Assessment of ventilation
Jonathan Dakin, Mark Mottershaw, Elena Kourteli in Making Sense of Lung Function Tests, 2017
Ventilation refers to the rate at which air is breathed in and out of the lungs. Alveolar ventilation is a parameter of fundamental importance, as it is the primary determinant of arterial CO2 concentration. Although each breath contains around 500 mL, approximately 150 mL do not reach the alveoli but remain within the dead space, which is comprised of the trachea and major airways. Because of the very large volume of CO2 held buffered in the body, it takes 20-30 minutes for a new steady state to be reached after a change in ventilation. There is increasing interest in use of venous blood gases for monitoring of PCO2 and pH in patients with acute respiratory failure, as these values correlate somewhat to the respective arterial values. Hypoventilation of gas-exchanging alveoli is the commonest mechanism of hypercapnia. Although chronic obstructive pulmonary disease is the commonest cause of hypercapnia, familiarity with this condition frequently leads doctors to miss other causes of hypercapnia.
Sleep and headache disorders
S.R. Pandi-Perumal, Meera Narasimhan, Milton Kramer in Sleep and Psychosomatic Medicine, 2017
The relationship between sleep and headache was recognized well over a century ago in medical texts and journals. Sleep apnea headache (SAH) is the only formal diagnosis of headache secondary to a sleep disorder, coded within “Headache attributed to hypoxia or hypercapnia,” although its mechanisms and criteria have not been validated. A comprehensive literature review concluded that it was unclear whether the mechanisms underlying SAH were hypoxemia or hypercapnia, or instead another non-respiratory consequence of sleep apnea. The parasomnia exploding head syndrome can present as sleep-related headache. Sleep triggers for migraine and tension-type headache were confirmed prospectively using time-series analysis. The convergence of sleep and headache disorders is generally believed to have its basis in neuroanatomical connections and neurophysiological mechanisms, particularly involving the hypothalamus, serotonin, and melatonin. Paper-and-pencil and electronic sleep diaries are probably the most commonly used systematic selfreport tools for sleep assessment.
Respiratory problems
Mervyn Dean, Juan-Diego Harris, Claud Regnard, Jo Hockley in Symptom Relief in Palliative Care, 2018
Breathlessness is the commonest respiratory problem. It is common in advanced disease, being present in 94% of chronic lung disease, 83% of heart failure patients and up to 70% of cancer patients, but it is also common in dementia, multiple sclerosis and Acquired Immune Deficiency Syndrome. Other respiratory problems include airway secretions, cough and hiccups. For many respiratory problems a clear history and bedside examination provide most of the information. Hypercapnia is most commonly seen in chronic respiratory failure due to conditions such as neuro-muscular disease or primary respiratory disease. Some of the patients are dependent on some hypoxia to stimulate respiration. If patients are given oxygen above 24% their hypercapnia will worsen and they will go into rapid respiratory failure. Pulmonary emboli can cause distressing pain and breathlessness. The standard practice is to anticoagulate, but in patients with advanced malignancy full anticoagulation causes new problems with bleeding or unstable anticoagulation control.
Interaction Between Vagal and Chemoreceptors Afferents in Ventilatory Response to Transient Hypercapnia (Anaesthetized Rabbit)
Published in Archives Internationales de Physiologie et de Biochimie, 1977
S. Delpierre, C. Guillot, Y. Jammes, C. Grimaud
In rabbits anaesthetized with ethyl-carbamate, stimulation of chemo-receptors afferents was allowed by transient hypercapnia, before and after vagal blockade by DC current. In these relatively fast breathing animals, the transient hypercapnia produced light changes of inspiratory tidal volume (VI) inspiratory (TI) and expiratory durations (TE). Despite the identity of transient hypercapnia, it ensued that : (1) the higher the spontaneous VI and the lower the respiratory frequencyfR, the greater their respective changes (δVI and δFR) during the ventilatory response; (2) after vagal blockade, greater changes in VI, TI, VE and mean inspiratory flow rate (VI / TI) occurred than in control state, while the relation between δFR and fR was more significant than in control state. Respective roles played by vagal and chemoreceptors afferents in the ventilatory response to transient hypercapnia are discussed.
Adenosine A
Published in Bioscience, Biotechnology, and Biochemistry, 2019
Huiming Ren, Xu Guo, Xiaotong Wang, Zhihui Cui
ABSTRACT This study aims to study the effects of adenosine A2A receptor (A2AR) on hippocampal cell apoptosis and the putative mechanisms in a mouse model of chronic hypoxic-hypercapnia. Wild-type (WT) or A2AR knockout (A2AR KO) mice were randomly divided into normal control (NC) groups and chronic hypoxic-hypercapnia (4HH) groups. Compared with their corresponding NC groups (WT-NC and KO-NC), the apoptosis index (AI), caspase-3 activity, Bax mRNA and P-p38 protein expression in the hippocampus of 4HH groups (WT-4HH and KO-4HH) were significantly increased, while Bcl2 mRNA expression was significantly decreased (P
Adenosine modifies canine myocardial blood flow response to hypocapnia and hypercapnia, while aminophylline and verapamil do not
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 1987
Variations of arterial Pco2 and pH are known to influence myocardial blood flow (MBF) in that hypercapnia results in a coronary vasodilatation, while hypocapnia possibly decreases MBF. The present study was performed to examine if hypocapnia and hypercapnia might influence the sensitivity to exogenous administration of adenosine. Aminophylline, an adenosine receptor blocking agent, was administered to rule out the effect of endogenously liberated adenosine during variations of Pco2 and pH. In the last part of the study, it was examined whether verapamil, a calcium-channel blocker, might influence the MBF response to variations in Pco2 and pH. Closed-chest dogs were anaesthetized with pentobarbital, and hypocapnia induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. In the control group hypocapnia did not significantly reduce MBF although a decrease in coronary sinus (CS) So2 indicated a coronary vasoconstriction. During continuous adenosine infusion (7.5 ± 0.3 mg/kg/h) which increased MBF 116% during normocapnia, creating hypocapnia caused a 40% decrease in MBF. Hypercapnia seemed to potentiate the vasodilating effect of adenosine. During administration of aminophylline hypocapnia did not cause any decrease in MBF, while hypercapnia increased MBF by 39%, and these results are in harmony with the results obtained in the control group without aminophylline. Verapamil did not result in any altered MBF response to hypocapnia and hypercapnia when compared to the unblocked control group. These observations do not support the idea of any major influence of the Ca2+ fluxes blocked by verapamil as the cause of MBF changes during variations in Pco2 and pH. In conclusion, the findings following aminophylline administration indicate that MBF regulation during variations in Pco2 and pH is not determined by altered endogenous adenosine formation. The altered sensitivity to exogenously administered adenosine observed during hypocapnia and hypercapnia indicates another mechanism by which adenosine might regulate MBF. Verapamil, a calcium-channel blocker, did not influence the response of MBF to variations of Pco2 and pH.
Related Knowledge Centers
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- Hypocapnia
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