scholarly journals COVID-19 pneumonia: pathophysiology and management

2021 ◽  
Vol 30 (162) ◽  
pp. 210138
Author(s):  
Luciano Gattinoni ◽  
Simone Gattarello ◽  
Irene Steinberg ◽  
Mattia Busana ◽  
Paola Palermo ◽  
...  
Keyword(s):  
Respiratory Mechanics ◽  
Underlying Mechanism ◽  
Carbon Dioxide Tension ◽  
Additional Patient ◽  
Normal Lung ◽  
Respiratory Drive ◽  
High Dependency ◽  
Severe Hypoxaemia ◽  
Peculiar Characteristic ◽  
Gas Volume

Coronavirus disease 2019 (COVID-19) pneumonia is an evolving disease. We will focus on the development of its pathophysiologic characteristics over time, and how these time-related changes determine modifications in treatment. In the emergency department: the peculiar characteristic is the coexistence, in a significant fraction of patients, of severe hypoxaemia, near-normal lung computed tomography imaging, lung gas volume and respiratory mechanics. Despite high respiratory drive, dyspnoea and respiratory rate are often normal. The underlying mechanism is primarily altered lung perfusion. The anatomical prerequisites for PEEP (positive end-expiratory pressure) to work (lung oedema, atelectasis, and therefore recruitability) are lacking. In the high-dependency unit: the disease starts to worsen either because of its natural evolution or additional patient self-inflicted lung injury (P-SILI). Oedema and atelectasis may develop, increasing recruitability. Noninvasive supports are indicated if they result in a reversal of hypoxaemia and a decreased inspiratory effort. Otherwise, mechanical ventilation should be considered to avert P-SILI. In the intensive care unit: the primary characteristic of the advance of unresolved COVID-19 disease is a progressive shift from oedema or atelectasis to less reversible structural lung alterations to lung fibrosis. These later characteristics are associated with notable impairment of respiratory mechanics, increased arterial carbon dioxide tension (PaCO2), decreased recruitability and lack of response to PEEP and prone positioning.

scholarly journals Ventilatory response to exercise in subjects breathing CO2 or HeO2

1997 ◽  
Vol 82 (3) ◽  
pp. 746-754 ◽  
Author(s):  
T. G. Babb
Keyword(s):  
Maximal Exercise ◽  
Respiratory Mechanics ◽  
Ventilatory Threshold ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Lung ◽  
Normal Lung Function ◽  
Older Subjects ◽  
Breathing Room ◽  
Response To Exercise

Babb, T. G. Ventilatory response to exercise in subjects breathing CO2 or HeO2. J. Appl. Physiol. 82(3): 746–754, 1997.—To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (V˙e) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase ( P < 0.001) inV˙e at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2,V˙e was increased ( P < 0.05) only during maximal exercise (24 ± 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2( P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2( P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater ( P < 0.01) when the subjects were breathing CO2 (22 ± 12%) than when breathing room air (12 ± 9%) or when breathing HeO2 (10 ± 7%) ( n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2( P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of V˙eduring maximal exercise and the regulation ofV˙e and respiratory mechanics during heavy-to-maximal exercise.

Neural respiratory drive, respiratory mechanics and breathlessness in COPD patients with comorbid heart failure

2020 ◽  
Author(s):  
Luis Estrada ◽  
Emily Lau ◽  
Manuel Lozano-Garcia ◽  
Anna Moore ◽  
Peter Cho ◽  
...  
Keyword(s):  
Heart Failure ◽  
Respiratory Mechanics ◽  
Respiratory Drive ◽  
Copd Patients

Severe tachypnoea and dyspnoea due to physiological hyperventilation in pregnancy

2021 ◽  
pp. 1753495X2110378
Author(s):  
Brady Thomson ◽  
Ragani Velusamy ◽  
Annabel Martin
Keyword(s):  
Daily Living ◽  
Renal Excretion ◽  
Underlying Mechanism ◽  
Normal Pregnancy ◽  
Respiratory Alkalosis ◽  
Respiratory Physiology ◽  
Respiratory Drive ◽  
Underlying Mechanisms ◽  
Underlying Pathology ◽  
In Pregnancy

Physiological hyperventilation and dyspnoea in pregnancy are well-established phenomena and commonly lead to a chronic respiratory alkalosis with compensatory renal excretion of bicarbonate. However, the underlying mechanism of dyspnoea during normal pregnancy remains largely undefined. Increasing progesterone levels are a primary factor leading to increased respiratory drive to ensure the rising metabolic demands of the pregnancy are met. Dyspnoea symptoms typically begin in the first or second trimester, are mild, and do not interfere with activities of daily living. We report the case of a 35-year-old female with severe physiological hyperventilation of pregnancy presenting with profound dyspnoea, tachypnoea, and presyncope from 18 weeks of gestation until delivery. Subsequent investigations revealed no identifiable underlying pathology. There remain limited reports of such severe physiological hyperventilation of pregnancy. This case highlights interesting questions regarding the respiratory physiology of pregnancy and underlying mechanisms.

scholarly journals Mechanisms, measurement and management of exertional dyspnoea in asthma

2017 ◽  
Vol 26 (144) ◽  
pp. 170015 ◽  
Author(s):  
Jason Weatherald ◽  
M. Diane Lougheed ◽  
Camille Taillé ◽  
Gilles Garcia
Keyword(s):  
Underlying Mechanism ◽  
Asthma Severity ◽  
Qualitative Description ◽  
Future Research ◽  
Dynamic Hyperinflation ◽  
Variable Degree ◽  
Respiratory Drive ◽  
Exertional Dyspnoea ◽  
Pharmacological Interventions ◽  
Physiological Mechanisms

Asthma is a heterogeneous condition, with dyspnoea during exercise affecting individuals to a variable degree. This narrative review explores the mechanisms and measurement of exertional dyspnoea in asthma and summarises the available evidence for the efficacy of various interventions on exertional dyspnoea. Studies on the mechanisms of dyspnoea in asthma have largely utilised direct bronchoprovocation challenges, rather than exercise, which may invoke different physiological mechanisms. Thus, the description of dyspnoea during methacholine challenge can differ from what is experienced during daily activities, including exercise. Dyspnoea perception during exercise is influenced by many interacting variables, such as asthma severity and phenotype, bronchoconstriction, dynamic hyperinflation, respiratory drive and psychological factors. In addition to the intensity of dyspnoea, the qualitative description of dyspnoea may give important clues as to the underlying mechanism and may be an important endpoint for future interventional studies. There is currently little evidence demonstrating whether pharmacological or non-pharmacological interventions specifically improve exertional dyspnoea, which is an important area for future research.

Influence of cerebral activity in wakefulness on regulation of breathing

1961 ◽  
Vol 16 (1) ◽  
pp. 15-20 ◽  
Author(s):  
B. Raymond Fink
Keyword(s):  
Carbon Dioxide ◽  
Control Volume ◽  
Control Level ◽  
Periodic Breathing ◽  
Carbon Dioxide Tension ◽  
Respiratory Drive ◽  
Healthy Men ◽  
Cerebral Activity ◽  
Control Frequency ◽  
Regulation Of Breathing

Thirteen healthy men, unaware of the objectives of this study, underwent passive or active overventilation lowering the end-expiration carbon dioxide tension to 25 mm. Hg or below. At the end of the period of hyperventilation, rhythmic respiration continued uninterrupted at approximately the control frequency. The volume of ventilation was above control during the first minute of recovery and then stabilized at about two-thirds of the control volume; it continued at this level for over 10 minutes during which time the end-expiration PCO2 gradually rose toward the control level. No instance of periodic breathing occurred. The absence of overventilatory apnea in the waking condition contrasts with its easy elicitation during general anesthesia. It is concluded that cerebral activity associated with wakefulness is a component of the normal respiratory drive, and that carbon dioxide acts by augmenting the effects of this component. Submitted on June 27, 1960

scholarly journals Effects on Lung Gas Volume, Respiratory Mechanics and Gas Exchange of a Closed-Circuit Suctioning System during Volume- and Pressure-Controlled Ventilation in ARDS Patients

2021 ◽  
Vol 10 (23) ◽  
pp. 5657
Author(s):  
Davide Chiumello ◽  
Luca Bolgiaghi ◽  
Paolo Formenti ◽  
Tommaso Pozzi ◽  
Manuela Lucenteforte ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Respiratory Mechanics ◽  
Pressure Control ◽  
Closed Circuit ◽  
Volume Control ◽  
Endotracheal Suctioning ◽  
Controlled Ventilation ◽  
Pressure Controlled Ventilation ◽  
Gas Volume ◽  
Pressure Controlled

Mechanically ventilated patients periodically require endotracheal suctioning. There are conflicting data regarding the loss of lung gas volume caused by the application of a negative pressure by closed-circuit suctioning. The aim of this study was to evaluate the effects of suctioning performed by a closed-circuit system in ARDS patients during volume- or pressure-controlled ventilation. In this prospective crossover-design study, 18 ARDS patients were ventilated under volume and pressure control applied in random order. Gas exchange, respiratory mechanics and EIT-derived end-expiratory lung volume (EELV) before the suctioning manoeuvre and after 5, 15 and 30 min were recorded. The tidal volume and respiratory rate were similar in both ventilation modes; in volume control, the EELV decreased by 31 ± 23 mL, 5 min after the suctioning, but it remained similar after 15 and 30 min; the oxygenation, PaCO2 and respiratory system elastance did not change. In the pressure control, 5 min after suctioning, EELV decreased by 35 (26–46) mL, the PaO2/FiO2 did not change, while PaCO2 increased by 5 and 30 min after suctioning (45 (40–51) vs. 48 (43–52) and 47 (42–54) mmHg, respectively). Our results suggest minimal clinical advantages when a closed system is used in volume-controlled compared to pressure-controlled ventilation.

scholarly journals PPA1 promotes NSCLC progression via a JNK- and TP53-dependent manner

Oncogenesis ◽  
2019 ◽  
Vol 8 (10) ◽  
Author(s):  
Dehong Luo ◽  
Daishun Liu ◽  
Wen Shi ◽  
Huimin Jiang ◽  
Wei Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Apoptosis ◽  
Ectopic Expression ◽  
Underlying Mechanism ◽  
Normal Lung ◽  
Inorganic Pyrophosphatase ◽  
Dependent Manner ◽  
Promising Target ◽  
Tumor Types ◽  
Inhibitor Treatment

Abstract Inorganic pyrophosphatase (PPA1) promotes tumor progression in several tumor types. However, the underlying mechanism remains elusive. Here, we disclosed that PPA1 expression is markedly upregulated in lung carcinoma tissue versus normal lung tissue. We also found that the non-small cell lung cancer (NSCLC) cell lines show increased PPA1 expression levels versus normal lung cell line control. Moreover, the knockdown of PPA1 promotes cell apoptosis and inhibits cell proliferation. Whereas, the ectopic expression of PPA1 reduces cell apoptosis and enhances cell proliferation. Most interestingly, the expression of mutant PPA1 (D117A) significantly abolishes PPA1-mediated effect on cell apoptosis and proliferation. The underlying mechanism demonstrated that TP53 expression deficiency or JNK inhibitor treatment could abolish PPA1-mediated NSCLC progression. In summary, the aforementioned findings in this study suggest a new pathway the PPA1 mediates NSCLC progression either via TP53 or JNK. Most important, the pyrophosphatase activity is indispensible for PPA1-mediated NSCLC progression. This may provide a promising target for NSCLC therapy.

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