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Cardiac arrest caused by subarachnoid haemorrhage

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We know that subarachnoid haemorrhage (SAH) can cause cardiac arrest. Some questions we may have about this are:

Questions

  • What proportion of out-of-hospital cardiac arrests (OOHCA) who achieve return of spontaneous circulation (ROSC) are caused by SAH?
  • What is the usual presenting arrest rhythm – VT/VF or non-shockable rhythms?
  • What is the outcome of these patients – do any survive?
  • Do they have other characteristic cardiac features, such as ECG or echo abnormalities?
  • Should we do a head CT on all survivors of out-of-hospital cardiac arrest of uncertain aetiology?

A recent Japanese article in Resuscitation1 is the third from that country to be published on the topic in three years, the other two2,3 coming from different centres and all demonstrating some consistent answers, as do papers published in recent years from Europe4 and North America5:

Answers

  • Rates of SAH in OOHCA patients who achieve ROSC and make it to CT range from 4-16% (even higher if other sources of intracranial haemorrhage are included).
  • Studies consistently demonstrate VT/VF to be very rare – PEA and asystole are by far the commonest presenting arrest rhythms.
  • Almost no patients with this presentation due to SAH survive to hospital discharge.
  • In the most recent study, all patients who survived long enough to get a 12 lead showed ST-T abnormalities and/or QT prolongation, although echocardiograms were mostly normal.
  • Rates of SAH in OOHCA patients who achieve ROSC seem to be sufficiently high to seriously consider head CT in these patients if there is no obvious alternate explanation for the arrest.

1. Clinical and cardiac features of patients with subarachnoid haemorrhage presenting with out-of-hospital cardiac arrest
Resuscitation. 2011 Oct;82(10):1294-7
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Background Subarachnoid haemorrhage (SAH) is known as one of the aetiologies of out-of-hospital cardiac arrest (OHCA). However, the mechanisms of circulatory collapse in these patients have remained unclear.

Methods and results We examined 244 consecutive OHCA patients transferred to our emergency department. Head computed tomography was performed on all patients and revealed the existence of SAH in 14 patients (5.9%, 10 females). Among these, sudden collapse was witnessed in 7 patients (50%). On their initial cardiac rhythm, all 14 patients showed asystole or pulseless electrical activity, but no ventricular fibrillation (VF). Return of spontaneous circulation (ROSC) was obtained in 10 of the 14 patients (14.9% of all ROSC patients) although all resuscitated patients died later. The ROSC rate in patients with SAH (71%) was significantly higher than that of patients with either other types of intracranial haemorrhage (25%, n = 2/8) or presumed cardiovascular aetiologies (22%, n = 23/101) (p < 0.01). On electrocardiograms, ST-T abnormalities and/or QT prolongation were found in all 10 resuscitated patients. Despite their electrocardiographic abnormalities, only 3 patients showed echocardiographic abnormalities.

Conclusions The frequency of SAH in patients with all causes of OHCA was about 6%, and in resuscitated patients was about 15%. The initial cardiac rhythm revealed no VF even though half had a witnessed arrest. A high ROSC rate was observed in patients with SAH, although none survived to hospital discharge.

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2. Assessing outcome of out-of-hospital cardiac arrest due to subarachnoid hemorrhage using brain CT during or immediately after resuscitation
Signa Vitae 2010; 5(2): 21 – 24 Full Text
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Objectives. The clinical course and outcome of out-of-hospital cardiopulmonary arrest (OHCPA) due to subarachnoid hemorrhage (SAH) is unclear. The objective of this study is to clarify them.

Study design. Single- center, observational study. Setting. We usually perform a brain computed tomography (CT) in OHCPA patients who present without a clear etiology (42% of all OHCPA), such as trauma, to determine the cause of OHCPA and to guide treatment.

Patients. The study included OHCPA patients without a clear etiology, who were transferred to our center and who underwent a brain CT during resuscitation.

Methods of measurement. Patients’ records were reviewed; initial cardiac rhythm, existence of a witness and bystander cardiopulmonary resuscitation efforts (CPR) were compared with patients’ outcomes.

Results. Sixty-six patients were enrolled. 72.7% achieved return of spontaneous circulation (ROSC), 71.2% were admitted, 30.3% survived more than 7 days, and 9.1. survived-to-discharge. In 41 witnessed OHCPA, 87.8% obtained ROSC, 85.4% were admitted, and 14.6% survived-to-discharge. All survivors were witnessed. In 25 non-witnessed OHCPA, 48% obtained ROSC and were admitted, and no patients were discharged. Initial cardiac rhythm was ventricular fibrillation (VF), pulseless electrical activity (PEA) and asystole in 3.0%, 39.4%, and 47.0%. In 2 VF patients 50.0% survived-to- discharge, and there was no survivor with PEA or asystole.

Conclusion. This study shows a high rate of ROSC and admission in OHCPA patients with a SAH, and also reveals their very poor neurological outcome. We conclude that the detection of a SAH in OHCPA patients is important to determine the accurate frequency of SAH in this patient group and to guide appropriate treatment of all OHCPA patients.

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3. Subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest: A prospective computed tomography study
Resuscitation. 2009 Sep;80(9):977-80
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Aim Aneurysmal subarachnoid haemorrhage (SAH) is a relatively common cause of out-of-hospital cardiac arrest (OHCA). Early identification of SAH-induced OHCA with the use of brain computed tomography (CT) scan obtained immediately after resuscitation may help emergency physicians make therapeutic decision as quickly as they can.

Methods During the 4-year observation period, brain CT scan was obtained prospectively in 142 witnessed non-traumatic OHCA survivors who remained haemodynamically stable after resuscitation. Demographics and clinical characteristics of SAH-induced OHCA survivors were compared with those with “negative” CT finding.

Results Brain CT scan was feasible with an average door-to-CT time of 40.0min. SAH was found in 16.2% of the 142 OHCA survivors. Compared with 116 survivors who were negative for SAH, SAH-induced OHCA survivors were significantly more likely to be female, to have experienced a sudden headache, and trended to have achieved return of spontaneous circulation (ROSC) prior to arrival in the emergency department less frequently. Ventricular fibrillation (VF) was significantly less likely to be seen in SAH-induced than SAH-negative OHCA (OR, 0.06; 95% CI, 0.01–0.46). Similarly, Cardiac Trop-T assay was significantly less likely to be positive in SAH-induced OHCA (OR, 0.08; 95% CI, 0.01–0.61).

Conclusion Aneurysmal SAH causes OHCA more frequently than had been believed. Immediate brain CT scan may particularly be useful in excluding SAH-induced OHCA from thrombolytic trial enrollment, for whom the use of thrombolytics is contraindicated. The low VF incidence suggests that VF by itself may not be a common cause of SAH-induced OHCA.

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4. Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest
Resuscitation. 2001 Oct;51(1):27-32
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Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest.

Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features.

Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome.

Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

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5. Cranial computed tomography in the resuscitated patient with cardiac arrest
Am J Emerg Med. 2009 Jan;27(1):63-7
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Introduction The incidence of out-of-hospital and in-hospital cardiorespiratory arrest from all causes in the United States occurs not infrequently. Postresuscitation care should include the identification of the inciting arrest event as well as therapy tailored to support the patient and treat the primary cause of the decompensation. The application of one particular testing modality, cranial computed tomography (CT) of the head, has not yet been determined. We undertook an evaluation of the use of head CT in patients who were resuscitated from cardiac arrest.

Methods Prehospital (emergency medical services), ED, and hospital records were reviewed for patients of all ages with cardiorespiratory arrest over a 4-year period (July 1996-June 2000). Information regarding diagnosis, management, and outcome was recorded. The results of cranial CT, if performed, and any apparent resulting therapeutic changes were recorded. Patients with a known traumatic mechanism for the cardiorespiratory arrest were excluded.

Results A total of 454 patients (mean age 58.3 years with 60% male) with cardiorespiratory arrest were entered in the study with 98 (22%) individuals (mean age 58.5 years with 53% male) undergoing cranial CT. Arrest location was as follows: emergency medical services, 41 (42%); ED, 11 (11%); and hospital, 46 (47%). Seventy-eight (79%) patients demonstrated 111 CT abnormalities: edema, 35 (32%); atrophy, 24 (22%); extra-axial hemorrhage, 14 (13%); old infarct, 12 (11%); new infarct, 11 (10%); intraparenchymal hemorrhage, 6 (5%); skull fracture, 5 (4%); mass, 3 (2%); and foreign body, 1 (1%). Therapeutic and diagnostic alterations in care were made in 38 (39%) patients—35 abnormal and 3 normal CTs. The following alterations occurred: medication administration, 26; withdrawal of life support, 7; additional diagnostic study, 6; neurologic consultation, 6; and intracranial pressure monitoring. 4. No patient survived to discharge.

Conclusion In this subset of resuscitated patients with cardiac arrest, abnormalities on the head CT were not uncommon. Alterations in management did occur in those patients with abnormalities. The indications and impact of head CT in the population of resuscitated patients with cardiac arrest remain unknown, warranting further investigation.

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Acute Med, All Updates, Guidelines, ICU, Resus

Myoclonus no longer a show-stopper

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In comatose survivors of cardiac arrest, myoclonus is considered a grave prognostic sign. The American Academy of Neurology stated in 20061 that:
After cardiac arrest, the following clinical findings accurately predict poor outcome;

  • myoclonus status epilepticus within the first 24 hours in patients with primary circulatory arrest
  • absence of pupillary responses within days 1 to 3 after CPR
  • absent corneal reflexes within days 1 to 3 after CPR
  • and absent or extensor motor responses after 3 days.

However in the age of targeted temperature management the presence and/or timing of these signs needs to be re-evaluated. It has been suggested that therapeutic hypothermia and sedation required for induced cooling might delay recovery of motor reactions up to 5–6 days after cardiac arrest. Now a series of three survivors of cardiac arrest who had massive myoclonus in the first four hours after return of spontaneous circulation (ROSC) is reported2, all of whom were treated with TTM and experienced good neurologic outcomes.


Early myoclonus in comatose survivors of cardiac arrest, even when it is not myoclonic status epilepticus (MSE), is considered a sign of severe global brain ischemia and has been associated with high rates of mortality and poor neurologic outcomes. We report on three survivors of primary circulatory cardiac arrests who had good neurologic outcomes (two patients with a CPC score=1 and one patient with a CPC score=2) after mild therapeutic hypothermia, despite exhibiting massive myoclonus within the first four hours after return of spontaneous circulation. The concept that early myoclonus heralds a uniformly poor prognosis may need to be reconsidered in the era of post-cardiac arrest mild therapeutic hypothermia.

1. Practice Parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): Report of the Quality Standards Subcommittee of the American Academy of Neurology
Neurology. 2006 Jul 25;67(2):203-10 Full Text
2. Neurologic Recovery After Therapeutic Hypothermia in Patients with Post-Cardiac Arrest Myoclonus
Resuscitation published on line 03 October 2011

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Pre-hospital thoracotomy

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The London Helicopter Emergency Medical Service provides a physician / paramedic team to victims of trauma. One of the interventions performed by their physicians is pre-hospital resuscitative thoracotomy to patients with cardiac arrest due to penetrating thoracic trauma. They have published the outcomes from this procedure over a 15 year period which show an 18% survival to discharge rate, with a high rate of neurologically intact survivors1.
The article was submitted for publication on February 1, 2010, and in the discussion mentions a further two survivors from the procedure performed after conducting the study. It is likely therefore in the year and a half since submission still more patients have been saved. It will be interesting to read future reports from this team as the numbers accumulate; penetrating trauma missions are sadly increasing in frequency.
Having worked for these guys and performed this procedure in the field a few times myself, I can attest to the training and governance surrounding this system. The technique of clamshell thoracotomy is well described 2 and one I would recommend for the non-surgeon.

BACKGROUND: Prehospital cardiac arrest associated with trauma almost always results in death. A case of survival after prehospital thoracotomy was published in 1994 and several others have followed. This article describes the result of prehospital thoracotomy in a physician-led system for patients with stab wounds to the chest who suffered cardiac arrest on scene.
METHODS: A 15-year retrospective prehospital trauma database review identified victims of stab wounds to the chest who suffered cardiac arrest on scene and had thoracotomy performed according to local standard operating procedures.
RESULTS: Overall, 71 patients met inclusion criteria. Thirteen patients (18%) survived to hospital discharge. Neurologic outcome was good in 11 patients and poor in 2. Presenting cardiac rhythm was asystole in four patients, pulseless electrical activity in five, and unrecorded in the remaining four. All survivors had cardiac tamponade. The medical team was present at the time of cardiac arrest for six survivors (good neurologic outcome): arrived in the first 5 minutes after arrest in three patients (all good neurologic outcome), arrived 5 minutes to 10 minutes after arrest in two patients (one poor neurologic outcome), and in one patient (poor neurologic outcome) the period was unknown. Of the survivors, seven thoracotomies were performed by emergency physicians and six by anesthesiologists.
CONCLUSIONS: Prehospital thoracotomy is a well-established procedure in this physician-led prehospital service. Results from this and other similar systems suggest that when performed for the subgroup of patients described, significant numbers of survivors with good neurologic outcome can be expected.

1. Thirteen Survivors of Prehospital Thoracotomy for Penetrating Trauma: A Prehospital Physician-Performed Resuscitation Procedure That Can Yield Good Results
J Trauma. 2011 May;70(5):E75-8
2. Emergency thoracotomy: “how to do it”
Emerg Med J. 2005 January; 22(1):22–24
Full text available here

All Updates, PHARM, Resus, Trauma

Exsanguinating cardiac arrest not always fatal

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The British Military has developed a reputation for aggressive pre-hospital critical care including (but not limited to) the use of blood products and tourniquets, and coordinated field hospital trauma care. They now report the outcomes for patients with traumatic cardiac arrest, mainly from improvised explosive devices. Of 52 patients, 14 (27%) demonstrated return of spontaneous circulation (ROSC), of whom four (8%) survived to hospital discharge with a neurologically good recovery. Resuscitative thoracotomy (RT) was performed on 12 patients (8 in the ED), including all four survivors. RT enabled open-chest CPR, release of pericardial tamponade, lung resection and compression of the descending thoracic aorta for haemorrhage control.
No patients who arrested in the field survived, although one of the neurologically well-recovered survivors arrested during transport to hospital and was in cardiac arrest for 24 minutes. The authors propose this individual’s survival was in part due to ‘the high level of care that he received during retrieval, including haemorrhage control, tracheal intubation and transfusion of blood products‘.
Asystole was universally associated with death but agonal / bradycardic rhythms were not. In keeping with other studies, cardiac activity on ultrasound was associated with ROSC.


AIM: To determine the characteristics of military traumatic cardiorespiratory arrest (TCRA), and to identify factors associated with successful resuscitation.

METHODS: Data was collected prospectively for adult casualties suffering TCRA presenting to a military field hospital in Helmand Province, Afghanistan between 29 November 2009 and 13 June 2010.

RESULTS: Data was available for 52 patients meeting the inclusion criteria. The mean age (range) was 25 (18-36) years. The principal mechanism of injury was improvised explosive device (IED) explosion, the lower limbs were the most common sites of injury and exsanguination was the most common cause of arrest. Fourteen (27%) patients exhibited ROSC and four (8%) survived to discharge. All survivors achieved a good neurological recovery by Glasgow Outcome Scale. Three survivors had arrested due to exsanguination and one had arrested due to pericardial tamponade. All survivors had arrested after commencing transport to hospital and the longest duration of arrest associated with survival was 24min. All survivors demonstrated PEA rhythms on ECG during arrest. When performed, 6/24 patients had ultrasound evidence of cardiac activity during arrest; all six with cardiac activity subsequently exhibited ROSC and two survived to hospital discharge.

CONCLUSION: Overall rates of survival from military TCRA were similar to published civilian data, despite military TCRA victims presenting with high Injury Severity Scores and exsanguination due to blast and fragmentation injuries. Factors associated with successful resuscitation included arrest beginning after transport to hospital, the presence of electrical activity on ECG, and the presence of cardiac movement on ultrasound examination.

Outcomes following military traumatic cardiorespiratory arrest: A prospective observational study
Resuscitation. 2011 Sep;82(9):1194-7

Acute Med, All Updates, Guidelines, ICU, PHARM, Resus

Still no cardiac arrest survival benefit from epinephrine?

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A double blind randomised controlled trial showed significantly better rates of return of spontaneous circulation and hospital admission with the use of adrenaline (epinephrine) compared with placebo. This effect was observed with both shockable and non-shockable initial cardiac arrest rhythms. There was no statistically significant difference in the primary outcome of survival to hospital discharge.
Interesting but unfortunate political factors appear to have prevented recruitment to the required numbers of patients for this study so it is underpowered for its primary outcome of survival to hospital discharge, which in the adrenaline group was double that in the placebo group, although this did not reach statistical significance. What was supposed to be a multi-centre study became a single centre one and it was not possible to continue as the study drugs reached their expiry date and no additional funding was available.
So do ROSC and survival to admission matter? The authors make the following point:


While not the primary outcome of our study, ROSC is an increasingly important clinical endpoint as the influence of post resuscitation care interventions (i.e.: therapeutic hypothermia, managing underlying cause, organ perfusion and oxygenation) on survival to hospital discharge are recognised.

Optimum dose and timing of adrenaline remain unknown, along with whether it impacts on long-term outcomes.


BACKGROUND: There is little evidence from clinical trials that the use of adrenaline (epinephrine) in treating cardiac arrest improves survival, despite adrenaline being considered standard of care for many decades. The aim of our study was to determine the effect of adrenaline on patient survival to hospital discharge in out of hospital cardiac arrest.

METHODS: We conducted a double blind randomised placebo-controlled trial of adrenaline in out-of-hospital cardiac arrest. Identical study vials containing either adrenaline 1:1000 or placebo (sodium chloride 0.9%) were prepared. Patients were randomly allocated to receive 1ml aliquots of the trial drug according to current advanced life support guidelines. Outcomes assessed included survival to hospital discharge (primary outcome), pre-hospital return of spontaneous circulation (ROSC) and neurological outcome (Cerebral Performance Category Score – CPC).

RESULTS: A total of 4103 cardiac arrests were screened during the study period of which 601 underwent randomisation. Documentation was available for a total of 534 patients: 262 in the placebo group and 272 in the adrenaline group. Groups were well matched for baseline characteristics including age, gender and receiving bystander CPR. ROSC occurred in 22 (8.4%) of patients receiving placebo and 64 (23.5%) who received adrenaline (OR=3.4; 95% CI 2.0-5.6). Survival to hospital discharge occurred in 5 (1.9%) and 11 (4.0%) patients receiving placebo or adrenaline respectively (OR=2.2; 95% CI 0.7-6.3). All but two patients (both in the adrenaline group) had a CPC score of 1-2.

CONCLUSION: Patients receiving adrenaline during cardiac arrest had no statistically significant improvement in the primary outcome of survival to hospital discharge although there was a significantly improved likelihood of achieving ROSC.

Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Resuscitation. 2011 Sep;82(9):1138-43

Acute Med, All Updates, ICU, Kids, PHARM, Resus

Pre-hospital ECMO

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Two cases are reported of the pre-hospital institution of venoarterial extracorporeal membrane oxygenation (ECMO) for patients in cardiac arrest. One was from France and the other from Germany – both countries with mature physician-staffed pre-hospital systems. The two cases were a 9 yr old drowning victim1 and a 48 year old marathon runner2. They each received BLS then ACLS then ECMO, and both went from asystole to sinus rhythm after the institution of ECMO. Sadly both failed to neurologically recover and died in hospital.
If irreversible anoxic encephalopathy could be detected in the field, patients could be better selected for this intervention. An editorialist3 states:


Until we have a hand held device which can measure neuronal integrity on a cellular level in the field we must use our best judgement, and in many cases give the patient the benefit of the doubt by cannulating them, cooling for 24 h and then making a neurological assessment and withdrawing ECLS if necessary.

Other issues to consider are:

  • Can society afford this level of intervention?
  • Could this intervention, when associated with brain death, result in sufficiently recovered organs for transplantation?
  • How can the infrastructure be created to enable rapid institution of pre-hospital ECMO?

I suspect as the equipment becomes even more portable and self-maintaining, pre-hospital / retrieval physicians already expert in critical care interventions such as seldinger-guided vascular access will be the ones instituting this therapy. In the meantime, we await evidence of outcome benefit and some objective means of case selection.
1. Out-of-hospital extracorporeal life support for cardiac arrest—A case report
Resuscitation. 2011 Sep;82(9):1243-5
2. Out-of-hospital extra-corporeal life support implantation during refractory cardiac arrest in a half-marathon runner
Resuscitation. 2011 Sep;82(9):1239-42
3. Community extracorporeal life support for cardiac arrest – When should it be used?
Resuscitation. 2011 Sep;82(9):1117

Acute Med, All Updates, ICU, Resus

Verapamil vs adenosine for SVT

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Most people reach for the adenosine once vagotonic manouevres have failed in SVT, but some patients find the side effects – albeit short-lived – pretty unpleasant. For this reason I’ve heard Jerry Hoffman espouse the relative benefits of verapamil in patients without contra-indications. A recent meta-analysis suggests both verapamil and adenosine have about a 90% success rate. The study did not look at recurrence rates of SVT, which one might expect to be higher with the shorter-acting adenosine.
The authors conclude:
The choice between the agents should be made on a case by case basis with awareness of the respective adverse effect profiles, and should involve informed discussion with the patient where appropriate.

OBJECTIVE: Verapamil and adenosine are the most common agents used to treat paroxysmal supraventricular tachycardia (PSVT). We performed a systematic review and meta-analysis to determine the relative effectiveness of these drugs and to examine their respective adverse effect profiles.
METHODS: We searched MEDLINE, EMBASE, CINAHL, the Cochrane database, and international clinical trial registers for randomized controlled trials comparing adenosine (or adenosine compounds) with verapamil for the treatment of PSVT in stable adult patients. The primary outcome was rate of reversion to sinus rhythm. Secondary outcome was occurrence of pooled adverse events. Odds ratios and 95% confidence intervals (CIs) were calculated using a random effects model (RevMan v5).
RESULTS: Eight trials were appropriate and had the available data. The reversion rate for adenosine was 90.8% (95% CI: 87.3-93.4%) compared with 89.9% for verapamil (95% CI: 86.0-92.9%). The pooled odds ratio for successful reversion was 1.27 (95% CI: 0.63-2.57) favouring adenosine. This was not statistically significant. There was a higher rate of minor adverse effects described with adenosine (16.7-76%) compared with verapamil (0-9.9%). The rate of hypotension was lower with adenosine [0.6% (95% CI: 0.1-2.4%)] compared with verapamil [3.7% (95% CI: 1.9-6.9%)].
CONCLUSION: Adenosine and verapamil have similar efficacy in treating PSVT. Adenosine has a higher rate of minor adverse effects, and of overall adverse effects, whereas verapamil has a higher rate of causing hypotension. A decision between the two agents should be made on a case-by-case basis and ideally involve informed discussion with the patient where appropriate.

The relative efficacy of adenosine versus verapamil for the treatment of stable paroxysmal supraventricular tachycardia in adults: a meta-analysis
Eur J Emerg Med. 2011 Jun;18(3):148-52

Acute Med, All Updates, ICU, PHARM, Resus

How much oxygen after ROSC?

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I reported a previous JAMA publication demonstrating an association between hyperoxia and mortality in patients resuscitated post-cardiac arrest. The same authors have published furthur data to better define the relationship between supranormal oxygen tension and outcome in postresuscitation patients. They hypothesised that a linear dose-dependent relationship would be present in the association between supranormal oxygen tension and in-hospital mortality.

Background– Laboratory and recent clinical data suggest that hyperoxemia after resuscitation from cardiac arrest is harmful; however, it remains unclear if the risk of adverse outcome is a threshold effect at a specific supranormal oxygen tension, or is a dose-dependent association. We aimed to define the relationship between supranormal oxygen tension and outcome in postresuscitation patients.

Methods and Results– This was a multicenter cohort study using the Project IMPACT database (intensive care units at 120 US hospitals). Inclusion criteria were age >17 years, nontrauma, cardiopulmonary resuscitation preceding intensive care unit arrival, and postresuscitation arterial blood gas obtained. We excluded patients with hypoxia or severe oxygenation impairment. We defined the exposure by the highest partial pressure of arterial oxygen (PaO(2)) over the first 24 hours in the ICU. The primary outcome measure was in-hospital mortality. We tested the association between PaO(2) (continuous variable) and mortality using multivariable logistic regression adjusted for patient-oriented covariates and potential hospital effects. Of 4459 patients, 54% died. The median postresuscitation PaO(2) was 231 (interquartile range 149 to 349) mm Hg. Over ascending ranges of oxygen tension, we found significant linear trends of increasing in-hospital mortality and decreasing survival as functionally independent. On multivariable analysis, a 100 mm Hg increase in PaO(2) was associated with a 24% increase in mortality risk (odds ratio 1.24 [95% confidence interval 1.18 to 1.31]. We observed no evidence supporting a single threshold for harm from supranormal oxygen tension.

Conclusion– In this large sample of postresuscitation patients, we found a dose-dependent association between supranormal oxygen tension and risk of in-hospital death.

Relationship Between Supranormal Oxygen Tension and Outcome After Resuscitation From Cardiac Arrest
Circulation. 2011 Jun 14;123(23):2717-2722
Australasian investigators provided the following critique of the original JAMA study:

Unfortunately, these investigators used only the first set of arterial blood gases in the ICU to assess oxygenation, excluded close to 30% of patients because of lack of arterial blood gas data and did not adjust for standard illness severity scores. Their conclusion that hyperoxia is a robust predictor of mortality in patients after resuscitation form cardiac arrest was therefore potentially affected by selection bias and by insufficient adjustment for major confounders. Thus, their results are of uncertain significance and require confirmation.
They undertook their own study of 12,108 patients:

INTRODUCTION: Hyperoxia has recently been reported as an independent risk factor for mortality in patients resuscitated from cardiac arrest. We examined the independent relationship between hyperoxia and outcomes in such patients.
METHODS: We divided patients resuscitated from nontraumatic cardiac arrest from 125 intensive care units (ICUs) into three groups according to worst PaO2 level or alveolar-arterial O2 gradient in the first 24 hours after admission. We defined ‘hyperoxia’ as PaO2 of 300 mmHg or greater, ‘hypoxia/poor O2 transfer’ as either PaO2 < 60 mmHg or ratio of PaO2 to fraction of inspired oxygen (FiO2 ) < 300, ‘normoxia’ as any value between hypoxia and hyperoxia and ‘isolated hypoxemia’ as PaO2 < 60 mmHg regardless of FiO2. Mortality at hospital discharge was the main outcome measure.

RESULTS: Of 12,108 total patients, 1,285 (10.6%) had hyperoxia, 8,904 (73.5%) had hypoxia/poor O2 transfer, 1,919 (15.9%) had normoxia and 1,168 (9.7%) had isolated hypoxemia (PaO2 < 60 mmHg). The hyperoxia group had higher mortality (754 (59%) of 1,285 patients; 95% confidence interval (95% CI), 56% to 61%) than the normoxia group (911 (47%) of 1,919 patients; 95% CI, 45% to 50%) with a proportional difference of 11% (95% CI, 8% to 15%), but not higher than the hypoxia group (5,303 (60%) of 8,904 patients; 95% CI, 59% to 61%). In a multivariable model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95% CI, 1.1 to 1.6). However, once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxemia, time period matching and hyperoxia defined as PaO2 > 400 mmHg, hyperoxia had no independent association with mortality. Importantly, after adjustment for FiO2 and the relevant covariates, PaO2 was no longer predictive of hospital mortality (P = 0.21).

CONCLUSIONS: Among patients admitted to the ICU after cardiac arrest, hyperoxia did not have a robust or consistently reproducible association with mortality. We urge caution in implementing policies of deliberate decreases in FiO2 in these patients.

Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest.
Crit Care. 2011 Mar 8;15(2):R90. [Epub ahead of print]
Open Access Full Text
What’s the best approach in the light of these differing results? My approach is to avoid hypoxia, since that’s probably bad, and to actively avoid overoxygenating as part of my general neuroprotection checklist in a post-cardiac arrest patient. It would seem prudent to follow the recommendations of ILCOR, summarised by the European Resuscitation Council guidelines as:

Recognition of the potential harm caused by hyperoxaemia after ROSC is achieved: once ROSC has been established and the oxygen saturation of arterial blood (SaO2) can be monitored reliably (by pulse oximetry and/or arterial blood gas analysis), inspired oxygen is titrated to achieve a SaO2 of 94–98%

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Targeted temperature management guidelines

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Okay – rather than ‘therapeutic hypothermia’, the recommended phrase now is ‘targeted temperature management’. Several critical care authorities got together to produce clinical recommendations on this topic. Here are a few interesting points from the document:
On coagulation:
Hypothermia affects platelet function and prolongs the prothrombin time and partial thromboplastin time. These effects are masked when laboratory analysis is performed at 37°C, suggesting that any risk will be mitigated by rewarming.
Although not mentioned in the abstract, the authors examined the role of TTM in raised intracranial pressure (ICP):
Sufficient evidence exists to conclude that TTM does decrease ICP compared to unstructured temperature management. However, there is no sufficient evidence to make a recommendation regarding the use of targeted hypothermia to control elevated ICP to improve patent-important outcomes in TBI. The jury makes NO RECOMMENDATION regarding the use of TTM as an ICP control strategy to improve outcomes in brain injuries regardless of cause (trauma, hemorrhage, or ischemic stroke).
Regarding acute liver failure with severe cerebral edema:
there are currently no RCTs. There is a case series suggesting a strongly favorable effect. This is a powerful argument for support of an RCT evaluating TTM alone or in combination with hepatic dialysis strategies

OBJECTIVE: Representatives of five international critical care societies convened topic specialists and a nonexpert jury to review, assess, and report on studies of targeted temperature management and to provide clinical recommendations.
DATA SOURCES: Questions were allocated to experts who reviewed their areas, made formal presentations, and responded to questions. Jurors also performed independent searches. Sources used for consensus derived exclusively from peer-reviewed reports of human and animal studies.
STUDY SELECTION: Question-specific studies were selected from literature searches; jurors independently determined the relevance of each study included in the synthesis.
CONCLUSIONS AND RECOMMENDATIONS:

  1. The jury opines that the term “targeted temperature management” replace “therapeutic hypothermia.”
  2. The jury opines that descriptors (e.g., “mild”) be replaced with explicit targeted temperature management profiles.
  3. The jury opines that each report of a targeted temperature management trial enumerate the physiologic effects anticipated by the investigators and actually observed and/or measured in subjects in each arm of the trial as a strategy for increasing knowledge of the dose/duration/response characteristics of temperature management. This enumeration should be kept separate from the body of the report, be organized by body systems, and be made without assertions about the impact of any specific effect on the clinical outcome.
  4. The jury STRONGLY RECOMMENDS targeted temperature management to a target of 32°C-34°C as the preferred treatment (vs. unstructured temperature management) of out-of-hospital adult cardiac arrest victims with a first registered electrocardiography rhythm of ventricular fibrillation or pulseless ventricular tachycardia and still unconscious after restoration of spontaneous circulation (strong recommendation, moderate quality of evidence).
  5. The jury WEAKLY RECOMMENDS the use of targeted temperature management to 33°C-35.5°C (vs. less structured management) in the treatment of term newborns who sustained asphyxia and exhibit acidosis and/or encephalopathy (weak recommendation, moderate quality of evidence).

Targeted temperature management in critical care: A report and recommendations from five professional societies
Crit Care Med. 2011 May;39(5):1113-1125

Acute Med, All Updates, Guidelines, ICU, PHARM, Resus

Drugs in cardiac arrest – guess what works?

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Just like epinephrine (adrenaline), amiodarone does not increase survival to hospital discharge in cardiac arrest patients. I doubt his will deter the people in the resuscitation room with their stopwatches from handing me these drugs and telling me I ought to be giving them though.

Amiodarone - a load of balls

 

AIMS: In adult cardiac arrest, antiarrhythmic drugs are frequently utilized in acute management and legions of medical providers have memorized the dosage and timing of administration. However, data supporting their use is limited and is the focus of this comprehensive review.

METHODS: Databases including PubMed, Cochrane Library (including Cochrane database for systematic reviews and Cochrane Central Register of Controlled Trials), Embase, and AHA EndNote Master Library were systematically searched. Further references were gathered from cross-references from articles and reviews as well as forward search using SCOPUS and Google scholar. The inclusion criteria for this review included human studies of adult cardiac arrest and anti-arrhythmic agents, peer-review. Excluded were review articles, case series and case reports.

RESULTS: Of 185 articles found, only 25 studies met the inclusion criteria for further review. Of these, 9 were randomised controlled trials. Nearly all trials solely evaluated Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF), and excluded Pulseless Electrical Activity (PEA) and asystole. In VT/VF patients, amiodarone improved survival to hospital admission, but not to hospital discharge when compared to lidocaine in two randomized controlled trials.

CONCLUSION: Amiodarone may be considered for those who have refractory VT/VF, defined as VT/VF not terminated by defibrillation, or VT/VF recurrence in out of hospital cardiac arrest or in-hospital cardiac arrest. There is inadequate evidence to support or refute the use of lidocaine and other antiarrythmic agents in the same settings.

The use of antiarrhythmic drugs for adult cardiac arrest: A systematic review
Resuscitation. 2011 Jun;82(6):665-70