Minimizing pre- and post-defibrillation pauses increases the likelihood of return of spontaneous circulation (ROSC)

Background

The three-phase model of ventricular fibrillation (VF) arrest suggests a period of compressions to “prime” the heart prior to defibrillation attempts. In addition, post-shock compressions may increase the likelihood of return of spontaneous circulation (ROSC). The optimal intervals for shock delivery following cessation of compressions (pre-shock interval) and resumption of compressions following a shock (post-shock interval) remain unclear.

Objective

To define optimal pre- and post-defibrillation compression pauses for out-of-hospital cardiac arrest (OOHCA).

Methods

All patients suffering OOHCA from VF were identified over a 1-month period. Defibrillator data were abstracted and analyzed using the combination of ECG, impedance, and audio recording. Receiver-operator curve (ROC) analysis was used to define the optimal pre- and post-shock compression intervals. Multiple logistic regression analysis was used to quantify the relationship between these intervals and ROSC. Covariates included cumulative number of defibrillation attempts, intubation status, and administration of epinephrine in the immediate pre-shock compression cycle. Cluster adjustment was performed due to the possibility of multiple defibrillation attempts for each patient.

Results

A total of 36 patients with 96 defibrillation attempts were included. The ROC analysis identified an optimal pre-shock interval of <3 s and an optimal post-shock interval of <6 s. Increased likelihood of ROSC was observed with a pre-shock interval <3 s (adjusted OR 6.7, 95% CI 2.0-22.3, p = 0.002) and a post-shock interval of <6 s (adjusted OR 10.7, 95% CI 2.8-41.4, p = 0.001). Likelihood of ROSC was substantially increased with the optimization of both pre- and post-shock intervals (adjusted OR 13.1, 95% CI 3.4-49.9, p < 0.001).

Conclusions

Decreasing pre- and post-shock compression intervals increases the likelihood of ROSC in OOHCA from VF.     

Survival does not improve when therapeutic hypothermia is added to post-cardiac arrest care

Background

We investigated whether the use of therapeutic hypothermia improves the outcome after cardiac arrest (CA) under routine clinical conditions.

Method

In a retrospective study, data of CA survivors treated from 2003 to 2010 were analysed. Of these, 143 patients were treated with hypothermia at 33 ± 0.5 °C for 24 h according to predefined inclusion criteria, while 67 who did not fulfil these criteria received comparable therapy without hypothermia.

Results

210 patients were included, 143 in the hypothermia group (HG) and 67 in the normothermia group (NG). There was no significant difference in mortality between the groups; 69 (48.2%) in the HG died in the first four weeks, compared to 30 patients (44.8%) in the NG (p = 0.659). Patients in the NG were older and more seriously ill, and CA occurred more often in-hospital. Binary logistic regression revealed ventricular fibrillation (p = 0.044), NSE serum level <33 ng ml⁻¹ (p < 0.001), age (p = 0.035) and witnessed cardiac arrest (p = 0.043) as independent factors significantly improving survival after CA, whereas hypothermia was not (p = 0.69). The target temperature was maintained for a significantly longer time (19.5 h vs. 15.2 h; p = 0.003) in hypothermia patients with a favourable outcome than in those with an unfavourable outcome.

Conclusion

There was no improvement in survival rates when hypothermia was added to standard therapy in this case series, as compared to standard therapy alone. The time at target temperature may be of relevance. We need better evidence in order to expand the recommendations for hypothermia after CA.     

Therapeutic hypothermia is associated with improved neurologic outcome and survival in cardiac arrest survivors of non-shockable rhythms

Background

Therapeutic hypothermia improves neurologic outcomes in patients resuscitated from cardiac arrest due to ventricular fibrillation. However, its role in patients with cardiac arrest due to non-shockable rhythms (pulseless electrical activity (PEA) and asystole) is unclear. We hypothesized that therapeutic hypothermia favorably impacts neurologic outcome and survival in patients resuscitated from cardiac arrest due to non-shockable rhythms.

Methods

Retrospectively collected data on consecutive adult patients admitted to Hartford Hospital from 1/1/2004 to 11/1/2010 who survived a cardiac arrest due to PEA or asystole were analyzed. Patients who underwent therapeutic hypothermia (1/1/2007-11/1/2010) formed the hypothermia group while patients admitted prior to the institution of therapeutic hypothermia (1/1/2004-1/1/2007) at Hartford Hospital formed the control group. The primary end-point was measured using the Pittsburgh cerebral performance category (CPC) scale and patients were assessed for a good (CPC 1 and 2) or poor (CPC 3-5) neurological outcome prior to discharge from hospital. A secondary end-point was measured as survival at discharge from hospital.

Results

Of 100 post-cardiac arrest patients included in the study, 15/52 (29%) patients in the hypothermia group had a good neurologic outcome as compared to 5/43 (10%) patients in the control group (P = 0.021). On multivariate analysis, the odds ratio for good neurologic outcome and survival at discharge from the hospital with therapeutic hypothermia as compared to control were 4.35 (95% CI 1.10-17.24, P = 0.04) and 5.65 (CI 1.66-19.23, P = 0.006) respectively.

Conclusion

Therapeutic hypothermia is associated with favorable neurologic outcome and survival in patients resuscitated after cardiac arrest due to non-shockable rhythms.     

Serum matrix metalloproteinases in patients resuscitated from cardiac arrest. The association with therapeutic hypothermia

Aim

To study the systemic levels of matrix metalloproteinases (MMP) -7, -8 and -9 and their inhibitor TIMP-1 in cardiac arrest patients and the association with mild therapeutic hypothermia treatment on the serum concentration of these enzymes.

Methods

MMP-7, -8 and -9 and tissue inhibitor of metalloproteinases-1 (TIMP-1) were analysed in blood samples obtained from 51 patients resuscitated from cardiac arrest. The samples were taken at 24 and 48 h from restoration of spontaneous circulation (ROSC). The biomarker levels were compared between patients (N = 51) and healthy controls (N = 10) and between patients who did (N = 30) and patients who did not (N = 21) receive mild therapeutic hypothermia.

Results

MMP-7 (median 0.47 ng/ml), MMP-8 (median 31.16 ng/ml) and MMP-9 (median 253.00 ng/ml) levels were elevated and TIMP-1 levels suppressed (median 78.50 ng/ml) in cardiac arrest patients as compared with healthy controls at 24 h from ROSC. Hypothermia treatment associated with attenuated elevation of MMP-9 (p = 0.001) but not MMP-8 (p = 0.02) or MMP-7 (p = 0.69). Concentrations of MMPs -7, -8 and -9 correlated with the leukocyte count but not with C-reactive protein (CRP) or neurone-specific enolase (NSE) levels.

Conclusion

We demonstrated that the systemic levels of MMP-7, -8 and -9 but not TIMP-1 are elevated in cardiac arrest patients in the 48 h post-resuscitation period relative to the healthy controls. Patients who received therapeutic hypothermia had lower MMP-9 levels compared to non-hypothermia treated patients, which generates hypothesis about attenuation of inflammatory response by hypothermia treatment.     

Antiplatelet effect of clopidogrel is reduced in patients treated with therapeutic hypothermia after cardiac arrest

Background

The platelet inhibitor clopidogrel is administered to patients treated with therapeutic hypothermia following cardiac arrest due to acute coronary syndromes. Interactions with proton pump inhibitors and genetics are factors with a known potential to attenuate the platelet inhibition of clopidogrel. In patients treated with therapeutic hypothermia, reduced gastrointestinal function and hypothermia may also reduce the effect of clopidogrel. To investigate the net platelet inhibition of clopidogrel, we have measured the platelet reactivity index in patients treated with therapeutic hypothermia.

Methods and results

Twenty-five Caucasian patients treated with clopidogrel and therapeutic hypothermia were prospectively included. Therapeutic hypothermia was defined as 33-34 °C and delivered for 24 h. Clopidogrel loading doses (300-600 mg) were administered enterally the day of admission and followed by 75 mg daily. Blood samples were collected on day 1 (n = 25) and day 3 (n = 16). The samples were analysed for inhibition by clopidogrel with a vasodilator stimulated phosphoprotein phosphorylation kit. On day 1 and day 3, platelet reactivity index was 0.77 ± 0.09 and 0.57 ± 0.16, respectively. The number of patients with a satisfactory antiplatelet effect (defined as platelet reactivity index <0.5) were 0 (0%) and 5 (31%), respectively.

Conclusion

In patients treated with therapeutic hypothermia after cardiac arrest, the effect of clopidogrel on platelets was virtually nonexistent on day 1 after administration, with some improvement on day 3.     

Severe QTc prolongation under mild hypothermia treatment and incidence of arrhythmias after cardiac arrest--a prospective study in 34 survivors with continuous Holter ECG

Background

Mild hypothermia treatment (32-34 °C) in survivors after cardiac arrest (CA) is clearly recommended by the current guidelines. The effects of cooling procedure towards QT interval have not been evaluated so far outside of case series. In a prospective study 34 consecutive survivors after cardiac arrest were continuously monitored with Holter ECG over the first 48 h.

Patients and methods

A total of 34 patients were analysed and received mild therapeutic hypothermia treatment (MTH) according to the current guidelines and irrespective of the initial rhythm. At admission to hospital and in the field in case of OHCA, a 12-lead ECG was performed in all patients.

Results

During cooling the incidence of ventricular tachycardia was low (8.8%) and in none of the patients Torsade de pointes occurred. The QTc interval was within normal range at first patient contact with EMS in the field (440.00 ms; IQR 424.25-476.75; n = 17) but during hypothermia treatment the QTc interval was significantly prolonged at 33 °C after 24 h of cooling (564.47 ms; IQR 512.41-590.00; p = 0.0001; n = 34) and decreased after end of hypothermia to baseline levels (476.74 ms; 448.71-494.97; p = 0.15).

Conclusion

The QTc interval was found to be significantly prolonged during MTH treatment, and some severe prolongations >670 ms were observed, without a higher incidence of life-threatening arrhythmias, especially no Torsade des pointes were detected. However, routine and frequent ECG recording with respect to the QTc interval should become part of any hypothermia standard operation protocol and should be recommended by official guidelines.     

Therapeutic hypothermia and prevention of acute kidney injury: a meta-analysis of randomized controlled trials

Background

Therapeutic hypothermia has been shown to reduce neurological morbidity and mortality in the setting of out-of-hospital cardiac arrest and may be beneficial following brain injury and cardiopulmonary bypass. We conducted a systematic review to ascertain the effect of therapeutic hypothermia on development of acute kidney injury (AKI) and mortality.

Methods

We searched for randomized controlled trials in MEDLINE through February 2011. We included trials comparing hypothermia to normothermia that reported kidney-related outcomes including, development of AKI, dialysis requirement, changes in serum creatinine, and mortality. We performed Peto fixed-effect and random-effects model meta-analyses, and meta-regressions.

Results

Nineteen trials reporting on 2218 patients were included; in the normothermia group, the weighted rate of AKI was 4.2%, dialysis requirement 3.7%, and mortality 10.8%. By meta-analysis, hypothermia was not associated with a lower odds of AKI (odds ratio [OR] 1.01, 95% confidence interval [CI] 0.68, 1.51; P = 0.95) or dialysis requirement (OR 0.81; 95% CI 0.30, 2.19; P = 0.68); however, by meta-regression, a lower target cooling temperature was associated with a lower odds of AKI (P = 0.01). Hypothermia was associated with lower mortality (OR 0.69; 95% CI 0.51, 0.92; P = 0.01).

Conclusions

In trials that ascertained kidney endpoints, therapeutic hypothermia prevented neither the development of AKI nor dialysis requirement, but was associated with lower mortality. Different definitions and rates of AKI, differences in mortality rates, and concerns about the optimal target cooling temperature preclude definitive conclusions.     

Association between clinical examination and outcome after cardiac arrest

Background

Neurologic prognostication after cardiac arrest relies on clinical examination findings derived before the advent of therapeutic hypothermia (TH). We measured the association between clinical examination findings at hospital arrival, 24, and 72 h after cardiac arrest in a modern intensive care unit setting.

Methods

Between 1/1/2005 and 3/31/2009, hospital charts were reviewed in 272 subjects for neurologic examination findings (Glasgow Coma Score - motor examination, pupil response, corneal response) at hospital arrival, 24, and 72 h following cardiac arrest. Primary outcome was survival to hospital discharge. Secondary outcome was “good outcome,” defined as discharge to home or acute rehabilitation facility.

Results

Mean age was 61 years; 155 (57%) were male. Most were treated with TH (N = 161; 59%) and 100 subjects (37%) were in ventricular fibrillation/ventricular tachycardia. Out-of-hospital cardiac arrest was common (N = 169; 62%). Ninety-one (33%) survived, with 54 (20%) experiencing a good outcome.In subjects with a GCS Motor score ≤3 at 24 and 72 h survival was 17% (13/76; 95% CI 7.9-26.2%) and 20% (6/27; 95% CI 6.3-33.6%), respectively. Subjects with a GCS Motor score ≤2 at 24 and 72 h survived in 14% (9/66; 95% CI 4.6-22.6%) and 18% (6/33; 95% CI 3.5-32.8%), respectively. Absent pupil reactivity on arrival did not exclude survival (7/65; 11%; 95% CI 2.4-19%). A lack of pupil reactivity or corneal response at 72 h was associated with death (pupil: 0/17; 95% CI 0, 2.9%; corneal: 0/21; 95% CI 0, 2.4%).

Conclusions

GCS Motor score ≤3 or ≤2 at 24 or 72 h following cardiac arrest does not exclude survival or good outcome. However, absent pupil or corneal response at 72 h appears to exclude survival and good outcome.     

Repeated magnetic resonance imaging and cerebral performance after cardiac arrest--a pilot study

Aim of the study

Prognostication may be difficult in comatose cardiac arrest survivors. Magnetic resonance imaging (MRI) is potentially useful in the prediction of neurological outcome, and it may detect acute ischemia at an early stage. In a pilot setting we determined the prevalence and development of cerebral ischemia using serial MRI examinations and neurological assessment.

Methods

Ten witnessed out-of-hospital cardiac arrest patients were included. MRI was carried out approximately 2 h after admission to the hospital, repeated after 24 h of therapeutic hypothermia and 96 h after the arrest. The images were assessed for development of acute ischemic lesions. Neurophysiological and cognitive tests as well as a self-reported quality-of-life questionnaire, Short Form-36 (SF-36), were administered minimum 12 months after discharge.

Results

None of the patients had acute cerebral ischemia on MRI at admission. Three patients developed ischemic lesions after therapeutic hypothermia. There was a change in the apparent diffusion coefficient, which significantly correlated with the temperature (p < 0.001). The neurophysiological tests appeared normal. The patients scored significantly better on SF 36 than the controls as regards both bodily pain (p = 0.023) and mental health (p = 0.016).

Conclusions

MRI performed in an early phase after cardiac arrest has limitations, as MRI performed after 24 and 96 h revealed ischemic lesions not detectable on admission. ADC was related to the core temperature, and not to the volume distributed intravenously. Follow-up neurophysiologic tests and self-reported quality of life were good.     

Relationship between blood, nasopharyngeal and urinary bladder temperature during intravascular cooling for therapeutic hypothermia after cardiac arrest

Objectives

Therapeutic hypothermia improves survival and neurological outcome in patients successfully resuscitated after cardiac arrest. Accurate temperature control during cooling is essential to prevent cooling-related side effects.

Methods

Prospective observational study of 12 patients assessed during therapeutic hypothermia (32-34 °C) achieved by intravascular cooling following cardiac arrest. Simultaneous temperature measurements were taken using a Swan-Ganz catheter (blood temperature BLT), nasopharyngeal probe (nasopharyngeal temperature NPT) and the urinary bladder catheter (urinary bladder temperature UBT). A total of 1728 measurements (144 measurements per patient) were recorded over a 48-h period and analyzed. Blood temperature was considered as the reference measurement.

Results

Temperature profiles obtained from BLT, NPT and UBT compared with the use of analysis of variance did not differ significantly. Pearson correlation revealed that the correlation between BLT and NPT as well as BLT and UBT was statistically significant (r = 0.96, p < 0.001 and r = 0.95, p < 0.001, respectively). Bland-Altman analysis proved that the agreement between all measurements was satisfactory and the differences were not clinically important.

Conclusions

In 12 post-cardiac arrest patients undergoing intravascular cooling, both nasopharyngeal and urinary bladder temperature measurements were similar to blood temperatures measured using a pulmonary artery catheter.     

Choline for diagnosis and prognostication of acute coronary syndromes in the Emergency Department

Objectives

Choline has been identified as a promising marker of coronary inflammation, plaque destabilisation and ischaemia. We sought to evaluate plasma choline levels for rapid confirmation or exclusion of acute myocardial infarction (AMI) in the Emergency Department (ED) and for predicting major adverse cardiac events (MACE).

Methods

We prospectively recruited 361 patients who presented to the ED with suspected cardiac chest pain within the previous 24 h. Blood was drawn at the time of presentation for plasma choline levels. All patients underwent troponin T testing ≥ 12 h after symptom onset and were followed up for the occurrence of MACE within 6 months. Whole blood choline (WBCho) levels were also measured in a convenience sample of 39 patients.

Results

Plasma choline levels did not help to predict a diagnosis of AMI (odds ratio (OR) 1.00 (95% confidence intervals (CI) 0.91-1.10, p = 0.98). For a diagnosis of AMI the area under the receiver operating characteristic (ROC) curve was 0.48. Plasma choline was not predictive of the combined endpoint of MACE (OR 1.03, 95% CI 0.95-1.12, p = 0.45) but predicted AMI within 6 months (OR 1.31, 95% CI 1.09-1.56, p = 0.003). WBCho levels were significantly different to plasma levels and were predictive of MACE.

Conclusions

Plasma choline, measured at the time of ED presentation, is not a diagnostic marker of AMI but predicts AMI within 6 months. While plasma choline failed to predict MACE, WBCho was predictive and warrants further evaluation.     

Examining the contextual effects of neighborhood on out-of-hospital cardiac arrest and the provision of bystander cardiopulmonary resuscitation

Objective

To understand the association between neighborhood and individual characteristics in determining whether or not bystanders perform cardiopulmonary resuscitation (CPR) in cases of out-of-hospital cardiac arrest (OHCA).

Methods

Between October 1, 2005 to November 30, 2008, 1108 OHCA cases from Fulton County (Atlanta), GA, were eligible for bystander CPR. We conducted multi-level non-linear regression analysis and derived Empirical Bayes estimates for bystander CPR by census tract.

Results

279 (25%) cardiac arrest victims received bystander CPR. Provision of bystander CPR was significantly more common in witnessed events (odds ratio [OR] 1.64; 95% confidence interval [CI] 1.21-2.22, p < 0.001) and those that occurred in public locations (OR 1.67; 95% CI 1.16-2.40, p < 0.001). Other individual-level characteristics were not significantly associated with bystander CPR. Cardiac arrests in the census tracts that rank in the highest income quintile, as compared to the lowest income quintile were much more likely (OR 4.98; 95% CI 1.65-15.04) to receive bystander CPR.

Conclusion

Cardiac arrest victims in the highest income census tracts were much more likely to receive bystander CPR than in the lowest income census tracts, even after controlling for individual and arrest characteristics. Low-income neighborhoods may be particularly appropriate targets for community-based CPR training and awareness efforts.     

Feasibility and safety of combined percutaneous coronary intervention and therapeutic hypothermia following cardiac arrest

Review

Mild therapeautic hypothermia (MTH) has been associated with cardiac dysrhythmias, coagulopathy and infection. After restoration of spontaneous circulation (ROSC), many cardiac arrest patients undergo percutaneous coronary intervention (PCI). The safety and feasibility of combined MTH and PCI remains unclear. This is the first study to evaluate whether PCI increases cardiac risk or compromises functional outcomes in comatose cardiac arrest patients who undergo MTH.

Methods

Ninety patients within a 6-h window following cardiac arrest and ROSC were included. Twenty subjects (23%) who underwent PCI following MTH induction were compared to 70 control patients who underwent MTH without PCI. The primary endpoint was the rate of dysrhythmias; secondary endpoints were time-to-MTH induction, rates of adverse events (dysrhythmia, coagulopathy, hypotension and infection) and mortality.

Results

Patients who underwent PCI plus MTH suffered no statistical increase in adverse events (P = .054). No significant difference was found in the rates of dysrhythmias (P = .27), infection (P = .90), coagulopathy (P = .90) or hypotension (P = .08). The PCI plus MTH group achieved similar neurological outcomes (modified Rankin Scale (mRS) ≤3 (P = .42) and survival rates (P = .40). PCI did not affect the speed of MTH induction; the target temperature was reached in both groups without a significant time difference (P = .29).

Conclusion

Percutaneous coronary intervention seems to be feasible when combined with MTH, and is not associated with increased cardiac or neurological risk.     

The incidence and significance of accidental hypothermia in major trauma--a prospective observational study

Background

Serious sequelae have been associated with injured patients who are hypothermic (<35 °C) including coagulopathy, acidosis, decreased myocardial contractility and risk of mortality.

Aim

Establish the incidence of accidental hypothermia in major trauma patients and identify causative factors.

Method

Prospective identification and subsequent review of 732 medical records of major trauma patients presenting to an Adult Major Trauma Centre was undertaken between January and December 2008. Multivariate analysis was performed using logistic regression. Significant and clinically relevant variables from univariate analysis were entered into multivariate models to evaluate determinants for hypothermia and for death. Goodness of fit was determined with the use of the Hosmer-Lemeshow statistic.

Main results

Overall mortality was 9.15%. The incidence of hypothermia was 13.25%. The mortality of patients with hypothermia was 29.9% with a threefold independent risk of death: OR (CI 95%) 3.44 (1.48-7.99), P = 0.04. Independent determinants for hypothermia were pre-hospital intubation: OR (CI 95%) 5.18 (2.77-9.71), P < 0.001, Injury Severity Score (ISS): 1.04 (1.01-1.06), P = 0.01, Arrival Systolic Blood Pressure (ASBP) < 100 mm Hg: 3.04 (1.24-7.44), P = 0.02, and wintertime: 1.84 (1.06-3.21), P = 0.03.Of the 87 hypothermic patients who had repeat temperatures recorded in the Emergency Department, 77 (88.51%) patients had a temperature greater than the recorded arrival temperature. There was no change in recorded temperature for four (4.60%) patients, whereas six (6.90%) patients were colder at Emergency Department discharge.

Conclusion

Seriously injured patients with accidental hypothermia have a higher mortality independent of measured risk factors. For patients with multiple injuries a coordinated effort by paramedics, nurses and doctors is required to focus efforts toward early resolution of hypothermia aiming to achieve a temperature >35 °C.     

Neurologic prognostication and bispectral index monitoring after resuscitation from cardiac arrest

Objective

While the use of therapeutic hypothermia (TH) has improved outcomes after resuscitation from cardiac arrest, prognostication of survival and neurologic function remains difficult during the post-arrest time period. Bispectral index (BIS) monitoring, a non-invasive measurement of simplified electroencephalographic data, is increasingly being considered for post-arrest neurologic assessment and outcomes prediction, although data supporting the technique are limited. We hypothesized that BIS values within 24 h after resuscitation would correlate with neurologic outcomes at discharge.

Methods

We prospectively collected BIS data in consecutive patients initially resuscitated from cardiac arrest and treated with TH in one academic medical center. We assessed BIS values in context of cerebral performance category (CPC) assessment on the day of discharge.

Results

Data were collected in 62 post-arrest patients, of whom 26/62 (42%) survived to hospital discharge. Mean BIS values at 24 h post-resuscitation were significantly different in the survivors with CPC 1-2 (“good” outcome) vs those with CPC 3-5 (“poor” outcome) or death during hospitalization (49 ± 13 vs 30 ± 20; p < 0.001). Receiver operator characteristic analysis suggested that 24 h BIS was most predictive of CPC 1-2 outcome compared to the other timepoints; a BIS cutpoint of 45 exhibited a sensitivity of 63% and a specificity of 86%, with a positive likelihood ratio of 4.67. Sixteen patients exhibited a BIS of zero during at least one timepoint; all of these patients died during hospitalization.

Conclusions

BIS monitoring values at 24 h post-resuscitation are correlated with neurologic outcomes in patients undergoing TH treatment. In 16/62 patients, a BIS of zero at any timepoint was observed, which was uniformly correlated with poor outcome after resuscitation from cardiac arrest; however, a non-zero BIS is insufficient as a sole predictor of good neurologic survival.     

Assessment of risk factors for post-rewarming “rebound hyperthermia” in cardiac arrest patients undergoing therapeutic hypothermia

Introduction

The outcomes associated with therapeutic hypothermia (TH) after cardiac arrest, while overwhelmingly positive, may be associated with adverse events. The incidence of post-rewarming rebound hyperthermia (RH) has been relatively unstudied and may worsen survival and neurologic outcome. The purpose of this study was to determine the incidence and risk factors associated with RH as well as its relationship to mortality, neurologic morbidity, and hospital length of stay (LOS).

Methods

A retrospective, observational study was performed of adult patients who underwent therapeutic hypothermia after an out-of-hospital cardiac arrest. Data describing 17 potential risk factors for RH were collected. The primary outcome was the incidence of RH while the secondary outcomes were mortality, discharge neurologic status, and LOS.

Results

141 patients were included. All 17 risk factors for RH were analyzed and no potential risk factors were found to be significant at a univariate level. 40.4% of patients without RH experienced any cause of death during the initial hospitalization compared to 64.3% patients who experienced RH (OR: 2.66; 95% CI: 1.26–5.61; p = 0.011). The presence of RH is not associated with an increase in LOS (10.67 days vs. 9.45 days; absolute risk increase = −1.21 days, 95% CI: −1.84 to 4.27; p = 0.434). RH is associated with increased neurologic morbidity (p = 0.011).

Conclusions

While no potential risk factors for RH were identified, RH is a marker for increased mortality and worsened neurologic morbidity in cardiac arrest patients who have underwent TH.     

Therapeutic hypothermia after cardiac arrest: A retrospective comparison of surface and endovascular cooling techniques

Objectives

Therapeutic hypothermia (32-34 °C) is recommended for comatose survivors of cardiac arrest; however, the optimal technique for cooling is unknown. We aimed to compare therapeutic hypothermia using either surface or endovascular techniques in terms of efficacy, complications and outcome.

Design

Retrospective cohort study.

Setting

Thirty-bed teaching hospital intensive care unit (ICU).

Patients

All patients (n = 83) undergoing therapeutic hypothermia following cardiac arrest over a 2.5-year period. The mean age was 61 ± 16 years; 88% of arrests occurred out of hospital, and 64% were ventricular fibrillation/tachycardia.

Interventions

Therapeutic hypothermia was initiated in the ICU using iced Hartmann's solution, followed by either surface (n = 41) or endovascular (n = 42) cooling; choice of technique was based upon endovascular device availability. The target temperature was 32-34 °C for 12-24 h, followed by rewarming at a rate of 0.25 °C h⁻¹.

Measurements and main results

Endovascular cooling provided a longer time within the target temperature range (p = 0.02), less temperature fluctuation (p = 0.003), better control during rewarming (0.04), and a lower 48-h temperature load (p = 0.008). Endovascular cooling also produced less cooling-associated complications in terms of both overcooling (p = 0.05) and failure to reach the target temperature (p = 0.04). After adjustment for known confounders, there were no differences in outcome between the groups in terms of ICU or hospital mortality, ventilator free days and neurological outcome.

Conclusion

Endovascular cooling provides better temperature management than surface cooling, as well as a more favorable complication profile. The equivalence in outcome suggested by this small study requires confirmation in a randomized trial.     

Post-resuscitation electrocardiograms,acute coronary findings and in-hospital prognosis of survivors of out-of-hospital cardiac arrest

Background

Identification of acute coronary lesions amenable to urgent intervention in survivors of out-of-hospital cardiac arrest is crucial. We aimed to compare the clinical and electrocardiographic characteristics to urgent coronary findings, and to analyze in-hospital prognosis of these patients.

Methods

From January 2005 to December 2012 we retrospectively identified consecutive patients resuscitated from out-of-hospital cardiac arrest, and analyzed the clinical characteristics, post-resuscitation electrocardiogram and coronary angiogram of those who underwent emergent angiography. Mortality and neurologic status at discharge were also assessed.

Results

Patients with ST-elevation more frequently had obstructive coronary artery disease (89% vs. 51%, p < 0.001) or acute coronary occlusions (83% vs. 8%, p < 0.001) than patients without ST-elevation. Independent predictors of an acute coronary occlusion were chest pain before arrest (OR 0.16, 95% CI 0.04–0.7, p = 0.01), a shockable initial rhythm (OR 0.16, 95% CI 0.03–0.9, p = 0.03), and ST-elevation on the post-resuscitation electrocardiogram (OR 0.02, 95% CI 0.004–0.13, p < 0.001). Survival with favorable neurologic recovery at discharge was 59%. Independent predictors of mortality or unfavorable neurological outcome at discharge were absence of basic life support (OR 0.2, 95% CI 0.06–0.9, p = 0.04), prolonged resuscitation time (OR 0.9, 95% CI 0.8–0.9, p = 0.01), and necessity of vasopressors (OR 14.8, 95% CI 3.3–65.4, p = 0.001).

Conclusions

Most patients with ST-elevation on the post-resuscitation electrocardiogram had an acute coronary occlusion, as opposed to patients without ST-elevation. Absence of basic life support, prolonged resuscitation time and use of vasopressors were independent predictors of worse in-hospital outcome.     

The LA story: What happened after a new policy allowing paramedics to forgo resuscitation attempts in prehospital cardiac arrest

Background

Despite potential harm to patients, families, and emergency personnel, a low survival rate, and high costs and intensity of care, attempting resuscitation after prehospital cardiac arrest is the norm, unless there are signs of irreversible death or the presence of a valid, state-issued DNR.

Objective

To determine whether there was a change in the rate of forgoing resuscitation attempts in prehospital cardiac arrest after implementation of a new policy allowing paramedics to forgo resuscitation based on a verbal family request or the presence of certain arrest characteristics.

Methods and results

All prehospital run sheets for cardiac arrest in Los Angeles County were reviewed for the first seven days of each month August 2006-January 2007 (pre-policy) and January-June 2008 (post-policy). Paramedics were more likely to forgo resuscitation attempts after the policy change (13.3% vs. 8.5%, p < 0.01). In addition, the percentage of patients with documented signs of irreversible death decreased post-policy, from 50.4% to 35.8%, p < 0.01. After adjustment for potential confounders (patient demographics, clinical characteristics and EMS factors), as well as exclusion of patients with signs of irreversible death, paramedics are significantly more likely to forgo a resuscitation, and less likely to attempt resuscitation, after the policy change (OR 1.67 [95% CI 1.07, 2.61], p = 0.024).

Conclusions

Paramedics are more likely to forgo, and less likely to attempt, resuscitation in victims of cardiac arrest after implementation of a new policy. There was also an associated decrease in the percentage of patients who had signs of irreversible death, which might reflect a change in paramedic behavior.     

Sublingual and muscular microcirculatory alterations after cardiac arrest: a pilot study

Aims of the study

Post-cardiac arrest resuscitated patients often develop a “sepsis-like” syndrome, which may be associated with organ dysfunction. Impaired microcirculatory blood flow is thought to play a key role in sepsis-induced organ failure; however, few data are available on the microcirculation after cardiac arrest. We investigated microvascular density and reactivity in the early phase following cardiac arrest.

Methods

We prospectively evaluated the sublingual microcirculation in 10 patients admitted to the intensive care unit (ICU) after cardiac arrest using a Sidestream Dark Field device. Thenar oxygen saturation (StO₂) was also measured using a tissue spectrometer and a vaso-occlusive test was performed by rapid inflation of a pneumatic cuff around the arm to evaluate the StO₂ reperfusion rate, reflecting microvascular reactivity. In all patients, measurements were performed within the first 12 h after admission (T1) and 24-48 h thereafter (T2).

Results

There was a significant increase in functional capillary density (FCD, 7.2 ± 1.9-10.0 ± 1.4 N/mm, p = 0.001), in the proportion of small perfused vessels (PSPV, 76 ± 13-92 ± 3%, p = 0.004) and in the mean microvascular flow index (MFI, 2.1 ± 0.5-2.8 ± 0.2, p = 0.003) at T2 compared to T1. FCD and PSPV were significantly correlated to body temperature, but not to cardiac output or mean arterial pressure. The StO₂ reperfusion rate did not change over the study period and showed considerable inter-individual variability.

Conclusions

The early post-resuscitation phase is characterised by significant abnormalities in microvascular density and flow, which return to normal within 48 h after cardiac arrest. These changes may be influenced by body temperature. Microvascular reactivity is impaired after cardiac arrest.