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Hypoventilation

About: Hypoventilation is a research topic. Over the lifetime, 1772 publications have been published within this topic receiving 40799 citations. The topic is also known as: respiratory depression.


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TL;DR: Positive pressure ventilation is currently the primary recommendation for all patients with sleep-disordered breathing (CSA included), and in some patients may effectively reduce the apnea-hypopnea index, and significant research is ongoing to determine how to treat this complex patient population.
Abstract: Central sleep apnea (CSA) is a common and under-diagnosed condition commonly associated with Cheyne-Stokes respiration. It is particularly prevalent in the heart failure population affecting up to 40 % of all patients with heart failure. The pathophysiology associated with CSA is based on the underlying effects of hypoventilation and hyperventilation, with neurologic dysregulation of respiratory control as the primary defect. However, therapeutic options are limited because of the prevailing perception that CSA is a consequence, rather than cause of morbidity and mortality. At present, the main focus remains treating the underlying problem (ie, intensifying heart failure therapeutics, decongestion), whereas additional suggestions of using acetazolamide, progesterone, nocturnal oxygen, and theophylline have not been validated with contemporary clinical trials. Positive pressure ventilation is currently the primary recommendation for all patients with sleep-disordered breathing (CSA included), and in some patients may effectively reduce the apnea-hypopnea index. However, significant research is ongoing to determine how to treat this complex patient population.

9 citations

Journal ArticleDOI
TL;DR: Two small, human studies on male volunteers conducted in The Netherlands on a promising new breathing stimulant compound, GAL021, are presented, which was well tolerated with "sweating and feeling warm" and "infusion site pain" as its main adverse effects.
Abstract: As anesthesiologists, we routinely administer drugs that compromise a patient's ability to breathe, and dealing with the consequences can be a challenge. However, our jobs may be getting easier. In this issue, Roozekrans et al. present two small, human studies on male volunteers conducted in The Netherlands on a promising new breathing stimulant compound, GAL021, being developed by Galleon Pharmaceuticals (Horsham, PA).1Additional first-in-human safety and pharmacokinetic studies of GAL021 conducted in Belgium are to be published in an upcoming issue of the British Journal of Anaesthesia. Opioids are the most effective drugs for acute pain management. However, they cause opioid induced respiratory depression (OIRD), which is a significant contributor to many adverse perioperative respiratory events.2Opioid sensitivity is unpredictable and impacted by polypharmacy, age, and co-morbidities including obesity and sleep apnea. Opioids, along with analgesia, cause sedation, hypoventilation, loss of responsiveness to hypoxia and to hypercapnia, irregular breathing with periods of apnea, and loss of upper airway muscle tone. A drug that minimizes OIRD would have significant clinical utility. Naloxone is effective, reliable, and widely-available to reverse OIRD, but, unfortunately, it reverses analgesia, as well. GAL021 is being developed as an agent to treat OIRD with no effect on opioid analgesia. In this well-conducted, two-part study, patients received steady-state drug infusions of low- or high-dose alfentanil co-administered with steady-state infusions of placebo or low- or high-dose GAL021. Study 1 tested GAL021 efficacy in reversing established OIRD. Study 2 addressed non-respiratory end points such as hemodynamics, analgesia, and sedation. In short, without altering analgesia, sedation, or hemodynamics, GAL021 reversed some of the hypoventilation induced by alfentanil. GAL021 was well tolerated with "sweating and feeling warm" and "infusion site pain" as its main adverse effects.

9 citations

Journal ArticleDOI
TL;DR: It is the impression that topical anesthesia has several advantages, not the least of which is the ability to perform the examination without depending on assisted ventilation, and the effect of topical anesthesia and bronchoscopy on the arterial oxygen pressure is investigated.
Abstract: IT IS well recognized that the perfect anesthesia for bronchoscopy has yet to be found. 1 Recently general anesthesia has gained popularity for endoscopic procedures. A number of techniques to overcome the hypoventilation associated with the administration of a general anesthetic have been reported. 2-5 Normal arterial oxygen saturation and adequate carbon dioxide removal during bronchoscopy have been considered by some to be one of the advantages of general anesthesia with assisted ventilation. It is our impression that topical anesthesia has several advantages, not the least of which is the ability to perform the examination without depending on assisted ventilation. Failure to provide adequate ventilation and prevent respiratory acidosis may predispose the patient to cardiac arrest, especially since many of the patients who require bronchoscopic examination have pulmonary insufficiency and chronic respiratory acidosis. In order to investigate the effect of topical anesthesia and bronchoscopy on the arterial oxygen pressure (P

9 citations

Journal ArticleDOI
TL;DR: Gabapentin (GBP) is indicated as an adjunctive therapy in the treatment of partial seizures with and without secondary generalization in adults with epilepsy and has been shown to be effective in the management of behavioral agitation and neuropathic pains.
Abstract: To the Editor: Gabapentin (GBP) is indicated as an adjunctive therapy in the treatment of partial seizures with and without secondary generalization in adults with epilepsy.1 GBP has been shown to be effective in the management of behavioral agitation2,3 and neuropathic pains including postherpetic neuralgia,4 painful diabetic neuropathy,5 trigeminal neuralgia,6 and reflex sympathetic dystrophy.7 GBP, 1-(aminomethyl)cyclohexane acetate is structurally related to the neurotransmitter gamma-aminobutyric acid (GABA), but it does not interact with GABA receptors or affect GABA metabolism or reuptake.1 GBP is lipophilic and readily crosses the bloodbrain barrier.8 Its mechanism of action is unknown.1 GBP does not interact with common receptor sites, including benzodiazepine, beta adrenergic, histamine H1, muscarinic acetylcholine, serotonin S1 or S2, or opiate mu or kappa.1 GBP is not metabolized in humans, is minimally protein bound, and has little drug interaction potential.9 Clinical trials data do not indicate that routine monitoring of clinical laboratory parameters is essential for the safe use of GBP.1 A 69-year-old man with chronic obstructive pulmonary disease (COPD), insomnia, and anxiety disorder was admitted for 5 days for worsening shortness of breath and wheezing. He denied fever, cough, or increased sputum production. He was a former 50-pack/year smoker but had quit 5 years ago. In the previous 3 years, he had required four hospitalizations for COPD exacerbation due to pneumonia. He was chronically maintained on albuterol and ipratropium bromide inhalers, clonazepam, and zolpidem. Two months previously, he had been started on GBP 300 mg three times daily for painful peripheral neuropathy. Five weeks later, he was hospitalized for 10 days for severe hypercapnia, and he required mechanical ventilation (MV) for the first time. On admission, his respiration rate was 30/minute. Arterial blood gases (ABGs) revealed pH 7.38, partial pressure of carbon dioxide (PCO2) 53 mmHg, and partial pressure of oxygen (PO2) 124 mmHg on two liters of oxygen via nasal cannula. Chest X-ray (CXR) showed no infiltrates. Complete blood count and chemistry were normal. Bronchodilator nebulizers, intravenous steroid, levofloxacin, clonazepam, zolpidem, and GBP were started. On day 3, he was put on MV for lethargy, respiratory distress, and hypercapnia (PCO2 5 72 mmHg). His CXR was unchanged. Four attempts at extubation, after he seemed to be doing well on MV, failed because of respiratory distress, expiratory wheezing, and hypercapnia (PCO2 5 89–116 mm Hg). His baseline ABGs were normal before GBP therapy. On day 10, GBP was discontinued and 2 days later he was extubated. His PCO2 levels were normalized, and he continued to improve despite continued treatment with the other medications. He remained stable after 8 months of follow-up. For most adults, glomerular filtration rate decreases with aging. GBP elimination half-life is 5 to 9 hours.9 It is eliminated from the systemic circulation by renal excretion as unchanged drug.1,9 In older patients, and in patients with impaired renal function, GBP renal clearance is reduced; therefore, dosage adjustment of GBP is necessary in patients who have ageor disease-related decline in renal function.1,9 In clinical studies, the most-commonly observed adverse events associated with the use of GBP were somnolence, dizziness, ataxia, nystagmus, and headache;1,10 rare adverse events involving the respiratory system include bronchospasm and hypoventilation.1 In older patients with exacerbation of chronic medical problems, a careful review and assessment of medications as potential etiological factors should always be considered. In our patients, a causal relationship between the use of GBP and hypercapnic respiratory failure may be established because there was a temporal relationship between the introduction of GBP and the onset of hypoventilation and subsequent respiratory failure. This was supported by this patient’s recovery following GBP withdrawal. Rechallenge with GBP was not attempted for ethical reasons. The mechanism by which GBP may cause bronchospasm is unknown. GABA is the major rapid inhibitory neurotransmitter of the mammalian brain.8 GABA transaminase (GABA-T) is the principal enzyme that degrades GABA in the brain.8 GBP is a reversible inhibitor of GABA-T in the mammalian brain;8 through this mechanism of action, GBP modulates neurotransmitter GABA, which has an inhibitory effect on the respiratory center in the medulla. This effect may be exaggerated in patients with COPD. The preexisting COPD in our patient may have predisposed him to hypoventilation and respiratory failure during GBP therapy. Therefore, older patients with COPD should not be considered good candidates for the use of GBP. Although GBP appears to be safe, physicians prescribing GBP should be aware of this potential, serious adverse event and may choose to communicate it to their patients and care providers.

9 citations

Journal ArticleDOI
TL;DR: The recently published American Academy of Neurology guidelines for the management of ALS recommends the following:Serial measures of pulmonary function to guide management and determine prognosis, and noninvasive ventilatory support—an effective initial therapy for symptomatic chronic hypoventilation and prolonged survival.
Abstract: •Respiratory complications account for the majority of deaths occurring in patients suffering from amyotrophic lateral sclerosis (ALS). Patients normally succumb to their illness within an average of 3 to 5 years from the time of diagnosis from complications such as hypoventilation, hypoxemia, hypercarbia, aspiration, and other pneumonia and pulmonary emboli [1]. Although invariably disabling, ALS need not be fatal if respiratory involvement is detected early, which will allow sufficient time to discuss and implement treatment options. The recently published American Academy of Neurology guidelines for the management of ALS recommends the following: •Serial measures of pulmonary function to guide management and determine prognosis. •Noninvasive ventilatory support—an effective initial therapy for symptomatic chronic hypoventilation and prolonged survival. •Invasive ventilatory support when long-term survival is the goal and noninvasive support is no longer sufficient. •Physicians respect the right of the patient to choose, refuse, or withdraw ventilatory support. •Liberal use of opiates and anxiolytics to relieve dyspnea and anxiety when ventilatory support is refused or withdrawn.

8 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023114
2022173
202173
202071
201949
201860