Willmar, MN, United States
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Mansukhani M.P.,Affiliated Communities Medical Center | Kolla B.P.,Affiliated Communities Medical Center | Olson E.J.,Center for Sleep Medicine | Olson E.J.,Mayo Medical School | And 4 more authors.
Expert Review of Medical Devices | Year: 2014

For most patients with obstructive sleep apnea syndrome (OSA), continuous positive airway pressure (CPAP) is an effective therapy. However, for a subset of individuals, CPAP is either not effective or is poorly tolerated. Bilevel positive airway pressure (BPAP) is potentially capable of treating OSA at a lower mean pressure than CPAP and can help augment ventilation via pressure support. This review summarizes the evidence for the use of BPAP in spontaneous mode in the initial treatment of patients with OSA and in those who are poorly compliant with CPAP therapy. It also examines evidence regarding use of BPAP in OSA with associated hypoventilation, such as in chronic obstructive pulmonary disease or severe obesity. Finally, current clinical guidelines that help determine which patients would be candidates for a BPAP device and how to manually titrate BPAP to determine the optimal settings to be prescribed are also discussed. © Informa UK, Ltd.


Mansukhani M.P.,Affiliated Communities Medical Center | Kara T.,St Annes University Hospital Brno | Kara T.,Mayo Medical School | Caples S.M.,Center for Sleep Medicine | Somers V.K.,Mayo Medical School
Current Hypertension Reports | Year: 2014

Obstructive sleep apnea (OSA) and hypertension are closely linked conditions. Disordered breathing events in OSA are characterized by increasing efforts against an occluded airway while asleep, resulting in a marked sympathetic response. This is predominantly due to hypoxemia activating the chemoreflexes, resulting in reflex increases in sympathetic neural outflow. In addition, apnea – and the consequent lack of inhibition of the sympathetic system that occurs with lung inflation during normal breathing – potentiates central sympathetic outflow. Sympathetic activation persists into the daytime, and is thought to contribute to hypertension and other adverse cardiovascular outcomes. This review discusses chemoreflex physiology and sympathetic modulation during normal sleep, as well as the sympathetic dysregulation seen in OSA, its extension into wakefulness, and changes after treatment. Evidence supporting the role of the peripheral chemoreflex in the sympathetic dysregulation seen in OSA, including in the context of comorbid obesity, metabolic syndrome, and systemic hypertension, is reviewed. Finally, alterations in cardiovascular variability and other potential mechanisms that may play a role in the autonomic imbalance in OSA are also discussed. © 2014, Springer Science+Business Media New York.


Mansukhani M.P.,Affiliated Communities Medical Center | Kolla B.P.,Affiliated Communities Medical Center | Ramar K.,Rochester College
Sleep Medicine Clinics | Year: 2014

Although current evidence suggests reasonable treatment of CSAS with PAP therapy, further long-term studies are required to address the effects on hospital admission rates, morbidity, and mortality. Also, additional studies comparing the relative cost-effectiveness, risks, and benefits of various treatment modalities are needed. More research on multimodality titration polysomnograms that use a different device when the previous one is unsuccessful may eventually help reduce testing time and health care costs. Complex sleep apnea, the persistence or worsening of central sleep disordered breathing events on PAP in a patient with predominantly obstructive sleep apnea, was not addressed separately in the ICSD-2 or AASM practice parameters, but is a condition that is being increasingly encountered in clinical practice. Research is urgently desired to determine the need for and efficacy of treatment options for complex sleep apnea, particularly in the long term. At present, there is a paucity of literature on pharmacologic treatments for CSAS, especially CSAS not caused by CHF. Further studies are needed to evaluate the long-term harms and benefits of these treatments as well as new therapies such as exercise therapy and novel ventilation devices. © 2014 Elsevier Inc. All rights reserved.


Mansukhani M.P.,Affiliated Communities Medical Center | Kara T.,Affiliated Communities Medical Center | Caples S.M.,Affiliated Communities Medical Center | Somers V.K.,Affiliated Communities Medical Center
Current hypertension reports | Year: 2014

Obstructive sleep apnea (OSA) and hypertension are closely linked conditions. Disordered breathing events in OSA are characterized by increasing efforts against an occluded airway while asleep, resulting in a marked sympathetic response. This is predominantly due to hypoxemia activating the chemoreflexes, resulting in reflex increases in sympathetic neural outflow. In addition, apnea - and the consequent lack of inhibition of the sympathetic system that occurs with lung inflation during normal breathing - potentiates central sympathetic outflow. Sympathetic activation persists into the daytime, and is thought to contribute to hypertension and other adverse cardiovascular outcomes. This review discusses chemoreflex physiology and sympathetic modulation during normal sleep, as well as the sympathetic dysregulation seen in OSA, its extension into wakefulness, and changes after treatment. Evidence supporting the role of the peripheral chemoreflex in the sympathetic dysregulation seen in OSA, including in the context of comorbid obesity, metabolic syndrome, and systemic hypertension, is reviewed. Finally, alterations in cardiovascular variability and other potential mechanisms that may play a role in the autonomic imbalance in OSA are also discussed.


Mansukhani M.P.,Affiliated Communities Medical Center | Wang S.,Mayo Medical School | Somers V.K.,Mayo Medical School
Experimental Physiology | Year: 2015

New Findings: What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho-inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study. © 2014 The Physiological Society.


PubMed | Affiliated Communities Medical Center
Type: Journal Article | Journal: Experimental physiology | Year: 2015

What is the topic of this review? This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. What advances does it highlight? Chemoreflex mechanisms are thought to contribute significantly to the pathophysiology and adverse outcomes seen in sleep apnoea. Clinical implications of altered chemoreflex function in sleep apnoea from recent studies in humans, including cardiac arrhythmias, coronary artery disease, systolic/diastolic heart failure and sudden cardiac death are highlighted. Activation of the chemoreflex in response to hypoxaemia results in an increase in sympathetic neural outflow. This process is predominantly mediated by the peripheral chemoreceptors in the carotid bodies and is potentiated by the absence of the sympatho-inhibitory influence of ventilation during apnoea, as is seen in patients with sleep apnoea. In these patients, repetitive nocturnal hypoxaemia and apnoea elicit sympathetic activation, which may persist into wakefulness and is thought to contribute to the development of systemic hypertension and cardiac and vascular dysfunction. Chemoreflex activation could possibly lead to adverse cardiovascular outcomes, such as nocturnal myocardial infarction, systolic and/or diastolic heart failure, cardiac arrhythmias and sudden death in patients with sleep apnoea. This review summarizes chemoreflex physiology in health and disease, with specific focus on chemoreflex-mediated pathophysiology in obstructive and central sleep apnoea. Measurement of the chemoreflex response may serve as a potential avenue for individualized screening for cardiovascular disease. Whether modulation of this response in sleep apnoea may aid in the prevention and treatment of adverse cardiovascular consequences will require further study.

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