Interobserver Agreement of the Echocardiographic Diagnosis of LV Hypertrabeculation/Noncompaction.

OBJECTIVES: The aim of the study was to assess interobserver agreement (IOA) between 3 observers from 2 laboratories. BACKGROUND: IOA of left ventricular hypertrabeculation/noncompaction (LVHT) in adults has only been studied within single echocardiographic laboratories. METHODS: Echocardiographic recordings with and without LVHT were selected and anonymized. The "not-LVHT" cases were matched for age and systolic function. Each observer reviewed the recordings, blinded to the initial diagnosis and the other observers' results. Pre-defined criteria for LVHT were: 1) >3 prominent trabeculae at end-diastole, distinct from papillary muscles, false tendons, or aberrant bands; 2) a noncompacted part of a 2-layered myocardial structure formed by these trabeculations; 3) a ratio of >2:1 of noncompacted to compacted layer at end-systole; and 4) perfusion of the intertrabecular spaces from the ventricular cavity. IOA was estimated using the kappa measure of concordance. RESULTS: Cine-loops of 100 patients (42 women, ages 16 to 92 years), 50 from each center, and 51 with LVHT as the initial diagnosis, were reviewed. The left ventricular end-diastolic diameter was 32 to 78 mm, and ejection fraction, 4% to 88%. The observers agreed about presence (n = 29) or absence (n = 36) of LVHT and disagreed in 35 cases. Agreement was higher among the 2 observers from the same laboratory (kappa 0.793 [95% confidence interval (CI): 0.672 to 0.915]) than from different laboratories (kappa 0.628 [95% CI: 0.472 to 0.784], kappa 0.669 [95% CI: 0.521 to 0.818]). The observers agreed with the initial report of LVHT-presence in 53% and of absence in 67%. By reviewing the discordant cases, consensus was achieved about LVHT presence (n = 8) or absence (n = 16); in 11 cases, the diagnosis remained questionable. Discordance was due to poor image quality, lack of views in different apical planes, aberrant bands and chordae tendineae, abnormally sized or inserting papillary muscles, and localized calcifications of the endocardium. CONCLUSIONS: IOA was substantial for diagnosing LVHT. However, even the application of pre-defined criteria yielded disagreement in 35% of cases; and after mutual review, there were still 11% questionable cases.

Survivors of cardiac arrest with good neurological outcome show considerable impairments of memory functioning.

BACKGROUND: Deficits in cognitive function are a well-known dysfunction in survivors of cardiac arrest. However, data concerning memory function in this neurological vulnerable patient collective remain scarce and inconclusive. Therefore, we aimed to assess multiple aspects of retrospective and prospective memory performance in patients after cardiac arrest. METHODS: We prospectively enrolled 33 survivors of cardiac arrest, with cerebral performance categories (CPC) 1 and 2 and a control-group (n=33) matched in sex, age and educational-level. To assess retrospective and prospective memory performance we administrated 4 weeks after cardiac arrest the "Rey Adult Learning Test" (RAVLT), the "Digit-Span-Backwards Test", the "Logic-Memory Test" and the "Red-Pencil Test". RESULTS: Results indicate an impairment in immediate and delayed free recall, but not in recognition. However, the overall impairment in immediate recall was qualified by analyzing RAVLT performance, showing that patients were only impaired in trials 4 and 5 of the learning sequence. Moreover, working and prospective memory as well as prose recall were worse in cardiac arrest survivors. Cranial computed tomography was available in 61% of all patients (n=20) but there was no specific neurological damage detectable that could be linked to this cognitive impairment. CONCLUSION: Episodic long-term memory functioning appears to be particularly impaired after cardiac arrest. In contrast, short-term memory storage, even tested via free-call, seems not to be affected. Based on cranial computed tomography we suggest that global brain ischemia rather than focal brain lesions appear to underlie these effects.

Head and neck cooling after cardiac arrest results in lower jugular bulb than esophageal temperature.

PURPOSE: To determine whether during the initial phase of head and neck cooling, jugular bulb temperature (Tjb; which may reflect brain temperature) is lower than esophageal temperature (Tes). BASIC PROCEDURES: To compare Tes and Tjb, patients received head or head and neck cooling after cardiac arrest. MAIN FINDINGS: The first series with head cooling (n = 5; mean age 54 with a range of 41-62 years; 1 female and 4 males; mean body weight 80 kg with a range of 70-85 kg) showed a mean difference of 0.22 degrees C (95% CI, -1.14 to 0.70; P = .55; limits of agreement, -3.17 to 2.73) between Tes and Tjb over 12 hours. For the second series, with head and neck cooling (n = 6, mean age 65 with a range of 56-76 years; 3 females and 3 males; mean body weight 75 kg with a range of 65-91 kg), Tjb was lower than Tes with a difference of 0.60 degrees C (95% CI, 0.22 to 0.99; P = .01; limits of agreement, -3.10 to 4.30). During the first 3 hours, Tjb decreased faster than Tes (1.1 degrees C/h [95% CI, 0.4 to 1.8; P < .01]). PRINCIPAL CONCLUSION: During the initial phase of therapeutic hypothermia, Tjb seems to be lower than Tes.

Cardiopulmonary resuscitation and the 2005 universal algorithm: has the quality of CPR improved?

BACKGROUND AND AIM: Chest compressions are crucial in cardiopulmonary resuscitation (CPR), although the optimal number, rate and sequence are unknown. The 2005 CPR guidelines of the European Resuscitation Council (ERC) brought major changes to the basic life support algorithm. One of the major aims of the ERC was to decrease hands-off time in order to improve perfusion of the coronary vessels and the brain. Using a manikin model of basic life support in simulated cardiac arrest, we compared hands-off time and total number of chest compressions according to the guidelines of 2000 and those of 2005. METHODS: A total of 50 volunteers performed CPR according to the guidelines of 2000 (Group 2000) and 2005 (Group 2005) in a randomized unblinded cross-over study. Volunteers received 10 min of standardized teaching and 10 min of training, including corrective feedback, for each set of guidelines before performing 5 min of basic life support on a manikin. We compared hands-off time as the primary outcome parameter and the total number of chest compressions as the secondary outcome parameter. RESULTS: Fifty volunteers were enrolled in the study, one individual dropped out after randomization. In Group 2005, hands-off time was significantly lower (mean 107 +/- 19 [SD] s vs. 139 +/- 15 s in Group 2000 (P < 0.0001) and the total number of chest compressions was significantly higher (347 +/- 64 compressions vs. 233 +/- 51 compressions; P < 0.0001). CONCLUSION: In this manikin setting, both hands-off time and the total number of chest compressions improved with basic life support performed according to the ERC guidelines of 2005.

Pronounced platelet hyperfunction in patients with cardiac arrest achieving restoration of spontaneous circulation.

OBJECTIVE: Markers of platelet activation are increased in patients undergoing cardiopulmonary resuscitation. Hyperfunctional platelets may contribute to impairment of microcirculatory function and overall poor outcome despite restoration of spontaneous circulation (ROSC). Patients with myocardial infarction have hyperfunctional platelets, which predict the degree of myocardial necrosis. Thus, we hypothesized that platelets may be even more activated in patients whose myocardial infarction leads to cardiac arrest and compared them with patients whose cardiac arrest was due to a noncardiac origin. DESIGN: Prospective observational study. SETTING: Emergency department of a tertiary care hospital. PATIENTS: One hundred four patients with witnessed cardiac arrest who achieved ROSC. INTERVENTIONS: Blood sampling. MEASUREMENTS AND MAIN RESULTS: We assessed collagen adenosine diphosphate closure time with the platelet function analyzer-100, and measured plasma levels of von Willebrand factor: ristocetin cofactor activity levels by turbidometry. Independent physicians diagnosed the origin of cardiac arrest. The majority of cardiac arrests were caused by myocardial ischemia. Invariably, collagen adenosine diphosphate closure time values (55 seconds; 95% confidence interval: 52-58 seconds) were much shorter in these patients compared with patients with other causes of cardiac arrest (110 seconds; 95% confidence interval: 84-135 seconds, p < 0.001). von Willebrand factor: ristocetin cofactor activity plasma levels were more than three-fold above normal values in both groups. CONCLUSIONS: Patients with myocardial ischemia-triggered cardiac arrest had the highest degree of platelet hyperfunction under high shear rates, which was not solely due to increased von Willebrand factor. Future trials are necessary to clarify whether rapid, more aggressive antiplatelet therapy improves outcome after cardiac arrest.

Thoracic-impedance changes measured via defibrillator pads can monitor signs of circulation.

AIMS: To investigate the potential for finding an alternative for the 'pulse check' during CPR, we studied the use of thoracic impedance measured via the defibrillator pads for circulation assessment during CPR. MATERIALS AND METHODS: Transthoracic impedance, ECG and arterial pressures were recorded on 69 patients with a resulting data set of 434 segments. The circulatory-related impedance waveform was first isolated manually and features characterising its shape were suggested. RESULTS: The features were correlated with corresponding blood pressure measurements, where a low, but significant, correlation coefficient (0.3) was found. By dividing the data set in groups of sufficient and insufficient circulation and using a neural network, we found that trends in features of the impedance waveform showed a discriminative potential for the two groups. Our classifier achieved a sensitivity of 90% for recognising insufficient circulation with a specificity of 82%. CONCLUSIONS: We have shown that the circulation-related information found in the impedance signal may be used for circulatory assessment, especially the recognition of restoration of spontaneous circulation after cardiac arrest.

Cold infusions alone are effective for induction of therapeutic hypothermia but do not keep patients cool after cardiac arrest.

AIM OF THE STUDY: Cold infusions have proved to be effective for induction of therapeutic hypothermia after cardiac arrest but so far have not been used for hypothermia maintenance. This study investigates if hypothermia can be induced and maintained by repetitive infusions of cold fluids and muscle relaxants. MATERIAL AND METHODS: Patients were eligible, if they had a cardiac arrest of presumed cardiac origin and no clinical signs of pulmonary oedema or severely reduced left ventricular function. Rocuronium (0.5 mg/kg bolus, 0.5 mg/kg/h for maintenance) and crystalloids (30 ml/kg/30 min for induction, 10 ml/kg every 6h for 24h maintenance) were administered via large bore peripheral venous cannulae. If patients failed to reach 33+/-1 degrees C bladder temperature within 60 min, endovascular cooling was applied. RESULTS: Twenty patients with a mean age of 57 (+/-15) years and mean body mass index of 27 (+/-4)kg/m(2) were included (14 males). Mean temperature at initiation of cooling (median 27 (IQR 16; 87)min after admission) was 35.4 (+/-0.9) degrees C. In 13 patients (65%) the target temperature was reached within 60 min, 7 patients (35%) failed to reach the target temperature. Maintaining the target temperature was possible in three (15%) patients and no adverse events were observed. CONCLUSION: Cold infusions are effective for induction of hypothermia after cardiac arrest, but for maintenance additional cooling techniques are necessary in most cases.

Gender modifies the influence of age on outcome after successfully resuscitated cardiac arrest: a retrospective cohort study.

Age is an important risk factor for mortality and unfavorable outcome after successfully resuscitated cardiac arrest. Other risk factors may interact with this relationship. We conducted the current study to quantify the influence of age on mortality and unfavorable neurologic outcome of patients surviving out-of-hospital cardiac arrest, and to determine the role of other confounding variables. This study was based on a cardiac arrest registry comprising all patients with witnessed out-of-hospital cardiac arrest of cardiac origin after successful resuscitation admitted to a department of emergency medicine between September 1991 and December 2004. We assessed the association between age and mortality and the degree of neurologic impairment, adjusting for multiple risk factors. We tested for interaction between age and all other risk factors with outcome. With each year of age the adjusted odds ratio for in-hospital death increased by 1.05 (95% confidence interval [CI], 1.04-1.07), and the adjusted odds ratio for an unfavorable neurologic outcome increased by 1.04 (95% CI, 1.03-1.06). Interaction between age and sex was present, and the analysis was stratified to sex. For men we found a steep risk increase for death and unfavorable outcome after being resuscitated from cardiac arrest, with the highest risk in the oldest age quartile. For women we observed only a slight risk increase for death and almost no risk increase for unfavorable outcome. Age is a strong independent risk factor for mortality and neurologic impairment after successfully resuscitated cardiac arrest. The risk increase with advancing age is much greater in men than in women. Therefore, in women, the influence of age on prognosis after cardiac arrest may not be very important, while in men it still plays an important role. This should be considered especially when treating successfully resuscitated women and discussing the prognosis with the medical team or the patient's family.

Thoracic impedance changes measured via defibrillator pads can monitor ventilation in critically ill patients and during cardiopulmonary resuscitation.

OBJECTIVE: Monitoring of ventilation performance during cardiopulmonary resuscitation would be desirable to improve the quality of cardiopulmonary resuscitation. To investigate the potential for measuring ventilation rate and inspiration time, we calculated the correlation in waveform between transthoracic impedance measured via defibrillator pads and tidal volume given by a ventilator. DESIGN: Clinical study. SETTING: Emergency department of a tertiary care university hospital. PATIENTS: A convenience sample of mechanical ventilated patients (n = 32), cardiac arrest patients (n = 20), and patients after restoration of spontaneous circulation (n = 31) older than 18 were eligible. INTERVENTIONS: The Heartstart 4000SP defibrillator (Laerdal Medical Cooperation, Stavanger, Norway) with additional capabilities of recording thoracic impedance changes was used. MEASUREMENTS AND MAIN RESULTS: The relationship between impedance change and tidal volume (impedance coefficient) was calculated. The mean (sd) correlations between the impedance waveform and the tidal volume waveform in the patient groups studied were .971 (.027), .969 (.032), and .967 (.035), respectively. The mean (sd) impedance coefficient for all patients in the study was .00194 (.0078) Omega/mL, and the mean (sd) specific (weight-corrected) impedance coefficient was .152 (.048) Omega/kg/mL. The measured thorax impedance change for different tidal volumes (400-1000 mL) was approximately linear. CONCLUSIONS: The impedance sensor of a defibrillator is accurate in identifying tidal volumes, when chest compressions are interrupted. This also allows quantifying ventilation rates and inspiration times. However this technology, at its present state, provides only limited practical means for exact tidal volume estimation.