The use of inhaled nitric oxide is established in certain groups of patients: it improves oxygenation (but not survival) in patients with acute respiratory distress syndrome(1), and it is used in neonatology for management of persistent pulmonary hypertension of the newborn(2). But it can be applied in other resuscitation settings: in arrested or peri-arrest patients with pulmonary hypertension.
Read this (modified) description of a case managed by one of my resuscitationist friends from an overseas location:
A young lady suffered a placental abruption requiring emergency hysterectomy. She arrested twice in the operating room after suspected amniotic fluid embolism. She had fixed dilated pupils.
She developed extreme pulmonary hypertension with suprasystemic pulmonary artery pressures, and she went down the pulmonary HT spiral as I stood there. On ultrasound her distended RV was making her LV totally collapse. She arrested. Futile CPR was started.
I have never had an extreme pulmonary HT survive an arrest. I grabbed a bag and rapidly set up a manual inhaled Nitric Oxide system and bagged and begged…
She achieved ROSC after some minutes. A repeat ultrasound showed a well functioning LV and less dilated RV.
Today, after 12 hours she is opening her eyes and obeying commands. Still a long way to go, but alive.
It sounds impressive. I don’t have more case details, and don’t know how confident they could be about the diagnosis of amniotic fluid embolism but the presentation certainly fits with acute pulmonary hypertension with RV failure. The use of inhaled nitric oxide has certainly been described for similar scenarios before(3). But it raises bigger questions: is this something we should all be capable of? Are there cardiac arrests involving or caused by pulmonary hypertension that will not respond to resuscitation without nitric oxide?
Inhaled nitric oxide is a pulmonary vasodilator. It decreases right-ventricular afterload and improves cardiac index by selectively decreasing pulmonary vascular resistance without causing systemic hypotension(4).
RV failure and pulmonary hypertension
Patients may become shocked or suffer cardiac arrest due to acute right ventricular dysfunction. This may be due to a primary cardiac cause such as right ventricular infarction (always consider this in a hypotensive patient with inferior STEMI, and confirm with a right ventricular ECG and/or echo). Alternatively it could be due to a pulmonary or systemic cause resulting in severe pulmonary hypertension, causing secondary right ventricular dysfunction. The commonest causes of acute pulmonary hypertension are massive PE, sepsis, and ARDS(5).
The haemodynamic consequences of RV failure are reduced pulmonary blood flow and inadequate left ventricular filling, leading to decreased cardiac output, shock, and arrest. In severe acute pulmonary hypertension the RV distends, resulting in a shift of the interventricular septum which compresses the LV and further inhibits LV filling (the concept of ventricular interdependence).
What’s wrong with standard ACLS?
In some patients with PHT who arrest, CPR may be ineffective due to a failure to achieve adequate pulmonary blood flow and ventricular filling. In one study of patients with known chronic PHT who arrested in the ICU, survival rates even for ventricular fibrillation were extremely poor and when measured end tidal carbon dioxide levels were very low. In the same study it was noted that some of the survivors had received an intravenous bolus administration of iloprost, a prostacyclin analogue (and pulmonary vasodilator) during CPR(6).
CPR may therefore be ineffective. Intubation and positive pressure ventilation may also be associated with haemodynamic deterioration in PHT patients(7), and intravenous epinephrine (adrenaline) has variable effects on the pulmonary circulation which could be deleterious(8).
If inhaled nitric oxide (iNO) can improve pulmonary blood flow and reduce right ventricular afterload, it could theoretically be of value in cases of shock or arrest with RV failure, especially in cases of pulmonary hypertension; these are patients who otherwise have poor outcomes and may not benefit from CPR.
Is the use of iNO described in shock or arrest?
Numerous case reports and series demonstrate recovery from shock or arrest following nitric oxide use in various situations of decompensated right ventricular failure from pulmonary hypertension secondary to pulmonary fibrotic disease(9), pneumonectomy surgery(10), and pulmonary embolism(11) including post-embolectomy(12).
Acute hemodynamic improvement was demonstrated following iNO therapy in a series of right ventricular myocardial infarction patients with cardiogenic shock(13).
A recent systematic review of inhaled nitric oxide in acute pulmonary embolism documented improvements in oxygenation and hemodynamic variables, “often within minutes of administration of iNO”. The authors state that these case reports underscore the need for randomised controlled trials to establish the safety and efficacy of iNO in the treatment of massive acute PE(14).
Why aren’t they telling us to use it?
If iNO may be helpful in certain cardiac arrest patients, why isn’t ILCOR recommending it? Actually it is mentioned – in the context of paediatric life support. The European Resuscitation Council states:
ERC Guideline: (Paediatric) Pulmonary hypertension
There is an increased risk of cardiac arrest in children with pulmonary hypertension.
Follow routine resuscitation protocols in these patients with emphasis on high FiO2 and alkalosis/hyperventilation because this may be as effective as inhaled nitric oxide in reducing pulmonary vascular resistance.
Resuscitation is most likely to be successful in patients with a reversible cause who are treated with intravenous epoprostenol or inhaled nitric oxide.
If routine medications that reduce pulmonary artery pressure have been stopped, they should be restarted and the use of aerosolised epoprostenol or inhaled nitric oxide considered.
Right ventricular support devices may improve survival
Should we use it?
So if acute (or acute on chronic) pulmonary hypertension can be suspected or demonstrated based on history, examination, and echo findings, and the patient is in extremis, it might be anticipated that standard ACLS approaches are likely to be futile (as they often are if the underlying cause is not addressed). One might consider attempts to induce pulmonary vasodilation to improve pulmonary blood flow and LV filling, improving oxygenation, and reducing RV afterload as means of reversing acute cor pulmonale.
Are there other pulmonary vasodilators we can use?
iNO is not the only means of inducing pulmonary vasodilation. Oxygen, hypocarbia (through hyperventilation)(15), and alkalosis are all known pulmonary vasodilators, the latter providing an argument for intravenous bicarbonate therapy from some quarters(16). Prostacyclin is a cheaper alternative to iNO(17) and can be given by inhalation or intravenously, although is more likely to cause systemic hypotension than iNO. Some inotropic agents such as milrinone and levosimendan can lower pulmonary vascular resistance(18).
What’s the take home message?
The take home message for me is that acute pulmonary hypertension provides yet another example of a condition that requires the resuscitationist to think beyond basic ACLS algorithms and aggressively pursue and manage the underlying cause(s) of shock or arrest. Inhaled pulmonary vasodilators may or may not be available but, as always, whatever resources and drugs are used, they need to be planned for well in advance. What’s your plan?
1. Adhikari NKJ, Dellinger RP, Lundin S, Payen D, Vallet B, Gerlach H, et al.
Inhaled Nitric Oxide Does Not Reduce Mortality in Patients With Acute Respiratory Distress Syndrome Regardless of Severity.
Critical Care Medicine. 2014 Feb;42(2):404–12
2. Steinhorn RH.
Neonatal pulmonary hypertension.
Pediatric Critical Care Medicine. 2010 Mar;11:S79–S84 Full text
3. McDonnell NJ, Chan BO, Frengley RW.
Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism.
International Journal of Obstetric Anesthesia. 2007 Jul;16(3):269–73
4. Creagh-Brown BC, Griffiths MJ, Evans TW.
Bench-to-bedside review: Inhaled nitric oxide therapy in adults.
Critical Care. 2009;13(3):221 Full text
5. Tsapenko MV, Tsapenko AV, Comfere TB, Mour GK, Mankad SV, Gajic O.
Arterial pulmonary hypertension in noncardiac intensive care unit.
Vasc Health Risk Manag. 2008;4(5):1043–60 Full text
6. Hoeper MM, Galié N, Murali S, Olschewski H, Rubenfire M, Robbins IM, et al.
Outcome after cardiopulmonary resuscitation in patients with pulmonary arterial hypertension.
American Journal of Respiratory and Critical Care Medicine. 2002 Feb 1;165(3):341–4.
7. Höhn L, Schweizer A, Morel DR, Spiliopoulos A, Licker M.
Circulatory failure after anesthesia induction in a patient with severe primary pulmonary hypertension.
Anesthesiology. 1999 Dec;91(6):1943–5 Full text
8. Witham AC, Fleming JW.
The effect of epinephrine on the pulmonary circulation in man.
J Clin Invest. 1951 Jul;30(7):707–17 Full text
9. King R, Esmail M, Mahon S, Dingley J, Dwyer S.
Use of nitric oxide for decompensated right ventricular failure and circulatory shock after cardiac arrest.
Br J Anaesth. 2000 Oct;85(4):628–31. Full text
10. Fernández-Pérez ER, Keegan MT, Harrison BA.
Inhaled nitric oxide for acute right-ventricular dysfunction after extrapleural pneumonectomy.
Respir Care. 2006 Oct;51(10):1172–6 Full text
11. Summerfield DT, Desai H, Levitov A, Grooms DA, Marik PE.
Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series.
Respir Care. 2012 Mar 1;57(3):444–8 Full text
12. Schenk P, Pernerstorfer T, Mittermayer C, Kranz A, Frömmel M, Birsan T, et al.
Inhalation of nitric oxide as a life-saving therapy in a patient after pulmonary embolectomy.
Br J Anaesth. 1999 Mar;82(3):444–7 Full text
13. Inglessis I, Shin JT, Lepore JJ, Palacios IF, Zapol WM, Bloch KD, et al.
Hemodynamic effects of inhaled nitric oxide in right ventricular myocardial infarction and cardiogenic shock.
Journal of the American College of Cardiology. 2004 Aug;44(4):793–8 Full text
14. Bhat T, Neuman A, Tantary M, Bhat H, Glass D, Mannino W, Akhtar M, Bhat A, Teli S, Lafferty J.
Inhaled nitric oxide in acute pulmonary embolism: a systematic review.
Rev Cardiovasc Med 2015;16(1):1–8.
15. Mahdi M, Joseph NJ, Hernandez DP, Crystal GJ, Baraka A, Salem MR.
Induced hypocapnia is effective in treating pulmonary hypertension following mitral valve replacement.
Middle East J Anaesthesiol. 2011 Jun;21(2):259-67
16. Evans S, Brown B, Mathieson M, Tay S.
Survival after an amniotic fluid embolism following the use of sodium bicarbonate.
BMJ Case Rep. 2014;2014
17. Fuller BM, Mohr NM, Skrupky L, Fowler S, Kollef MH, Carpenter CR.
The Use of Inhaled Prostaglandins in Patients With ARDS: A Systematic Review and Meta-analysis.
Chest. 2015 Jun;147(6):1510–22 Full text
18. LITFL: Right Ventricular Failure
Life In The Fast Lane iNO info
Comments Off on Post-arrest hypothermia in children did not improve outcome
Many clinicians extrapolate adult research findings to paediatric patients because there’s no alternative, and until now we’ve had to do that with post-cardiac arrest therapeutic hypothermia after paediatric cardiac arrest.
However the THAPCA trial in the New England Journal of Medicine now provides child-specific data.
It was a multicentre trial in the US which included children between 2 days and 18 years of age, who had had an out-of-hospital cardiac arrest and remained comatose after return of circulation. They were randomised to therapeutic hypothermia (target temperature, 33.0°C) or therapeutic normothermia (target temperature, 36.8°C) within 6 hours after the return of circulation.
Therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit with respect to survival with good functional outcome at 1 year, and survival at 12 months did not differ significantly between the treatment groups.
These findings are similar to the adult TTM trial, although there are some interesting differences. In the paediatric study, the duration of temperature control was longer (120 hrs vs 36 hrs in the adult study), respiratory conditions were the predominant cause of paediatric cardiac arrest (72%), and there were only 8% shockable rhythms in the paediatric patients, compared with 80% in the adult study.
The full text is available here.
Therapeutic Hypothermia after Out-of-Hospital Cardiac Arrest in Children
N Engl J Med. 2015 Apr 25
Background: Therapeutic hypothermia is recommended for comatose adults after witnessed out-of-hospital cardiac arrest, but data about this intervention in children are limited.
Methods: We conducted this trial of two targeted temperature interventions at 38 children’s hospitals involving children who remained unconscious after out-of-hospital cardiac arrest. Within 6 hours after the return of circulation, comatose patients who were older than 2 days and younger than 18 years of age were randomly assigned to therapeutic hypothermia (target temperature, 33.0°C) or therapeutic normothermia (target temperature, 36.8°C). The primary efficacy outcome, survival at 12 months after cardiac arrest with a Vineland Adaptive Behavior Scales, second edition (VABS-II), score of 70 or higher (on a scale from 20 to 160, with higher scores indicating better function), was evaluated among patients with a VABS-II score of at least 70 before cardiac arrest.
Results: A total of 295 patients underwent randomization. Among the 260 patients with data that could be evaluated and who had a VABS-II score of at least 70 before cardiac arrest, there was no significant difference in the primary outcome between the hypothermia group and the normothermia group (20% vs. 12%; relative likelihood, 1.54; 95% confidence interval [CI], 0.86 to 2.76; P=0.14). Among all the patients with data that could be evaluated, the change in the VABS-II score from baseline to 12 months was not significantly different (P=0.13) and 1-year survival was similar (38% in the hypothermia group vs. 29% in the normothermia group; relative likelihood, 1.29; 95% CI, 0.93 to 1.79; P=0.13). The groups had similar incidences of infection and serious arrhythmias, as well as similar use of blood products and 28-day mortality.
Conclusions: In comatose children who survived out-of-hospital cardiac arrest, therapeutic hypothermia, as compared with therapeutic normothermia, did not confer a significant benefit in survival with a good functional outcome at 1 year.
Comments Off on CPR in Pectus Excavatum
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
Comments Off on London Cardiac Arrest Symposium 2014
The focus of the entire day is cardiac arrest and this is the second day of the London Cardiac Arrest Symposium.
Professor Niklas Nielsen kicked off with a presentation of his Targeted Temperature Management trial. It seems that even now there is uncertainty in the interpretation of this latest study. I take heart from the knowledge that Prof Nielsen has changed the practice of his institution to reflect the findings of his study – I have certainly changed my practice. But we need to remain aware that there is more work to be done to answer the multiple questions that remain and the need for further RCTs is recognised.
The management of Cardiac arrest after avalanche is not a clinical scenario that I imagine I’ll ever find myself in. The management is well documented in the ICAR MEDCOM guidelines 2012. Dr Peter Paal reminded us that you’re not dead until you’re rewarmed and dead unless: with asystole, CPR may be terminated (or withheld) if a patient is lethally injured or completely frozen, the airway is blocked and duration of burial >35 min, serum potassium >12 mmol L(-1), risk to the rescuers is unacceptably high or a valid do-not-resuscitate order exists.
The age old question about prognostication after cardiac arrest was tackled by Prof Mauro Oddo. He covered the evidence for clinical examination, SSPE, EEG, and neurone specific enolase. Bottom line, all of these modalities are useful but none are specific enough to be used as a stand alone test so multiple modalities are required.
SAMU is leading the way with prehospital ECMO. They have mastered the art of cannulation (in the Louvre no less!) but there haven’t enough cases to demonstrate a mortality benefit. The commencement of ECMO prehospital reduces low flow time and theoretically should improve outcomes. This is begging for a RCT.
The experience of the Italians with in hospital ECMO shoes a better survival rate for in-hospital rather than out of hospital cardiac arrests, explained Dr Tomasso Mauri. They treat patients with a no flow time of <6min and low flow rate of <45min and had a 31% ICU survival rate. If you want to learn more about ED ECMO go to http://edecmo.org.
The Douglas Chamberlain lecture this year was Selective aortic arch perfusion presented by Prof James Manning. He spoke about the use of this technique in cardiac arrest and also in trauma (where it is known to you as Zone 1 REBOA).
In cardiac arrest the aim is to improve coronary perfusion, to preserve perfusion to the heart and the brain, offer a route of rapid temperature control and offer a direct route of administration of adrenaline. Coronary perfusion is seen to be supra normal after SAAP. And the suggested place for SAAP is prior to ECMO.
It’s more familiar ground talking about SAAP in trauma. This Zone 1 occlusion preserves cerebral and cardiac perfusion while blood loss is limited and rapid fluid resuscitation can occur.
You can hear Prof Manning on SAAP over at EMCrit (of course!).
It’s been another great conference. Put the dates for next year’s London Trauma & Cardiac Arrest Conferences in your diary: 8th-10th December 2015!
Happy Holidays & Keep Well
Comments Off on Left Ventricular Assist Device for Cardiac Arrest?
An interesting case report by Dr Heidlebaugh and colleagues from the Department of Emergency Medicine at the William Beaumont Hospital describes a 72 year old marathon runner who arrested during cardiac catheterisation. It suggests a possible novel alternative to ECMO for cardiac arrest.
The patient became bradycardic then asystolic during catheterisation of his right coronary artery. High quality CPR was initiated and an Impella LV assist device was placed. This restored cardiac output which was followed by episodes of venticular fibrillation and then ROSC. His initial low ejection fraction of 15% recovered after targeted temperature management on ICU to 50% and he fully recovered neurologically.
This patient already had femoral arterial access for introduction of the Impella, since he was in a cath lab. He also had immediate CPR on arresting, and was an abnormally fit 72 year old. It remains to be seen whether this procedure can be applied to other patients in cardiac arrest. The authors state:
“..until ECLS is readily available, poor survival and neurological outcome after cardiac arrest might be avoided in many patients by the use of pLVAD to offload the LV and enhance perfusion. Furthermore, there may be a subset of patients, in whom the support that pLVAD offers is sufficient to optimize hemodynamic parameters and bridge to ROSC, thus reducing the need for ECLS.”
This video by Dr. I-Wen Wang from the Barnes-Jewish Hospital explains how the Impella is inserted and how it works.
Full Neurologic Recovery and Return of Spontaneous Circulation Following Prolonged Cardiac Arrest Facilitated by Percutaneous Left Ventricular Assist Device
Ther Hypothermia Temp Manag. 2014 Sep 3. [Epub ahead of print]
Sudden cardiac arrest is associated with high early mortality, which is largely related to postcardiac arrest syndrome characterized by an acute but often transient decrease in left ventricular (LV) function. The stunned LV provides poor cardiac output, which compounds the initial global insult from hypoperfusion. If employed early, an LV assist device (LVAD) may improve survival and neurologic outcome; however, traditional methods of augmenting LV function have significant drawbacks, limiting their usefulness in the periarrest period. Full cardiac support with cardiopulmonary bypass is not always readily available but is increasingly being studied as a tool to intensify resuscitation. There have been no controlled trials studying the early use of percutaneous LVADs (pLVADs) in pericardiac arrest patients or intra-arrest as a bridge to return of spontaneous circulation. This article presents a case study and discussion of a patient who arrested while undergoing an elective coronary angioplasty and suffered prolonged cardiopulmonary resuscitation. During resuscitation, treatment included placement of a pLVAD and initiation of therapeutic hypothermia. The patient made a rapid and full recovery.
Image is of M. Joshua Morris, a happy LVAD recipient (not the patient in the described study) who kindly alerted me to this article. Used with permission.
Comments Off on Blunt traumatic arrest in kids
Traumatic cardiac arrest outcomes are not great, but they’re not so bad that resuscitation is futile – a subject I’ve ranted about before.
The largest study on blunt traumatic arrest in children to date has been published, showing that 340 / 7766 kids without signs of life in the field survived to hospital discharge. Neurological status at discharge was not documented. However, this represents 4.4%, or in other words for every 22 blunt traumatically arrested children who underwent prehospital resuscitation, one survived to discharge. The authors describe this survival as ‘dismal’. It’s not great, but my take on it is that survival is possible and in most cases resuscitation should be attempted.
The authors state:
“Based on these data, EMS providers should not be discouraged from resuscitating blunt pediatric trauma patients found in the field with no signs of life“
While the major focus should be on injury prevention, it is worthwhile considering whether more advanced resuscitation in the field could be provided to further increase the number of neurologically intact survivors.
Survival of pediatric blunt trauma patients presenting with no signs of life in the field
J Trauma Acute Care Surg. 2014 Sep;77(3):422-6
BACKGROUND: Prehospital traumatic cardiopulmonary arrest is associated with dismal prognosis, and patients rarely survive to hospital discharge. Recently established guidelines do not apply to the pediatric population because of paucity of data. The study objective was to determine the survival of pediatric patients presenting in the field with no signs of life after blunt trauma.
METHODS: We conducted a retrospective analysis of the National Trauma Data Bank research data set (2002-2010). All patients 18 years and younger with blunt traumatic injuries were identified (DRG International Classification of Diseases-9th Rev. codes 800-869). No signs of life (SOL) was defined on physical examination findings and included the following: pulse, 0; respiratory rate, 0; systolic blood pressure, 0; and no evidence of neurologic activity. These same criteria were reassessed on arrival at the emergency department (ED). Furthermore, we examined patients presenting to the ED who underwent resuscitative thoracotomy (Current Procedural Terminology code 34.02). Our primary outcome was survival to discharge from the hospital.
RESULTS: There were a total of 3,115,597 pediatric patients who were found in the field after experiencing blunt trauma. Of those, 7,766 (0.25%) had no SOL. Seventy percent of the patients with no SOL in the field were male. Survival to hospital discharge of all patients presenting with no SOL was 4.4% (n = 340). Twenty-five percent of the patients in the field with no SOL were successfully resuscitated in the field and regained SOL by the time they arrived to the ED (n = 1,913). Of those patients who regained SOL, 13.8% (n = 265) survived to hospital discharge. For patients in the field with no SOL, survival to discharge was significantly higher in patients who did not receive a resuscitative thoracotomy than in those who did.
CONCLUSION: Survival of pediatric blunt trauma patients in the field without SOL is dismal. Resuscitative thoracotomy poses a heightened risk of blood-borne pathogen exposure to involved health care workers and is associated with a significantly lower survival rate.
Patients in cardiac arrest due to severe hypothermia benefit from extracorporeal rewarming, and it is often recommended that they are treated at centres capable of providing cardiopulmonary bypass or extracorporeal membrane oxygenation (ECMO).
But what if they’re brought to a centre that doesn’t have those facilities?
If you work in such a centre do you have a plan, and are you familiar with what equipment you could use?
One option if you have an ICU is to provide extracorporeal warming using a haemofiltration machine used for renal replacement therapy(1). A double lumen haemofiltration catheter is inserted into a central vein and an ICU nurse can often do the rest, although some variables have to be set by the intensivist, often aided by a standard renal replacement therapy prescription chart. The machines are mobile and can be wheeled into the resus room (I have practiced this set up in resus). It might be worth discussing and practicing this option with your ICU.
Another extracorporeal option is to rig up a rapid infusion device such as a ‘Level 1’ to connect to arterial and venous catheters so that blood from the patient flows through and is warmed by the machine before being returned to the patient(2). Rapid rewarming has been achieved by this method but it requires some modification to the usual set up and so is much less likely to be a realistic option for most teams doing this on very rare occasions.
Less technical options are the traditionally taught warm saline lavage of body cavities such as the thorax and the peritoneal cavity. These can be achieved with readily available catheters and of course should be combined with ventilation with warmed gas and administration of warm intravenous fluid.
Thoracic lavage can be achieved with open thoracotomy or tube thoracostomy. One or two chest tubes can be placed on each side. One technique was described as:
Two 36 French chest tubes were placed in each hemithorax. One tube was placed in the fourth intercostal space in the mid-clavicular line. Another tube was placed into the sixth intercostal space in the mid-axillary line. Sterile saline at 39.0◦C was infused by gravity into each superior chest tube and allowed to drain passively through each inferior tube.(3)
Rapid rewarming at a rate of 6.8◦C per hour was achieved in an arrested hypothermic man using peritoneal lavage. It was done in the operating room with peritoneal lavage (saline 40◦C) with a rapid infusion system (Level 1) through two laparoscopic access sites. It was combined with external forced air rewarming and warm intravenous infusions(4).
Finally some devices manufactured for inducing hypothermia in post-cardiac arrest patients can also be used to rewarm patients, which might be endovascular devices, such as the Cool Line® catheter(5), or external, such as the Arctic Sun® Temperature Management System(6). It’s definitely worth finding out what your critical care services have as far as this equipment goes.
In summary, although the ‘exam answer’ for cardiac arrest due to profound hypothermia is often ECMO/cardiopulmonary bypass, in most centres that’s not an option. It’s helpful to remind ourselves that (1) other extracorporeal rewarming options exist and (2) non-extracorporeal techniques can provide rapid rewarming.
1. Spooner K, Hassani A. Extracorporeal rewarming in a severely hypothermic patient using venovenous haemofiltration in the accident and emergency department. J Accid Emerg Med. 2000 Nov;17(6):422–4. Full text
2. Gentilello LM, Cobean RA, Offner PJ, Soderberg RW, Jurkovich GJ. Continuous arteriovenous rewarming: rapid reversal of hypothermia in critically ill patients. The Journal of Trauma: Injury, Infection, and Critical Care. 1992 Mar;32(3):316–25 PubMed
3. Plaisier BR. Thoracic lavage in accidental hypothermia with cardiac arrest — report of a case and review of the literature. Resuscitation. 2005 Jul;66(1):99–104. PubMed
4. Gruber E, Beikircher W, Pizzinini R, Marsoner H, Pörnbacher M, Brugger H, et al. Non-extracorporeal rewarming at a rate of 6.8°C per hour in a deeply hypothermic arrested patient. Resuscitation. 2014 Aug;85(8):e119–20. PubMed
5. Kiridume K, Hifumi T, Kawakita K, Okazaki T, Hamaya H, Shinohara N, et al. Clinical experience with an active intravascular rewarming technique for near-severe hypothermia associated with traumatic injury. Journal of Intensive Care. BioMed Central Ltd; 2014;2(1):11. link to abstract
6. Cocchi MN, Giberson B, Donnino MW. Rapid rewarming of hypothermic patient using arctic sun device. Journal of Intensive Care Medicine. 2012 Mar;27(2):128–30. PubMed
A man in his 40s has a witnessed collapse and CPR is immediately started. Paramedics are on scene within 5 minutes and initiate advanced cardiac life support. He has refractory ventricular fibrillation which degenerates to asystole. He arrives in an emergency department where, with good ongoing CPR, he appears reasonably well perfused and even demonstrates some spontaneous movements and reactive pupils. He is placed on a mechanical CPR device and activation of the cardiac cath lab is requested. The patient has been in cardiac arrest now for 32 minutes. The cardiology fellow appears and asks: ‘what’s the down time?’
What’s the right answer? Would you say ‘half an hour’? ’32 minutes’?
And does it matter? Why is the cardiology fellow asking? Does she have an arbitrary cut off in mind, over which emergency coronary reperfusion will be denied?
I think there are several problems with conversations like these.
The first, is what does ‘down time’ even mean?
The second, is how relevant is a cardiac arrest time interval to prognosis in an individual patient?
The third, is what is the significance of any time interval in a patient who at the time of assessment has some signs that CPR is providing some perfusion and there is some evidence of brain function?
Let’s take the first. The definition of ‘down time’ does not appear to be standardised:
In this publication it appears to refer to the time before resuscitation is commenced, where it is demonstrated to be prognostically important.
Similarly, in this medical dictionary, it is defined as the ‘temporal duration from cardiac arrest until beginning cardiopulmonary resuscitation or advanced cardiac life support.‘
However, a post in Life in the Fast Lane defines it as ‘time to return of spontaneous circulation‘
This appears to agree with The New South Wales Government’s Intensive Care Monitoring and Coordination Unit who define it as ‘the time from when a person’s heart stops beating to the time it starts beating again‘
Yet another definition is used in King County, Washington, where it is defined as ‘the time interval from collapse to call 911‘.
So the first thing is to clarify what we’re talking about: “This patient received immediate bystander CPR. He has had resuscitation for 32 minutes”. My friend in the UK, nurse resuscitationist Fernando Candal Carballido, coined the term ‘Time of Supported Circulation‘, or TOSC. I quite like this and think it could catch on.
The next question is so what? What if it was 90 minutes? At what point do we declare futility? This is where I believe the game has changed. Multiple survivors of prolonged resuscitation are springing up in the news and in the literature. Particularly in the subgroup of patients with minimal comorbidity, early CPR, and who receive circulatory support via ECMO or mechanical CPR while they undergo coronary reperfusion.
For a great example of a prolonged CPR survivor, check out paramedic Wayne Schneider’s story,
…or listen to Steven Bernard describe amazing results from ECMO used in Melbourne in the CHEER study, which includes survivors of over two hours of CPR.
So, in summary:
- Be clear on your definitions when communicating with colleagues. ‘Down time’ does not appear to have a standard definition, so I would avoid its use.
- Some patients without comorbidities who have had early bystander CPR may survive despite long periods of CPR (or ‘TOSC’), provided the underlying cause can be treated or is reversible.
- ECMO and even more widely available mechanical CPR devices are extending the period in which these causes can be addressed.
- Bear in mind, that even if there is a period between collapse and initiation of CPR, the point that arrest occurred may not be known, and laypersons may overestimate time intervals in cardiac arrest.