Perioperative Point-of-Care Ultrasound Use by Anesthesiologists.

Point-of-Care ultrasound (POCUS) is the bedside utilization of ultrasound, in real-time, to aid in the diagnosis and treatment of patients. Image acquisition from POCUS utilization by anesthesiologists involves the assessment of multiple organs in different perioperative situations. POCUS can be utilized to enhance clinical decision-making in a variety of perioperative situations due to its ability to assess endotracheal tube placement, cardiac function, pulmonary function, aspiration risk, hemodynamics, vascular access, and nerve visualization for regional procedures. The mounting clinical evidence for the value of POCUS in perioperative settings, its growing affordability, and its low associated risks are responsible for the nationwide movement across many anesthesiology residency programs to increase the focus on perioperative ultrasound training. The purpose of this review is to present to current anesthesiologists and anesthesiology trainees, a broad discussion regarding the diverse utility and importance of POCUS in perioperative settings.

Vascular-Cognitive Impairment following High-Thoracic Spinal Cord Injury Is Associated with Structural and Functional Maladaptations in Cerebrovasculature.

Individuals living with chronic spinal cord injury (SCI) often exhibit impairments in cognitive function, which impede their rehabilitation and transition into the community. Although a number of clinical studies have demonstrated the impact of impaired cardiovascular control on cognitive impairment, the mechanistic understanding of this deleterious relationship is still lacking. The present study investigates whether chronic disruption of cardiovascular control following experimental SCI results in cerebrovascular decline and vascular cognitive impairment. Fourteen weeks following a high thoracic SCI (at the third thoracic segment), rats were subjected to a battery of in vivo and in vitro physiological assessments, cognitive-behavioral tests, and immunohistochemical approaches to investigate changes in cerebrovascular structure and function in the middle cerebral artery (MCA). We show that in the MCA of rats with SCI, there is a 55% (SCI vs. control: 13.4 ± 1.9% vs. 29.63 ± 2.8%, respectively) reduction in the maximal vasodilator response to carbachol, which is associated with reduced expression of endothelial marker cluster of differentiation 31 (CD31) and transient receptor potential cation channel 4 (TRPV 4) channels. Compared with controls, MCAs in rats with SCI were found to have 50% (SCI vs. control: 1.5 ± 0.2 vs. 1 ± 0.1 a.u., respectively) more collagen 1 in the media of vascular wall and 37% (SCI vs. control: 30.5 ± 2.9% vs. 42.0 ± 4.0%, respectively) less distensibility at physiological intraluminal pressure. Further, the cerebral blood flow (CBF) in the hippocampus was reduced by 32% in the SCI group (SCI vs. control: 44.3 ± 4.5 mL/100 g/min vs. 65.0 ± 7.2 mL/100 g/min, respectively) in association with impairment of short-term memory based on a novel object recognition test. There were no changes in the sympathetic innervation of the vasculature and passive structure in the SCI group. Chronic experimental SCI is associated with structural alterations and endothelial dysfunction in cerebral arteries that likely contribute to significantly reduced CBF and vascular cognitive impairment.

Is Technology for Orthostatic Hypotension Ready for Primetime?

Spinal cord injury (SCI) often results in the devastating loss of motor, sensory, and autonomic function. After SCI, the interruption of descending sympathoexcitatory pathways disrupts supraspinal control of blood pressure (BP). A common clinical consequence of cardiovascular dysfunction after SCI is orthostatic hypotension (OH), a debilitating condition characterized by rapid profound decreases in BP when assuming an upright posture. OH can result in a diverse array of insidious and pernicious health consequences. Acute effects of OH include decreased cardiac filling, cerebral hypoperfusion, and associated presyncopal symptoms such as lightheadedness and dizziness. Over the long term, repetitive exposure to OH is associated with a drastically increased prevalence of heart attack and stroke, which are leading causes of death in those with SCI. Current recommendations for managing BP after SCI primarily include pharmacologic interventions with prolonged time to effect. Because most episodes of OH occur in less than 3 minutes, this delay in action often renders most pharmacologic interventions ineffective. New innovative technologies such as epidural and transcutaneous spinal cord stimulation are being explored to solve this problem. It might be possible to electrically stimulate sympathetic circuitry caudal to the injury and elicit rapid modulation of BP to manage OH. This review describes autonomic control of the cardiovascular system before injury, resulting cardiovascular consequences after SCI such as OH, and the clinical assessment tools for evaluating autonomic dysfunction after SCI. In addition, current approaches for clinically managing OH are outlined, and new promising interventions are described for managing this condition.

Transient Hypertension after Spinal Cord Injury Leads to Cerebrovascular Endothelial Dysfunction and Fibrosis.

We aimed to create a clinically relevant pre-clinical model of transient hypertension, and then evaluate the pathophysiological cerebrovascular processes resulting from this novel stimulus, which has recently been epidemiologically linked to cerebrovascular disease. We first developed a clinically relevant model of transient hypertension, secondary to induced autonomic dysreflexia after spinal cord injury and demonstrated that in both patients and rats, this stimulus leads to drastic acute cerebral hyperperfusion. For this, iatrogenic urodynamic filling/penile vibrostimulation was completed while measuring beat-by-beat blood pressure and cerebral blood flow (CBF) in patients. We then developed a rodent model mimicking the clinical reality by performing colorectal distention (to induce autonomic dysreflexia) using pre-clinical beat-by-beat blood pressure and CBF assessments. We then performed colorectal distension in rats for four weeks (6x/day) to evaluate the long-term cerebrovascular consequences of transient hypertension. Outcome measures included middle cerebral artery endothelial function, remodeling, profibrosis and perivascular innervation; measured via pressure myography, immunohistochemistry, molecular biology, and magnetic resonance imaging. Our model demonstrates that chronic repetitive cerebral hyperperfusion secondary to transient hypertension because of autonomic dysreflexia: (1) impairs cerebrovascular endothelial function; (2) leads to profibrotic cerebrovascular stiffening characterized by reduced distensibility and increased collagen deposition; and (3) reduces perivascular sympathetic cerebrovascular innervation. These changes did not occur concurrent to hallmark cerebrovascular changes from chronic steady-state hypertension, such as hypertrophic inward remodeling, or reduced CBF. Chronic exposure to repetitive transient hypertension after spinal cord injury leads to diverse cerebrovascular impairment that appears to be unique pathophysiology compared with steady-state hypertension in non-spinal cord injured models.