Johnson, Bruce D.

Abstract Background: Occupational stress in resident physicians has profound implications for wellness, professionalism, and patient care. This observational pilot trial measured psychological and physiological stress biomarkers before, during, and after the start of anesthesia residency. Methods: Eighteen physician interns scheduled to begin anesthesia residency were recruited for evaluation at three time points: baseline (collected remotely before residency in June 2013); first-month visit 1 (July); and follow-up visit 2 (residency months 3 to 5, September–November). Validated scales were used to measure stress, anxiety, resilience, and wellness at all three time points. During visits 1 and 2, the authors measured resting heart-rate variability, responses to laboratory mental stress (hemodynamic, catecholamine, cortisol, and interleukin-6), and chronic stress indices (C-reactive protein, 24-h ambulatory heart rate and blood pressure, 24-h urinary cortisol and catecholamines, overnight heart-rate variability). Results: Thirteen interns agreed to participate (72% enrollment). There were seven men and six women, aged 27 to 33 yr. The mean ± SD of all study variables are reported. Conclusion: The novelty of this report is the prospective design in a defined cohort of residents newly exposed to the similar occupational stress of the operating environment. Because of the paucity of literature specific to the measures and stress conditions in this investigation, no data were available to generate a priori definition of primary outcomes and a data analytic plan. These findings will allow power analysis for future design of trials examining occupational stress and stress-reducing interventions. Given the importance of physician burnout in our country, the impact of chronic stress on resident wellness requires further study.

New FindingsWhat is the central question of this study?Patients with heart failure often develop ventilatory abnormalities at rest and during exercise, but the mechanisms underlying these abnormalities remain unclear. This study investigated the influence of inhibiting afferent neural feedback from locomotor muscles on the ventilatory response during exercise in heart failure patients.What is the main finding and its importance?Our results suggest that inhibiting afferent feedback from locomotor muscle via intrathecal opioid administration significantly reduces the ventilatory response to exercise in heart failure patients.Patients with heart failure (HF) develop ventilatory abnormalities at rest and during exercise, but the mechanism(s) underlying these abnormalities remain unclear. We examined whether the inhibition of afferent neural feedback from locomotor muscles during exercise reduces exercise ventilation in HF patients. In a randomized, placebo‐controlled design, nine HF patients (age, 60 ± 2 years; ejection fraction, 27 ± 2%; New York Heart Association class 2 ± 1) and nine control subjects (age, 63 ± 2 years) underwent constant‐work submaximal cycling (65% peak power) with intrathecal fentanyl (impairing the cephalad projection of opioid receptor‐sensitive afferents) or sham injection. The hypercapnic ventilatory response was measured to determine whether cephalad migration of fentanyl occurred. There were no differences in hypercapnic ventilatory response within or between groups in either condition. Despite a lack of change in ventilation, tidal volume or respiratory rate, HF patients had a mild increase in arterial carbon dioxide () and a decrease in oxygen (;P< 0.05 for both) at rest. The control subjects demonstrated no change in,, ventilation, tidal volume or respiratory rate at rest. In response to fentanyl during exercise, HF patients had a reduction in ventilation (63 ± 6versus44 ± 3 l min−1,P< 0.05) due to a lower respiratory rate (30 ± 1versus26 ± 2 breaths min−1,P< 0.05). The reduced ventilation resulted in lower(97.6 ± 2.5versus79.5 ± 3.0 mmHg,P< 0.05) and increased(37.3 ± 0.9versus43.5 ± 1.1 mmHg,P< 0.05), with significant improvement in ventilatory efficiency (reduction in the ventilatory equivalent for carbon dioxide;P< 0.05 for all). The control subjects had no change in ventilation or measures of arterial blood gases. These data suggest that inhibition of afferent feedback from locomotor muscle significantly reduces the ventilatory response to exercise in HF patients.

We determined whether a non-invasive gas exchange based estimate of pulmonary vascular (PV) capacitance [PV CAP = stroke volume (SV) x pulmonary arterial pressure (Ppa)] (GX CAP ) tracked the PV response to exercise in heart-failure (HF) patients. Pulmonary wedge pressure (Ppw), Ppa, PV resistance (PVR), and gas exchange were measured simultaneously during cycle exercise in 42 HF patients undergoing right-heart catheterization. During exercise, P ET CO 2 and V E /VCO 2 were related to each other ( r= -0.93, P < 0.01) and similarly related to mean Ppa (mPpa) ( r = -0.39 and 0.36; P < 0.05); P ET CO 2 was subsequently used as a metric of mPpa. Oxygen pulse (O 2 pulse) tracked the SV response to exercise (r = 0.91, P < 0.01). Thus, GX CAP was calculated as O 2 pulse x P ET CO 2 . During exercise, invasively determined PV CAP and non-invasive GX CAP were related (r = 0.86, P < 0.01), and GX CAP correlated with mPpa and PVR (r = -0.46 and -0.54; P < 0.01). In conclusion, noninvasive gas exchange measures may represent a simple way to track the PV response to exercise in HF.

Objective Although the majority of high altitude studies have used doubly labeled water to assess energy expenditure (EE), minimal research has examined variation in intensity levels while participating in such an expedition. The purpose of this study was to use ambulatory monitoring technology to assess EE and time spent in moderate (3.0–6.0 METS), vigorous (6.0–9.0 METS), and very vigorous (>9.0 METS) intensities during an expedition to summit a 6170-m peak in Northern Pakistan. Methods Twelve men and 2 women were studied. Their EE was determined from galvanic skin response, heat flux, and biaxial accelerometry using a multisensor armband. Lake Louise Scores for altitude illness assessment were obtained each morning. Results Average daily total EE and number of steps taken was 4173 ± 848 kcal/d (range, 3332 to 4838 kcal/d) and 26,232 ± 7210 steps/d (range, 11,788 to 34,979 steps/d), respectively. On average, subjects spent approximately 7.7 h/d performing physical activity (>3.0 METS). Of this, subjects spent 399 ± 107, 61 ± 77, and 3 ± 10 min/d at moderate, vigorous, and very vigorous intensity levels, respectively, corresponding to 88%, 11%, and 1% of total physical activity time. During summit day, subjects climbed at an intensity equivalent to approximately 42% of their high altitude predicted maximal oxygen consumption at 5100 m). Conclusions During a high altitude expedition, subjects predominantly exercise at a moderate intensity, with limited time spent at higher intensity levels. Use of accelerometer-based technology may provide more cost-effective and logistically easier means of assessing EE in extreme environments.

Background The heart and lungs are intimately linked anatomically and physiologically, and, as a result, heart failure (HF) patients often develop changes in pulmonary function. This study examined the prognostic value of resting pulmonary function (PF) in HF. Methods and Results In all, 134 HF patients (enrolled from January 1, 1999 Through December 31, 2005; ejection fraction (EF) = 29% ± 11%; mean age = 55 ± 12 years; 65% male) were followed for 67 ± 34 months with death/transplant confirmed via the Social Security Index and Mayo Clinic registry. PF included forced vital capacity (FVC), forced expiratory volume in 1 second (FEV 1 ), diffusing capacity of the lungs for carbon monoxide (DL CO ), and alveolar volume (VA). Patients were divided in tertiles according to PF with survival analysis via log-rank Mantel-Cox test with chi-square analysis. Groups for FVC included (1) >96%, (2) 96% to 81%, and (3) <81% predicted (chi-square = 18.9, P< 0.001). Bonferroni correction for multiple comparisons (BC) suggested differences between groups 1 and 3 (P < 0.001) and 2 and 3 ( P = 0.008). Groups for FEV 1 included (1) >94%, (2) 94% to 77%, and (3) <77% predicted (chi-square = 17.3, P < 0.001). BC suggested differences between groups 1 and 3 ( P < 0.001). Groups for DL CO included (1) >90%, (2) 90% to 75%, and (3) <75% predicted (chi-square = 11.9, P = 0.003). BC suggested differences between groups 1 and 3 >( P < 0.001). Groups for VA included (1) <97%, (2) 97% to 87%, and (3) <87% predicted (Chi-square = 8.5, P = 0.01). BC suggested differences between groups 1 and 2 ( P = 0.014) and 1 and 3 >( P = 0.003). Conclusions In a well-defined cohort of HF patients, resting measures of PF are predictive of all-cause mortality.

Abstract Aims Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF), yet its mechanisms remain unclear. The current study sought to determine whether increases in cardiac output (CO) during exercise are appropriately matched to metabolic demands in HFpEF. Methods and results Patients with HFpEF (n = 109) and controls (n = 73) exercised to volitional fatigue with simultaneous invasive (n = 96) or non-invasive (n = 86) haemodynamic assessment and expired gas analysis to determine oxygen consumption (VO2) during upright or supine exercise. At rest, HFpEF patients had higher LV filling pressures but similar heart rate, stroke volume, EF, and CO. During supine and upright exercise, HFpEF patients displayed lower peak VO2 coupled with blunted increases in heart rate, stroke volume, EF, and CO compared with controls. LV filling pressures increased dramatically in HFpEF patients, with secondary elevation in pulmonary artery pressures. Reduced peak VO2 in HFpEF patients was predominantly attributable to CO limitation, as the slope of the increase in CO relative to VO2 was 20% lower in HFpEF patients (5.9 ± 2.5 vs. 7.4 ± 2.6 L blood/L O2, P = 0.0005). While absolute increases in arterial–venous O2 difference with exercise were similar in HFpEF patients and controls, augmentation in arterial–venous O2 difference relative to VO2 was greater in HFpEF patients (8.9 ± 3.4 vs. 5.5 ± 2.0 min/dL, P &lt; 0.0001). These differences were observed in the total cohort and when upright and supine exercise modalities were examined individually. Conclusion While diastolic dysfunction promotes congestion and pulmonary hypertension with stress in HFpEF, reduction in exercise capacity is predominantly related to inadequate CO relative to metabolic needs.

Patients with pulmonary arterial hypertension (PAH) and heart failure (HF) display many abnormalities in respiratory gas exchange. These abnormalities are accentuated with exercise and track with disease severity. However, use of gas exchange measures in day-to-day clinical practice is limited by several issues, including the large number of variables available and difficulty in data interpretation. Moreover, maximal exercise testing has limitations in clinical populations due to their complexity, patient anxiety and variability in protocols and cost. Therefore, a multivariable gas exchange index (MVI) that integrates key gas exchange variables obtained during submaximal exercise into a severity score that ranges from normal to severe-very-severe is proposed. To demonstrate the usefulness of this index, we applied this to 2 groups (PAH,n=42and HF,n=47) as well as to age matched healthy controls (n=25). We demonstrate that this score tracks WHO classification and right ventricular systolic pressure in PAH (r=0.53and 0.73,P≤0.01) and NYHA and cardiac index in HF (r=0.49and 0.74,P≤0.01). This index demonstrates a stronger relationship than any single gas exchange variable alone. In conclusion, MVI obtained from light, submaximal exercise gas exchange is a useful approach to simplify data interpretation in PAH and HF populations.