Respiratory centre will offer support to leave hospital

2014 ◽  
Vol 29 (9) ◽  
pp. 11-11
Keyword(s):  
1928 ◽  
Vol 74 (306) ◽  
pp. 443-453 ◽  
Author(s):  
F. Golla ◽  
S. A. Mann ◽  
F. Golla ◽  
R. G. B. Marsh

The preceding studies on the acid-base equilibrium in psychotics have made it evident that the failure to adjust must be attributed in the first instance to an inadequacy of the respiratory compensatory mechanism, and can be in no sense attributable to either a deficiency in the buffering power of the blood itself or to an increased organic acid production (acidosis). We have endeavoured to determine the excitability of the respiratory centre to the stimulus created by CO2. For this purpose a number of psychotic patients were tested as to the excitability of the respiratory centre to air containing 2% CO2 and the reaction compared with that obtaining in a number of normal subjects.


1974 ◽  
Vol 8 (4) ◽  
pp. 466-466 ◽  
Author(s):  
J Cosgrove ◽  
P Cooper ◽  
A C Bryan ◽  
N Neuburger ◽  
H Levison

1961 ◽  
Vol 38 (1) ◽  
pp. 79-92
Author(s):  
G. SHELTON

1. The medulla of the tench brain was searched systematically by means of needle electrodes for rhythmic bursts of action potential activity coinciding with the breathing movements. 2. The neurones which produced these rhythmic bursts of activity were located in the grey matter, mainly beneath the IXth and Xth motor nuclei and in the region round the VIIth motor nucleus. This type of activity was also found in some of the neurones forming the Vth and VIIth motor nuclei. 3. The respiratory neurones were not arranged in a discrete and homogenous nucleus anywhere in the medulla, but were scattered through the grey matter. The distribution was not uniform, the neurones tending to occur in very small groups. There was also a relatively higher density of respiratory neurones in the central, as compared with the more anterior and posterior, parts of the respiratory region. The possibility that variations may occur in the constitution of the respiratory centre, in different individuals and in the same individual at different times, is considered. 4. The manner in which neurones of the respiratory centre function to produce the rhythmic activity is discussed. Localized destruction of active respiratory regions, over a wide area of the medulla in different fish, was never followed by a breakdown in the rhythmic movements. This is interpreted as evidence against the existence of a pacemaker and favouring the hypothesis that the rhythm is produced by a general reciprocal interaction of large numbers of respiratory neurones.


2008 ◽  
pp. 170-183
Author(s):  
D. Ewen Cameron
Keyword(s):  

Author(s):  
Samantha Prigmore ◽  
Vikki Knowles,

This chapter addresses the fundamental nursing in managing breathlessness. Every nurse should possess the knowledge and skills to assess patients holistically, to select and implement evidence-based strategies, to manage breathlessness, and to review the effectiveness of these to inform any necessary changes in care. The nurse has a key role in managing this often frightening symptom, which may be caused by many disorders, including certain heart and respiratory conditions, strenuous exercise, or anxiety. Breathlessness is described as a distressing subjective sensation of uncomfortable breathing (Mosby, 2009) and can be expressed as an unpleasant or uncomfortable awareness of breathing, or of the need to breathe (Gift, 1990). The term dyspnoea, also meaning breathlessness, is derived from the Greek word for difficulty in breathing. Whilst it is difficult to estimate the prevalence of dyspnoea, it is apparent when we exercise beyond our normal tolerance levels; pathologically, dyspnoea occurs with little or no exertion and is a symptom response to different aetiologies (causes of illness). Breathlessness is a common symptom in patients with both cardiac (McCarthy et al., 1996) and respiratory disease (Dean, 2008), and also in people with neuromuscular diseases approaching the end of life; this can prove difficult and distressing to manage (see Chapter 18 Managing End-of-Life Care). There is a peak incidence of chronic dyspnoea in the 55–69 age group (Karnani, 2005), and the prevalence and severity of dyspnoea increases with age. This is associated with an increase in mortality and reduction in quality of life (Huijnen et al., 2006). It is estimated that 70% of all terminal cancer patients experience breathlessness in their last 6 weeks of life (Davis, 1997). Both physiological and psychological responses (including pain, emotion, and anxiety) can lead to an increase in respiratory rate. Breathing is controlled by the respiratory centre in the medulla of the brain. Higher centres in the cerebral hemispheres can voluntarily control respiratory rate so that breathing can be temporarily stopped, slowed, or increased. The respiratory centre generates the basic rhythm of breathing, with the depth and rate being altered in response to the body’s requirements, mainly by nervous and chemical control (Ward and Linden, 2008).


1940 ◽  
Vol 86 (361) ◽  
pp. 276-280 ◽  
Author(s):  
Leslie Dundonald MacLeod ◽  
Max Reiss

Since Hildebrandt (1926) described the convulsant effect of cardiazol injection, several studies have been carried out on the mechanism of such convulsions. Zung and Tremonti (1931) suggested a direct action on the respiratory centre when cardiazol is used as a stimulant; Kerr and Antaki (1937) found no effect on brain glycogen or phosphocreatine in cardiazol-induced convulsions; Hashimoto (1937) found differences in distribution of calcium and potassium ions in the central nervous system after cardiazol. Goodwin and Lloyd (1938) recorded a direct effect on brain potential changes as shown on oscillographic records. Leibel and Hall (1938) found a large (75 per cent.) diminution of cerebral blood-flow at the onset of cardiazol convulsions. Weigand (1938) found no effect on liver glycogen or vitamin A content, reducing power of suprarenal cortex or blood picture. Denyssen and Watterson (1938) and Watterson and Macdonald (1939) attribute the convulsions to action on the vasomotor centre and note the action of vasodilator drugs in inhibiting convulsions. Wortis (1938) quoted by Quastel (1939) found no effect on brain respiration.


1992 ◽  
Vol 1 (2) ◽  
pp. 94-97 ◽  
Author(s):  
D C Currie ◽  
C M Prendergast ◽  
M C Pearson

1975 ◽  
Vol 49 (1) ◽  
pp. 57-68 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell

1. A technique has been developed for assessing CO2 responsiveness by measuring the maximum rate of isometric inspiratory pressure change at the mouth [(dP/dt)max.]. 2. By use of a rebreathing technique, the (dP/dt)max. response to CO2 was shown to correlate well with the ventilatory response in thirty-two normal subjects. 3. The addition of an external flow resistance sufficient to reduce the ventilatory response by a mean of 33.4% produced no significant mean change in the (dP/dt)max. response in thirty subjects. 4. In six patients recovering from bronchial asthma, reduction of airways obstruction led to a mean increase in the ventilatory response of 109% without any significant mean change in the (dP/dt)max. response. 5. An increase in lung volume did not reduce the (dP/dt)max. response in five normal subjects. 6. At very high lung volumes, six normal subjects were able to develop a higher (dP/dt)max. during voluntary inspiratory efforts than has been recorded during spontaneous breathing response to CO2. 7. It is believed that (dP/dt)max. represents the initial rate of development of force by the inspiratory muscles before this can be modified by mechanical loading, proprioceptive feedback mechanisms or conscious response and can therefore be used to study changes in the motor output of the respiratory centre in response to ventilatory stimuli independently of pulmonary mechanics.


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