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Sleep disorders and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Obesity has been shown to have a causal association with sleep apnea (38,39). Pregnancy is associated with weight gain, which may exceed 20% or more by term (40). A recently published study suggests that the prevalence of pre-gravid obesity (defined as BMI>29 kg/m2) in the United States has increased significantly from 13% immediately before pregnancy in 1993 to 22% immediately before pregnancy in 2002/2003 (41). Rapid gain in weight is known to be associated with a higher incidence of obstructive sleep apnea (OSA). It has not, however, been established by sleep studies whether excessive weight gain during pregnancy causes sleep apnea. In 1992, Feinsilver et al. (42) reviewed the physiologic adaptations in pregnancy and suggested an increased likelihood of sleep-disordered breathing in pregnant women. Upper airway changes, as described earlier, would predispose the patient to snoring and OSA. In addition, the respiratory alkalosis resulting from augmented minute ventilation and the enhanced sensitivity of the respiratory center to CO2, as occurs in pregnancy, could predispose to central sleep apnea. On the other hand, there are physiologic adaptations, such as increased minute ventilation and pharyngeal muscle tone, due to elevated progesterone levels during pregnancy (43), which may be protective against sleep-disordered breathing. There is reduction in REM sleep (22) during pregnancy, which may protect against sleep apnea. Additionally, in late pregnancy, there is a greater tendency for women to sleep on their sides, thereby reducing the tendency to manifest severe sleep apnea.
Symptom Control in Hospice-State of the Art
Published in Inge B. Corless, Zelda Foster, The Hospice Heritage: Celebrating Our Future, 2020
J. Cameron Muir, Lisa M. Krammer, Jacqueline R. Cameron, Charles F. von Gunten
The pathophysiology of dyspnea is not fully understood (see Figure 2). Either separately or in combination the stimulation of cortical centers (anxiety or somatization), lung mechanoreceptors (embolism, edema, other) and lung chemoreceptors (abnormal serum gases) can trigger the respiratory center of the medulla to affect both respiratory drive and the sensation of breathlessness.29
Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Paralysis of the respiratory center is thought by some authors to be at least a contributory factor. After toxin exposure, efferent inspiratory fibers of the brainstem are not responsive to normal stimuli (Ado and Abrosimov, 1964). One study using parenteral toxin shows depression of cortical electrical activity in monkeys with otherwise stable vital signs just before respiratory failure and may suggest a direct central nervous system toxicity of botulinal toxins (Polley et al., 1965).
Respiratory disturbances in fibromyalgia: A systematic review and meta-analysis of case control studies
Published in Expert Review of Respiratory Medicine, 2021
Araceli Ortiz-Rubio, Irene Torres-Sánchez, Irene Cabrera-Martos, Laura López-López, Janet Rodríguez-Torres, María Granados-Santiago, Marie Carmen Valenza
Respiration is a complex function involving the absolute and strict cooperation of muscular, skeletal, and nervous systems [8]. It is rarely completely regular, except in deep non-REM sleep and under anesthesia [11]. Moderate instability reflects a mechanism that is termed dynamic homeostasis. Respiratory function can be influenced by biochemical, biomechanical, and psychological factors, showing an open loop system, vulnerable to adaptations [12–14]. The increased levels of baseline respiratory instability are often associated with pathophysiology either at the level of the sensors of the regulation system (such as hypersensitivity or hyposensitivity of peripheral and central CO2 sensors or proprioceptive afferents) or at the effectors (such as stiffness in the diaphragm or intercostals or inhibited nerve transmission to them) [15]. Additionally, there is a rich network for cortical and subcortical projections to the brain stem (the respiratory center) that can likely influence movement to moment breathing [16].
Mouth occlusion pressure at 100ms (P0.1) as a respiratory biomarker in amyotrophic lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2021
Susana Pinto, Michael Swash, Mamede De Carvalho
Older female ALS patients with bulbar-onset had abnormally high values of P0.1, greater than 147% of predicted, and these were associated with a lower functional score, including the respiratory subscore (SG1). In these patients, a significant reduction of all respiratory function tests, including FVC, MEP and MIP, and MeanPhrenAmpl, was identified and consistent with weakness of the respiratory muscles, including the diaphragm and the expiratory muscles, and thus translating into marked involvement of respiratory function. The resulting increase of pCO2 in these patients probably drives the activation of the respiratory center. In healthy subjects, augmentation of the central respiratory drive is normally seen under stressful conditions (21,22). In our patients, P0.1/MIP was particularly increased in SG1 population (7.92 ± 4.62), representing a compensatory inverse relation between inspiratory power and central respiratory drive. Female gender, greater age, bulbar-onset, and diaphragmatic weakness were independent predictors for a higher P0.1/MIP ratio. Lower bulbar functional abnormality as quantified by the ALSFRSb was not an independent predictor for higher %P0.1, suggesting that this subsection of the ALSFRS has low sensitivity.
Dopamine β hydroxylase as a potential drug target to combat hypertension
Published in Expert Opinion on Investigational Drugs, 2020
Sanjay Kumar Dey, Manisha Saini, Pankaj Prabhakar, Suman Kundu
The arterial baro- and chemo-reflexes are negative feedback mechanisms to maintain the beat-to-beat homeostasis in ABP [21]. Sudden change in ABP is detected by baroreceptors in the circulatory walls of the carotid sinus and aortic arch. These afferent baroreceptors then induce a sympatho-inhibitory reflex, known as baroreflex from carotid sinus and aorta using glossopharyngeal and vagus nerves, respectively, toward NTS and normalizes BP by adjusting cardiac output and vascular resistance [22–24]. In case of chronic hypertension, baroreceptors loses sensitivity and remains unable to prevent sudden variation in BP [22–24]. On the other hand, chemoreflexes are induced by the chemoreceptors which sense the changes in arterial PO2, PCO2, and pH at their distinct vassal locations in the carotid bodies and aortic bodies [18,23]. Respiratory center in the brain is stimulated by chemoreflex due to decrease in PO2 and pH or increase in PCO2, which in turn induces the sympathetic outflow. In obstructive sleep apnea patients, repeated stimulation of chemoreflex by chronic hypoxia and hypercapnia increases the chance of hypertension [21,25].