Sublingual microcirculation is impaired in post-cardiac arrest patients

Aim

We hypothesized that microcirculatory dysfunction, similar to that seen in sepsis, occurs in post-cardiac arrest patients and that better microcirculatory flow will be associated with improved outcome. We also assessed the association between microcirculatory dysfunction and inflammatory markers in the post-cardiac arrest state.

Methods

We prospectively evaluated the sublingual microcirculation in post-cardiac arrest patients, severe sepsis/septic shock patients, and healthy control patients using Sidestream Darkfield microscopy. Microcirculatory flow was assessed using the microcirculation flow index (MFI) at 6 and 24 h in the cardiac arrest patients, and within 6 h of emergency department admission in the sepsis and control patients.

Results

We evaluated 30 post-cardiac arrest patients, 16 severe sepsis/septic shock patients, and 9 healthy control patients. Sublingual microcirculatory blood flow was significantly impaired in post-cardiac arrest patients at 6 h (MFI 2.6 [IQR: 2–2.9]) and 24 h (2.7 [IQR: 2.3–2.9]) compared to controls (3.0 [IQR: 2.9–3.0]; p < 0.01 and 0.02, respectively). After adjustment for initial APACHE II score, post-cardiac arrest patients had significantly lower MFI at 6-h compared to sepsis patients (p < 0.03). In the post-cardiac arrest group, patients with good neurologic outcome had better microcirculatory blood flow as compared to patients with poor neurologic outcome (2.9 [IQR: 2.4–3.0] vs. 2.6 [IQR: 1.9–2.8]; p < 0.03). There was a trend toward higher median MFI at 24 h in survivors vs. non-survivors (2.8 [IQR: 2.4–3.0] vs. 2.6 [IQR: 2.1–2.8] respectively; p < 0.09). We found a negative correlation between MFI-6 and vascular endothelial growth factor (VEGF) (r = −0.49, p = 0.038). However, after Bonferroni adjustment for multiple comparisons, this correlation was statistically non-significant.

Conclusion

Microcirculatory dysfunction occurs early in post-cardiac arrest patients. Better microcirculatory function at 24 h may be associated with good neurologic outcome.     

Markers of intestinal injury are associated with endotoxemia in successfully resuscitated patients

Aims

Gut dysfunction is suspected to play a major role in the pathophysiology of post-resuscitation disease through an increase in intestinal permeability and endotoxin release. However this dysfunction often remains occult and is poorly investigated. The aim of this pilot study was to explore intestinal failure biomarkers in post-cardiac arrest patients and to correlate them with endotoxemia.

Methods

Following resuscitation after cardiac arrest, 21 patients were prospectively studied. Urinary intestinal fatty acid-binding protein (IFABP), which marks intestinal permeability, plasma citrulline, which reflects the functional enterocyte mass, and whole blood endotoxin were measured at admission, days 1–3 and 6. We explored the kinetics of release and the relationship between IFABP, citrulline and endotoxin values.

Results

IFABP was extremely high at admission and normalized at D3 (6668 pg/mL vs 39 pg/mL, p = 0.01). Lowest median of citrulline (N = 20–40 μmol/L) was attained at D2 (11 μmol/L at D2 vs 24 μmol/L at admission, p = 0.01) and tended to normalize at D6 (21 μmol/L). During ICU stay, 86% of patients presented a detectable endotoxemia. Highest endotoxin level was positively correlated with highest IFABP level (R² = 0.31, p = 0.01) and was inversely correlated with lowest plasma citrulline levels (R² = 0.55, p < 0.001). Endotoxin levels increased between admission and D2 in patients with post-resuscitation shock, whereas it decreases in patients with no shock (median +0.33 EU vs −0.19 EU, p = 0.03). Highest endotoxin level was positively correlated with D3 SOFA score (R² = 0.45, p = 0.004).

Conclusion

Biomarkers of intestinal injury are altered after cardiac arrest and are associated with endotoxemia. This could worsen post-resuscitation shock and organ failure.     

Percutaneous left ventricular assistance in post cardiac arrest shock: Comparison of intra aortic blood pump and IMPELLA Recover LP2.5

Aim

To compare the feasibility, safety and outcome of IMPELLA Recover LP2.5 cardiac assistance and intra aortic balloon pump (IABP) in patients with post-cardiac arrest shock.

Background

The high early mortality rate of post-cardiac arrest patients is attributed to a “post cardiac arrest syndrome” characterized by an acute and transient left ventricular (LV) systolic dysfunction. LV assistance with IMPELLA Recover LP2.5 is proposed in most severe patients.

Methods

Retrospective single center registry from January 2007 to October 2010. All survivors of out-of-hospital cardiac arrest with patent or predictive factors for the occurrence of post-resuscitation shock assisted by either IMPELLA or intra aortic balloon pump (IABP) device immediately after the coronary angiogram were included.

Results

78 post-cardiac arrest patients were assisted by one of the devices (35 by IMPELLA and 43 by IABP). Median “no flow” and median “low flow” were similar at admission as were hemodynamic parameters. The feasibility of IMPELLA implantation was good (97%). At 28 days, the survival rate without sequellae was 23.0% in the IMPELLA and 29.5% in the IABP group (p = 0.61). Vascular complications were observed equally in both groups (3 vs 2, p = 0.9). Serious bleeding complications occurred in 26% of IMPELLA patients vs 9% of IABP patients (p = 0.06).

Conclusion

Early LV assistance by the IMPELLA LP2.5 is feasible in patients with post-resuscitation shock. The rate of complications did not differ substantially in the two groups, except for a trend toward a higher rate of bleeding events with IMPELLA. These encouraging findings must be confirmed in a larger clinical study.     

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.     

A feasibility study of cerebral oximetry monitoring during the post-resuscitation period in comatose patients following cardiac arrest

Background

One of the major causes of death and neurological injury after cardiac arrest is delayed ischemia combined with oxygen free radical mediated reperfusion injury. Consequently determining the optimal balance between oxygen delivery and uptake in the brain using a reliable non-invasive monitoring system during the post-resuscitation period is of importance. In this observational study, we evaluated the feasibility of using cerebral oximetry during the post-resuscitation period in order to identify changes in regional cerebral oxygen saturation (rSO₂) and its association with survival to discharge.

Methods

21 consecutive patients admitted to the intensive care units following cardiac arrest had cerebral oximetry monitoring carried out for 48 h. Mean rSO₂ values were collected during the first 24 h and then again during the subsequent 24–48 h of the post-resuscitation period.

Results

43% (n = 9) patients survived to hospital discharge and 57% (n = 12) died. Amongst all patients the median (IQR) rSO₂% was 65.5% (62.6–68.2) in the first 24-h following ROSC and increased to 72.1% (64.6–73.7) (p = 0.11) in the subsequent 24–48 h. The median (IQR) rSO₂% during the first 24 h in patients who survived to discharge compared to those who did not survive were significantly higher 68.2% (66.0–71.0) vs. 62.9% (56.5–66.0), p = 0.01). During the subsequent 24–48 h period, while a difference in the rSO₂ between survivors and non-survivors was noted, this did not achieve statistical significance (median (IQR): 73.7 (70.2–74.0) vs. 66.5 (58.2–72.1), p = 0.11).

Conclusions

Our study indicates that the use of cerebral oximetry is feasible during the post resuscitation period after cardiac arrest. Further studies are needed to determine whether cerebral oximetry may be used as a novel non-invasive monitoring system to evaluate changes in the balance between cerebral oxygen delivery and uptake during the post-resuscitation period.     

Serum procalcitonin as a marker of post-cardiac arrest syndrome and long-term neurological recovery,but not of early-onset infections,in comatose post-anoxic patients treated with therapeutic hypothermia

Objective

To examine the relationship of early serum procalcitonin (PCT) levels with the severity of post-cardiac arrest syndrome (PCAS), long-term neurological recovery and the risk of early-onset infections in patients with coma after cardiac arrest (CA) treated with therapeutic hypothermia (TH).

Methods

A prospective cohort of adult comatose CA patients treated with TH (33 °C, for 24 h) admitted to the medical/surgical intensive care unit, Lausanne University Hospital, was studied. Serum PCT was measured early after CA, at two time-points (days 1 and 2). The SOFA score was used to quantify the severity of PCAS. Diagnosis of early-onset infections (within the first 7 days of ICU stay) was made after review of clinical, radiological and microbiological data. Neurological recovery at 3 months was assessed with Cerebral Performance Categories (CPC), and was dichotomized as favorable (CPC 1–2) vs. unfavorable (CPC 3–5).

Results

From December 2009 to April 2012, 100 patients (median age 64 [interquartile range 55–73] years, median time from collapse to ROSC 20 [11–30] min) were studied. Peak PCT correlated with SOFA score at day 1 (Spearman's R = 0.44, p < 0.0001) and was associated with neurological recovery at 3 months (peak PCT 1.08 [0.35–4.45] ng/ml in patients with CPC 1–2 vs. 3.07 [0.89–9.99] ng/ml in those with CPC 3–5, p = 0.01). Peak PCT did not differ significantly between patients with early-onset vs. no infections (2.14 [0.49–6.74] vs. 1.53 [0.46–5.38] ng/ml, p = 0.49).

Conclusions

Early elevations of serum PCT levels correlate with the severity of PCAS and are associated with worse neurological recovery after CA and TH. In contrast, elevated serum PCT did not correlate with early-onset infections in this setting.     

Haemodynamic variables and functional outcome in hypothermic patients following out-of-hospital cardiac arrest

Aim of the study

To evaluate the association between haemodynamic variables during the first 24 h after intensive care unit (ICU) admission and neurological outcome in out-of-hospital cardiac arrest (OHCA) victims undergoing therapeutic hypothermia.

Methods

In a multi-disciplinary ICU, records were reviewed for comatose OHCA patients undergoing therapeutic hypothermia. The hourly variable time integral of haemodynamic variables during the first 24 h after admission was calculated. Neurologic outcome was assessed at day 28 and graded as favourable or adverse based on the Cerebral Performance Category of 1–2 and 3–5. Bi- and multivariate regression models adjusted for confounding variables were used to evaluate the association between haemodynamic variables and functional outcome.

Results

67/134 patients (50%) were classified as having favourable outcome. Patients with adverse outcome had a higher mean heart rate (73 [62–86] vs. 66 [60–78] bpm; p = 0.04) and received noradrenaline more frequently (n = 17 [25.4%] vs. n = 9 [6%]; p = 0.02) and at a higher dosage (128 [56–1004] vs. 13 [2–162] μg h⁻¹; p = 0.03) than patients with favourable outcome. The mean perfusion pressure (mean arterial blood pressure minus central venous blood pressure) (OR = 1.001, 95% CI  = 1–1.003; p = 0.04) and cardiac index time integral (OR = 1.055, 95% CI = 1.003–1.109; p = 0.04) were independently associated with adverse outcome at day 28.

Conclusion

Mean perfusion pressure and cardiac index during the first 24 h after ICU admission were weakly associated with neurological outcome in an OHCA population undergoing therapeutic hypothermia. Further studies need to elucidate whether norepinephrine-induced increases in perfusion pressure and cardiac index may contribute to adverse neurologic outcome following OHCA.     

Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients

Aim of the study

This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest.

Methods

We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO₂) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO₂ (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming.

Results

At the start of mechanically induced TH, SctO₂ was 68% (65–72) and PaCO₂ was 47.2 mmHg (36.9 – 51.4). SctO₂ and PaCO₂ significantly decreased to 59% (57–64; p = 0.006) and 36.6 mmHg (33.9–44.7; p = 0.002), respectively, within the first 3 h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n = 10) compared with survivors (n = 18) at 3 h after induction of hypothermia (p = 0.02) while the decrease in PaCO₂ was similar in both groups. During TH maintenance, SctO₂ gradually returned to baseline values (69% (63–72)) at 24 h, with no differences between survivors and non-survivors (p = 0.65). Carbon dioxide remained within the range of mild hypocapnia (32–38 mmHg) throughout the hypothermic period. During rewarming, SctO₂ further increased to 71% (67–78).

Conclusions

Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO₂ was less pronounced in patients surviving to hospital discharge.     

Myocardial infarction is a frequent cause of exercise-related resuscitated out-of-hospital cardiac arrest in a general non-athletic population

Background

Performing exercise is shown to prevent cardiovascular disease, but the risk of an out-of-hospital cardiac arrest (OHCA) is temporarily increased during strenuous activity. We examined the etiology and outcome after successfully resuscitated OHCA during exercise in a general non-athletic population.

Methods

Consecutive patients with OHCA were admitted with return of spontaneous circulation (ROSC) or on-going resuscitation at hospital arrival (2002–2011). Patient charts were reviewed for post-resuscitation data. Exercise was defined as moderate/vigorous physical activity.

Results

A total of 1393 OHCA-patients were included with 91(7%) arrests occurring during exercise. Exercise-related OHCA-patients were younger (60 ± 13 vs. 65 ± 15, p < 0.001) and predominantly male (96% vs. 69%, p < 0.001). The arrest was more frequently witnessed (94% vs. 86%, p = 0.02), bystander CPR was more often performed (88% vs. 54%, p < 0.001), time to ROSC was shorter (12 min (IQR: 5–19) vs. 15 (9–22), p = 0.007) and the primary rhythm was more frequently shock-able (91% vs. 49%, p < 0.001) compared to non-exercise patients. Cardiac etiology was the predominant cause of OHCA in both exercise and non-exercise patients (97% vs. 80%, p < 0.001) and acute coronary syndrome was more frequent among exercise patients (59% vs. 38%, p < 0.001). One-year mortality was 25% vs. 65% (p < 0.001), and exercise was even after adjustment associated with a significantly lower mortality (HR = 0.40 (95%CI: 0.23–0.72), p = 0.002).

Conclusions

OHCA occurring during exercise was associated with a significantly lower mortality in successfully resuscitated patients even after adjusting for confounding factors. Acute coronary syndrome was more common among exercise-related cardiac arrest patients.     

Improving the quality of cardiopulmonary resuscitation by training dedicated cardiac arrest teams incorporating a mechanical load-distributing device at the emergency department

Objective

Determine if implementing cardiac arrest teams trained with a ‘pit-crew’ protocol incorporating a load-distributing band mechanical CPR device (Autopulse™ ZOLL) improves the quality of CPR, as determined by no-flow ratio (NFR) in the first 10 min of resuscitation.

Methods

A phased, prospective, non-randomized, before–after cohort evaluation. Data collection was from April 2008 to February 2011. There were 100 before and 148 after cases. Continuous video and chest compression data of all study subjects were analyzed. All non-traumatic, collapsed patients aged 18 years and above presenting to the emergency department were eligible. Primary outcome was NFR. Secondary outcomes were return of spontaneous circulation (ROSC), survival to hospital admission and neurological outcome at discharge.

Main results

After implementation, mean total NFR for the first 5 min decreased from 0.42 to 0.27 (decrease = 0.15, 95% CI 0.10–0.19, p < 0.005), and from 0.24 to 0.18 (decrease = 0.06, 95% CI 0.01–0.11, p = 0.02) for the next 5 min. The mean time taken to apply Autopulse™ decreased from 208.8 s to 141.6 s (decrease = 67.2, 95% CI, 22.3–112.1, p < 0.005). The mean CPR ratio increased from 46.4% to 88.4% (increase = 41.9%, 95% CI 36.9–46.9, p < 0.005) and the mean total NFR for the first 10 min decreased from 0.33 to 0.23 (decrease = 0.10, 95% CI 0.07–0.14, p < 0.005).

Conclusion

Implementation of cardiac arrest teams was associated with a reduction in NFR in the first 10 min of resuscitation. Training cardiac arrest teams in a ‘pit-crew’ protocol may improve the quality of CPR at the ED.     

Post-resuscitation myocardial microcirculatory dysfunction is ameliorated with eptifibatide

Background

The post-cardiac arrest syndrome includes a decline in myocardial microcirculation function. Inhibition of the platelet IIb/IIIa glycoprotein receptor has improved myocardial microvascular function post-percutaneous coronary intervention. Therefore, we evaluated such inhibition with eptifibatide for its effect on myocardial microcirculation function post-cardiac arrest and resuscitation.

Methods

Four groups of swine were studied in a prospective, randomized, blinded, placebo-controlled protocol including; eptifibatide administered during CPR (Group 1, n = 5), after resuscitation (Group 2, n = 4), during and after resuscitation (Group 3, n = 5), or placebo (Group 4, n = 10). CPR was initiated following 12 min of untreated VF. Those successfully resuscitated were studied during a 4-h post-resuscitation period. Coronary flow reserve, a measure of microcirculation function (in the absence of coronary obstruction), as well as parameters of left ventricular systolic and diastolic function, were measured pre-arrest and serially post-resuscitation.

Results

Coronary flow reserve was preserved during the post-resuscitation period, indicating normal microcirculatory function in the eptifibatide-treated animals, but not in the placebo-treated group. However, LV function declined equally in both groups during the first 4 h after cardiac arrest.

Conclusion

Inhibition of platelet IIb/IIIa glycoprotein receptors with eptifibatide post-resuscitation prevented myocardial microcirculation dysfunction. Left ventricular dysfunction post-resuscitation was not improved with eptifibatide, and perhaps transiently worse at 30 min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration.     

Ability of code leaders to recall CPR quality errors during the resuscitation of older children and adolescents

Aim

Performance of high quality CPR is associated with improved resuscitation outcomes. This study investigates code leader ability to recall CPR error during post-event interviews when CPR recording/audiovisual feedback-enabled defibrillators are deployed.

Patients and methods

Physician code leaders were interviewed within 24 h of 44 in-hospital pediatric cardiac arrests to assess their ability to recall if CPR error occurred during the event. Actual CPR quality was assessed using quantitative recording/feedback-enabled defibrillators. CPR error was defined as an overall average event chest compression (CC) rate <95/min, depth <38 mm, ventilation rate >10/min, or any interruptions in CPR >10 s. We hypothesized that code leaders would recall error when it actually occurred ≥75% of the time when assisted by audiovisual alerts from a CPR recording feedback-enabled defibrillators (analysis by χ²).

Results

810 min from 44 cardiac arrest events yielded 40 complete data sets (actual and interview); ventilation data was available in 24. Actual CPR error was present in 3/40 events for rate, 4/40 for depth, 32/40 for interruptions >10 s, and 17/24 for ventilation frequency. In post-event interviews, code leaders recalled these errors in 0/3 (0%) for rate, 0/4 (0%) for depth, and 19/32 (59%) for interruptions >10 s. Code leaders recalled these CPR quality errors less than 75% of the time for rate (p = 0.06), for depth (p < 0.01), and for CPR interruption (p = 0.04). Quantification of errors not recalled: missed rate error median = 94 CC/min (IQR 93–95), missed depth error median = 36 mm (IQR 35.5–36.5), missed CPR interruption >10 s median = 18 s (IQR 14.4–28.9). Code leaders did recall the presence of excessive ventilation in 16/17 (94%) of events (p = 0.07).

Conclusion

Despite assistance by CPR recording/feedback-enabled defibrillators, pediatric code leaders fail to recall important CPR quality errors for CC rate, depth, and interruptions during post-cardiac arrest interviews.     

Factors associated with quality of bystander CPR: The presence of multiple rescuers and bystander-initiated CPR without instruction

Aims

To identify the factors associated with good-quality bystander cardiopulmonary resuscitation (BCPR).

Methods

Data were prospectively collected from 553 out-of-hospital cardiac arrests (OHCAs) managed with BCPR in the absence of emergency medical technicians (EMT) during 2012. The quality of BCPR was evaluated by EMTs at the scene and was assessed according to the standard recommendations for chest compressions, including proper hand positions, rates and depths.

Results

Good-quality BCPR was more frequently confirmed in OHCAs that occurred in the central/urban region (56.3% [251/446] vs. 39.3% [42/107], p = 0.0015), had multiple rescuers (31.8% [142/446] vs. 11.2% [12/107], p < 0.0001) and received bystander-initiated BCPR (22.0% [98/446] vs. 5.6% [6/107], p < 0.0001). Good-quality BCPR was less frequently performed by family members (46.9% [209/446] vs. 67.3% [72/107], p = 0.0001), elderly bystanders (13.5% [60/446] vs. 28.0% [30/107], p = 0.0005) and in at-home OHCAs (51.1% [228/446] vs. 72.9% [78/107], p < 0.0001). BCPR duration was significantly longer in the good-quality group (median, 8 vs. 6 min, p = 0.0015). Multiple logistic regression analysis indicated that multiple rescuers (odds ratio = 2.8, 95% CI 1.5–5.6), bystander-initiated BCPR (2.7, 1.1–7.3), non-elderly bystanders (1.9, 1.1–3.2), occurrence in the central region (2.1, 1.3–3.3) and duration of BCPR (1.1, 1.0–1.1) were associated with good-quality BCPR. Moreover, good-quality BCPR was initiated earlier after recognition/witness of cardiac arrest compared with poor-quality BCPR (3 vs. 4 min, p = 0.0052). The rate of neurologically favourable survival at one year was 2.7 and 0% in the good-quality and poor-quality groups, respectively (p = 0.1357).

Conclusions

The presence of multiple rescuers and bystander-initiated CPR are predominantly associated with good-quality BCPR.     

A comparison of etanercept vs. infliximab for the treatment of post-arrest myocardial dysfunction in a swine model of ventricular fibrillation

Aims

To compare the effects of two TNF-α antagonists, etanercept and infliximab, on post-cardiac arrest hemodynamics and global left ventricular function (LV) in a swine model following ventricular fibrillation (VF).

Methods

Domestic swine (n = 30) were placed under general anesthesia and instrumented before VF was induced electrically. After 7 min of VF, standard ACLS resuscitation was performed. Animals achieving return of spontaneous circulation (ROSC) were randomized to immediately receive infliximab (5 mg/kg, n = 10) or etanercept (0.3 mg/kg [4 mg/m²], n = 10) or vehicle (250 mL normal saline [NS], n = 10) and LV function and hemodynamics were monitored for 3 h.

Results

Following ROSC, mean arterial pressure (MAP), stroke work (SW), and LV dP/dt fell from pre-arrest values in all groups. However, at the 30 min nadir, infliximab-treated animals had higher MAP than either the NS group (difference 14.4 mm Hg, 95% confidence interval [CI] 4.2–24.7) or the etanercept group (19.2 mm Hg, 95% CI 9.0–29.5), higher SW than the NS group (10.3 gm-m, 95% CI 5.1–15.5) or the etanercept group (8.9 gm-m, 95% CI 4.0–14.4) and greater LV dP/dt than the NS group (282.9 mm Hg/s, 95% CI 169.6–386.1 higher with infliximab) or the etanercep group (228.9 mm Hg/s, 95% CI 115.6–342.2 higher with infliximab).

Conclusions

Only infliximab demonstrated a beneficial effect on post cardiac arrest hemodynamics and LV function in this swine model. Etanercept was no better in this regard than saline.     

Continuous neuromuscular blockade is associated with decreased mortality in post-cardiac arrest patients

Aim

Neuromuscular blockade may improve outcomes in patients with acute respiratory distress syndrome. In post-cardiac arrest patients receiving therapeutic hypothermia, neuromuscular blockade is often used to prevent shivering. Our objective was to determine whether neuromuscular blockade is associated with improved outcomes after out-of-hospital cardiac arrest.

Methods

A post hoc analysis of a prospective observational study of comatose adult (>18 years) out-of-hospital cardiac arrest at 4 tertiary cardiac arrest centers. The primary exposure of interest was neuromuscular blockade for 24 h following return of spontaneous circulation and primary outcomes were in-hospital survival and functional status at hospital discharge. Secondary outcomes were evolution of oxygenation (PaO₂:FiO₂), and change in lactate. We tested the primary outcomes of in-hospital survival and neurologically intact survival with multivariable logistic regression. Secondary outcomes were tested with multivariable linear mixed-models.

Results

A total of 111 patients were analyzed. In patients with 24 h of sustained neuromuscular blockade, the crude survival rate was 14/18 (78%) compared to 38/93 (41%) in patients without sustained neuromuscular blockade (p = 0.004). After multivariable adjustment, neuromuscular blockade was associated with survival (adjusted OR: 7.23, 95% CI: 1.56–33.38). There was a trend toward improved functional outcome with neuromuscular blockade (50% versus 28%; p = 0.07). Sustained neuromuscular blockade was associated with improved lactate clearance (adjusted p = 0.01).

Conclusions

We found that early neuromuscular blockade for a 24-h period is associated with an increased probability of survival. Secondarily, we found that early, sustained neuromuscular blockade is associated with improved lactate clearance.     

Impact of a standardized nurse observation protocol including MEWS after Intensive Care Unit discharge

Background

Analysis of in-hospital mortality after serious adverse events (SAE's) in our hospital showed the need for more frequent observation in medical and surgical wards. We hypothesized that the incidence of SAE's could be decreased by introducing a standard nurse observation protocol.

Aim

To investigate the effect of a standard nurse observation protocol implementing the Modified Early Warning Score (MEWS) and a color graphic observation chart.

Methods

Pre- and post-intervention study by analysis of patients records for a 5-day period after Intensive Care Unit (ICU) discharge to 14 medical and surgical wards before (n = 530) and after (n = 509) the intervention.

Results

For the total study population the mean Patient Observation Frequency Per Nursing Shift (POFPNS) during the 5-day period after ICU discharge increased from .9993 (95% C.I. .9637–1.0350) in the pre-intervention period to 1.0732 (95% C.I. 1.0362–1.1101) (p = .005) in the post-intervention period. There was an increased risk of a SAE in patients with MEWS 4 or higher in the present nursing shift (HR 8.25; 95% C.I. 2.88–23.62) and the previous nursing shift (HR 12.83;95% C.I. 4.45–36.99). There was an absolute risk reduction for SAE's within 120 h after ICU discharge of 2.2% (95% C.I. −0.4–4.67%) from 5.7% to 3.5%.

Conclusion

The intervention had a positive impact on the observation frequency. MEWS had a predictive value for SAE's in patients after ICU discharge. The drop in SAE's was substantial but did not reach statistical significance.     

Post-resuscitation intestinal microcirculation: Its relationship with sublingual microcirculation and the severity of post-resuscitation syndrome

Objective

Post-resuscitation syndrome has been recognized as one of the major causes of the poor outcomes of cardiopulmonary resuscitation. The aims of this study were to investigate the intestinal microcirculatory changes following cardiopulmonary resuscitation and relate those changes to sublingual microcirculation and the severity of post-resuscitation syndrome as measured by myocardial function and serum inflammatory cytokine levels.

Methods

Twenty-five rats were randomized into three groups: (1) short duration of cardiac arrest (n = 10): ventricular fibrillation (VF) was untreated for 4 min prior to 6 min of cardiopulmonary resuscitation (CPR); (2) long duration of cardiac arrest (n = 10): VF was untreated for 8 min followed by 8 min of CPR; (3) sham control group (n = 5): a sham operation was performed without VF induction and CPR. Intestinal and sublingual microcirculatory blood flow was visualized by a sidestream dark-field (SDF) imaging device at baseline and 1, 2, 4, 6, 8 h post-resuscitation. Myocardial function was measured by echocardiography and serum cytokine levels (TNF-α and IL-6) were measured by enzyme-linked immunosorbent assay (ELISA).

Results

Both intestinal and sublingual microcirculatory blood flow decreased significantly with increasing duration of cardiac arrest and resuscitation. The decreases in intestinal microcirculatory blood flow were closely correlated with the reductions of sublingual microcirculatory blood flow (perfused small vessels density: r = 0.772, p < 0.01; microcirculatory flow index: r = 0.821, p < 0.01). The decreased microcirculatory blood flow was closely correlated with weakened myocardial function and elevated inflammatory cytokine levels.

Conclusions

The severity of post-resuscitation intestinal microcirculatory dysfunction is closely correlated with that of myocardial function and inflammatory cytokine levels. The measurement of sublingual microcirculation reflects changes of intestinal microcirculation and may therefore provide a new option for post-resuscitation monitoring.     

Arterial carbon dioxide tension and outcome in patients admitted to the intensive care unit after cardiac arrest

Background

Arterial carbon dioxide tension (PaCO₂) affects neuronal function and cerebral blood flow. However, its association with outcome in patients admitted to intensive care unit (ICU) after cardiac arrest (CA) has not been evaluated.

Methods and results

Observational cohort study using data from the Australian New Zealand (ANZ) Intensive Care Society Adult-Patient-Database (ANZICS-APD). Outcomes analyses were adjusted for illness severity, co-morbidities, hypothermia, treatment limitations, age, year of admission, glucose, source of admission, PaO₂ and propensity score.We studied 16,542 consecutive patients admitted to 125 ANZ ICUs after CA between 2000 and 2011. Using the APD-PaCO₂ (obtained within 24 h of ICU admission), 3010 (18.2%) were classified into the hypo- (PaCO₂ < 35 mmHg), 6705 (40.5%) into the normo- (35–45 mmHg) and 6827 (41.3%) into the hypercapnia (>45 mmHg) group. The hypocapnia group, compared with the normocapnia group, had a trend toward higher in-hospital mortality (OR 1.12 [95% CI 1.00–1.24, p = 0.04]), lower rate of discharge home (OR 0.81 [0.70–0.94, p < 0.01]) and higher likelihood of fulfilling composite adverse outcome of death and no discharge home (OR 1.23 [1.10–1.37, p < 0.001]). In contrast, the hypercapnia group had similar in-hospital mortality (OR 1.06 [0.97–1.15, p = 0.19]) but higher rate of discharge home among survivors (OR 1.16 [1.03–1.32, p = 0.01]) and similar likelihood of fulfilling the composite outcome (OR 0.97 [0.89–1.06, p = 0.52]). Cox-proportional hazards modelling supported these findings.

Conclusions

Hypo- and hypercapnia are common after ICU admission post-CA. Compared with normocapnia, hypocapnia was independently associated with worse clinical outcomes and hypercapnia a greater likelihood of discharge home among survivors.     

Benefit of an early and systematic imaging procedure after cardiac arrest: Insights from the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) registry

Aims

Identification of the cause of out-of-hospital cardiac arrest (OHCA) is of paramount importance. We investigated the ability of our imaging strategy to provide an early etiological diagnosis of OHCA and the influence of this strategy on ICU survival.

Methods

Retrospective review of a prospectively acquired ICU database (01/2000–12/2010) including all OHCA patients without obvious extracardiac cause, for which an early diagnosis research was conducted (coronary angiography and/or brain and chest CT scan) within 24 h after resuscitation. These procedures could be performed separately or be combined, according to a decision algorithm.

Results

Of the 1274 patients admitted after OHCA during this 10-year period, the imaging strategy was applied in 896 patients. Patients who benefited from coronary angiography and/or CT scan were admitted to our ICU after a median delay of 180 [130–220] min after resuscitation. Seven hundred and forty-five coronary angiographies were performed, of which 452 (61%) identified at least one significant coronary lesion deemed responsible for the OHCA. CT-scan was performed in 355 patients and provided a diagnosis in 72 patients (20%), mainly stroke (n = 38) and pulmonary embolism (n = 19). Overall, this strategy allowed early diagnosis in 524 patients (59%). ICU survival was significantly higher for patients with a diagnosis identified by coronary angiography as compared with CT-scan (43% vs 10%, p < 0.001).

Conclusion

The use of an early diagnosis protocol with immediate coronary angiography and/or CT scan provided the etiology of nearly two thirds of OHCA cases. In this large retrospective database, coronary angiography yielded a better diagnostic value than brain and/or chest CT-scan.     

A pilot study examining the role of regional cerebral oxygen saturation monitoring as a marker of return of spontaneous circulation in shockable (VF/VT) and non-shockable (PEA/Asystole) causes of cardiac arrest

Background

Non-invasive monitoring of cerebral perfusion and oxygen delivery during cardiac arrest is not routinely utilized during cardiac arrest resuscitation. The objective of this study was to investigate the feasibility of using cerebral oximetry during cardiac arrest and to determine the relationship between regional cerebral oxygen saturation (rSO2) with return of spontaneous circulation (ROSC) in shockable (VF/VT) and non-shockable (PEA/asystole) types of cardiac arrest.

Methods

Cerebral oximetry was applied to 50 in-hospital and out-of-hospital cardiac arrest patients.

Results

Overall, 52% (n = 26) achieved ROSC and 48% (n = 24) did not achieve ROSC. There was a significant difference in mean ± SD rSO2% in patients who achieved ROSC compared to those who did not (47.2 ± 10.7% vs. 31.7 ± 12.8%, p < 0.0001). This difference was observed during asystole (median rSO2 (IQR) ROSC versus no ROSC: 45.0% (35.1–48.8) vs. 24.9% (20.5–32.9), p < 0.002) and PEA (50.6% (46.7–57.5) vs. 31.6% (18.8–43.3), p = 0.02), but not in the VF/VT subgroup (43.7% (41.1–54.7) vs. 42.8% (34.9–45.0), p = 0.63). Furthermore, it was noted that no subjects with a mean rSO2 < 30% achieved ROSC.

Conclusions

Cerebral oximetry may have a role as a real-time, non-invasive predictor of ROSC during cardiac arrest. The main utility of rSO2 in determining ROSC appears to apply to asystole and PEA subgroups of cardiac arrest, rather than VF/VT. This observation may reflect the different physiological factors involved in recovery from PEA/asytole compared to VF/VT. Whereas in VF/VT, successful defibrillation is of prime importance, however in PEA and asytole achieving ROSC is more likely to be related to the quality of oxygen delivery. Furthermore, a persistently low rSO2 <30% in spite of optimal resuscitation methods may indicate futility of resuscitation efforts.