Detection of ROSC in Patients with Cardiac Arrest During Chest Compression Using NIRS: A Pilot Study.

Return of spontaneous circulation (ROSC) during chest compression is generally detected by arterial pulse palpation and end-tidal CO2 monitoring; however, it is necessary to stop chest compression during pulse palpation, and to perform endotracheal intubation for monitoring end-tidal CO2. In the present study, we evaluated whether near-infrared spectroscopy (NIRS) allows the detection of ROSC during chest compression without interruption. We monitored cerebral blood oxygenation in 19 patients with cardiac arrest using NIRS (NIRO-200NX, Hamamatsu Photonics, Japan). On arrival at the emergency room, the attending physicians immediately assessed whether a patient was eligible for this study after conventional advanced life support (ALS) and employed NIRS to measure cerebral blood oxygenation (CBO) in the bilateral frontal lobe in patients. We found cerebral blood flow waveforms in synchrony with chest compressions in all patients. In addition, we observed abrupt increases of oxy-hemoglobin concentration and tissue oxygen index (TOI), which were associated with ROSC detected by pulse palpation. The present findings indicate that NIRS can be used to assess the quality of chest compression in patients with cardiac arrest as demonstrated by the detection of synchronous waveforms during cardiopulmonary resuscitation (CPR). NIRS appears to be applicable for detection of ROSC without interruption of chest compression and without endotracheal intubation.

The relationship between hyperlactatemia and microcirculation in the thenar eminence as measured using near-infrared spectroscopy in patients with sepsis.

OBJECTIVE: Near-infrared spectroscopy (NIRS)-derived variables during a vascular occlusion test (VOT) have recently been used to evaluate peripheral circulatory insufficiency in patients with sepsis. We investigated the relationship between NIRS-derived variables and the lactate concentration during sepsis. METHODS: This was a prospective observational study. Forty-one patients with sepsis were divided into two groups according to their blood lactate concentration: a high lactate group (≥2.0 mmol/l; n=15) and a normal lactate group (<2.0 mmol/l; n=26). NIRS was used to evaluate the tissue oxygen index (TOI) at the thenar eminence before and after a VOT. VOT was performed by sphygmomanometer cuff inflation around upper arm for 3 min. The TOI value before VOT was defined as the TOI baseline, the TOI value immediately after VOT was defined as the minimum TOI and the TOI value after releasing the muscle from the VOT was defined as the TOI after VOT. The ΔTOI was defined as the difference between the TOI after VOT and minimum TOI. RESULTS: NIRS-derived variables had significant differences between the normal lactate group and the high lactate group with respect to the TOI baseline (median: 65% vs 55%, p=0.01), TOI after VOT (median: 65% vs 46%, p<0.001) and ΔTOI (median: 19% vs 6%, p<0.001). The lactate concentration was significantly correlated with the TOI after VOT (R=0.594, p<0.001), TOI baseline (R=0.513, p<0.001), ΔTOI (R=0.488, p=0.001) and minimum TOI (R=0.377, p=0.02). CONCLUSIONS: We revealed a significant correlation between NIRS-derived variables and the lactate concentration during sepsis.

Changes of cerebral oxygen metabolism and hemodynamics during ECPR with hypothermia measured by near-infrared spectroscopy: a pilot study.

BACKGROUND: The 2010 CPR Guidelines recommend that extracorporeal cardiopulmonary resuscitation (ECPR) using an emergency cardiopulmonary bypass (CPB) should be considered for patients with cardiac arrest. However, it is not yet clear whether this therapy can improve cerebral circulation and oxygenation in these patients. To clarify this issue, we evaluated changes of cerebral blood oxygenation (CBO) during ECPR using near-infrared spectroscopy (NIRS). METHODS: We employed NIRS to measure CBO in the bilateral frontal lobe in patients transported to the emergency room (ER) after out-of-hospital cardiac arrest between November 2009 and June 2011. RESULTS: Fifteen patients met the above criteria. The tissue oxygenation index (TOI) on arrival at the ER was 36.5 %. This increased to 67.8 % during ECPR (P < 0.001). The one patient whose TOI subsequently decreased had a favorable neurological outcome. CONCLUSION: Increase of TOI during ECPR might reflect an improvement in cerebral blood flow, while decrease of TOI after ECPR might reflect oxygen utilization by the brain tissue as a result of neuronal cell survival. NIRS may be useful for monitoring cerebral hemodynamics and oxygen metabolism during CPR.

Neurological benefit of therapeutic hypothermia following return of spontaneous circulation for out-of-hospital non-shockable cardiac arrest.

BACKGROUND: Although therapeutic hypothermia is an effective therapy for comatose adults experiencing out-of-hospital shockable cardiac arrest, there is insufficient evidence that is also applicable for those with out-of-hospital non-shockable cardiac arrest. METHODS AND RESULTS: Of 452 comatose adults treated with therapeutic hypothermia after return of spontaneous circulation (ROSC) subsequent to an out-of-hospital cardiac arrest of cardiac etiology, 372 who had a bystander-witnessed cardiac arrest, target core temperature of 32-34°C and cooling duration of 12-72 h were eligible for this study (75 cases of non-shockable cardiac arrest, 297 cases of shockable cardiac arrest). The median collapse-to-ROSC interval was significantly longer in the non-shockable group than in the shockable group (30 min vs. 22 min, P=0.008), resulting in a significantly lower frequency of 30-day favorable neurological outcome in the non-shockable group compared with the shockable group (32% vs. 66%, P<0.001). However, an analysis of data in quartiles assigned to varying lengths of collapse-to-ROSC interval revealed a similar frequency of 30-day favorable neurological outcome among both groups when the collapse-to-ROSC interval was ≤16 min (90% non-shockable group vs. 92% shockable group; odds ratio 0.80, 95% confidence interval 0.09-7.24, P=0.84). CONCLUSIONS: Post-ROSC cooling is an effective treatment for patients with non-shockable cardiac arrest when the time interval from collapse to ROSC is short.

Prognostic value of venous blood ammonia in patients with out-of-hospital cardiac arrest.

BACKGROUND: Although studies have shown there is a correlation between increased blood ammonia level and hepatic encephalopathy, little information is available for patients with out-of-hospital cardiac arrest. METHODS AND RESULTS: We did a prospective study of 357 adult patients with out-of-hospital cardiac arrest whose venous blood ammonia levels were measured on arrival at the emergency room. The primary endpoint was favorable of neurological outcome to hospital discharge. Of the 357 patients, 25 (7%) had a favorable neurological outcome. The venous ammonia levels were lower in the favorable neurological outcome group than in the unfavorable neurological outcome group (median, 50 µg/dl vs. 210 µg/dl, P<0.0001). The adjusted odds ratio of ammonia levels for favorable neurological outcome was 0.98 (95% confidence interval, 0.96-0.99; P<0.0001). The ammonia cutoff value of 93.0 µg/dl for the identification of favorable neurological outcome had the highest combined sensitivity and specificity, and higher ammonia levels were associated with more accurate negative predictive values (for ammonia levels of 192.5 µg/dl, the negative predictive value was 100%). Hyperammonemia was significantly related to patient variables that had a poor outcome (R=0.439, P<0.001). In addition, there was a significant correlation between venous ammonia level and arterial pH on emergency room arrival (R=0.633, P<0.0001). CONCLUSIONS: The measurement of ammonia was found to provide valuable information regarding neurological outcome to hospital discharge in adult patients with out-of-hospital cardiac arrest.

Early induction of hypothermia during cardiac arrest improves neurological outcomes in patients with out-of-hospital cardiac arrest who undergo emergency cardiopulmonary bypass and percutaneous coronary intervention.

BACKGROUND: Therapeutic hypothermia for comatose survivors of out-of-hospital cardiac arrest has demonstrated neurological benefits. Although early cooling during cardiac arrest enhances efficacy in animal studies, few clinical studies are available. METHODS AND RESULTS: The 171 patients who failed to respond to conventional cardiopulmonary resuscitation were studied prospectively. Patients underwent emergency cardiopulmonary bypass (CPB) plus intra-aortic balloon pumping, with subsequent percutaneous coronary intervention (PCI) if needed. Mild hypothermia (34 degrees C for 3 days) was induced during cardiac arrest or after return of spontaneous circulation. Of the 171 patients, 21 (12.3%) had a favorable neurological outcome at hospital discharge. An unadjusted rate of favorable outcome decreased in a stepwise fashion for increasing quartiles of collapse-to-34 degrees C interval (P=0.016). An adjusted odds ratio for favorable outcome after collapse-to-CPB interval was 0.89 (95% confidence interval (CI) 0.82-0.97) and after CPB-to-34 degrees C interval, 0.99 (95%CI 0.98-0.99) when collapse-to-34 degrees C interval was divided into 2 components. Favorable neurological accuracy of a collapse-to-CPB interval at a cutoff of 55.5 min and CPB-to-34 degrees C interval at a cutoff of 21.5 min was 85.4% and 89.5%, respectively. CONCLUSIONS: Early attainment of a core temperature had neurological benefits for patients with out-of-hospital cardiac arrest who underwent CPB and PCI. (Circ J 2010; 74: 77 - 85).

Right atrial free-floating thrombus in a patient with massive pulmonary embolism: a case of 'emboli in transit'.

A 78-year-old man was admitted with sudden onset of dyspnea followed by syncope. Contrast-enhanced computed tomography showed embolism in the right main pulmonary artery and left upper pulmonary artery. Echocardiography revealed a large, free-floating thrombus and cine magnetic resonance imaging showed highly mobile, low-signal intensity mass in the right atrium, which protruded into the right ventricle during diastole. During surgery the thrombus migrated into the pulmonary artery trunk, but it was successfully removed.

Ulinastatin alone does not reduce caspase 3-mediated apoptosis in protease-positive Aeromonas hydrophilia-induced sepsis.

BACKGROUND/PURPOSE: To evaluate the effect of ulinastatin, a protease inhibitor, on survival and apoptosis in protease-positive Aeromonas hydrophilia (PPAH)-induced sepsis. METHODS: Thirty mice were randomly allocated to receive intraperitoneal injection of either phosphate buffered saline (PBS) (control mice, n = 10) or PPAH (PPAH mice, n = 20). After 30 minutes, control mice received an additional intraperitoneal PBS injection, 10 PPAH mice received intraperitoneal PBS injection (non-treated PPAH mice), and the remaining 10 PPAH mice received an intraperitoneal injection of ulinastatin (ulinastatin-treated PPAH mice). RESULTS: Survival at 24 hours was 100% in control mice, and 35% (p < 0.05) in PPAH mice; the survival rate in non-treated and ulinastatin-treated PPAH mice were 30% and 40% (p > 0.05), respectively. The thymus weight (mg) decreased significantly in PPAH mice (51.1 +/- 14.9) compared to control mice (69.7 +/- 14.4; p < 0.001); there was no difference between ulinastatin-treated (52 +/- 13.9; p > 0.05) and non-treated PPAH mice (50.4 +/- 16). The thymus gland cell count reduced significantly in PPAH mice (8.1 +/- 4.7 x 10(7)) compared to control mice (12.8 +/- 6.6 x 10(7); p < 0.01), and immunofluorescence analysis demonstrated that the reduced cells were mostly CD4+ CD8+, in contrast to the increase in CD4+ CD8- cells. There was no difference in cell count between ulinastatin-treated (8.7 +/- 4.9 x 10(7)) and non-treated PPAH mice (7.4 +/- 4.6 x 10(7); p > 0.05). Caspase 3-mediated apoptosis was not detectable in control mice in contrast to the pronounced manifestation in PPAH mice. CONCLUSION: PPAH-induced sepsis has a high mortality that is related to lymphocyte apoptosis. Ulinastatin alone does not significantly reduce caspase 3-mediated lymphocyte apoptosis.