Some pectus excavatum patients have a metal ‘Nuss bar’ inserted below the sternum which can make chest compressions more difficult. In those without one, standard compression depths compress the left ventricle more than in non-pectus subjects, and might lead to myocardial injury.
This has led to a recommendation in the journal Resuscitation:
“Until further studies are available, we recommend strong chest compressions, according to the current guidelines, in PE patients with a sternal Nuss bar and, to minimize the risk of myocardial injury, we suggest a reduced chest compression depth (approximately 3–4 cm) at the level of lower half of the sternum in PE patients who have not had corrective surgery.”
Cardiopulmonary resuscitation in pectus excavatum patients: Is it time to say more?
Resuscitation. 2014 Dec 10.[Epub ahead of print]
Already well publicised on social media, the team at Hennepin County published a retrospective comparison between patients with refractory VF who received esmolol with those who did not(1). The results are impressive and I look forward to further studies on this.
I work in an ED in a hospital with no cath lab and no access to extracorporeal life support, limiting our options for patients who remain in shockable rhythms despite ACLS interventions. We now have esmolol available in our resus room. You might want to keep it in your list of options for ACLS-refractory VF, which might also include double sequential external defibrillation(2) and even stellate ganglion block.
The dose of esmolol used was: loading dose 500 mcg/kg, followed by infusions of 0, 50, or 100 mcg/kg/min
An important point to note in the esmolol study is that almost all patients received high-quality mechanical CPR with the combined use of an impedence threshold device to augment venous return and cardiac output. The authors “speculate that this additional hemodynamic support may be essential given the hypotensive effects of esmolol.”
1. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation
Resuscitation. 2014 Oct;85(10):1337-41
INTRODUCTION: We compare the outcomes for patients who received esmolol to those who did not receive esmolol during refractory ventricular fibrillation (RVF) in the emergency department (ED).
METHODS: A retrospective investigation in an urban academic ED of patients between January 2011 and January 2014 of patients with out-of-hospital or ED cardiac arrest (CA) with an initial rhythm of ventricular fibrillation (VF) or ventricular tachycardia (VT) who received at least three defibrillation attempts, 300mg of amiodarone, and 3mg of adrenaline, and who remained in CA upon ED arrival. Patients who received esmolol during CA were compared to those who did not.
RESULTS: 90 patients had CA with an initial rhythm of VF or VT; 65 patients were excluded, leaving 25 for analysis. Six patients received esmolol during cardiac arrest, and nineteen did not. All patients had ventricular dysrhythmias refractory to many defibrillation attempts, including defibrillation after administration of standard ACLS medications. Most received high doses of adrenaline, amiodarone, and sodium bicarbonate. Comparing the patients that received esmolol to those that did not: 67% and 42% had temporary return of spontaneous circulation (ROSC); 67% and 32% had sustained ROSC; 66% and 32% survived to intensive care unit admission; 50% and 16% survived to hospital discharge; and 50% and 11% survived to discharge with a favorable neurologic outcome, respectively.
CONCLUSION: Beta-blockade should be considered in patients with RVF in the ED prior to cessation of resuscitative efforts.
2. Double Sequential External Defibrillation in Out-of-Hospital Refractory Ventricular Fibrillation: A Report of Ten Cases.
Prehosp Emerg Care. 2015 January-March;19(1):126-130
Background. Ventricular fibrillation (VF) is considered the out-of-hospital cardiac arrest (OOHCA) rhythm with the highest likelihood of neurologically intact survival. Unfortunately, there are occasions when VF does not respond to standard defibrillatory shocks. Current American Heart Association (AHA) guidelines acknowledge that the data are insufficient in determining the optimal pad placement, waveform, or energy level that produce the best conversion rates from OOHCA with VF.
Objective. To describe a technique of double sequential external defibrillation (DSED) for cases of refractory VF (RVF) during OOHCA resuscitation.
Methods. A retrospective case series was performed in an urban/suburban emergency medical services (EMS) system with advanced life support care and a population of 900,000. Included were all adult OOHCAs having RVF during resuscitation efforts by EMS providers. RVF was defined as persistent VF following at least 5 unsuccessful single shocks, epinephrine administration, and a dose of antiarrhythmic medication. Once the patient was in RVF, EMS personnel applied a second set of pads and utilized a second defibrillator for single defibrillation with the new monitor/pad placement. If VF continued, EMS personnel then utilized the original and second monitor/defibrillator charged to maximum energy, and shocks were delivered from both machines simultaneously. Data were collected from electronic dispatch and patient care reports for descriptive analysis.
Results. From 01/07/2008 to 12/31/2010, a total of 10 patients were treated with DSED. The median age was 76.5 (IQR: 65-82), with median resuscitation time of 51minutes (IQR: 45-62). The median number of single shocks was 6.5 (IQR: 6-11), with a median of 2 (IQR: 1-3) DSED shocks delivered. VF broke after DSED in 7 cases (70%). Only 3 patients (30%) had ROSC in the field, and none survived to discharge.
Conclusion. This case series demonstrates that DSED may be a feasible technique as part of an aggressive treatment plan for RVF in the out-of-hospital setting. In this series, RVF was terminated 70% of the time, but no patient survived to discharge. Further research is needed to better understand the characteristics of and treatment strategies for RVF.
This idea was provoked by a colleague some years ago who could not achieve a palpable pulse during CPR of an arrested asthmatic child. He wondered whether the severe hyperinflation was rendering external cardiac compressions ineffective and whether he should have done a (prehospital) thoracotomy.
The literature is not strong. The 2010 AHA Guidelines rightly focus on reducing hyperinflation by disconnecting the tracheal tube from the ventilator circuit, and they mention ECMO for refractory cases, but there is no mention of open chest CPR.
I can only find two papers discussing it, both pretty old. A case series in the British Medical Journal from 1968 describes three patients with asthma who had asystolic arrests but did not achieve femoral pulses with external compressions(1). In two, open cardiac massage was performed resulting in restoration of sinus rhythm and cardiac output, and one appeared to make a neurological recovery.
A case report in 1987 describes a 32 year old man in asystolic cardiac arrest due to asthma(2):
“Ventilation required very high inflation pressures and little air movement was heard within the chest despite the administration of Adrenaline 1 mg and Aminophylline 250mg intravenously, and Adrenaline 1mg via the endotracheal tube. This was followed by an intravenous infusion of 100 ml of 8.4% Sodium Bicarbonate solution. External cardiac massage failed to produce a palpable pulse in the carotid area. The chest was, therefore, opened through a left anterolateral thoracotomy. The lungs appeared hyperinflated, bulky and tense and did not collapse when the pleural cavity was opened. The pericardium was opened and asystole confirmed, following eight to ten compressions of the heart some intrinsic activity commenced, ventilation also became much easier.”
He achieved ROSC and became haemodynamically stable but failed to wake up and treatment was withdrawn some days later.
Neither reports include mention of disconnection strategies to reduce hyperinflation. The lack of neurological recovery is not surprising given the apparent prolonged state of arrest the patients were resuscitated from. However there does appear to be a survivor who may not have made it had standard resuscitation (at the time) been continued.
Does this mean I would open the chest in an arrested asthma patient?
Not straight away, no. I would treat dynamic hyperinflation with tube disconnection and external compressions. I would correct absolute and relative hypovolaemia with crystalloid. I would treat bronchospasm (and possible anaphylaxis) with intravenous adrenaline/epinephrine. And I would exclude pneumothorax, possibly with ultrasound or more likely with bilateral open thoracostomies. If however these measures resulted in no detectable carotid flow with external cardiac compressions, ECMO was not available, and the arrest was not prolonged, I would definitely consider doing internal cardiac massage via thoracotomy.
What about you?
1. Grant IW, Kennedy WP, Malone DN
Deaths from asthma
Br Med J. 1968 May 18;2(5602):429–30
2. Diament RH, Sloan JP
Failed resuscitation in acute severe asthma: a medical indication for emergency thoracotomy?
Arch Emerg Med. 1987 Dec;4(4):233–5