Despite calls for more interprofessional and intraprofessional team-based approaches in healthcare, we lack sufficient understanding of how this happens in the context of patient care teams. This multi-perspective, team-based interview study examined how medical teams negotiated collaborative tensions. From 2011 to 2013, 50 patients across five sites in three Canadian provinces were interviewed about their care experiences and were asked to identify members of their health care teams. Patient-identified team members were subsequently interviewed to form 50 "Team Sampling Units" (TSUs), consisting of 209 interviews with patients, caregivers and healthcare providers. Results are gathered from a focused analysis of 13 TSUs where intraprofessional collaborative tensions involved treating fluid overload, or edema, a common HF symptom. Drawing on actor-network theory (ANT), the analysis focused on intraprofessional collaboration between specialty care teams in cardiology and nephrology. The study found that despite a shared narrative of common purpose between cardiology teams and nephrology teams, fluid management tools and techniques formed sites of collaborative tension. In particular, care activities involved asynchronous clinical interpretations, geographically distributed specialist care, fragmented forms of communication, and uncertainty due to clinical complexity. Teams 'disentangled' fluid in order to focus on its physiological function and mobilisation. Teams also used distinct 'framings' of fluid management that created perceived collaborative tensions. This study advances collaborative entanglement as a conceptual framework for understanding, teaching, and potentially ameliorating some of the tensions that manifest during intraprofessional care for patients with complex, chronic disease.

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Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (∆CVRi/∆T)/∆BP]. The BHD demonstrated slower RoR than controls ( P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls ( P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls ( P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.

Changes in vascular resistance and vascular compliance contribute to the regulation of cerebral perfusion. While changes in vascular resistance are known to be mediated by vasodilatation, the mechanisms contributing to changes in vascular compliance are complex. In particular, whether vasodilatation affects compliance of the vasculature within the cranium remains unknown. Therefore, the present study examined the impact of two vasodilatation pathways on cerebrovascular compliance in humans. Fifteen young, healthy adults (26 ± 5 years, seven females) completed two protocols: (i) sublingual sodium nitroglycerin (SNG; 0.4 mg) and (ii) hypercapnia(5-6% carbon dioxide gas mixture for 4 min). Blood pressure waveforms (finger photoplethysmography) and middle cerebral artery blood velocity waveforms (transcranial Doppler ultrasound) were input into a modified Windkessel model and an index of cerebrovascular compliance (Ci) was calculated. During the SNG protocol, Ci decreased 24 ± 17% from baseline ((5.0 ± 2.3) × 10 -4 cm s -1 mmHg -1 ) to minute 10 ((3.6 ± 1.2) × 10 -4 cm s -1 mmHg -1 ; P = 0.009). During the hypercapnia protocol, Ci decreased 28 ± 9% from baseline ((4.4 ± 1.9) × 10 -4 cm s -1 mmHg -1 ) to minute 4 ((3.1 ± 1.4) × 10 -4 cm s -1 mmHg -1 ; P < 0.001). Cerebral vasodilatory stimuli induced by nitric oxide and carbon dioxide mechanisms reduced compliance of the cerebral vascular bed by approximately 26% from supine baseline values.