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.     

The adipocyte–myocyte axis in insulin resistance

Insulin resistance in skeletal muscle is linked to an elevated adipose tissue mass, as is found in obesity, but can also be observed in lipodystrophy, in which adipose tissue is greatly reduced. Adipose tissue releases endocrine and metabolic mediators and is actively involved in crosstalk with skeletal muscle, a process that precedes and underlies the development of insulin resistance in muscles. Adipokines including tumor necrosis factor alpha, interleukin-6, leptin and adiponectin influence insulin signaling in skeletal muscle. Free fatty acids, their metabolites and ectopic fat in muscle also contribute to insulin resistance. Recent research indicates inflammation, endoplasmic reticulum stress and oxidative stress could be underlying mechanisms at the center of the development of insulin resistance. Insights into the role of macrophages in adipose tissue add to the complicated interplay between adipose tissue and skeletal muscle.     

Derivation of hepatocytes from bone marrow cells in mice after radiation-induced myeloablation

Following a report of skeletal muscle regeneration from bone marrow cells, we investigated whether hepatocytes could also derive in vivo from bone marrow cells. A cohort of lethally irradiated B6D2F1 female mice received whole bone marrow transplants from age-matched male donors and were sacrificed at days 1, 3, 5, and 7 and months 2, 4, and 6 posttransplantation (n = 3 for each time point). Additionally, 2 archival female mice of the same strain who had previously been recipients of 200 male fluorescence-activated cell sorter (FACS)-sorted CD34(+)lin(-) cells were sacrificed 8 months posttransplantation under the same protocol. Fluorescence in situ hybridization (FISH) for the Y-chromosome was performed on liver tissue. Y-positive hepatocytes, up to 2.2% of total hepatocytes, were identified in 1 animal at 7 days posttransplantation and in all animals sacrificed 2 months or longer posttransplantation. Simultaneous FISH for the Y-chromosome and albumin messenger RNA (mRNA) confirmed male-derived cells were mature hepatocytes. These animals had received lethal doses of irradiation at the time of bone marrow transplantation, but this induced no overt, histologically demonstrable, acute hepatic injury, including inflammation, necrosis, oval cell proliferation, or scarring. We conclude that hepatocytes can derive from bone marrow cells after irradiation in the absence of severe acute injury. Also, the small subpopulation of CD34(+)lin(-) bone marrow cells is capable of such hepatic engraftment.