Willadsencohen5723

Recent consensus guidelines highlight these and other knowledge gaps that are the focus of active research efforts. This chapter outlines important general principles to consider when initiating, titrating, and discontinuing mechanical ventilation in patients with acute neurologic injuries. Important disease-specific considerations are also reviewed where appropriate.In humans, several respiratory viruses can have neurologic implications affecting both central and peripheral nervous system. Neurologic manifestations can be linked to viral neurotropism and/or indirect effects of the infection due to endothelitis with vascular damage and ischemia, hypercoagulation state with thrombosis and hemorrhages, systemic inflammatory response, autoimmune reactions, and other damages. Among these respiratory viruses, recent and huge attention has been given to the coronaviruses, especially the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic started in 2020. Besides the common respiratory symptoms and the lung tropism of SARS-CoV-2 (COVID-19), neurologic manifestations are not rare and often present in the severe forms of the infection. The most common acute and subacute symptoms and signs include headache, fatigue, myalgia, anosmia, ageusia, sleep disturbances, whereas clinical syndromes include mainly encephalopathy, ischemic stroke, seizures, and autoimmune peripheral neuropathies. Although the pathogenetic mechanisms of COVID-19 in the various acute neurologic manifestations are partially understood, little is known about long-term consequences of the infection. These consequences concern both the so-called long-COVID (characterized by the persistence of neurological manifestations after the resolution of the acute viral phase), and the onset of new neurological symptoms that may be linked to the previous infection.The respiratory and the nervous systems are closely interconnected and are maintained in a fine balance. Central mechanisms maintain strict control of ventilation due to the high metabolic demands of brain which depends on a continuous supply of oxygenated blood along with glucose. Moreover, brain perfusion is highly sensitive to changes in the partial pressures of carbon dioxide and oxygen in blood, which in turn depend on respiratory function. selleck Ventilatory control is strictly monitored and regulated by the central nervous system through central and peripheral chemoreceptors, baroreceptors, the cardiovascular system, and the autonomic nervous system. Disruption in this delicate control of respiratory function can have subtle to devastating neurological effects as a result of ensuing hypoxia or hypercapnia. In addition, pulmonary circulation receives entire cardiac output and this may act as a conduit to transmit infections and also for metastasis of malignancies to brain resulting in neurological dysfunction. Furthermore, many neurological paraneoplastic syndromes can have underlying lung malignancies resulting in respiratory dysfunction. It is essential to understand the underlying mechanisms and the resulting manifestations in order to prevent and effectively manage the many neurological effects of respiratory dysfunction. This chapter explores the various neurological effects of respiratory dysfunction with focus on their pathophysiology, etiologies, clinical features and long-term neurological sequelae.Neuromuscular disorders frequently compromize pulmonary function and effective ventilation, and a thorough respiratory evaluation often can assist in diagnosis, risk assessment, and prognostication. Since many of these disorders can be progressive, serial assessments may be necessary to best define a trajectory of impairment or improvement with therapy. Patients with neuromuscular diseases may have few respiratory symptoms and limited signs of skeletal muscle weakness, but can have significant respiratory muscle weakness. A single testing modality may fail to elucidate true respiratory compromise, and often a combination of tests is recommended to fully evaluate these patients. Common tests performed in this population include measurement of flow rates, lung volumes, maximal pressures, and airways resistance. This review covers the major respiratory testing modalities available in the evaluation of these patients, emphasizing both the benefits and shortcomings of each approach. The majority of parameters are available in a standard pulmonary laboratory (flows, volumes, static pressures), although referral to a specialized center may be necessary to conclusively evaluate a given patient.Sleep disorders are prevalent in heart failure and include insomnia, poor sleep architecture, periodic limb movements and periodic breathing, and encompass both obstructive (OSA) and central sleep apnea (CSA). Polysomnographic studies show excess light sleep and poor sleep efficiency particularly in those with heart failure. Multiple studies of consecutive patients with heart failure show that about 50% of patients suffer from either OSA or CSA. While asleep, acute pathological consequences of apneas and hypopneas include altered blood gases, sleep fragmentation, and large negative swings in intrathoracic pressure. These pathological consequences are qualitatively similar in both types of sleep apnea, though worse in OSA than CSA. Sleep apnea results in oxidative stress, inflammation, and endothelial dysfunction, best documented in OSA. Multiple studies show that both OSA and CSA are associated with excess hospital readmissions and premature mortality. However, no randomized controlled trial (RCT) has been reported for OSA, but sensitivity analysis of two randomized controlled trials has concluded that use of positive airway pressure devices is associated with excess mortality in patients with heart failure and CSA. Phrenic nerve stimulation has shown improvement in sleep apnea events and daytime sleepiness; however, no randomized controlled trials have demonstrated improvement in survival in patients with heart failure. The correct identification and treatment of heart failure patients with sleep and breathing disorders could affect the long-term outcomes of these patients.Phrenic nerve injury results in paralysis of the diaphragm muscle, the primary generator of an inspiratory effort, as well as a stabilizing muscle involved in postural control and spinal alignment. Unilateral deficits often result in exertional dyspnea, orthopnea, and sleep-disordered breathing, whereas oxygen or ventilator dependency can occur with bilateral paralysis. Common etiologies of phrenic injuries include cervical trauma, iatrogenic injury in the neck or chest, and neuralgic amyotrophy. Many patients have no identifiable etiology and are considered to have idiopathic paralysis. Diagnostic evaluation requires radiographic and pulmonary function testing, as well as electrodiagnostic assessment to quantitate the nerve deficit and determine the extent of denervation atrophy. Treatment for symptomatic diaphragm paralysis has traditionally been limited. Medical therapies and nocturnal positive airway pressure may provide some benefit. Surgical repair of the nerve injury to restore functional diaphragmatic activity, termed phrenic nerve reconstruction, is a safe and effective alternative to static repositioning of the diaphragm (diaphragm plication), in properly selected patients. Phrenic nerve reconstruction has increasingly become a standard surgical treatment for diaphragm paralysis due to phrenic nerve injury. A multidisciplinary approach at specialty referral centers combining diagnostic evaluation, surgical treatment, and rehabilitation is required to achieve optimal long-term outcomes.In amyotrophic lateral sclerosis (ALS), Guillain-Barré syndrome (GBS), and neuromuscular junction disorders, three mechanisms may lead, singly or together, to respiratory emergencies and increase the disease burden and mortality (i) reduced strength of diaphragm and accessory muscles; (ii) oropharyngeal dysfunction with possible aspiration of saliva/bronchial secretions/drink/food; and (iii) inefficient cough due to weakness of abdominal muscles. Breathing deficits may occur at onset or more often along the chronic course of the disease. Symptoms and signs are dyspnea on minor exertion, orthopnea, nocturnal awakenings, excessive daytime sleepiness, fatigue, morning headache, poor concentration, and difficulty in clearing bronchial secretions. The "20/30/40 rule" has been proposed to early identify GBS patients at risk for respiratory failure. The mechanical in-exsufflator is a device that assists ALS patients in clearing bronchial secretions. Noninvasive ventilation is a safe and helpful support, especially in ALS, but has some contraindications. Myasthenic crisis is a clinical challenge and is associated with substantial morbidity including prolonged mechanical ventilation and 5%-12% mortality. Emergency room physicians and consultant pulmonologists and neurologists must know such respiratory risks, be able to recognize early signs, and treat properly.Spinal cord injury (SCI) often results in impaired respiratory function. Paresis or paralysis of inspiratory and expiratory muscles can lead to respiratory dysfunction depending on the level and severity of the injury, which can affect the management and care of SCI patients. Respiratory dysfunction after SCI is more severe in high cervical injuries, with vital capacity (VC) being an essential indicator of overall respiratory health. Respiratory complications include hypoventilation, a reduction in surfactant production, mucus plugging, atelectasis, and pneumonia. Respiratory management includes mechanical ventilation and tracheostomy in high cervical SCI, while noninvasive ventilation is more common in patients with lower cervical and thoracic injuries. Mechanical ventilation can negatively impact the function of the diaphragm and weaning should start as soon as possible. Patients can sometimes be weaned from mechanical ventilation with assistance of electrical stimulation of the phrenic nerve or the diaphragm. Respiratory muscle training regimens may also improve patients' inspiratory function following SCI. Despite the critical advances in preventing, diagnosing, and treating respiratory complications, they continue to significantly affect persons living with SCI. Additional studies of interventions to reduce respiratory complications are likely to further decrease the morbidity and mortality associated with these injuries.Neurodegenerative disorders are a diverse group of conditions caused by progressive degeneration of neurons resulting in cognitive, motor, sensory, and autonomic dysfunction, leading to severe disability and death. Pulmonary dysfunction is relatively common in these conditions, may be present early in the disease, and is less well recognized and treated than other symptoms. There are variable disorders of upper and lower airways, central control of ventilation, strength of respiratory muscles, and breathing during sleep which further impact daily activities and quality of life and have the potential to injure vulnerable neurons. Laryngopharyngeal dysfunction affects speech, swallowing, and clearance of secretions, increases the risk of aspiration pneumonia, and can cause stridor and sudden death. In Parkinson's disease, L-Dopa benefits some pulmonary symptoms but there are limited pharmacological treatment options for pulmonary dysfunction. Targeted treatments include strengthening of respiratory muscles, positive airway pressure in sleep and techniques to improve cough efficacy.