Menstrual phase and the vascular response to acute resistance exercise

Abstract

Introduction

Aerobic exercise has a favorable effect on systemic vascular function, reducing both central (large elastic artery) and peripheral (smaller muscular artery) stiffness. The effects of resistance exercise (RE) on arterial stiffness are more complex. Acute RE increases central artery stiffness while decreasing peripheral stiffness. To date, the majority of studies have been performed in predominantly male participants.

Purpose

To examine the effect of acute RE on central and peripheral arterial stiffnesses in women, a secondary purpose was to explore the influence of cyclic changes in estrogen status across the menstrual cycle on the arterial response to acute RE.

Methods

18 healthy women [28 ± 7 years, body mass index (BMI) 22.6 ± 2.9 kg/m²] completed an acute RE bout during the early follicular and the early luteal phase of their menstrual cycle. Salivary 17β-Estradiol concentration was measured during each phase, using a passive drool technique. Pulse-wave velocity (PWV) was obtained from the carotid–femoral and carotid–radial pulse sites to measure central and peripheral stiffness, respectively, using applanation tonometry. PWV was measured at rest, immediately, 10, 20, and 30 min post-RE.

Results

17β-Estradiol concentration was significantly lower in the early follicular vs. the early luteal phase of the menstrual cycle (1.78 ± 0.51 vs. 2.40 ± 0.26 pg/ml, p = 0.01). Central PWV significantly increased (p < 0.05) and peripheral PWV significantly decreased (p < 0.05) post-RE in both the early follicular and early luteal phases. No phase-by-time interaction was detected for either vascular segment (p > 0.05).

Conclusion

Women experience increases in central arterial stiffness and reductions in peripheral arterial stiffness following acute RE. Menstrual cycle phase may not influence changes in arterial stiffness in response to acute RE.

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Post-Cardiac Arrest Management: Time to Cool It on Cooling?

No abstract available

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Targeted Temperature Management After Cardiac Arrest: Systematic Review and Meta-analyses

BACKGROUND: Targeted temperature management (TTM) with therapeutic hypothermia is an integral component of postarrest care for survivors. However, recent randomized controlled trials (RCTs) have failed to demonstrate the benefit of TTM on clinical outcomes. We sought to determine if the pooled data from available RCTs support the use of prehospital and/or in-hospital TTM after cardiac arrest. METHODS: A comprehensive search of SCOPUS, Elsevier's abstract and citation database of peer-reviewed literature, from 1966 to November 2016 was performed using predefined criteria. Therapeutic hypothermia was defined as any strategy that aimed to cool post–cardiac arrest survivors to a temperature ≤34°C. Normothermia was temperature of ≥36°C. We compared mortality and neurologic outcomes in patients by categorizing the studies into 2 groups: (1) hypothermia versus normothermia and (2) prehospital hypothermia versus in-hospital hypothermia using standard meta-analytic methods. A random effects modeling was utilized to estimate comparative risk ratios (RR) and 95% confidence intervals (CIs). RESULTS: The hypothermia and normothermia strategies were compared in 5 RCTs with 1389 patients, whereas prehospital hypothermia and in-hospital hypothermia were compared in 6 RCTs with 3393 patients. We observed no difference in mortality (RR, 0.88; 95% CI, 0.73–1.05) or neurologic outcomes (RR, 1.26; 95% CI, 0.92–1.72) between the hypothermia and normothermia strategies. Similarly, no difference was observed in mortality (RR, 1.00; 95% CI, 0.97–1.03) or neurologic outcome (RR, 0.96; 95% CI, 0.85–1.08) between the prehospital hypothermia versus in-hospital hypothermia strategies. CONCLUSIONS: Our results suggest that TTM with therapeutic hypothermia may not improve mortality or neurologic outcomes in postarrest survivors. Using therapeutic hypothermia as a standard of care strategy of postarrest care in survivors may need to be reevaluated.

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Perioperative Cardiac Arrest: Focus on Malignant Hyperthermia (MH)

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Perioperative Cardiac Arrest: Focus on Local Anesthetic Systemic Toxicity (LAST)

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Perioperative Cardiac Arrest: Focus on Anaphylaxis

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Cardiac Arrest in the Operating Room: Part 2—Special Situations in the Perioperative Period

As noted in part 1 of this series, periprocedural cardiac arrest (PPCA) can differ greatly in etiology and treatment from what is described by the American Heart Association advanced cardiac life support algorithms, which were largely developed for use in out-of-hospital cardiac arrest and in-hospital cardiac arrest outside of the perioperative space. Specifically, there are several life-threatening causes of PPCA of which the management should be within the skill set of all anesthesiologists. However, previous research has demonstrated that continued review and training in the management of these scenarios is greatly needed and is also associated with improved delivery of care and outcomes during PPCA. There is a growing body of literature describing the incidence, causes, treatment, and outcomes of common causes of PPCA (eg, malignant hyperthermia, massive trauma, and local anesthetic systemic toxicity) and the need for a better awareness of these topics within the anesthesiology community at large. As noted in part 1 of this series, these events are always witnessed by a member of the perioperative team, frequently anticipated, and involve rescuer–providers with knowledge of the patient and the procedure they are undergoing or have had. Formulation of an appropriate differential diagnosis and rapid application of targeted interventions are critical for good patient outcome. Resuscitation algorithms that include the evaluation and management of common causes leading to cardiac in the perioperative setting are presented. Practicing anesthesiologists need a working knowledge of these algorithms to maximize good outcomes.

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