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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74

Animal studies have demonstrated that activation of the baroreflex by increases in arterial pressure inhibits cardiovascular and ventilatory responses to activation of peripheral chemoreceptors (PC) with hypoxia. In this study, we examined the influences of baroreflex activation on the sympathetic response to stimulation of PC and central chemoreceptors in humans. PC were stimulated by hypoxia (10% O2/90% N2) (n = 6) and central chemoreceptors by hypercapnia (7% CO2/93% O2) (n = 6). Responses to a cold pressor stimulus were also obtained as an internal reflex control to determine the selectivity of the interactive influence of baroreflex activation. Baroreflex activation was achieved by raising mean blood pressure by greater than 10 mmHg with intravenous infusion of phenylephrine (PE). Sympathetic nerve activity (SNA) to muscle was recorded from a peroneal nerve (microneurography). During hypoxia alone, SNA increased from 255 +/- 92 to 354 +/- 107 U/min (P less than 0.05). During PE alone, mean blood pressure increased and SNA decreased to 87 +/- 45 U/min (P less than 0.05). With hypoxia during baroreflex activation with PE, SNA did not increase (50 +/- 23 U/min). During hypercapnia alone, SNA increased from 116 +/- 39 to 234 +/- 72 U/min (P less than 0.01). Hypercapnia during baroreflex activation with PE increased SNA from 32 +/- 25 U/min during PE alone to 61 +/- 26 U/min during hypercapnia and PE (P less than 0.05). Like hypercapnia (but unlike hypoxia) the cold pressor test also increased SNA during PE. We conclude that baroreflex activation selectively abolishes the SNA response to hypoxia but not to hypercapnia or the cold pressor test. The inhibitory interaction of the baroreflex and the peripheral chemoreflex may be explained by convergence of baroreceptor and peripheral chemoreceptor afferents on neurons in the medulla.
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PMID:Interaction of baroreceptor and chemoreceptor reflex control of sympathetic nerve activity in normal humans. 204 Jun 88

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

In the present study the functional and morphologic effects of two pulmoplegic solutions are evaluated. Single left-lung allotransplantation with ligation of the right pulmonary artery was performed in 15 piglets (13-20 kg). The lungs were preserved after donor prostaglandin E-1 treatment with single pulmonary artery flush with either modified Euro-Collins solution (mECS) (9 pigs) or oxygenated fluorocarbon emulsion (FC-43) (6 pigs) and transplanted after 6-hr storage in cold Physiosol solution. Tidal volumes of 15 ml/kg x fr (18) with 40% inspired oxygen were used for ventilation during reperfusion. Function of the transplanted lung was monitored for 4 hr postoperatively by determining pa CO2 and pa O2 levels from arterial samples and by noninvasive monitoring of end-tidal CO2 values and arterial oxygen saturations. Sequential morphologic changes in pulmonary artery flow surface and lung tissue were studied after 6-hr storage and 4-hr reperfusion, using light, scanning, and transmission electron microscopy (LM, SEM, TEM). There was no mortality. After transplantation the mECS group experienced significant hypoxia and hypercarbia and had low end-tidal CO2 values as signs of defective oxygenation and gas exchange, whereas the FC-43 group was normoxic and normoventilated without disturbed elimination of carbon dioxide. After storage and reperfusion, LM showed signs of increased vascular permeability and reperfusion damage--more evident in the mECS group compared with the FC-43 group--while the lymphoid cell population was more intensely activated in the latter group. Electron microscopy after storage showed good overall preservation of structures in both groups. After reperfusion preservation of pulmonary artery flow surface and lung tissue was estimated to be moderate in the mECS group, whereas it was good-to-moderate in the FC-43 group by SEM (NS). TEM of lung tissue, however, showed significantly better-preserved alveolar epithelial lining in the FC-43 group compared with the mECS group. In conclusion, oxygenated fluorocarbon (FC-43) pulmoplegia gave better functional and morphologic preservation of lung grafts compared with modified Euro-Collins solution.
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PMID:Single lung allotransplantation in pigs. A morphologic study of tissue preservation with modified Euro-Collins and fluorocarbon solutions. 236 Feb 50

Aortic chemoreceptor influences on vascular capacitance after changes in blood carbon dioxide and oxygen were studied in mongrel dogs anesthetized with methoxyflurane and nitrous oxide. The mean circulatory filling pressure (Pmcf), measured during transient cardiac fibrillation, provided a measure of capacitance vessel tone. Hypercapnia, hypoxia, and hypoxic hypercapnia significantly increased most variables, except that hypercapnia caused the total peripheral resistance (TPR) to decrease. Hypocapnia caused a significant decrease in mean systemic (Psa) and pulmonary (Ppa) arterial blood pressures, cardiac output (CO), and central blood volume and an increase in TPR and heart rate. The changes in Pmcf on changing blood gas tensions could be described by the equation delta Pmcf = -1.60 + 0.036 (arterial PCO2) + 50.8/arterial PO2. Thus a 10 mmHg increase in arterial PCO2 caused a 0.36 mmHg increase in Pmcf with receptors intact. Cold block (2 degrees C) of the cervical vagosympathetic trunks did not significantly influence the measured variables at control. During severe hypercapnia, vagal cooling caused a small but significant decrease in Pmcf, Psa, Ppa, and CO but not TPR. During hypoxia, vagal cooling caused the Pmcf, Psa, and TPR to decrease. We conclude that although hypercapnia or hypoxia acts reflexly to increase the capacitance vessel tone (an increase in Pmcf), the aortic and cardiopulmonary chemoreceptors with afferents in the vagi have only a small influence on the capacitance system, accounting for only approximately 25% of the total body response.
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PMID:Effects of hypercapnia and hypoxia on the cardiovascular system: vascular capacitance and aortic chemoreceptors. 239 98

To determine the functional significance of the cricothyroid muscle (CT) in respiration, laryngeal resistance was measured in anesthetized dogs, along with electromyographic activity of the posterior cricoarytenoid muscle (PCA) and CT. In two dogs the larynx was videotaped simultaneously via a telescope. Increased CT activity was induced by airway occlusion or hypercapnia. Observations were carried out before and during cold blockade of the recurrent laryngeal nerve (RLN) or the nerve to the CT (external branch of the superior laryngeal nerve [Ext SLN]). Paralysis of the CT had no effect on laryngeal resistance or glottic area, even at very high levels of CT activity. Blockade of the RLN increased inspiratory resistance, but did not have a significant effect on expiratory resistance. Electrical stimulation of the Ext SLN produced tetanic CT contraction, which increased laryngeal resistance in both inspiration and expiration. This was true even at very high levels of PCA activity. These results indicate that although artificially induced CT contraction markedly affects laryngeal resistance, physiologic levels of respiratory activity do not have a significant effect.
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PMID:Effects of cricothyroid muscle contraction on laryngeal resistance and glottic area. 291 22

The purpose of this study was to assess the relationship between the breathing pattern response to CO2 and the severity of mechanical impairment in twenty patients with COLD. The CO2 response was compared to that of a control group of twelve normal subjects. All patients had airway obstruction (FEV1 = 40 +/- 14% of predicted; means +/- SD) and hyperinflation (FRC = 154 +/- 23% of predicted). Tidal volume (VT), inspiratory and total cycle duration (TI, TT), occlusion pressure (P0.1) and endtidal PCO2 were measured at rest and during hyperoxic CO2 rebreathing. On the same day, in all patients, arterial blood gas analysis, spirometric and plethysmographic measurements were made. The slope (S) of the P0.1 response (SP 0.1) to increasing endtidal PCO2 was negatively correlated with airway resistance (r = -0.59; p less than 0.01). Although the flow response, S(VT/TI), was positively and closely correlated with SP 0.1 (r = 0.88; p less than 0.001), it also appeared to be independently influenced by obstruction (p less than 0.01). The tidal volume response, SVT, was principally correlated with inspiratory capacity (r = 0.90; p less than 0.001) and also, independently, with Vmax50 (p less than 0.01). SVT was diminished in seventeen patients, ten of whom only had a decreased S(VT/TI). The shortening in TI during hypercapnia was most marked in patients with the greatest S(P0.1), who did not have arterial hypercapnia at rest. These results suggest: that the poor VT response to CO2 in COLD patients is principally caused by a limitation in inspiratory volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the mechanical impairment on the ventilatory response to CO2 in chronic airway obstruction. 310 31

The effects of hypoxia (10% O2) on the thermosensitivities of preoptic neurons were studied in urethanized rats and compared to the effects of hypercapnia (10% CO2). This was examined by regression of neuronal activity on preoptic temperature. During hypoxia, the slope of the regression line increased significantly in 8 (23%) of 35 warm-sensitive neurons and decreased in eight other neurons (P less than 0.05). During hypercapnia, the slope of the regression line decreased significantly in 7 (30%) of the 23 warm-sensitive neurons (P less than 0.05). No neuron was found that significantly increased the slope of the regression line. The effects of hypoxia on thermosensitivities (i.e. the slope of the regression line) of PO neurons differed from those of hypercapnia in chi-square analysis (P less than 0.05). Responses of the cold-sensitive neurons to hypoxia or hypercapnia did not generally differ from those of the warm-sensitive neurons. During hypoxia and hypercapnia, arterial blood pressure, respiratory frequency, heart rate, and EEG were recorded to examine their relations to neuronal activity. The present results indicate that the thermosensitivities of preoptic neurons are modified by both hypoxia and hypercapnia, but that hypoxic differ from hypercapnic effects.
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PMID:Effects of air constituents on thermosensitivities of preoptic neurons: hypoxia versus hypercapnia. 311 32

Single motor units of the cricothyroid muscle (CT), the contralateral CT electromyogram, and the posterior cricoarytenoid muscle (PCA) electromyogram were recorded in anesthetized, spontaneously breathing dogs. In quiet breathing the CT was active predominantly in inspiration, and distinct phasic expiratory activity was observed at lighter levels of anesthesia. Both the CT and PCA increased their inspiratory and expiratory activity with hypercapnia, whereas only their inspiratory activity increased in response to negative pressure and/or absence of volume feedback. Cold blockade of either the recurrent laryngeal nerves or the external branch of the superior laryngeal nerves did not modify CT or PCA activity. In general, activity of CT motor units reflected the behavior of the whole muscle, but different units were recruited at different levels of CT activity. Even though the majority exhibited similar thresholds for inspiration and expiration, some units showed a lower threshold for either one, suggesting some degree of specialization. However, for a few units with high threshold for inspiration the expiratory threshold could not be determined, since a comparable level of CT activity was not achieved in expiration.
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PMID:Respiratory activity of the cricothyroid muscle. 314 25

A thermal clearance technique for measuring cerebral blood flow is described and compared with the radiolabelled microsphere technique. The thermal technique involves measurement of the rewarming curve generated after bolus infusion of 4-5 ml of ice-cold saline into the common carotid artery with a subdural thermistor placed on the parietal cortex. Evaluation of the biexponential decay curves obtained with this technique demonstrated a close correlation with total hemispheric, parietal, and parietal gray blood flow determined by simultaneous microsphere measurement. Despite significant correlations (p less than 0.001), scatter in the data produced a broad 95% confidence interval, thus making interpretation of blood flow with the thermal clearance technique impossible. Furthermore, instrumentation with the thermal probe, which required opening of the dura, blunted the cerebral blood flow response to hypercapnia. We conclude that the major limitations of the thermal clearance technique include: nonhomogeneous clearance function, significant variability, and depression of CO2 reactivity. These limitations must be addressed before this technique can be used reliably in the laboratory.
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PMID:Comparison of thermal clearance measurement of regional cerebral blood flow with radiolabelled microspheres. 359 Feb 53


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