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Biomedical subjects

N A Perkins

Publications and source records attributed to N A Perkins.

7 recordsLinked to original sources
PubMed1994

Case-mix adjustment, claims data quality, and physician profiling.

On the surface, there are many ways in which case mix may be considered, but the key to any successful system often lies below the surface, in the way in which the available data feed the systems, and in the operational environment in which the output is to be used. This article will review terminology used in case-mix adjustment and profiling techniques, highlight some dangerous (and avoidable) data pitfalls, and emphasize reasonable goals that can be achieved through the use of case-mix adjusted profiling.

Data Collection↗
PubMed1991

Health insurance and outcomes: comprehensive assessment of health system outputs.

Outcomes analysis in health care has historically meant the examination of clinical results of inpatient hospitalization. In response to climbing health care and health insurance costs, the organization of health care providers, the location of service delivery and reimbursement mechanisms have changed. As the health care industry changes, so too must the definition of outcomes. This article presents a conceptual framework for the analysis of health outcomes as health industry outputs, with an emphasis on the ways in which such outputs are being assessed and improved.

Financial Audit↗
PubMed1985

Intravenous fluid loading as prophylaxis for paradoxical air embolism.

Paradoxical cerebral air embolism has been described in neurosurgical operations performed on patients in the seated position. This problem is thought to result most often from a probe-patent foramen ovale. It has been postulated that right atrial pressure exceeds left atrial pressure when paradoxical air embolism occurs. A study is described in which intravenous fluid loading is compared with routine fluid management in 20 patients undergoing neurosurgical operations in the seated position. In order to investigate if intravenous fluid loading would decrease the risk of paradoxical air embolism during neurosurgical operations on seated patients, 20 patients were assigned randomly to two groups: 10 patients received normal intravenous fluid replacement (1220 +/- 102 ml), and 10 received augmented fluid replacement (2800 +/- 400 ml). Right atrial and pulmonary capillary pressures were monitored for evidence of an interatrial pressure gradient that would force air emboli from the right atrium into the left atrium via a probe-patent foramen ovale. Four of 10 patients receiving routine fluid administration developed right atrial pressure greater than pulmonary capillary wedge pressure (and hence, indirectly, greater than left atrial pressure), whereas none of the 10 patients with augmented fluid loading developed this condition (p = 0.04). The authors conclude that augmented intravenous fluid loading may be effective in preventing systemic air embolism during neurosurgical operations performed on patients in the seated position.

Adolescent↗
PubMed1984

Hemodynamic consequences of PEEP in seated neurological patients--implications for paradoxical air embolism.

In order to better understand the hemodynamic consequences of the use of positive end-expiratory pressure (PEEP) in patients in the seated position, 11 patients undergoing neurosurgical operations were monitored with radial arterial and thermistor-tipped Swan-Ganz catheters both before and during 10-cm H2O PEEP. Significant (P less than 0.05) reductions in cardiac output (15%), stroke volume (15%), and mean arterial pressure (14%) occurred with the introduction of PEEP, while pulmonary vascular resistance increased 47% and right atrial pressure (RAP) increased from 3.6 +/- 0.7 SEM mm Hg to 8.9 +/- 0.9 SEM mm Hg (P less than 0.05). Pulmonary capillary wedge pressure (PCWP) did not increase significantly during PEEP. RAP exceeded PCWP in only two patients before PEEP, but RAP exceeded PCWP in seven patients during PEEP. We conclude that PEEP is potentially detrimental during operations in the seated position because it not only impairs hemodynamic performance, but might predispose patients with a probe-patent foramen ovale to the risk of paradoxical air embolism.

Adult↗
PubMed1979

Effect of prolactin on dopamine synthesis in medial basal hypothalamus: evidence for a short loop feedback.

Several procedures were utilized to study the effects of prolactin on dopamine synthesis in the medial basal hypothalamus of the rat. Elevation of serum prolactin was produced by the administration of trifluoperazine (5 mg/kg, i.p.) and resulted in a significant increase in the conversion of [3',5'-3H]tyrosine to dopamine when measured in slices of medial basal hypothalamus and striatum. Hypophysectomy abolished this effect of trifluoperazine in the medial basal hypothalamus but not in the striatum. In addition, the synthesis of dopamine was significantly elevated in slices of medial basal hypothalamus obtained from rats bearing pituitary tumor implants that secreted microgram quantities of prolactin. In contrast, the in vitro synthesis of dopamine in the striatum of such rats was increased by the secretory products in one tumor line but decreased in another compared to that observed in control animals. It is suggested that the ability of prolactin to accelerate the synthesis of dopamine in the medial basal hypothalamus might constitute a short loop feedback system that finely regulates prolactin secretion.

Animals↗
PubMed1979

Influence of cholinergic agents on dopamine release from medial basal hypothalamus.

The ability of acetylcholine to influence the stimulation-induced release of [3H]dopamine in medial basal hypothalamus was evaluated. A muscarinic facilitation of electrical field-stimulated but not potassium-stimulated release was observed. These data suggest a muscarinic enhancement of dopamine release perhaps via an action at the level of the cell body. These data suggest that observed effects of cholinergic agents on prolactin release may be mediated in part through such a cholinergic-dopaminergic interaction.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗