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Abstract Disclosure: L. Kattamuri: None. S. Duvvuru: None. R. Desai: None. M. Rajachandran: None. Background: Chronic suppression of the HPA axis due to prolonged use of exogenous steroids can blunt the physiological glucocorticoid response when abruptly discontinued during periods of illness or stress. This can lead to tertiary adrenal insufficiency (TAI), which may present as unexplained vasopressor-resistant shock in critical care patients. Clinical Case: 50-year-old female with a history of breast cancer, diabetes, hypertension, and chronic joint pain was admitted for debridement of left submandibular abscess. Her hospital course was complicated by a right upper extremity DVT recanalized with catheter-directed thrombolysis and balloon angioplasty, and by persistent hypotension with mean arterial pressure (MAP) of 40-50mmHg, refractory to standard fluid resuscitation and vasopressor therapy (epinephrine, norepinephrine and vasopressin). Patient was empirically treated with broad-spectrum antibiotics for possible septic shock though blood bacterial and fungal cultures were sterile. No signs of hemorrhagic shock were noted. Transthoracic echocardiogram revealed ejection fraction of 65-70%, inferior vena cava and tricuspid jet velocity (226.5 cm/sec) were normal. Right heart catheterization (RHC) to assess the etiology of the hypotension was offered but declined by the family. Further history from family members revealed that the patient had been taking “Ardosons,” an over-the-counter pill from Mexico containing indomethacin, methocarbamol and 0.75 mg of betamethasone, twice daily for several years. While indomethacin use was documented, the Betamethasone component was not previously known. She received treatment with intravenous glucocorticoids for TAI with improvement in MAP (65-70 mmHg). Despite achieving hemodynamic stability with minimal vasopressor support, she developed progressive multi-organ failure. The patient subsequently expired after the family withdrew supportive care. Conclusion: This case demonstrates the critical value of a detailed history in patient care. Careful review of the patient’s medications was of inestimable importance in this case. Physicians should have a low threshold for diagnosis of TAI in critically ill patients with vasopressor-resistant unexplained hypotension. RHC, which was declined in this case, may have been of value for the evaluation and optimization of hemodynamics, identifying the precise etiology of the hypotension and guiding therapy in this critically ill patient. Presentation: Saturday, July 12, 2025

Orthostatic hypotension is an unusually large decrease in blood pressure on standing that increases the risk of adverse outcomes even when asymptomatic. Improvements in haemodynamic profiling with continuous blood pressure measurements have uncovered four major subtypes: initial orthostatic hypotension, delayed blood pressure recovery, classic orthostatic hypotension, and delayed orthostatic hypotension. Clinical presentations are varied and range from cognitive slowing with hypotensive unawareness or unexplained falls to classic presyncope and syncope. Establishing whether symptoms are due to orthostatic hypotension requires careful history taking, a thorough physical examination, and supine and upright blood pressure measurements. Management and prognosis vary according to the underlying cause, with the main distinction being whether orthostatic hypotension is neurogenic or non-neurogenic. Neurogenic orthostatic hypotension might be the earliest clinical manifestation of Parkinson's disease or related synucleinopathies, and often coincides with supine hypertension. The emerging variety of clinical presentations advocates a stepwise, individualised, and primarily non-pharmacological approach to the management of orthostatic hypotension. Such an approach could include the cessation of blood pressure lowering drugs, adoption of lifestyle measures (eg, counterpressure manoeuvres), and treatment with pharmacological agents in selected cases.

Objectives: Hypotension is a common complication of spinal anesthesia. Imaging of inferior vena cava (IVC) and measurement of the IVC-collapsibility index (IVC-CI) by ultrasonography (USG) has been a widely used non-invasive, easy and reliable method for measurement of the fluid imbalance. In the present study, we aimed to investigate the predictive ability of the maximum IVC diameter (dIVCmax) and IVC-CI for hypotension after spinal anesthesia. Methods: The study was designed as prospective and observational. One hundred thirty-two patients aged 18-75 years with ASA I-II underwent inguinal hernia surgery with spinal anesthesia and recruited to the study. Maximum and minimum (dIVCmin) IVC diameters were measured. IVC-CI (%) was quantified according to the formula of [(dIVCmax - dIVCmin)/dIVKmax] × 100%. Results: The patients were grouped as hypotensive and non-hypotensive. In fifty-seven patients of 120 cases (47.5%), hypotension has emerged following spinal anesthesia. No significant differences in dIVCmax and IVC-CI were recorded between the study groups (p > 0.05). There were significant inverse correlation between age and IVC-CI. Significant positive correlation between the lowest values of the systolic arterial pressure, diastolic arterial pressure, mean arterial pressure and IVC-CI and significant positive correlation between dIVCmax and diastolic blood pressure, maximum and minimum values of the mean arterial pressure. Conclusions: We found that dIVCmax and IVC-CI values measured before spinal anesthesia were not sufficient parameters enough to predict hypotension after spinal anesthesia. Further studies investigating the IVC measurements under spinal anesthesia together with dynamic hemodynamic monitorization modalities are needed.

For this reason, women should not drink alcohol when taking flibanserin; about one in six persons taking this combination will experience clinically significant hypotension and syncope.1 Flibanserin should not be taken by women with hepatic impairment or women who are also taking moderate or strong cytochrome P450 3A4 inhibitors such as azole antifungals or protease inhibitors, which may increase serum levels.2 Flibanserin should be taken at night because adverse effects are more prominent when it is taken in the morning. About one in eight patients will discontinue treatment because of adverse effects.1 EFFECTIVENESS Flibanserin has been evaluated in three randomized, double-blind, placebo-controlled studies of 2,375 premenopausal women with acquired, generalized HSDD, defined as low sexual desire causing marked distress or interpersonal difficulties.2 Women in monogamous, heterosexual relationships with no known cause of HSDD reported an average increase of 1.6 to 2.5 additional satisfying sexual events per month with treatment, from a baseline of 2.5 to 3.0 per month. Certification is required of physicians before prescribing, and prescriptions can only be dispensed by pharmacists who have completed this training as well.3 Bottom Line Although flibanserin results in a modest improvement in the number of satisfying sexual events (approximately one more per month vs. placebo), it does not improve other measures, is considerably expensive, and has significant adverse effects.

Neurogenic orthostatic hypotension (nOH) is common in patients with neurodegenerative disorders such as Parkinson’s disease, multiple system atrophy, pure autonomic failure, dementia with Lewy bodies, and peripheral neuropathies including amyloid or diabetic neuropathy. Due to the frequency of nOH in the aging population, clinicians need to be well informed about its diagnosis and management. To date, studies of nOH have used different outcome measures and various methods of diagnosis, thereby preventing the generation of evidence-based guidelines to direct clinicians towards ‘best practices’ when treating patients with nOH and associated supine hypertension. To address these issues, the American Autonomic Society and the National Parkinson Foundation initiated a project to develop a statement of recommendations beginning with a consensus panel meeting in Boston on November 7, 2015, with continued communications and contributions to the recommendations through October of 2016. This paper summarizes the panel members’ discussions held during the initial meeting along with continued deliberations among the panel members and provides essential recommendations based upon best available evidence as well as expert opinion for the (1) screening, (2) diagnosis, (3) treatment of nOH, and (4) diagnosis and treatment of associated supine hypertension.

Abstract Hypotension is a leading cause of age-related cognitive impairment. The available literature evidences that vascular factors are associated with dementia and that hypotension alters cerebral perfusion flow and can aggravate the neurodegeneration of Alzheimer’s disease (AD). Despite the discovery of biomarkers and the recent progress made in neurovascular biology, epidemiology, and brain imaging, some key issues remain largely unresolved: the potential mechanisms underlying the neural deterioration observed in AD, the effect of cerebrovascular alterations on cognitive deficits, and the positive effects of hypotension treatment on cognition. Therefore, further well-designed studies are needed to unravel the potential association between hypotension and cognitive dysfunction and reveal the potential benefits of hypotension treatment for AD patients. Here, we review the current epidemiological, pathobiological, and treatment-related literature on neurovascular changes and hypotension-related cognitive dysfunction and highlight the unsettled but imminent issues that warrant future research endeavors.

This trial comparing treatment strategies that emphasized the use of vasopressors or intravenous fluids for early treatment of sepsis-induced hypotension showed no difference in 90-day mortality before discharge home.

IntroductionRecent decades have heralded remarkable advances in heart failure (HF) pharmacotherapy. Consequently, defining digoxin’s role amongst the array of contemporary compounds is challenging. Associated debate is mired in divisive opinion and ambiguous data. The ESC lends a class IIb recommendation for digoxin’s use in HFrEF patients who remain symptomatic despite Optimal Medical Therapy (OMT) and class IIa for rate control in atrial fibrillation (AF), where 1st line agents are inadequate or contraindicated.PurposeThe DIG Trial demonstrated that digoxin reduced hospitalisations, but not mortality in HFrEF patients in sinus rhythm, underpinning current guidelines. Subsequent observational data is contradictory. Although digoxin prescription has diminished, recent HF trials reveal that 10–20% patients continue to receive it. This prompted us to examine its usage at a large HF unit.MethodsThis was a single centre, retrospective, observational study conducted at St. Michael’s HF Unit, Dublin. Patients were identified by scanning the unit’s database for active digoxin prescriptions, specifically for de novo prescriptions in 2021, along with pre-existing ones. The database provided information on demographics, HF status, medications, comorbidities, echo parameters, lab values and a detailed clinical summaries. Data was stored on a password-protected file on-site. Analysis in the form of descriptive statistics was performed on Stata IC software. Regarding missing data, complete case analysis was employed, as data was complete for >90% patients.Results236 active prescriptions for digoxin were identified, 66 of these being issued in 2021. 219 patients were included in the final analysis. This was an elderly, symptomatic (88% ≥NYHAII) and comorbid population. 22.4% had experienced decompensated HF in the preceding year. 92.7% had AF. Correspondingly, rate control was the primary indication for digoxin in 84.5% of patients, with three distinct contexts: an adjunct where beta blocker (BB)/calcium channel blocker (CCB) was maximally dosed (50.7%); where hypotension precluded higher BB/CCB doses (16.9%); where contraindications/intolerances to BB/CCB existed (16.9%). In the remainder (32/219, 14.6%), the main rationale for prescription was HF. In this setting, digoxin was used to facilitate OMT in hypotension (7.3%), to tackle persistent symptoms in stable patients (4.1%) and in cases of unstable deterioration (3.2%). Amongst these 32 patients, 34.4% did not have AF and 25% had RV impairment (table 1). Improvement occurred in more than half of symptomatic patients.Abstract 54 Table 1Data analysisDiscussionWe find that digoxin is chiefly employed as an adjunctive therapy for rate control in AF. However, this study illustrates that a subset of patients with advanced HFrEF may continue to benefit from this unique drug. The limitations of this study are its retrospective nature with inherent associated biases and restriction to a single centre, where prescription bias could arise.

Orthostatic hypotension (OH) is an abnormal blood pressure response to standing, which is associated with an increased risk of adverse outcomes such as syncope, falls, cognitive impairment, and mortality. Medical therapy is one the most common causes of OH, since numerous cardiovascular and psychoactive medications may interfere with the blood pressure response to standing, leading to drug-related OH. Additionally, hypotensive medications frequently overlap with other OH risk factors (e.g., advanced age, neurogenic autonomic dysfunction, and comorbidities), thus increasing the risk of symptoms and complications. Consequently, a medication review is recommended as a first-line approach in the diagnostic and therapeutic work-up of OH, with a view to minimizing the risk of drug-related orthostatic blood pressure impairment. If symptoms persist after the review of hypotensive medications, despite adherence to non-pharmacological interventions, specific drug treatment for OH can be considered. In this narrative review we present an overview of drugs acting on the cardiovascular and central nervous system that may potentially impair the orthostatic blood pressure response and we provide practical suggestions that may be helpful to guide medical therapy optimization in patients with OH. In addition, we summarize the available strategies for drug treatment of OH in patients with persistent symptoms despite non-pharmacological interventions.