Intensive care unit rounding checklist implementation. Effect of accountability measures on physician compliance.

RATIONALE/OBJECTIVES: Checklist utilization has been shown to improve multiple processes of care in the intensive care unit (ICU). The ICU setting makes checklist implementation challenging, particularly when prompters are unavailable to ensure checklist compliance. We performed a prospective analysis on physician compliance reporting as a means to improve attending physician compliance with checklist use during ICU rounds. METHODS: We performed a prospective analysis of 14 attending physicians' compliance with checklist use before and after accountability measures employed at two urban academic hospitals in the United States. The accountability measures were bimonthly publication of physician checklist compliance via division e-mail and during a multidisciplinary division conference. MEASUREMENTS AND MAIN RESULTS: A total of 5,812 patient days of ICU care were assessed from April 2013 through March 2014. Compliance with checklist use during ICU rounds improved at both academic hospitals during the intervention phase. Initial compliance rates were 67% at both institutions and subsequently improved to 90 and 81%, respectively, after accountability measures were employed. During a 3-month washout phase in which no public accountability measures were employed, compliance was maintained at 89 and 78% at the two hospitals. Foley catheter, central venous catheter, and ventilator utilization rates decreased after initiation of public accountability at both hospitals. CONCLUSIONS: Physician compliance reporting can be used to improve ICU physician compliance with rounding checklists when prompters are unavailable. Improved physician compliance translated into decreased rates of Foley catheter, central venous catheter, and ventilator use. These results highlight the impact physician accountability can have on patient care in the ICU.

Neonatal hyperoxic lung injury favorably alters adult right ventricular remodeling response to chronic hypoxia exposure.

The development of pulmonary hypertension (PH) requires multiple pulmonary vascular insults, yet the role of early oxygen therapy as an initial pulmonary vascular insult remains poorly defined. Here, we employ a two-hit model of PH, utilizing postnatal hyperoxia followed by adult hypoxia exposure, to evaluate the role of early hyperoxic lung injury in the development of later PH. Sprague-Dawley pups were exposed to 90% oxygen during postnatal days 0-4 or 0-10 or to room air. All pups were then allowed to mature in room air. At 10 wk of age, a subset of rats from each group was exposed to 2 wk of hypoxia (Patm = 362 mmHg). Physiological, structural, and biochemical endpoints were assessed at 12 wk. Prolonged (10 days) postnatal hyperoxia was independently associated with elevated right ventricular (RV) systolic pressure, which worsened after hypoxia exposure later in life. These findings were only partially explained by decreases in lung microvascular density. Surprisingly, postnatal hyperoxia resulted in robust RV hypertrophy and more preserved RV function and exercise capacity following adult hypoxia compared with nonhyperoxic rats. Biochemically, RVs from animals exposed to postnatal hyperoxia and adult hypoxia demonstrated increased capillarization and a switch to a fetal gene pattern, suggesting an RV more adept to handle adult hypoxia following postnatal hyperoxia exposure. We concluded that, despite negative impacts on pulmonary artery pressures, postnatal hyperoxia exposure may render a more adaptive RV phenotype to tolerate late pulmonary vascular insults.

Estradiol improves right ventricular function in rats with severe angioproliferative pulmonary hypertension: effects of endogenous and exogenous sex hormones.

Estrogens are disease modifiers in PAH. Even though female patients exhibit better right ventricular (RV) function than men, estrogen effects on RV function (a major determinant of survival in PAH) are incompletely characterized. We sought to determine whether sex differences exist in RV function in the SuHx model of PAH, whether hormone depletion in females worsens RV function, and whether E2 repletion improves RV adaptation. Furthermore, we studied the contribution of ERs in mediating E2's RV effects. SuHx-induced pulmonary hypertension (SuHx-PH) was induced in male and female Sprague-Dawley rats as well as OVX females with or without concomitant E2 repletion (75 µg·kg(-1)·day(-1)). Female SuHx rats exhibited superior CI than SuHx males. OVX worsened SuHx-induced decreases in CI and SuHx-induced increases in RVH and inflammation (MCP-1 and IL-6). E2 repletion in OVX rats attenuated SuHx-induced increases in RV systolic pressure (RVSP), RVH, and pulmonary artery remodeling and improved CI and exercise capacity (V̇o2max). Furthermore, E2 repletion ameliorated SuHx-induced alterations in RV glutathione activation, proapoptotic signaling, cytoplasmic glycolysis, and proinflammatory cytokine expression. Expression of ERα in RV was decreased in SuHx-OVX but was restored upon E2 repletion. RV ERα expression was inversely correlated with RVSP and RVH and positively correlated with CO and apelin RNA levels. RV-protective E2 effects observed in females were recapitulated in male SuHx rats treated with E2 or with pharmacological ERα or ERß agonists. Our data suggest significant RV-protective ER-mediated effects of E2 in a model of severe PH.