization of the blood to reduce cardiotoxicity, there is a resultant left-shift of the oxyhemoglobin dissociation curve, and that leads to a decreased ability for oxygen to offload from the hemoglobin at the level of the tissue beds. This could potentially hamper our attempts to correct the massive hypoxia that’s developed, and so management is usually targeted at a pH of no higher than 7.50-7.55.

Intubation of this patient would also prove delicate, since critical hypotension and acidosis would likely be worsened by the use of most induction agents or paralytics, forcing providers to classify this as a physiologically difficult airway. For this reason, airway management should likely be accomplished using a resuscitate-before-you-intubate approach. Fluid resuscitation should be well underway before RSI, push-dose pressors should be at the ready, and providers should be aware that there’s a high-likelihood of this patient requiring vasopressor support, despite receiving a 20ml/kg crystalloid bolus.

In conclusion, the critically ill mixed-overdose patient requires aggressive yet calculated emergency management from first responders and physicians alike. A clinical understanding of the pathophysiology, as well as the implications of each aspect of treatment, is vitally important in caring for each of these patients.

Further reading on the subject

Cocaine Overdose Presents with Wide Complex Tachycardia – Alec Weir, M.D. ACLSMedicalTraining.com/Blog (2016)

Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmias – Michael E. O’Leary & Jules C. Hancox. British Journal of Clinical Pharmacology (Oct 2009)

Current Concepts: The Serotonin Syndrome – Edward W. Boyer M.D., Ph.D., Michael Shannon M.D., M.P.H. NEJM (2005)

Treatment of patients with cocaine-induced arrhythmias: bringing the bench to the bedside – Robert S Hoffman Br J Clin Pharmacol. (2010)

Tricyclic Overdose (Sodium-Channel Blocker Toxicity) – Edward Burns, M.D. LifeInTheFastLane.com

Ventricular Fibrillation is considered the most favorable cardiac arrest rhythm, and if treated promptly can result in ROSC with a favorable neurological outcome. Most survival rates are reported using witnessed arrest with a shockable rhythm as opposed to asystole or PEA, as the outcomes of these rhythms are comparatively very poor.

The Resuscitation Academy mantra “everyone in VF survives” has been adopted by many EMS systems around the world to emphasize that these patients can and do survive, and it’s up to us to save them.

Major advances have been made over the past 10 years but CPR and defibrillation are still the bedrock of resuscitation science. The attributes of high-quality CPR were re-affirmed in the 2015 AHA ECC Guidelines.

• Ensuring adequate rate (100-120)
• Ensuring adequate depth (2 to 2.4” or 5 to 6 cm)
• Allowing full chest recoil (avoid leaning)
• Minimizing interruptions to chest compressions
• Avoiding excessive ventilations

Is CPR Before Defibrillation Dogmatic?

In the context of a witnessed arrest by a trained first responder or bystander who has an AED or manual defibrillator, the importance of early defibrillation is irrefutable. We have been told repeatedly that early defibrillation saves lives.

I initially began my research under the assumption that providing 1.5 to 3 minutes of CPR before defibrillation provides oxygen and nutrients to the heart therefore making defibrillation more likely to be successful. However, recent evidence suggests that performing chest compressions while setting up the defibrillator and charging the capacitor may be adequate.

A “CPR first” approach is rooted in evidence suggesting the existence of 3 time-sensitive phases of VF arrest.

1. Electrical phase (0-4 minutes)
2. Circulatory phase (5-10 minutes)
3. Metabolic Phase (> 10 minutes)

Researchers suggested that a period of CPR prior to defibrillation might confer a benefit during the so-called “circulatory phase” of the cardiac arrest.

Evolution of American Heart Association Recommendations

Because it is rare for EMS to arrive on scene during the electrical phase, the 2005 AHA ECC Guidelines made this recommendation:

When an out-of-hospital cardiac arrest is not witnessed by EMS personnel, they may give about 5 cycles of CPR before checking the ECG rhythm and attempting defibrillation (Class IIb). One cycle of CPR consists of 30 compressions and 2 breaths. When compressions are delivered at a rate of about 100 per minute, 5 cycles of CPR should take roughly 2 minutes (range: about 1½ to 3 minutes). This recommendation regarding CPR prior to attempted defibrillation is supported by 2 clinical studies (LOE 2, LOE 3) of adult out-of-hospital VF SCA. In those studies when EMS call-to-arrival intervals were 4 to 5 minutes or longer, victims who received 1½ to 3 minutes of CPR before defibrillation showed an increased rate of initial resuscitation, survival to hospital discharge, and 1-year survival when compared with those who received immediate defibrillation for VF SCA. One randomized study, however, found no benefit to CPR before defibrillation for non-paramedic-witnessed SCA.

Fast forward 10 years to the 2015 Guidelines.

Observational clinical studies and mechanistic studies in animal models suggest that CPR under conditions of prolonged untreated VF might help restore metabolic conditions of the heart favorable to defibrillation…others have suggested that prolonged VF is energetically detrimental to the ischemic heart, justifying rapid defibrillation attempts regardless of the duration of arrest.

Evidence summary

Five RCTs, 4 observational cohort studies, 3 meta-analyses, and 1 subgroup analysis of an RCT addressed the question of CPR before defibrillation. The duration of CPR before defibrillation ranged from 90 to 180 seconds, with the control group having a shorter CPR interval lasting only as long as the time required for defibrillator deployment, pad placement, initial rhythm analysis, and AED charging. These studies showed that outcomes were not different when CPR was provided for a period of up to 180 seconds before attempted defibrillation compared with rhythm analysis and attempted defibrillation first for the various outcomes examined, ranging from 1-year survival with favorable neurologic outcome to ROSC. Subgroup analysis suggested potential benefit from CPR before defibrillation in patients with prolonged EMS response intervals (4 to 5 minutes or longer) and in EMS agencies with high baseline survival to hospital discharge, but these findings conflict with other subset analyses.  Accordingly, the current evidence suggests that for unmonitored patients with cardiac arrest outside of the hospital and an initial rhythm of VF or pVT, there is no benefit from a period of CPR of 90 to 180 seconds before attempted defibrillation.

Specifically, the ROC PRIMED trial concluded that:

Among patients who had an out-of-hospital cardiac arrest, we found no difference in the outcomes with a brief period, as compared with a longer period, of EMS-administered CPR before the first analysis of cardiac rhythm.

The ROC Investigators subsequently found that EMS systems with a VF survival rate < 20% appeared to do better with an “analyze first” strategy. Conversely, EMS systems with a VF survival rate > 20% appeared to do better with a “analyze late” strategy.

Can the VF Waveform Determine the Likelihood of Successful Defibrillation?

Ventricular fibrillation sometimes begins as ventricular tachycardia, and if left untreated deteriorates into fine VF. Fine VF predictably results in conversion to asystole or continued VF, but rarely to a perfusing rhythm.

Berg et al. performed a randomized, controlled trial using animals. After inducing VF in swine for 8 minutes, they were randomly assigned to either immediate defibrillation, or defibrillation provided after 90 seconds of CPR. Nine out of 15 attained ROSC in the CPR first group, and zero out of 15 who were defibrillated first resulted in ROSC. Their conclusion?

Pre-countershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.

Additionally, they determined there was a mathematical relationship between the VF waveform and chances of successful defibrillation. The animals who received CPR first had a much higher median frequency, and a much higher rate of ROSC than those that did not.

In the field, whether or not VF is “fine” or “coarse” is typically based on visual inspection of the waveform. What if there was a way to accurately determine which patients would benefit from defibrillation and those that would not, thus eliminating unnecessary pauses and ineffective shocks?

Callaway et al. and Eftestol et al. supported the theory that VF frequency and amplitude could be used to determine which patients will respond to countershock.

Eftestol et al. concluded:

CPR done by professionals can improve the chance for ROSC and ultimate survival of patients with prolonged cardiac arrest and significantly deteriorated myocardium. This study also indicates that CPR periods of 3 minutes might be better for the myocardium than shorter periods. Finally, together with the studies showing rapid deterioration of the myocardium in even a few seconds without CPR after a cardiac arrest, it gives the important message that periods without CPR (for ECG analysis, defibrillation charging, pulse checks, intubation attempts, etc) should be kept to a minimum. This is frequently not the case clinically.

As promising as this may have seemed, an article in Circulation by Freese et al. evaluated the theory of defibrillation based on waveform analysis, and the results were disappointing.

Use of a waveform analysis algorithm to guide the initial treatment of out-of-hospital cardiac arrest patients presenting in VF did not improve overall survival compared with a standard shock-first protocol. Further study is recommended to examine the role of waveform analysis for the guided management of VF.

The Bottom Line

The totality of the evidence suggests that defibrillation as soon as practicable (with the caveat that high quality chest compressions are performed while setting up the defibrillator) is equivalent to a prescribed interval of CPR prior to the first shock in most instances.

EMS systems that measure the “patient’s side to first shock” interval know that it usually takes at least 1 minute to power on the defibrillator, extend the cables, attach the pads, charge the capacitor, and deliver the shock. During that interval, there’s no reason that the patient can’t receive continuous chest compressions.

One benefit to emphasizing a “shock as soon as possible” approach is that it’s the same for EMS-witnessed cardiac arrest.

Alternatively, defibrillation can be delivered after the first 2-minute cycle. It seems likely that CPR quality plays a more important role than the exact timing of the first shock.

References

Baker PW, Conway J, Cotton C, Ashby DT, Smyth J, Woodman RJ, Grantham H; Clinical Investigators. Defibrillation or cardiopulmonary resuscitation first for patients with out-of-hospital cardiac arrests found by paramedics to be in ventricular fibrillation? A randomised control trial. Resuscitation. 2008;79:424–431. doi: 10.1016/j.resuscitation.2008.07.017.

Bradley SM, Gabriel EE, Aufderheide TP, Barnes R, Christenson J, Davis DP, Stiell IG, Nichol G; Resuscitation Outcomes Consortium Investigators. Survival increases with CPR by Emergency Medical Services before defibrillation of out-of-hospital ventricular fibrillation or ventricular tachycardia: observations from the Resuscitation Outcomes Consortium. Resuscitation. 2010;81:155–162. doi: 10.1016/j. resuscitation.2009.10.026.

Cobb LA, Fahrenbruch CE, Walsh TR, Copass MK, Olsufka M, Breskin M, Hallstrom AP. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA. 1999;281:1182–1188.

Freese J, Jorgenson D, Liu P et al. Waveform Analysis-Guided Treatment Versus a Standard Shock-First Protocol for the Treatment of Out-of-Hospital Cardiac Arrest Presenting in Ventricular Fibrillation: Results of an International Randomized, Controlled Trial. Circulation. 2013;128(9):995-1002. doi:10.1161/circulationaha.113.003273.

Gilmore C, Rea T, Becker L, Eisenberg M. Three-Phase Model of Cardiac Arrest: Time-Dependent Benefit of Bystander Cardiopulmonary Resuscitation. The American Journal of Cardiology. 2006;98(4):497-499. doi:10.1016/j.amjcard.2006.02.055.

Hayakawa M, Gando S, Okamoto H, Asai Y, Uegaki S, Makise H. Shortening of cardiopulmonary resuscitation time before the defibrilla- tion worsens the outcome in out-of-hospital VF patients. Am J Emerg Med. 2009;27:470–474. doi: 10.1016/j.ajem.2008.

Huang Y, He Q, Yang LJ, Liu GJ, Jones A. Cardiopulmonary resuscitation (CPR) plus delayed defibrillation versus immediate defibrillation for out-of-hospital cardiac arrest. Cochrane Database Syst Rev. 2014;9:CD009803. doi: 10.1002/14651858.CD009803.pub2.

Jacobs IG, Finn JC, Oxer HF, Jelinek GA. CPR before defibrillation in out-of-hospital cardiac arrest: a randomized trial. Emerg Med Australas. 2005;17:39–45. doi: 10.1111/j.1742-6723.2005.00694.x.

Kleinman M, Brennan E, Goldberger Z et al. Part 5: Adult Basic Life Support and Cardiopulmonary Resuscitation Quality. Circulation. 2015;132(18 suppl 2):S414-S435. doi:10.1161/cir.0000000000000259.

Koike S, Tanabe S, Ogawa T, Akahane M, Yasunaga H, Horiguchi H, Matsumoto S, Imamura T. Immediate defibrillation or defibrillation after cardiopulmonary resuscitation. Prehosp Emerg Care. 2011;15:393–400. doi: 10.3109/10903127.2011.569848.

Ma MH, Chiang WC, Ko PC, Yang CW, Wang HC, Chen SY, Chang WT, Huang CH, Chou HC, Lai MS, Chien KL, Lee BC, Hwang CH, Wang YC, Hsiung GH, Hsiao YW, Chang AM, Chen WJ, Chen SC. A randomized trial of compression first or analyze first strategies in patients with out-of-hospital cardiac arrest: results from an Asian community. Resuscitation. 2012;83:806–812. doi: 10.1016/j.resuscitation.2012.01.009.

Meier P, Baker P, Jost D, Jacobs I, Henzi B, Knapp G, Sasson C. Chest compressions before defibrillation for out-of-hospital cardiac arrest: a meta-analysis of randomized controlled clinical trials. BMC Med. 2010;8:52. doi: 10.1186/1741-7015-8-52.

When trying to decide on a subject for this blog post, I remembered an article I read a few months ago originally published in the Journal of Paramedic Practice, by Logarajah and Alinier titled ‘An Integrated ABCDE Approach To Managing Medical Emergencies Using CRM Principles’.

At the time I first read this article I was lucky enough to have the experience of undertaking a secondment on a Critical Care Paramedic unit and had attended a number of high acuity incidents, and felt the principles outlined assisted me in preparing when heading to these.

I feel using a structured approach can help break down the mental workload, especially when applied to incidents that involve a large degree of decision-making and prioritization. The principles described can be applied to all incidents you may attend as a Paramedic, however in keeping with the increasing focus on human factors and CRM in cardiac arrest management I have decided to tailor them to this area.

Its 17:00pm and nearing the end point of a tiring weekend day shift, just after arriving back on station for the first time since you left in the early hours of the morning you are called to a 51 year old male reported to be in cardiac arrest. Two local community responders and a Technician crew are also attending however you are the only Paramedic available. As you drive to the scene you start to mentally plan how you will approach this incident, what will you need to do, where will you transport the patient to…

ABCDE (alongside remembering how your crewmate likes their coffee) is a cornerstone of all levels of emergency medical care and the tried, tested and trusted tool we all use when we don’t know what to do next. Logarajah and Alinier (2014) proposed a modified version of this mnemonic, using CRM principles, as a tool ‘to remember the sequence in which to manage emergencies or difficult situations while ensuring effective and safe teamwork’ (pp.625).

These principles, in relation to thinking about cardiac arrest management, are as follows:

A: AWARENESS, ANTICIPATION & ALLOCATION OF ATTENTION

What details do you have? What are you anticipating you will find?

Awareness can be divided into two areas; self-awareness and situational awareness. Consideration of both these is vital to maintain control of complex situations and prevent the unanticipated development of additional problems. Anticipating what you will encounter on arrival at the scene is highly dependent on how much or little information you have received.

Try and think about what you would expect to find based upon factors such as the type of incident, the location, or the likely cause of cardiac arrest. This can help prepare you with making decisions such as what equipment to take in with you, treatment algorithms to use and logistical issues such as the locations of nearby hospitals and cath labs.

If you have received an update from resources already on scene you can start to plan how you are going to allocate your clinical attention once you arrive and discuss your plan of action.

B: ‘BE IN THE REQUIRED ROLE’ & BEHAVIOUR

What do you need to do for the team? How can you make the most of your skills? Are you required to be a leader or a follower?

Some of this is dependent on your clinical role however everybody needs to build and maintain a team effort. Does your service use a ‘pit-crew’ CPR approach? Knowing the role you need to assume beforehand can save vital time in decision-making and reduce disruption to already established and organized resuscitation attempts.

C: CALL FOR HELP, COMMUNICATION & COGNITIVE AIDS/CHECKLISTS

Are you going to be able to communicate effectively? What barriers will there be?

Factors such as noise, incidents involving multiple patients, a chaotic scene and poor lighting can all contribute to poor communication. Check your radio, do you know the correct channel to pass updates on? Use your awareness and anticipation to request extra assistance, such as enhanced care teams, early if you think it may be needed.

‘Medicine is not a memory game’

Ensure you have cognitive aids available. Cardiac arrest checklists, resuscitation algorithms and clinical guidelines all can save bandwidth and enable you and the team to focus on the task at hand without having to perform complex mental calculations such as drug doses or tube lengths.

D: DYNAMIC PRIORITISATION, DECISION MAKING & DELEGATION

Do you have enough help? Does everyone have a task?

Based on your awareness and anticipation of the resuscitation be decisive on your immediate priorities, make and execute a plan of action, but remember to also be prepared to change as required.

Ensure you have enough resources available for everybody to be able to concentrate on their task fully and not be overloaded. As the resuscitation progresses it is likely your priorities will change and require you to adapt to these and redistribute the workload accordingly.

E: ERROR WISDOM & ENVIRONMENT

What are the potential errors that could occur? Can you carry out effective resuscitation within the environment the patient is in? What needs to change?

‘Forewarned is forearmed’

Be aware of the potential for errors. During stressful events such as resuscitation attempts, with a number of interventions performed and drugs administered, it is easy for these to occur. Considering this risk beforehand and utilizing tools such as checklists and pocket books can help minimize the potential for mistakes and refresh things in your head that you may not encounter very often in practice.

If the patient you are attending is in an unusual environment, or a scene that may pose a danger, consider the options you have to minimize hazards and allow you and the team to carry out the resuscitation safely. Even in domestic locations, during the initial stages of resuscitation it is easy to forget about the environment you are working in. Ensure you have enough space to work in and if not, move something!

I hope you have found this interesting. It may all seem like common sense and I am sure we all give these factors consideration every day with every incident we attend, however personally I feel having a structured approach is worth thinking about to reduce mental overload in times when we all need a little bit of extra brain capacity!

Reference

Logarajah, S. and Alinier, G. (2014). An Integrated ABCDE Approach To Managing Medical Emergencies Using CRM Principles (PDF – Subscription Required). Journal of Paramedic Practice, 6(12), pp.620-625.