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Psychosocial Aspects of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Underlying mechanisms of panic attacks or panic disorder involve the hippocampus, anterior cingulate cortex, insula, amygdala, lateral prefrontal cortex, and periaqueductal gray matter. In a panic attack, there is usually elevated blood flow or metabolism. Insula hyperactivity is likely related to irregular norepinephrine activity. The periaqueductal gray matter is implicated in generating fear responses. There is an abnormally functioning “brain circuit” made up of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and locus coeruleus. Often, there are lower than normal levels of gamma-aminobutyric acid (GABA). Hyperventilation is a component of panic, and results in the exhalation of excessive carbon dioxide. There may be a feeling of being unable to “catch their breath.” The partial pressure of carbon dioxide is another mediator of panic disorder. Panic attacks may begin and worsen in association with diabetes progressing, increased complications, and loss of normal functioning. They are also accompany with depression in many patients.
Measuring and monitoring vital signs
Published in Nicola Neale, Joanne Sale, Developing Practical Nursing Skills, 2022
The person’s depth of breathing should be observed, which relates to the volume of air moving in and out of the respiratory tract with each breath – the tidal volume. An adult male’s tidal volume should be approximately 500 mL and a female’s, approximately 400 mL (Hallett et al. 2020). However, this can be altered to fit physiological needs, for example during exercise. The term hyperventilation refers to prolonged, rapid and deep ventilations that can occur during an anxiety attack, causing dizziness and fainting as the resulting low carbon dioxide level causes cerebral vasoconstriction.
Psychological Aspects of Trauma
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
These attacks usually peak within 10 minutes and are generally short-lived, but they may last for several hours. They are often aborted when the patient feels safe and secure. They may also be associated with hyperventilation, although it is not clear whether hyperventilation causes the panic attack or vice versa. Hyperventilation may also lead to the ‘hyper-ventilation syndrome’, characterized by palpitation, dizziness, faintness, tinnitus, peripheral tingling and chest pain. Physical causes should also be excluded, including pulmonary embolism, acute or chronic pulmonary disease, asthma and the excessive ingestion of aspirin.16
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Central neurogenic hyperventilation, a syndrome in which hyperpnea and associated respiratory alkalosis occur during both wakefulness and sleep, is considered a result of a pontine lesion, most commonly secondary to tumors.80,85 The exact pathophysiology beyond stimulation of respiratory control areas in the pons and medulla remains unclear.85 When this syndrome is suspected based on clinical presentation, other causes of hyperventilation, such as pulmonary embolus or respiratory disease, must first be ruled out.80 Lesions to the caudal respiratory neurons can cause an apneustic breathing pattern in which each inspiration is accompanied by a prolonged pause.80 As a FLS, this syndrome can also be caused by lower lesions. There have been five reported cases of such apneustic breathing in patients with achondroplasia, the pathophysiology being cervicomedullary compression rather than vagal or pneumotaxic center lesions.86 The lesion’s severity, location, and reversibility by decompression is variable.86 Central neurogenic hyperventilation can also result from thalamic lesions.85 Diagnosis involves polysomnography sleep studies, measuring somatosensory evoked potentials, and CT and MRI scans of the brain.85,86
Prehospital Manual Ventilation: An NAEMSP Position Statement and Resource Document
Published in Prehospital Emergency Care, 2022
John W. Lyng, Francis X. Guyette, Michael Levy, Nichole Bosson
Several studies have demonstrated that EMS and hospital-based clinicians manually ventilate patients with rates as high as 50 ventilations per minute (19, 20, 31, 55–60). In a study by Scott et al. only 42.3% of clinicians delivered tidal volumes at the target 5–8 ml/kg of ideal body weight and the majority of participants exceeded 20% variability among breaths (61). There are harmful physiologic effects of hyperventilation including increased intrathoracic pressure, decreased cerebral blood flow, impaired coronary perfusion pressure, barotrauma, and gastric insufflation increasing the risk for aspiration (20, 23, 62). Together these harmful effects have been shown to increase morbidity and mortality, particularly for patients with cardiac arrest and traumatic brain injuries (19, 20, 63).
Optimizing Physiology During Prehospital Airway Management: An NAEMSP Position Statement and Resource Document
Published in Prehospital Emergency Care, 2022
Daniel P. Davis, Nichole Bosson, Francis X. Guyette, Allen Wolfe, Bentley J. Bobrow, David Olvera, Robert G. Walker, Michael Levy
Hyperventilation is generally harmful but unfortunately common in prehospital ventilation (33). For most patients, achieving eucapnia with a target PaCO2 ∼40 mmHg is reasonable. End-tidal CO2 may not accurately reflect PaCO2 in critically ill and injured patients but can help avoid excessive ventilation rates (57). These are associated with inadvertent hypocapnia and elevated intrathoracic pressures, which may compromise cardiac output or result in lung injury via barotrauma. Patients with traumatic brain injury experience decreased cerebral blood flow, with increased ventilation rates leading to worse outcomes. Controversy exists for use of mild hyperventilation in patients with impending herniation; this is addressed elsewhere in this compendium (60). Patients with metabolic acidosis but without brain injury may require a lower PaCO2 target to provide partial respiratory alkalosis unless this relative hyperventilation results in hypotension. Patients with acute respiratory distress syndrome (ARDS) or multi-organ dysfunction syndrome benefit from low tidal volume ventilation and permissive hypercapnia to avoid the adverse systemic and/or pulmonary effects of positive-pressure ventilation.