Academic literature on the topic 'Paradoxical ventilation'

We investigated the differential effect of histamine and methacholine on spirometry and ventilation distribution (where indexes S cond and S acin represent conductive and acinar ventilation heterogeneity; Verbanck S, Schuermans D, Van Muylem A, Noppen M, Paiva M, and Vincken W. J Appl Physiol 83: 1807–1816, 1997). Thirty normal subjects were challenged with cumulative doses of 6.52 μmol histamine and, on a separate day, with either 6.67 μmol methacholine (equal-dose group; n = 15) or 13.3 μmol methacholine (double-dose group; n = 15). Largest average forced expiratory volume in 1 s (FEV1) decreases or S cond increases obtained in either group were −9% and +286%, respectively; S acin remained unaffected at all times. In the equal-dose group, a smaller FEV1 decline ( P= 0.002) after methacholine was paralleled by a smaller S cond increase ( P = 0.041) than with histamine. However, in the double-dose group, methacholine maintained a smaller FEV1 decline ( P = 0.009) while inducing a larger S cond increase ( P = 0.006) than did histamine. The differential action of histamine and methacholine is confined to the conductive airways, where histamine likely causes the greatest overall airway narrowing and methacholine induces the largest parallel heterogeneity in airway narrowing, probably at the level of the large and small conductive airways, respectively. The observed ventilation heterogeneities predict a risk for dissociation between ventilation-perfusion mismatch and spirometry, particularly after methacholine challenge.

Heterogeneity of airway constriction and regional ventilation in asthma are commonly studied under the paradigm that each airway's response is independent from other airways. However, some paradoxical effects and contradictions in recent experimental and theoretical findings suggest that considering interactions among serial and parallel airways may be necessary. To examine airway behavior in a bronchial tree with 12 generations, we used an integrative model of bronchoconstriction, including for each airway the effects of pressure, tethering forces, and smooth muscle forces modulated by tidal stretching during breathing. We introduced a relative smooth muscle activation factor (Tr) to simulate increasing and decreasing levels of activation. At low levels of Tr, the model exhibited uniform ventilation and homogeneous airway narrowing. But as Tr reached a critical level, the airway behavior suddenly changed to a dual response with a combination of constriction and dilation. Ventilation decreased dramatically in a group of terminal units but increased in the rest. A local increase of Tr in a single central airway resulted in full closure, while no central airway closed under global elevation of Tr. Lung volume affected the response to both local and global stimulation. Compared with imaging data for local and global stimuli, as well as for the time course of airway lumen caliber during bronchoconstriction recovery, the model predictions were similar. The results illustrate the relevance of dynamic interactions among serial and parallel pathways in airway interdependence, which may be critical for the understanding of pathological conditions in asthma.

We describe the care for an elderly woman who was admitted to the intensive care unit (ICU) to receive noninvasive ventilation for acute exacerbation of chronic obstructive pulmonary disease. After administration of the sleeping pill zopiclone, a nonbenzodiazepine receptor agonist (NBRA), the patient became agitated and was confused, a possible paradoxical reaction to benzodiazepines. These symptoms were immediately resolved after treatment with flumazenil, usually used to reverse the adverse effects of benzodiazepines or NBRAs and to reverse paradoxical reactions to benzodiazepines. This case indicates that zopiclone induced behavioral changes resembling a paradoxical reaction to benzodiazepines and these symptoms may be treated with flumazenil.

We studied both central conducting airway response and changes in the distribution of regional ventilation induced by inhaled histamine in healthy anesthetized and mechanically ventilated rabbit using a novel xenon-enhanced synchrotron radiation computed tomography (CT) imaging technique, K-edge subtraction imaging (KES). Images of specific ventilation were obtained using serial KES during xenon washin, in three axial lung slices, at baseline and twice after inhalation of histamine aerosol (50 or 125 mg/ml) in two groups of animals ( n = 6 each). Histamine inhalation caused large clustered areas of poor ventilation, characterized by a drop in average specific ventilation (sV̇m), but an increase in sV̇m in the remaining lung zones indicating ventilation redistribution. Ventilation heterogeneity, estimated as coefficient of variation (CV) of sV̇m significantly increased following histamine inhalation. The area of ventilation defects and CV were significantly larger with the higher histamine dose. In conducting airways, histamine inhalation caused a heterogeneous airway response combining narrowing and dilatation in individual airways of different generations, with the probability for constriction increasing peripherally. This finding provides further in vivo evidence that airway reactivity in response to inhaled histamine is complex and that airway response may vary substantially with location within the bronchial tree.

AbstractDiaphragmatic paralysis following phrenic nerve injury is a major complication following congenital cardiac surgery. In contrast to unilateral paralysis, patients with bilateral diaphragmatic paralysis present a higher risk group, require different management methods, and have poorer prognosis. We retrospectively analysed seven patients who had bilateral diaphragmatic paralysis following congenital heart surgery during the period from July, 2006 to July, 2014. Considerations were given to the time to diagnosis of diaphragm paralysis, total ventilator days, interval after plication, and lengths of ICU and hospital stays. The incidence of bilateral diaphragmatic paralysis was 0.68% with a median age of 2 months (0.6–12 months). There was one neonate and six infants with a median weight of 4 kg (3–7 kg); five patients underwent unilateral plication of the paradoxical diaphragm following recovery of the other side, whereas the remaining two patients who did not demonstrate a paradoxical movement were successfully weaned from the ventilator following recovery of function in one of the diaphragms. The median ventilation time for the whole group was 48 days (20–90 days). The median length of ICU stay was 46 days (24–110 days), and the median length of hospital stay was 50 days (30–116 days). None of the patients required tracheostomy for respiratory support and there were no mortalities, although all the patients except one developed ventilator-associated pneumonia. The outcome of different management options for bilateral diaphragmatic paralysis following surgery for CHD is discussed.

Breathing was monitored during normocarbia, hypercarbia (6% CO2 in air), and the period immediately after the return to normocarbic conditions in intact, olfactory-denervated, and vagotomized bullfrogs. In intact frogs, ventilation increased during hypercarbia, but the breathing pattern remained episodic. Immediately upon return to air, there was a further paradoxical increase in breathing frequency, and breathing became continuous in most frogs. Results obtained from animals after olfactory receptor denervation indicate that tonic stimulation of olfactory receptors by airway CO2 inhibited breathing during hypercarbia. Measurements of the kinetics of changes in airway and arterial blood CO2 levels support the suggestion that the sudden release of this inhibition on the return to normocarbic conditions was responsible for the posthypercarbic hyperpnea. Vagotomy increased ventilation during normocarbia. Hypercarbia now caused a change in breathing pattern but had no net effect on total ventilation, suggesting that pulmonary vagal feedback inhibited ventilation during normocarbia but stimulated ventilation during hypercarbia. Although olfactory and pulmonary receptor feed-back shape the breathing pattern, they were not responsible for initiating or terminating the episodes of breathing.

Spine stability is ensured through isometric coactivation of the torso muscles; however, these same muscles are used cyclically to assist ventilation. Our objective was to investigate this apparent paradoxical role (isometric contraction for stability or rhythmic contraction for ventilation) of some selected torso muscles that are involved in both ventilation and support of the spine. Eight, asymptomatic, male subjects provided data on low back moments, motion, muscle activation, and hand force. These data were input to an anatomically detailed, biologically driven model from which spine load and a lumbar spine stability index was obtained. Results revealed that subjects entrained their torso stabilization muscles to breathe during demanding ventilation tasks. Increases in lung volume and back extensor muscle activation coincided with increases in spine stability, whereas declines in spine stability were observed during periods of low lung inflation volume and simultaneously low levels of torso muscle activation. As a case study, aberrant ventilation motor patterns (poor muscle entrainment), seen in one subject, compromised spine stability. Those interested in rehabilitation of patients with lung compromise and concomitant back troubles would be assisted with knowledge of the mechanical links between ventilation during tasks that impose spine loading.

Melhor sincronia entre os compartimentos da caixa torácica tem sido identificada como um dos fatores para a redução da dispnéia e aumento da capacidade de exercício após a cirurgia de redução de volume pulmonar (CRVP).Para elucidar os efeitos da CRVP nas variações de volume da caixa torácica em repouso e durante exercício, seis pacientes (VEF1% 26,5 ± 5,5 e VR 224,6 ± 30,2%) foram avaliados antes CRVP, 1 e 3 meses após a cirurgia. Provas de função pulmonar e teste de caminhada de 6 minutos, mudanças de volume da caixa torácica pulmonar (RCp), caixa torácica abdominal (RCa) e abdome (AB) foram registradas pela Pletismografia Opto-Eletrônica (POE) em repouso e durante um teste de exercício incremental em esteira. Após a CRVP, todos os valores espirométricos, os volumes pulmonares, escores de dispnéia e teste de caminhada de 6 minutos melhoraram significativamente. Antes da cirurgia, volume expiratório final da caixa torácica tendeu a diminuir no início do exercício e aumentar depois. Por outro lado, após a cirurgia, o aumento do volume expiratório final foi significativa a partir de 1 mph para a velocidade máxima, o que foi totalmente devido as mudanças de volume do abdômen. O sincronismo entre PCR e AB também melhorou em 1 e 3 meses após o CRVP (p <0,001, p <0,05, respectivamente). Em conclusão, em pacientes com DPOC grave LVRS modifica a ação da musculatura abdominal expiratória e melhora a sincronização entre a caixa torácica pulmonar e o abdome. Estas melhorias são associadas e, possivelmente, explicam o aumento da capacidade de exercício e da diminuição da dispnéia.
Better-synchronized chest wall displacement has been identified as one of the factors for the reduction of dyspnea and increase in exercise capacity after Lung Volume Reduction Surgery (LVRS). To elucidate the effects of LVRS on chest wall volume variations at rest and during exercise six patients (FEV1 26.5±5.5 % and RV 224.6±30.2 %) were studied before LVRS, 1 and 3 months after the surgery. Pulmonary function test and 6-min walking test, volume changes of the pulmonary rib cage (RCp), abdominal rib cage and abdomen (AB) were recorded by Opto-Electronic-Plethysmography (OEP) at rest and during an incremental test on a treadmill. After LVRS, all spirometric and lung volume values, dyspnea scores and 6-minute walking distance significantly improved. Before surgery, end-expiratory volume of the chest wall tended to decrease at the onset of exercise and to increase thereafter. Conversely, after surgery, the increase of end-expiratory volume was significant from 1 mph to the maximum speed and it was totally due to the abdomen. The synchronism between RCp and AB also improved at 1 and 3 month after LVRS (p<0.001,p<0.05, respectively). In conclusion, in severe COPD patients LVRS determines a different action of the abdominal expiratory muscles and a better synchronization between the pulmonary rib cage and abdominal displacement. These improvements are associated to and possibly explain the increased exercise capacity and decreased dyspnea.

Under normal conditions, the right ventricle (RV) virtually acts as a passive conduit. In critically-ill patients many situations induce uncoupling between the right ventricle and pulmonary circulation, leading to RV systolic dysfunction, then failure. Mechanical ventilation has a major impact by decreasing RV preload, but also significantly increasing RV afterload. RV function should thus always be interpreted and re-evaluated in the light of respiratory mechanics and ventilator settings. RV systolic function is key to the patient’s haemodynamic profile and must be monitored to achieve optimal haemodynamic management. Echocardiography is the best compromise between clinical effectiveness and invasiveness to monitor RV function. A limitation is its inability to monitor haemodynamics continuously. Acute cor pulmonale is defined by the combination of RV dilatation with paradoxical septal motion during systole. In conclusion, RV function monitoring is strongly recommended in many situations encountered in the intensive care unit, such as ARDS, septic shock, and pulmonary embolism. Many devices are available, but echocardiography constitutes the best compromise between accuracy and invasiveness.