The negative impact of nurse-physician disruptive behavior on patient safety: a review of the literature.

OBJECTIVE: To review what is known about the impact of nurse-physician disruptive behavior on patient safety to inform appropriate intervention programs to address this health care problem. METHODS: A systematic review of the literature using the key words "disruptive physician behavior" and "physician verbal abuse" was conducted. RESULTS: Ten articles were reviewed. All were descriptive in nature and used a nonexperimental approach to measure the incidence of disruptive behavior and/or verbal abuse in various health care settings via self-report surveys. All studies confirmed the alarming prevalence of disruptive behavior. CONCLUSIONS: A standard definition of "disruptive behavior" is needed, as is a valid and reliable measure of the phenomenon before interventions to address the problem can be developed.

Genetic predisposition to hypertension sensitizes borderline hypertensive rats to the hypertensive effects of prenatal glucocorticoid exposure.

An adverse intrauterine environment can increase the incidence of hypertension and other cardiovascular disease risk factors. However, in clinical and experimental studies the magnitude of the effect is variable. Possibly, the relative influence of the prenatal environment on cardiovascular disease is determined in part by genetic factors that predispose individuals to the development of environmentally induced hypertension. We tested this hypothesis by comparing the effects of prenatal dexamethasone treatment (Dex, 300 microg kg(-1) i.p. on days 15 and 16 of gestation) in borderline hypertensive rats (BHR) and control Wistar-Kyoto (WKY) rats. Blood pressure, heart rate and plasma corticosterone values were measured at rest during the middle of the day, and during 1 h of restraint stress in the adult offspring using indwelling arterial catheters implanted at least 4 days prior to data collection. Compared with the saline (vehicle) control treatment, prenatal dexamethasone significantly (P < 0.05) increased baseline mean arterial pressure in male (123 +/- 2 versus 131 +/- 3 mmHg, saline versus Dex) and female (121 +/- 2 versus 130 +/- 2 mmHg, saline versus Dex) BHR, but not in male (108 +/- 3 versus 113 +/- 2 mmHg, saline versus Dex) or female (112 +/- 2 versus 110 +/- 2 mmHg, saline versus Dex) WKY rats. Relative to saline treatment, prenatal Dex also significantly increased baseline heart rate (328 +/- 6 versus 356 +/- 5 beats min(-1), saline versus Dex) and plasma corticosterone (5 +/- 2 versus 24 +/- 4 microg dl(-1), saline versus Dex), and prolonged the corticosterone response to acute stress, selectively in female BHR. However, prenatal Dex significantly enhanced the arterial pressure response to acute stress only in female WKY, while Dex augmented the elevation in heart rate during stress only in male rats. We conclude that prenatal dexamethasone increased baseline arterial pressure selectively in BHR, and plasma corticosterone only in female BHR. In contrast, prenatal Dex enhanced cardiovascular reactivity to stress in both BHR and WKY rats.

Baroreflex control of sympathetic nerve activity in hypertensive pregnant rats with reduced uterine perfusion.

OBJECTIVE: Baroreflex sensitivity is reduced in women with preeclampsia. The aim of this study was to determine whether baroreflex control of renal sympathetic nerve activity (RSNA) is altered in pregnant rats with reduced uterine perfusion (a model of human preeclampsia). METHODS: Uterine perfusion was reduced in the third trimester by clipping the distal aorta and uterine branches of the ovarian arteries. RSNA baroreflex parameters were compared at term gestation in rats with reduced uterine perfusion (n = 12), in normal pregnant rats (n = 14) and in nonpregnant rats (n = 14). RESULTS: Reduced perfusion rats were hypertensive (123.6 +/- 2.3 mm Hg), and normal pregnant rats were hypotensive (97.7 +/- 2.2 mm Hg), compared with controls. In rats with reduced perfusion, the baroreflex was shifted to a higher set-point, and maximum and minimum RSNA were increased compared with normal pregnant rats. CONCLUSION: The blunted baroreflex gain of normal pregnancy is maintained in rats with reduced uterine perfusion, but a hypertensive shift in baroreflex function exists in this rat model that is associated with a reversal of the reflex maximum and minimum RSNA observed in normal pregnancy.

The hypo-osmolality of pregnancy does not alter baroreceptor responses to acute changes in osmolality.

Reducing extracellular osmolality by 10-12 mOsm/L reduces baroreceptor firing in vitro in tissues from male rats. Pregnancy is associated with a similar reduction in plasma osmolality (pOsm) as well as with alterations in baroreceptor firing and reduced baroreceptor reflex activity. Mechanisms for reduced baroreflex activity are not yet understood, but they have important implications for maintenance of cardiovascular homeostasis in the pregnant female. Thus, this study was designed to test whether changes in plasma osmolality alter baroreceptor discharge during pregnancy. Late-gestation pregnant and virgin control rats were anesthetized, femoral vessels were cannulated for measurement of arterial pressure and drug infusion, and the aortic depressor nerve, containing baroreceptor afferents, was isolated and prepared for recording. Plasma osmolality was measured before and 30 min after graded intraperitoneal injections of NaCl (50-1500 mOsm/L). Arterial pressure, heart rate, and aortic depressor nerve activity (ADNA) were measured continuously before and after injections. A 50 mOsm/L NaCl injection significantly decreased pOsm but did not alter ADNA in either group. Likewise, 1200 mOsm/L NaCl injections significantly increased pOsm and had no effect on ADNA in either group. The 1500 mOsm salt load significantly increased pOsm and ADNA in pregnant rats, and in virgin animals, it increased pOsm but evoked a paradoxical decrease in ADNA. The authors' studies indicate that pOsm has minimal effects on baroreceptor activity, which are not significantly different during gestation. Their findings suggest that in vitro data from male rats indicating a correlation between pOsm and baroreceptor discharge are not applicable in anesthetized intact female animals.

Right atrial dimension-pressure relation during volume expansion is unaltered by pregnancy in the rat.

Blood volume expands significantly during pregnancy, but afferent signals from cardiac receptors are reduced. In addition, during exogenous volume expansion, right atrial pressure (RAP) increases more for equivalent volumes in pregnant animals, implying reduced atrial compliance. To examine possible gestational alterations in atrial dimension during volume expansion, we compared the effects of volume expansion on RAP and right atrial dimension (RAD) in pregnant vs. virgin rats. Anesthetized animals were ventilated and catheterized for measurement of arterial pressure and RAP and for drug infusion. Through a parasternal incision, ultrasonic crystals were glued to the medial and lateral surfaces of the right atrium for measurement of RAD. Plasma volume and hematocrit were determined before experimentation. RAP, RAD, and arterial pressure were recorded at baseline and during progressive volume expansion (6% dextran, 60% of initial blood volume). Baseline RAP was similar in the two groups: 2.82 +/- 0.40 and 2.72 +/- 0.47 mmHg in pregnant and virgin rats, respectively. Basal RAD was significantly larger in pregnant than in virgin rats: 4.36 +/- 0.66 vs. 3.36 +/- 0.48 mm. Despite increased basal RAD in pregnant rats, the slope of the RAD-RAP relation during volume expansion was similar in the two groups. Results indicate that resting RAD is increased in pregnant rats and that the change in dimension during volume loads is similar to that in virgin rats. Thus, during pregnancy, the right atrium appears to accommodate the increased blood volume, and reduced afferent signaling most likely is due to mechanisms other than mechanical alterations of the atrium by expanded volume.