Incidence of sudden infant death syndrome in Texas, 1969-1972; estimation by the surrogate method.
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Biomedical subjects
Publications and source records attributed to R Maxwell.
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A 30-year-old man had a long history of seizures that began with feelings of tightness in his throat and fear, followed by projectile vomiting and head and eye deviation to the left. These episodes were not completely controlled by antiepileptic medications. Video EEG monitoring confirmed his clinical description. Corticography was performed before and after temporal lobectomy and revealed residual spikes in the unresectable tissue of the insula. Three years postoperatively he has had no seizures with vomiting but has occasional 'auras' of throat tightening and fear. The case suggests that the insula may be a trigger area for emesis but requires anterior-mesial temporal cortex for completion.
Intravenous (i.v.) methohexital (MTH, Brevital) was found to have an effect on the intraoperative electrocorticogram (ECOG) of 63 patients who had temporal lobectomies performed under general anesthesia for intractable complex partial seizures. In the preresection ECOG, MTH increased the frequency of spikes in 78%, the area of cortical spiking in 30% and induced seemingly "new" spike foci in 43%. Similar although less dramatic changes occurred in the final (i.e., postresection) ECOG. Whether these changes induced by MTH, specifically the new spike foci, are significant was assessed by correlating surgical results with the presence of "residual spikes" (i.e., after all resections, not spontaneously occurring but activated by MTH). Surprisingly, nine patients with residual "MTH-spikes" did not have any postoperative seizures whereas two had some. This raises the question of whether MTH effects are significant overall. Caution is advised in the use of MTH in intraoperative assessment of interictal spike fields, especially when new spike foci are activated. Further study of the possibility of false activation, with a larger series, is advised.
Isoflurane, an inhalation agent often used for general anesthesia during craniotomy, has been reported to suppress spike activity in the intraoperative electrocorticogram (ECoG) during epilepsy surgery. We studied the effect of isoflurane concentrations of 0.25, 0.5, 0.75, 1, and 1.25% on the number of spike bursts per 5-min epochs in 15 patients undergoing ECoG during epilepsy surgery. N2O in O2 was maintained at 50% in 10 patients, at 60% in 2, and at 70% in 3. End tidal CO2 concentration was maintained in the hypocarbic range, and analgesia was maintained with the narcotic alfentanil in the range of 0.5-2 micrograms/min. The median number of spikes for each isoflurane concentration was 29 (range 3-107) at 0.25%, 27 (range 2-73) at 0.5%; 29 (range 5-90) at 0.75%, 33 (range 2-100) at 1%, and 40 (range 32-140) in 5 patients who tolerated 1.25% without occurrence of burst suppression pattern. No significant difference (Student's paired t test) was noted in the number of spikes for each isoflurane concentration. Therefore, if isoflurane concentrations are maintained between 0.25 and 1.25% or before burst suppression pattern occurs and N2O/O2 is maintained in the 50-70% range, isoflurane has no significant effect on spike activity.
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To summarize, five areas have been targeted by the AARP for improvement: Market and price stability Geriatric training for medical and support staff Emphasis on preventive care and maintenance programs Integration of health care services with social services Provision of useful consumer information on quality of care as a marketing tool AARP is concerned about the universe of health care problems facing this nation. I do not for an instant suggest that these issues will be easily resolved or resolved quickly. We are all anxious to find solutions that work. One of the most promising solutions is with you, in your experience, commitment and willingness to forge new ground. HMOs and Social HMOs serving this older population are leaders in the health care industry. Many of you have demonstrated that HMOs can provide quality medical care for elderly patients. It is AARP's hope that working together we can create an environment in which HMOs adopt policies and practices that ensure comprehensive quality health for the elderly.
After inducing an increase in pulmonary vascular resistance (Rp) in an isolated in situ lobe (LAIS) embolized with gelfoam (GE), the effect of dopamine infused at 12 mcg/kg/min in eight mongrel dogs was evaluated. We studied the rectilinear pressure-flow (QL/PL) relationship, the hemodynamic and blood gas before (condition A), 15 minutes later GE (condition B) and after dopamine infusion (condition C). After GE a decrease in QL and an increase in inflow (PL) and mean critical closing pressures (PLi) were noticed (p less than 0.01). Also decrease in pulmonary vascular conductance (1/Rp) was noted. At condition C a rise in QL and PL were noticed (p less than 0.01), but 1/Rp and PLi did not change. We concluded that dopamine in the LAIS with increased Rp at the used doses does not have vasoactive action for those vessels responsible for the phenomenons where flow resistance or mean critical closing pressure occurs.
To determine whether hydralazine (H) a systemic vasodilator, inhibits hypoxic pulmonary vasoconstriction (HPV) we studied in a canine model of lobar atelectasis (LA) the circulatory changes during the following interventions: a) control 1 (LA = HPV), b) during the acute effect produced by opening bilateral arteriovenous fistulas (OF), c) after the closure of the fistulas (CF) (control 2), d) after infusing H (0.33 mg/kg) and e) bleeding the animal at the end of the experiment (control 3). Once HPV was stabilized (control 1), both opening the fistulas and infusing H produced a similar and significant increase in cardiac output and a decrease in resistance (p less than 0.05). Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output (Qt). Intrapulmonary shunt (Qs/Qt) significantly increased (p less than 0.05) with the fistulas open and with H infusion. CF and bleeding the animal at the end of the experiment reversed the changes in Qt and Qs/Qt. The similar increases in Qt and Qs/Qt by OF or infusing H seems to be related to the levels of pVO2. Our data suggest that hydralazine inhibits pulmonary vasoconstriction probably by raising the level of pVO2 although a direct pulmonary vasodilatory effect of the drug could not be ruled out.
In order to evaluate the isolated hemodynamic effects of acute hypercapnea on pulmonary circulation, we designed a canine model in which vascular pressures. PaO2, and arterial pH were maintained within normal limits. Six mongrel dogs were studied. Hypercapnea was achieved by a single intravenous doses of acetazolamide (120 mg/Kg) while maintaining mechanical ventilation constant. Both arterial and mixed venous PCO2 increased from 27 to 41 mm Hg and from 31 to 46 mm Hg respectively, and remained constant through the rest of the experiment (up to 3 Hs). With hypercapnea, total pulmonary vascular resistance increased from 312 +/- 156 to 435 +/- 173 d.s.cm-5 (p less than 0.05) and the stroke index decreased from 20.7 +/- 8.3 to 13.2 +/- 4.8 ml/beat (p less than 0.05). There were no changes either in pulmonary capillary wedge pressure or in the right ventricular end diastolic pressure. The above changes suggest a pulmonary vasoconstrictor effect of hypercapnea in the absence of other known vasoactive factors.
In order to establish an animal model of pulmonary vasoconstriction we followed the time course of intrapulmonary shunt (Qs/Qt) in a canine model of lobar atelectasis with closed chest. Ten mongrel dogs were studied. Bronchial occlusion of the right lower lobe (RLL) was performed by inflating the balloon of a Foley catheter placed through a rigid bronchoscopy. Analysis of variance was used for statistical analysis. (15 minutes) After occlusion Qs/Qt reached its maximum increasing from 8.2 +/- 3.6 to 29.7 +/- 11.7% (p less than 0.05) and PaO2 decreased from 357 +/- 49 to 100 +/- 43 mm Hg (p less than 0.05). Afterwards, there was a progressive decline of Qs/QT accompanied by an also progressive increase in PaO2. At the end of the experiment (3 hrs post atelectasis) Qs/Qt was 11.2 +/- 4.9 and PaO2 251 +/- 124 mm Hg (p less than 0.05). Pulmonary vascular resistance increased post atelectasis from 439 +/- 168 to 598 +/- 256 d.s.cm-5 (p less than 0.05). Complete atelectasis of the RLL was confirmed postmortem. As the changes in Qs/Qt and PaO2 did not parallel the change in cardiac output we conclude that the mechanism of decrease in Qs/Qt was hypoxic vasoconstriction.