Opportunities for shared decision-making about major surgery with high-risk patients: a multi-method qualitative study.

BACKGROUND: Little is known about the opportunities for shared decision-making when older high-risk patients are offered major surgery. This study examines how, when, and why clinicians and patients can share decision-making about major surgery. METHODS: This was a multi-method qualitative study, combining video recordings of preoperative consultations, interviews, and focus groups (33 patients, 19 relatives, 36 clinicians), with observations and documentary analysis in clinics in five hospitals in the UK undertaking major orthopaedic, colorectal, and/or cardiac surgery. RESULTS: Three opportunities for shared decision-making about major surgery were identified. Resolution-focused consultations (cardiac/colorectal) resulted in a single agreed preferred option related to a potentially life-threatening problem, with limited opportunities for shared decision-making. Evaluative and deliberative consultations offered more opportunity. The former focused on assessing the likelihood of benefits of surgery for a presenting problem that was not a threat to life for the patient (e.g., orthopaedic consultations) and the latter (largely colorectal) involved discussion of a range of options while also considering significant comorbidities and patient preferences. The extent to which opportunities for shared decision-making were available, and taken up by surgeons, was influenced by the nature of the presenting problem, clinical pathway, and patient trajectory. CONCLUSIONS: Decisions about major surgery were not always shared between patients and doctors. The nature of the presenting problem, comorbidities, clinical pathways, and patient trajectories all informed the type of consultation and opportunities for sharing decision-making. Our findings have implications for clinicians, with shared decision-making about major surgery most feasible when the focus is on life-enhancing treatment.

Cerebral hemodynamics at altitude: effects of hyperventilation and acclimatization on cerebral blood flow and oxygenation.

OBJECTIVE: Alterations in cerebral blood flow (CBF) and cerebral oxygenation are implicated in altitude-associated diseases. We assessed the dynamic changes in CBF and peripheral and cerebral oxygenation engendered by ascent to altitude with partial acclimatization and hyperventilation using a combination of near-infrared spectroscopy, transcranial Doppler ultrasound, and diffuse correlation spectroscopy. METHODS: Peripheral (Spo2) and cerebral (Scto2) oxygenation, end-tidal carbon dioxide (ETCO2), and cerebral hemodynamics were studied in 12 subjects using transcranial Doppler and diffuse correlation spectroscopy (DCS) at 75 m and then 2 days and 7 days after ascending to 4559 m above sea level. After obtaining baseline measurements, subjects hyperventilated to reduce baseline ETCO2 by 50%, and a further set of measurements were obtained. RESULTS: Cerebral oxygenation and peripheral oxygenation showed a divergent response, with cerebral oxygenation decreasing at day 2 and decreasing further at day 7 at altitude, whereas peripheral oxygenation decreased on day 2 before partially rebounding on day 7. Cerebral oxygenation decreased after hyperventilation at sea level (Scto2 from 68.8% to 63.5%; P<.001), increased after hyperventilation after 2 days at altitude (Scto2 from 65.6% to 69.9%; P=.001), and did not change after hyperventilation after 7 days at altitude (Scto2 from 62.2% to 63.3%; P=.35). CONCLUSIONS: An intensification of the normal cerebral hypocapnic vasoconstrictive response occurred after partial acclimatization in the setting of divergent peripheral and cerebral oxygenation. This may help explain why hyperventilation fails to improve cerebral oxygenation after partial acclimatization as it does after initial ascent. The use of DCS is feasible at altitude and provides a direct measure of CBF indices with high temporal resolution.

High-intensity intermittent exercise increases pulmonary interstitial edema at altitude but not at simulated altitude.

OBJECTIVE: Ascent to high altitude leads to a reduction in ambient pressure and a subsequent fall in available oxygen. The resulting hypoxia can lead to elevated pulmonary artery (PA) pressure, capillary stress, and an increase in interstitial fluid. This fluid can be assessed on lung ultrasound (LUS) by the presence of B-lines. We undertook a chamber and field study to assess the impact of high-intensity exercise in hypoxia on the development of pulmonary interstitial edema in healthy lowlanders. METHODS: Thirteen volunteers completed a high-intensity intermittent exercise (HIIE) test at sea level, in acute normobaric hypoxia (12% O2, approximately 4090 m equivalent altitude), and in hypobaric hypoxia during a field study at 4090 m after 6 days of acclimatization. Pulmonary interstitial edema was assessed by the evaluation of LUS B-lines. RESULTS: After HIIE, no increase in B-lines was seen in normoxia, and a small increase was seen in acute normobaric hypoxia (2 ± 2; P < .05). During the field study at 4090 m, 12 participants (92%) demonstrated 7 ± 4 B-lines at rest, which increased to 17 ± 5 immediately after the exercise test (P < .001). An increase was evident in all participants. There was a reciprocal fall in peripheral arterial oxygen saturations (Spo2) after exercise from 88% ± 4% to 80% ± 8% (P < .01). B-lines and Spo2 in all participants returned to baseline levels within 4 hours. CONCLUSIONS: HIIE led to an increase in B-lines at altitude after subacute exposure but not during acute exposure at equivalent simulated altitude. This may indicate pulmonary interstitial edema.

Exercise limitation of acetazolamide at altitude (3459 m).

OBJECTIVE: To assess the effect of acetazolamide (Az) on exercise performance during early acclimatization to altitude. METHODS: Az (250 mg twice daily) or placebo was administered for 3 days in a double-blind, randomized manner followed by a rapid ascent to 3459 m in the Italian Alps. Twenty healthy adults (age range, 18-67 years) were tested at 60% of sea-level peak power output for 15 minutes on a bicycle ergometer after 16 to 27 hours of altitude exposure. Exercise performance was measured in relation to peripheral oxygen saturations measured from pulse oximetry (Spo2), Lake Louise acute mountain sickness (AMS) score, and perceived difficulty. RESULTS: At altitude, resting Spo2 was higher in the Az group compared with placebo (P < .001). The highest AMS scores were in 4 of the placebo individuals with the lowest resting Spo2 (P < .05). During the exercise test, Spo2 fell in all but 1 subject (P < .001) and was reduced more in the Az group (P < .01). Four Az and 1 placebo subject were unable to complete the exercise test; 4 of these 5 had the largest fall in Spo2. The perception of exercise difficulty was higher in the Az subjects compared with those taking the placebo (P < .01). There was an age relationship with exercise limitation; 4 of the 9 older than 50 years failed to complete the test whereas only 1 of 11 younger than 50 years failed, and there were no failures in the 6 younger than 30 years (P < .05). CONCLUSIONS: In this study group, and despite higher resting Spo2, Az may have compromised exercise at 3459 m altitude during early acclimatization, particularly in older subjects.

Improving sleep at altitude: a comparison of therapies.

OBJECTIVE: This study aimed to compare 3 treatment modalities during sleep at an altitude of 5300 m to identify strategies for reducing the incidence of periodic breathing at high altitude. METHODS: Fifteen trekkers, with identical ascent profiles and no signs or symptoms of altitude illness, served as subjects. All study participants arrived at 5300 m after a gradual ascent from 1300 m. On their second night at 5300 m, subjects were randomly assigned (with a computer-based random assignment procedure) to 1 of 4 different treatment groups: control (n = 4); 1 L/min O(2) via a demand system during sleep (n = 3); 1 L/min O(2)/CO(2) mix (1.5% CO(2)) via a demand system during sleep (n = 4); or 125 mg acetazolamide 30 minutes before bedtime (n = 4). Heart rate, respiration rate, blood oxygen saturation, tidal volume, minute volume, and apnea hypopnea index were measured. RESULTS: Upon comparing the 4 groups, there were no statistically significant differences between the variables. One-way analysis of variance indicated a trend toward statistical significance for SaO(2) between groups (F = 2.9, P = .08), and Tukey Honestly Significant Difference (HSD) post hoc tests indicated a trend in the SaO(2) difference between the 1 L/min oxygen and control groups (P = .07). While 1-way analysis of variance suggested no difference for respiratory rate between groups (F = 2.5, P = .1), Tukey HSD indicated a trend in statistical difference of the respiratory rate between 1 L/min O(2) and 1 L/min O(2)/CO(2) mixture (P = .08). CONCLUSIONS: These statistical trends found between control and treatment groups indicate that further study is warranted.

Cerebral artery dilatation maintains cerebral oxygenation at extreme altitude and in acute hypoxia--an ultrasound and MRI study.

Transcranial Doppler is a widely used noninvasive technique for assessing cerebral artery blood flow. All previous high altitude studies assessing cerebral blood flow (CBF) in the field that have used Doppler to measure arterial blood velocity have assumed vessel diameter to not alter. Here, we report two studies that demonstrate this is not the case. First, we report the highest recorded study of CBF (7,950 m on Everest) and demonstrate that above 5,300 m, middle cerebral artery (MCA) diameter increases (n=24 at 5,300 m, 14 at 6,400 m, and 5 at 7,950 m). Mean MCA diameter at sea level was 5.30 mm, at 5,300 m was 5.23 mm, at 6,400 m was 6.66 mm, and at 7,950 m was 9.34 mm (P<0.001 for change between 5,300 and 7,950 m). The dilatation at 7,950 m reversed with oxygen. Second, we confirm this dilatation by demonstrating the same effect (and correlating it with ultrasound) during hypoxia (FiO(2)=12% for 3 hours) in a 3-T magnetic resonance imaging study at sea level (n=7). From these results, we conclude that it cannot be assumed that cerebral artery diameter is constant, especially during alterations of inspired oxygen partial pressure, and that transcranial 2D ultrasound is a technique that can be used at the bedside or in the remote setting to assess MCA caliber.