Fellowship-trained physicians who let their geriatric medicine certification lapse: A national survey.

BACKGROUND: Only 62.6% of fellowship-trained and American Board of Internal Medicine (ABIM)-certified geriatricians maintain their specialty certification in geriatric medicine, the lowest rate among all internal medicine subspecialties and the only subspecialty in which physicians maintain their internal medicine certification at higher rates than their specialty certification. This study aims to better understand underlying issues related to the low rate of maintaining geriatric medicine certification in order to inform geriatric workforce development strategies. METHODS: Eighteen-item online survey of internists who completed a geriatric medicine fellowship, earned initial ABIM certification in geriatric medicine between 1999 and 2009, and maintained certification in internal medicine (and/or another specialty but not geriatric medicine). Survey domains: demographics, issues related to maintaining geriatric medicine certification, professional identity, and current professional duties. RESULTS: 153/723 eligible completed surveys (21.5% response). Top reasons for not maintaining geriatric medicine certification were time (56%), cost of maintenance of certification (MOC) (45%), low Medicare reimbursement for geriatricians' work (32%), and no employer requirement to maintain geriatric medicine certification (31%). Though not maintaining geriatric medicine certification, 68% reported engaging in professional activities related to geriatric medicine. Reflecting on career decisions, 56% would again complete geriatric medicine fellowship, 21% would not, and 23% were unsure. 54% considered recertifying in geriatric medicine. 49% reported flexible MOC assessment options would increase likelihood of maintaining certification. CONCLUSIONS: The value proposition of geriatric medicine certification needs strengthening. Geriatric medicine leaders must develop strategies and tactics to reduce attrition of geriatricians by enhancing the value of geriatric medicine expertise to key stakeholders.

GRECC Connect: Geriatrics Telehealth to Empower Health Care Providers and Improve Management of Older Veterans in Rural Communities.

A telehealth program supports meaningful partnerships between urban geriatric specialists and rural health care providers to facilitate increased access to specialty care.

Effects of sleep-disordered breathing on cerebrovascular regulation: A population-based study.

RATIONALE: Cerebrovascular regulation is impaired in patients with moderate to severe obstructive sleep apnea; however, it is unknown whether this impairment exists in individuals with less severe sleep-disordered breathing. OBJECTIVES: To test the hypothesis that cerebrovascular responses to hypercapnia are attenuated in a nonclinical population-based cohort. METHODS: A rebreathing test that raised end-tidal CO2 tension by 10 mm Hg was performed during wakefulness in 373 participants of the Wisconsin Sleep Cohort. MEASUREMENTS AND MAIN RESULTS: We measured cerebral flow velocity (transcranial Doppler ultrasound); heart rate (electrocardiogram); blood pressure (photoplethysmograph); ventilation (pneumotachograph); and end-tidal CO2 (expired gas analysis). Cerebrovascular CO2 responsiveness was quantified as the slope of the linear relationship between flow velocity and end-tidal CO2 during rebreathing. Linear regression analysis was performed using cerebrovascular CO2 responsiveness as the outcome variable. Main independent variables were the apnea-hypopnea index and the mean level of arterial oxygen saturation during sleep. We observed a positive correlation between cerebrovascular CO2 responsiveness and the mean level of oxygen saturation during sleep that was statistically significant in unadjusted analysis and after adjustment for known confounders and the increase in arterial pressure during rebreathing. Each 5% decrease in Sa(O2) during sleep predicted a decrease in cerebrovascular reactivity of 0.4 ± 0.2 cm/second/mm Hg P(ET)CO2. In contrast, the negative correlation between cerebrovascular CO2 responsiveness and apnea-hypopnea index was statistically significant only in the unadjusted analysis. CONCLUSIONS: Hypercapnic vasodilation in the cerebral circulation is blunted in individuals with sleep-disordered breathing. This impairment is correlated with hypoxemia during sleep.

Impaired vascular regulation in patients with obstructive sleep apnea: effects of continuous positive airway pressure treatment.

RATIONALE: Impaired endothelium-dependent vasodilation has been documented in patients with sleep apnea. This impairment may result in blood flow dysregulation during apnea-induced fluctuations in arterial blood gases. OBJECTIVES: To test the hypothesis that hypoxic and hypercapnic vasodilation in the forearm and cerebral circulation are impaired in patients with sleep apnea. METHODS: We exposed 20 patients with moderate to severe sleep apnea and 20 control subjects, to isocapnic hypoxia and hyperoxic hypercapnia. A subset of 14 patients was restudied after treatment with continuous positive airway pressure. MEASUREMENTS AND MAIN RESULTS: Cerebral flow velocity (transcranial Doppler), forearm blood flow (venous occlusion plethysmography), arterial pressure (automated sphygmomanometry), oxygen saturation (pulse oximetry), ventilation (pneumotachograph), and end-tidal oxygen and carbon dioxide tensions (expired gas analysis) were measured during three levels of hypoxia and two levels of hypercapnia. Cerebral vasodilator responses to hypoxia (-0.65 +/- 0.44 vs. -1.02 +/- 0.72 [mean +/- SD] units/% saturation; P = 0.03) and hypercapnia (2.01 +/- 0.88 vs. 2.57 +/- 0.89 units/mm Hg; P = 0.03) were smaller in patients versus control subjects. Hypoxic vasodilation in the forearm was also attenuated (-0.05 +/- 0.09 vs. -0.10 +/- 0.09 unit/% saturation; P = 0.04). Hypercapnia did not elicit forearm vasodilation in either group. Twelve weeks of continuous positive airway pressure treatment enhanced hypoxic vasodilation in the cerebral circulation (-0.83 +/- 0.32 vs. -0.46 +/- 0.29 units/% saturation; P = 0.01) and forearm (-0.19 +/- 0.15 vs. -0.02 +/- 0.08 units/% saturation; P = 0.003), and hypercapnic vasodilation in the brain showed a trend toward improvement (2.24 +/- 0.78 vs. 1.76 +/- 0.64 units/mm Hg; P = 0.06). CONCLUSIONS: Vasodilator responses to chemical stimuli in the cerebral circulation and the forearm are impaired in many patients with obstructive sleep apnea. Some of these impairments can be improved with continuous positive airway pressure.

Influence of cerebral blood flow on breathing stability.

Our previous work showed a diminished cerebral blood flow (CBF) response to changes in Pa(CO(2)) in congestive heart failure patients with central sleep apnea compared with those without apnea. Since the regulation of CBF serves to minimize oscillations in H(+) and Pco(2) at the site of the central chemoreceptors, it may play an important role in maintaining breathing stability. We hypothesized that an attenuated cerebrovascular reactivity to changes in Pa(CO(2)) would narrow the difference between the eupneic Pa(CO(2)) and the apneic threshold Pa(CO(2)) (DeltaPa(CO(2))), known as the CO(2) reserve, thereby making the subjects more susceptible to apnea. Accordingly, in seven normal subjects, we used indomethacin (Indo; 100 mg by mouth) sufficient to reduce the CBF response to CO(2) by approximately 25% below control. The CO(2) reserve was estimated during non-rapid eye movement (NREM) sleep. The apnea threshold was determined, both with and without Indo, in NREM sleep, in a random order using a ventilator in pressure support mode to gradually reduce Pa(CO(2)) until apnea occurred. results: Indo significantly reduced the CO(2) reserve required to produce apnea from 6.3 +/- 0.5 to 4.4 +/- 0.7 mmHg (P = 0.01) and increased the slope of the ventilation decrease in response to hypocapnic inhibition below eupnea (control vs. Indo: 1.06 +/- 0.10 vs. 1.61 +/- 0.27 l x min(-1) x mmHg(-1), P < 0.05). We conclude that reductions in the normal cerebral vascular response to hypocapnia will increase the susceptibility to apneas and breathing instability during sleep.

Cerebrovascular response to arousal from NREM and REM sleep.

STUDY OBJECTIVE: To determine the effect of arousal from sleep on cerebral blood flow velocity (CBFV) in relation to associated ventilatory and systemic hemodynamic changes. PARTICIPANTS: Eleven healthy individuals (6 men, 5 women). MEASUREMENTS: Pulsed Doppler ultrasonography was used to measure CBFV in the middle cerebral artery with simultaneous measurements of sleep state (EEG, EOG, and EMG), ventilation (inductance plethysmography), heart rate (ECG), and arterial pressure (finger plethysmography). Arousals were induced by auditory tones (range: 40-80 dB; duration: 0.5 sec). Cardiovascular responses were examined beat-by-beat for 30 sec before and 30 sec after auditory tones. RESULTS: During NREM sleep, CBFV declined following arousals (-15% +/- 2%; group mean +/- SEM) with a nadir at 9 sec after the auditory tone, followed by a gradual return to baseline. Mean arterial pressure (MAP; +20% +/- 1%) and heart rate (HR; +17% +/- 2%) increased with peaks at 5 and 3 sec after the auditory tone, respectively. Minute ventilation (VE) was increased (+35% +/- 10%) for 2 breaths after the auditory tone. In contrast, during REM sleep, CBFV increased following arousals (+15% +/- 3%) with a peak at 3 sec. MAP (+17% +/- 2%) and HR (+15% +/- 2%) increased during arousals from REM sleep with peaks at 5 and 3 sec post tone. VE increased (+16% +/- 7%) in a smaller, more sustained manner during arousals from REM sleep. CONCLUSIONS: Arousals from NREM sleep transiently reduce CBFV, whereas arousals from REM sleep transiently increase CBFV, despite qualitatively and quantitatively similar increases in MAP, HR, and VE in the two sleep states.