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.

Hypoventilation patterns during bronchoscopic sedation and their clinical relevance based on capnographic and respiratory impedance analysis

Abstract: Capnography involves the measurement of end-tidal CO2 (EtCO2) values to detect hypoventilation in patients undergoing sedation. In a previous study, we reported that initiating a flexible bronchoscopy (FB) examination only after detecting signs of hypoventilation could reduce the risk of hypoxemia without compromising the tolerance of the patient for this type of intervention. We hypothesize that hypoventilation status could be determined with greater precision by combining thoracic impedance-based respiratory signals, RESP, and EtCO2 signals obtained from a nasal-oral cannula. Retrospective analysis was conducted on RESP and EtCO2 waveforms obtained from patients during the induction of sedation using propofol for bronchoscopic examination in a previous study. EtCO2 waveforms associated with hypoventilation were then compared with RESP patterns, patient variables, and sedation outcomes. Signals suitable for analysis were obtained from 44 subjects, 42 of whom presented indications of hypoventilation, as determined by EtCO2 waveforms. Two subtypes of hypoventilation were identified by RESP: central-predominant (n = 22, flat line RESP pattern) and non-central-predominant (n = 20, RESP pattern indicative of respiratory effort with upper airway collapse). Compared to cases of non-central-predominant hypoventilation, those presenting central-predominant hypoventilation during induction were associated with a lower propofol dose (40.2 ± 18.3 vs. 60.8 ± 26.1 mg, p = 0.009), a lower effect site concentration of propofol (2.02 ± 0.33 vs. 2.38 ± 0.44 µg/ml, p = 0.01), more rapid induction (146.1 ± 105.5 vs. 260.9 ± 156.2 s, p = 0.01), and lower total propofol dosage (96.6 ± 41.7 vs. 130.6 ± 53.4 mg, p = 0.04). Hypoventilation status (as revealed by EtCO2 levels) could be further classified by RESP into central-predominant or non-central-predominant types. It appears that patients with central-predominant hypoventilation are more sensitive to propofol during the induction of sedation. RESP values could be used to tailor sedation management specifically to individual patients.

Primary central hyperventilation in a child with a brainstem glioma: management with continuous intravenous fentanyl.

Abstract: Alveolar ventilation and respiratory rate are regulated by central respiratory centers in the pons and medulla, which are influenced by both neural and humoral input. Aberrations in control mechanisms can lead to apnea, hypoventilation, or hyperventilation. Although hyperventilation usually occurs as a compensatory mechanism for metabolic derangements, primary central hyperventilation (CHV) has been reported with brainstem gliomas, central nervous system lymphoma, supratentorial lesions, and head trauma.1-3 We present an 11-year-old boy with a brainstem glioma whose initial symptoms included CHV. When CHV became unresponsive to primary tumor management with radiation therapy and administration of dexamethasone, oral morphine was administered in an attempt to decrease his respiratory rate.

The problem of obesity in anaesthesia for abdominal surgery.

Abstract: The physiological changes responsible for the syndrome of hypoventilation in obesity are discussed. This state may be intensified during anaesthesia for abdominal surgery, and an obese person not suffering from hypoventilation may readily develop this condition when anaesthetized. Further studies are in order to establish more clearly the effects of various types of anaesthesia on the altered lung volumes and mechanics of respiration occurring in fat people. It is proposed that relaxant drugs are hazardous. It is, our unconfirmed opinion that spinal and epidural anaesthesia allow establishment of adequate respiratory control, with a decreased hazard of immediate postoperative respirator) insufficiency.

Mechanical ventilation in a dog with acetylcholinesterase inhibitor toxicosis

Abstract: Background To describe a case of acetylcholinesterase inhibitor (AChEI) toxicosis with ventilatory failure that was successfully treated with mechanical ventilation (MV). Key Findings A 7-year-old, female spayed German Short-haired Pointer, presented with acute onset ptyalism, generalized muscle tremors, and diarrhea. Physical examination findings included evidence of muscarinic overstimulation in the parasympathetic nervous system (eg, diarrhea, ptyalism, lacrimation), and nicotinic overstimulation in the sympathetic nervous system (tachycardia), central nervous system (agitation), and the neuromuscular junction (eg, diffuse muscle fasciculations, tetraparesis). Point-of-care testing demonstrated hyperlactatemic metabolic acidosis and respiratory acidosis (hypoventilation). Hypoventilation progressed to respiratory failure and the dog lost its gag reflex necessitating emergency endotracheal intubation and MV. Additional treatments included atropine, parenteral antimicrobials (for aspiration pneumonia), pralidoxime, and supportive care. Weaning from the ventilator was achieved in 4 days. The dog was administered supplemental oxygen for 24 hours, and discharged 48 hours later with improved neurologic function and normal respiratory drive. Whole blood acetylcholinesterase activities measured on day 0, 2, and 4 and were consistent with AChEI toxicity. New or Unique Information Provided Specific AChEI toxicity (ie, carbamate and organophosphate) has been reported in the veterinary literature with good prognosis for survival and hospital discharge. While the existing veterinary literature suggests that ventilatory failure is rare in this disease syndrome, consideration for treatment with MV must be made for patients that develop respiratory failure (associated with hypoventilation, bronchoconstriction, bronchorrhea, or aspiration pneumonia).