Outcomes with Tibial and Humeral Intraosseous Access Compared to Peripheral Intravenous Access in Out-of-Hospital Cardiac Arrest.

BACKGROUND: The optimal initial vascular access strategy for out-of-hospital cardiac arrest (OHCA) remains unknown. Our objective was to evaluate the association between peripheral intravenous (PIV), tibial intraosseous (TIO), or humeral intraosseous (HIO) as first vascular attempt strategies and outcomes for patients suffering OHCA. METHOD: This was a secondary analysis of the Portland Cardiac Arrest Epidemiologic Registry, which included adult patients (≥18 years-old) with EMS-treated, non-traumatic OHCA from 2018-2021. The primary independent variable in our analysis was the initial vascular access strategy, defined as PIV, TIO, or HIO based on the first access attempt. The primary outcome for this study was the return of spontaneous circulation (ROSC) at emergency department (ED) arrival (a palpable pulse on arrival to the hospital). Secondary outcomes included survival to: admission, discharge, and discharge with a favorable outcome (Cerebral Perfusion Category score of ≤2). We conducted multivariable logistic regressions, adjusting for confounding variables and for clustering using a mixed-effects approach, with prespecified subgroup analyses by initial rhythm. RESULTS: We included 2,993 patients with initial vascular access strategies of PIV (822 [27.5%]), TIO (1,171 [39.1%]), and HIO (1,000 [33.4%]). Multivariable analysis showed lower odds of ROSC at ED arrival (adjusted odds ratio [95% CI]) with TIO (0.79 [0.64-0.98]) or HIO (0.75 [0.60-0.93]) compared to a PIV-first strategy. These associations remained in stratified analyses for those with shockable initial rhythms (0.60 [0.41-0.88] and 0.53 [0.36-0.79]) but not in patients with asystole or pulseless electrical activity for TIO and HIO compared to PIV, respectively. There were no statistically significant differences in adjusted odds for survival to admission, discharge, or discharge with a favorable outcome for TIO or HIO compared to the PIV-first group in the overall analysis. Patients with shockable initial rhythms had lower adjusted odds of survival to discharge (0.63 [0.41-0.96] and 0.64 [0.41-0.99]) and to discharge with a favorable outcome (0.60 [0.39-0.93] and 0.64 [0.40-1.00]) for TIO and HIO compared to PIV, respectively. CONCLUSIONS: TIO or HIO as first access strategies in OHCA were associated with lower odds of ROSC at ED arrival compared to PIV.

Abnormal Regulation of Microvascular Tone in a Murine Model of Sickle Cell Disease Assessed by Contrast Ultrasound.

BACKGROUND: Microvascular dysregulation, abnormal rheology, and vaso-occlusive events play a role in the pathophysiology of sickle cell disease (SCD). The aim of this study was to test the hypothesis that abnormalities in skeletal muscle perfusion in a murine model of SCD could be parametrically assessed by quantitative contrast-enhanced ultrasound perfusion imaging. METHODS: A murine model of moderate SCD without anemia produced by homozygous ß-globin deletion replaced by human ßs-globin transgene (NY1DD-/-; n = 18), heterozygous transgene replacement (NY1DD+/-; n = 19), and C57Bl/6 control mice (n = 14) was studied. Quantitative contrast-enhanced ultrasound of the proximal hindlimb skeletal muscle was performed at rest and during contractile exercise (2 Hz). Time-intensity data were analyzed to measure microvascular blood volume (MBV), microvascular blood transit rate (ß), and microvascular blood flow. Erythrocyte deformability was measured by elongation at various rotational shears. RESULTS: At rest, muscle MBV was similar between strains, whereas ß was significantly (P = .0015, analysis of variance) reduced to a similar degree in NY1DD-/- and NY1DD+/- compared with wild-type mice (0.24 ± 0.10, 0.16 ± 0.07, and 0.34 ± 0.14 sec(-1), respectively), resulting in a reduction in microvascular blood flow. During contractile exercise, there were no groupwise differences in ß (1.43 ± 0.67, 1.09 ± 0.42, and 1.36 ± 0.49 sec(-1) for NY1DD-/-, NY1DD+/-, and wild-type mice, respectively) or in microvascular blood flow or MBV. Erythrocyte deformability at high shear stress (≥5 Pa) was mildly reduced in both transgenic groups, although it was not correlated with blood flow or ß. CONCLUSIONS: Contrast-enhanced ultrasound in skeletal muscle revealed a lower microvascular blood transit rate in the NY1DD model of SCD and sickle trait but no alterations in MBV. The abnormality in microvascular blood transit rate was likely due to vasomotor dysfunction, because it was abrogated by contractile exercise and at rest was only weakly related to erythrocyte deformability.

Dysregulated selectin expression and monocyte recruitment during ischemia-related vascular remodeling in diabetes mellitus.

OBJECTIVE: Diabetes mellitus (DM) is associated with impaired ischemia-related vascular remodeling and also dysregulation of the inflammatory response. We sought to determine whether impaired selectin-mediated monocyte recruitment in ischemic tissues contributes to blunted ischemia-mediated angiogenesis in DM. METHODS AND RESULTS: Contrast-enhanced ultrasound perfusion imaging and molecular imaging of endothelial P-selectin expression in the proximal hindlimb were performed at 1, 3, and 21 days after arterial ligation in wild-type and db/db mice. Ligation reduced muscle blood flow to ≈0.05 mL/minute per gram in both strains. Significant recovery of flow occurred only in wild-type mice (60%-65% of baseline flow). On molecular imaging, baseline P-selectin signal was 4-fold higher in db/db compared with wild-type mice (P<0.01) but increased minimally at day 1 after ischemia, whereas signal increased approximately 10-fold in wild-type mice (P<0.01). Immunohistology of the hindlimb skeletal muscle demonstrated severely reduced monocyte recruitment in db/db mice compared with wild-type mice. Local treatment with monocyte chemotactic protein-1 corrected the deficits in postischemic P-selectin expression and monocyte recruitment in db/db mice and led to greater recovery in blood flow. CONCLUSION: In DM, there is dysregulation of the selectin response to limb ischemia, which leads to impaired monocyte recruitment, which may be mechanistically related to reduced vascular remodeling in limb ischemia.