Początek formularza
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Dół formularza
Received 30 November 2011; received in revised form 15 February 2012; accepted 27 February 2012. published online 19 March 2012.
Abstract
Objectives
To review the literature addressing whether the use of vasopressors improves outcomes in patients who suffer cardiac arrest.
Methods
Databases were searched using the terms: “(adrenaline or noradrenaline or vasopressor) and (heart arrest or cardiac arrest) and therapy”. Inclusion criteria were human studies, controlled trials, meta-analysis or case series. Exclusion criteria were articles with no abstract, abstract-only citations without accompanying article, non-English abstracts, vasopressor studies without human clinical trials, case reports, reviews, and articles addressing traumatic arrest.
Results
1603 papers were identified of which 53 articles were included for review. The literature addressed 5 main therapeutic questions. (1) Outcomes comparing any vasopressor to placebo. (2) Outcomes comparing vasopressin (alone or in combination with epinephrine) to epinephrine. (3) Outcomes comparing high dose epinephrine to standard dose epinephrine. (4) Outcomes comparing any alternative vasopressor to epinephrine. (5) Outcomes examining vasopressor use in pediatric cardiac arrest.
Conclusion
There are few studies that compare vasopressors to placebo in resuscitation from cardiac arrest. Epinephrine is associated with improvement in short term survival outcomes as compared to placebo, but no long-term survival benefit has been demonstrated. Vasopressin is equivalent for use as an initial vasopressor when compared to epinephrine during resuscitation from cardiac arrest. There is a short-term, but no long-term, survival benefit when using high dose vs. standard dose epinephrine during resuscitation from cardiac arrest. There are no alternative vasopressors that provide a long-term survival benefit when compared to epinephrine. There is limited data on the use of vasopressors in the pediatric population.
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Początek formularza
Dół formularza
Division of Critical Care Neurology, Mayo Clinic, Rochester, MN 55905, United States
Received 11 January 2012; received in revised form 6 February 2012; accepted 15 March 2012. published online 23 March 2012.
Abstract
Persistent coma from a major anoxic-ischemic injury to the brain may indicate there is less chance for full recovery. The tools of prognostication to assess comatose survivors of cardiopulmonary resuscitation have developed over several decades. Physicians would initially base their judgment on experience and data on outcome in these patients in the early years were merely on awakening not on disability.
In the late 1970s, a large multicenter prospective study was performed on outcome in nontraumatic coma. The impetus for this study was the result of Plum and Jennet's collaboration. In 1981 - for the first time - complex statistics were used to improve the accuracy of prognosis and became known as the “Levy algorithms.” These early seminal studies shaped the prediction models and implied that clinical information alone could assist physicians in making a prediction. Later, probabilistic methods became more commonplace.
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Dynamic effects of adrenaline (epinephrine) in out-of-hospital cardiac arrest with initial pulseless electrical activity (PEA)☆
Początek formularza
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Dół formularza
Received 23 October 2011; received in revised form 6 February 2012; accepted 23 February 2012. published online 19 March 2012.
Abstract
Background
In cardiac arrest, pulseless electrical activity (PEA) is a challenging clinical syndrome. In a randomized study comparing intravenous (i.v.) access and drugs versus no i.v. access or drugs during advanced life support (ALS), adrenaline (epinephrine) improved return of spontaneous circulation (ROSC) in patients with PEA. Originating from this study, we investigated the time-dependent effects of adrenaline on clinical state transitions in patients with initial PEA, using a non-parametric multi-state statistical model.
Methods and results
Patients with available defibrillator recordings were included, of whom 101 received adrenaline and 73 did not. There were significantly more state transitions in the adrenaline group than in the no-adrenaline group (rate ratio
=
1.6, p
<
0.001). Adrenaline markedly increased the rate of transition from PEA to ROSC during ALS and slowed the rate of being declared dead; e.g. by 20
min 20% of patients in the adrenaline group had been declared dead and 25% had obtained ROSC, whereas 50% in the no-adrenaline group have been declared dead and 15% had obtained ROSC. The differential effect of adrenaline could be seen after approx. 10
min of ALS for most transitions. For both groups the probability of deteriorating from PEA to asystole was highest during the first 15
min. Adrenaline increased the rate of transition from PEA to ventricular fibrillation or -tachycardia (VF/VT), and from ROSC to VF/VT.
Conclusions
Adrenaline has notable clinical effects during ALS in patients with initial PEA. The drug extends the time window for ROSC to develop, but also renders the patient more unstable. Further research should investigate the optimal dose, timing and mode of adrenaline administration during ALS.
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Assessment of CPR interruptions from transthoracic impedance during use of the LUCAS™ mechanical chest compression system☆
Początek formularza
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Dół formularza
Received 5 August 2011; received in revised form 10 December 2011; accepted 16 January 2012. published online 06 February 2012.
Abstract
Background
Quality of cardiopulmonary resuscitation (CPR) is a key determinant of outcome following out-of-hospital cardiac arrest (OHCA). Recent evidence shows manual chest compressions are typically too shallow, interruptions are frequent and prolonged, and incomplete release between compressions is common. Mechanical chest compression systems have been developed as adjuncts for CPR but interruption of CPR during their use is not well documented.
Aim
Analyze interruptions of CPR during application and use of the LUCAS™ chest compression system.
Methods
54 LUCAS 1 devices operated on compressed air, deployed in 3 major US emergency medical services systems, were used to treat patients with OHCA. Electrocardiogram and transthoracic impedance data from defibrillator/monitors were analyzed to evaluate timing of CPR. Separately, providers estimated their CPR interruption time during application of LUCAS, for comparison to measured application time.
Results
In the 32 cases analyzed, compressions were paused a median of 32.5
s (IQR 25-61) to apply LUCAS. Providers' estimates correlated poorly with measured pause length; pauses were often more than twice as long as estimated. The average device compression rate was 104/min (SD 4) and the average compression fraction (percent of time compressions were occurring) during mechanical CPR was 0.88 (SD 0.09).
Conclusions
Interruptions in chest compressions to apply LUCAS can be <20
s but are often much longer, and users do not perceive pause time accurately. Therefore, we recommend better training on application technique, and implementation of systems using impedance data to give users objective feedback on their mechanical chest compression device use.
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Początek formularza
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Dół formularza
Received 2 November 2011; received in revised form 3 January 2012; accepted 23 January 2012. published online 03 February 2012.
Abstract
Context
Extracorporeal cardiopulmonary resuscitation (ECPR) refers to emergent percutaneous veno-arterial cardiopulmonary bypass to stabilize and provide temporary support of patients who suffer cardiopulmonary arrest. Initiation of ECPR by emergency physicians with meaningful long-term patient survival has not been demonstrated.
Objective
To determine whether emergency physicians could successfully incorporate ECPR into the resuscitation of patients who present to the emergency department (ED) with cardiopulmonary collapse refractory to traditional resuscitative efforts.
Design
A three-stage algorithm was developed for ED ECPR in patients meeting inclusion/exclusion criteria. We report a case series describing our experience with this algorithm over a 1-year period.
Results
42 patients presented to our ED with cardiopulmonary collapse over the 1-year study period. Of these, 18 patients met inclusion/exclusion criteria for the algorithm. 8 patients were admitted to the hospital after successful ED ECPR and 5 of those patients survived to hospital discharge neurologically intact. 10 patients were not started on bypass support because either their clinical conditions improved or resuscitative efforts were terminated.
Conclusion
Emergency physicians can successfully incorporate ED ECPR in the resuscitation of patients who suffer acute cardiopulmonary collapse. More studies are necessary to determine the true efficacy of this therapy.
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Efficacy of veno-arterial extracorporeal membrane oxygenation in acute myocardial infarction with cardiogenic shock
Początek formularza
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Dół formularza
Received 21 September 2011; received in revised form 24 January 2012; accepted 29 January 2012. published online 10 February 2012.
Abstract
Aim
We analyzed the results of acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) necessitating extracorporeal membrane oxygenation (ECMO), and investigated for the associated risk factors for poor clinical outcomes.
Methods
We retrospectively reviewed the medical records of 27 patients who required ECMO for AMI associated with CS between April 2006 and July 2010. Mean age was 63.7
±
11.0 (range: 45-81) years, and there were 16 males (59.3%).
Results
The mean duration of ECMO support was 30.2
±
30.1 (range: 1-141)
h. Cardiopulmonary resuscitations (CPR) were performed in 21 patients (77.8%) before ECMO initiation. Twenty-two patients (81.5%) were successfully weaned off ECMO, and 16 patients (59.3%) survived to discharge. The 30-day mortality was 37.0% (10/27 patients). Complications developed in 17 patients (63.0%: pneumonia in 10 patients, acute renal failure in 10 patients, massive bleeding in 4 patients, and thromboembolic event in 1 patient). The period between CPR initiation and ECMO commencement was a significant risk factor for ECMO weaning failure. High pre-ECMO serum lactate level was identified as a significant risk factor for poor survival on univariated and multivariated analysis.
Conclusion
ECMO support could improve survival in patients who suffer AMI associated with CS, and early ECMO initiation yields better outcomes (successful ECMO weaning).
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Resuscitation of non-postcardiotomy cardiogenic shock or cardiac arrest with extracorporeal life support: The role of bridging to intervention☆
Początek formularza
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Dół formularza
Received 20 August 2011; received in revised form 6 January 2012; accepted 8 January 2012. published online 24 January 2012.
Abstract
Background
To investigate the predictors of adverse outcomes of extracorporeal life support (ECLS) in rescuing adult non-postcardiotomy cardiogenic shock or cardiac arrest (non-PC CS/CA).
Materials and methods
This retrospective study included 60 adult patients receiving ECLS for non-PC CS/CA in a single institution between June 2003 and June 2010. The exclusion criteria were (1) pre-ECLS cardiac surgeries in the same admission and (2) age
<
18
years. Pre-ECLS and ECLS characteristics were compared in patients surviving to hospital discharge and those who did not. Mortalities after hospital discharge were also investigated.
Results
Of the 38 patients weaned from ECLS, 32 survived to discharge. Acute myocardial infarction (AMI) and myocarditis were the most common aetiologies in this study. Forty patients experienced pre-ECLS conventional cardiopulmonary resuscitation (C-CPR) and 29 required an ECLS-assisted CPR (E-CPR). Thirteen patients who received E-CPR had profound anoxic encephalopathy later. In-hospital mortality was similar in AMI patients who underwent emergent coronary artery bypass grafting (CABG) after a failed percutaneous coronary intervention (PCI, 43%, 5/11) and those who underwent PCI only (58%, 7/12). Aetiologies other than myocarditis (odds ratio (OR) 11.0, 95% confidence interval (CI) 1.5-78.5), requirement for E-CPR (OR 5.6, 95% CI 1.5-22.0) and profound anoxic encephalopathy (OR 8.9, 95% CI 2.0-40.5) were predictors of in-hospital mortality. No risk factors of mortality after hospital discharge were identified.
Conclusion
ECLS was effective in bridging adults with non-PC CS/CA to definite treatments. Their prognosis depended on the cause of collapse and the severity of the post-cardiac arrest syndrome.
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A feasibility study evaluating the role of cerebral oximetry in predicting return of spontaneous circulation in cardiac arrest☆
Początek formularza
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Dół formularza
Resuscitation Research Group, Department of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794, United States
Received 28 October 2011; received in revised form 27 January 2012; accepted 29 January 2012. published online 10 February 2012.
Abstract
To date there has been no reliable noninvasive real time monitoring available to determine cerebral perfusion during cardiac arrest.
Objectives
To investigate the feasibility of using a commercially available cerebral oximeter during in-hospital cardiac arrest, and determine whether this parameter predicts return of spontaneous circulation (ROSC).
Methods
Cerebral oximetry was incorporated in cardiac arrest management in 19 in-hospital cardiac arrest cases, five of whom had ROSC. The primary outcome measure was the relationship between rSO2 and ROSC.
Results
The use of cerebral oximetry was found to be feasible during in hospital cardiac arrest and did not interfere with management. Patients with ROSC had a significantly higher overall mean
±
SE rSO2 (35
±
5 vs. 18
±
0.4, p
<
0.001). The difference in mean rSO2 between survivors and non-survivors was most pronounced in the final 5
min of cardiac arrest (48
±
1 vs. 15
±
0.2, p
<
0.0001) and appeared to herald imminent ROSC. Although spending a significantly higher portion of time with an rSO2
>
40% was found in survivors (p
<
0.0001), patients with ROSC had an rSO2 above 30% for >50% of the duration of cardiac arrest, whereas non-survivors had an rSO2 that was below 30%
>
50% of their cardiac arrest. Patients with ROSC also had a significantly higher change in rSO2 from baseline compared to non-survivors (310%
±
60% vs. 150%
±
27%, p
<
0.05).
Conclusion
Cerebral oximetry may have a role in predicting ROSC and the optimization of cerebral perfusion during cardiac arrest.
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Początek formularza
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Dół formularza
Received 27 January 2012; received in revised form 26 March 2012; accepted 6 April 2012. published online 20 April 2012.
Abstract
Introduction
Treatment with hypothermia has been shown to improve outcome after cardiac arrest (CA). Current consensus is to rewarm at 0.25-0.5
°C/h and avoid fever. The aim of this study was to investigate whether active rewarming, the rate of rewarming or development of fever after treatment with hypothermia after CA was correlated with poor outcome.
Methods
This retrospective cohort study included adult patients treated with hypothermia after CA and admitted to the intensive care unit between January 2006 and January 2009. The average rewarming rate from end of hypothermia treatment (passive rewarming) or start active rewarming until 36
°C was dichotomized in a high (≥0.5
°C/h) or normal rate (<0.5
°C/h). Fever was defined as >
38
°C within 72
h after admission. Poor outcome was defined as death, vegetative state, or severe disability after 6
months.
Results
From 128 included patients, 56% had a poor outcome. Actively rewarmed patients (38%) had a higher risk for poor outcome, OR 2.14 (1.01-4.57), p
<
0.05. However, this effect disappeared after adjustment for the confounders age and initial rhythm, OR 1.51 (0.64-3.58). A poor outcome was found in 15/21 patients (71%) with a high rewarming rate, compared to 54/103 patients (52%) with a normal rewarming rate, OR 2.61 (0.88-7.73), p
=
0.08. Fever was not associated with outcome, OR 0.64 (0.31-1.30), p
=
0.22.
Conclusions
This study showed that patients who needed active rewarming after therapeutic hypothermia after CA did not have a higher risk for a poor outcome. In addition, neither speed of rewarming, nor development of fever had an effect on outcome.
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Long-term prognosis following resuscitation from out-of-hospital cardiac arrest: Role of aetiology and presenting arrest rhythm☆
Początek formularza
,
Dół formularza
Received 20 September 2011; received in revised form 17 January 2012; accepted 23 January 2012. published online 03 February 2012.
Abstract
Objective
Little is known about long-term prognosis following resuscitation from out-of-hospital cardiac arrest, especially as it relates to the presenting rhythm or arrest aetiology. We investigated long-term survival among those discharged alive following resuscitation according to presenting rhythm and arrest aetiology.
Methods
We conducted a cohort investigation of all non-traumatic adult out-of-hospital cardiac arrest patients resuscitated and discharged alive from hospital between January 1, 2001 and December 31, 2009 in a large metropolitan emergency medical service system. Information about demographics, circumstances, presenting arrest rhythm and aetiology was collected using the dispatch, EMS, and hospital records. Long-term vital status was ascertained using state death records and the Social Security Death Index through 31st December 2010. We used Kaplan Meier to evaluate survival.
Results
During the study period, a total of 1001/5958 (17%) persons were resuscitated and discharged alive, of whom 313/1001 (31%) presented with a non-shockable rhythm and 210/1001 (21%) had a non-cardiac aetiology. Overall median survival was 9.8 years with 64% surviving >5 years. Five-year survival was 43% for non-shockable rhythms compared to 73% for shockable rhythms, and 45% for non-cardiac aetiology compared to 69% for cardiac aetiology (p
<
0.001 respectively).
Conclusion
Cardiac arrest due to non-shockable rhythm or non-cardiac aetiology comprises a substantial proportion of those who survive to hospital discharge. Although long-term survival in these groups is less than their shockable or cardiac aetiology counterparts, nearly half are alive 5 years following discharge. The findings support efforts to improve resuscitation care for those with non-shockable rhythms or non-cardiac cause.
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Początek formularza
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Dół formularza
Received 25 July 2011; received in revised form 19 December 2011; accepted 16 January 2012. published online 06 February 2012.
Abstract
Aim
Determine the impact of backboard placement, torso weight and bed compression on chest compression (CC) depth feedback in simulated cardiac arrest patients.
Methods
Epochs of 50 high quality CCs with real-time feedback of sternum-to-spine compression depth were provided by a blinded BLS/ACLS/PALS certified provider on manikins of two torso weights (25 vs. 50
kg), using three bed surfaces (stretcher, Stryker hospital bed with Impression mattress, soft Total Care ICU bed), with/without a backboard (BB). Two BB sizes were tested (small: 60
cm
×
50
cm; large: 89
cm
×
50
cm) in vertical vs. horizontal orientation. Mattress displacement was measured using an accelerometer placed internally on the spine plate of the manikin. Mattress displacement of ≥5
mm was prospectively defined as the minimal clinically important difference.
Results
During CPR (CC depth: 51.8
±
2.8
mm), BB use significantly reduced mattress displacement only for soft ICU beds. Mattress displacement was reduced (vs. no BB) for 25
kg torso weight: small BB12.3
mm (95%CI 11.9-12.6), horizontally oriented large BB 11.2
mm (95%CI 10.8-11.7), and vertically oriented large BB 12.2
mm (95%CI 11.8-12.6), and for 50
kg torso weight: small BB 7.4
mm (95%CI 7.1-7.8), horizontally oriented large BB 7.9
mm (95%CI 7.6-8.3), and vertically oriented large BB 6.2
mm (95%CI 5.8-6.5; all p
<
0.001). BB size and orientation did not significantly affect mattress displacement. Lighter torso weight was associated with larger displacement in soft ICU beds without BB (difference: 6.9
mm, p
<
0.001).
Conclusion
BB is important for CPR when performed on soft surfaces, such as ICU beds, especially when torso weight is light. BB may not be needed on stretchers, relatively firm hospital beds, or for patients with heavy torso weights.
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Potential negative effects of epinephrine on carotid blood flow and ETCO2 during active compression-decompression CPR utilizing an impedance threshold device☆
Początek formularza
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Dół formularza
Received 18 January 2012; received in revised form 25 February 2012; accepted 5 March 2012. published online 22 March 2012.
Abstract
Objectives
This study examines the effects of IV epinephrine administration on carotid blood flow (CBF) and end tidal CO2 (ETCO2) production in a swine model of active compression-decompression CPR with an impedance threshold device (ACD-CPR
+
ITD).
Methods
Six female swine (32
±
1
kg) were anesthetized, intubated and ventilated. Intracranial, thoracic aorta and right atrial pressures were measured via indwelling catheters. CBF was recorded. ETCO2, SpO2 and EKG were monitored. V-fib was induced and went untreated for 6
min. Three minutes each of standard CPR (STD), STD-CPR
+
impedance threshold device (ITD) and active compression-decompression (ACD)-CPR
+
ITD were performed. At minute 9 of the resuscitation, 40
μg/kg of IV Epinephrine was administered and ACD-CPR
+
ITD was continued for 1
min. Statistical analysis was performed with a paired t-test. p values of <0.05 were considered statistically significant and all values are reported in mmHg unless otherwise noted.
Results
Aortic pressure, cerebral and coronary perfusion pressures increased from STD
<
STD
+
ITD
<
ACD-CPR
+
ITD (p
<0.001). Epinepherine administered during ACD-CPR
+
ITD signficantly increased mean aortic pressure (29
±
5 vs 42
±
12, p
=
0.01), cerebral perfusion pressure (12
±
5 vs 22
±
10, p
=
0.01), and coronary perfusion pressure (8
±
7 vs 17
±
4, p
=
0.02); however, mean CBF and ETCO2 decreased (respectively 29
±
15 vs 14
±
7.0
ml/min, p
=
0.03; 20
±
7 vs 18
±
6, p
=
0.04).
Conclusions
In this model, administration of epinepherine during ACD-CPR
+
ITD signficantly increased markers of macrocirculation, while significantly decreasing carotid blood flow and ETCO2. This calls into question the ability of calculated perfusion pressures to accurately reflect oxygen delivery to end organs. The administration of epinepherine during ACD-CPR
+
ITD does not improve cerebral tissue perfusion.
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