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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Pathophysiological mechanisms that influence the development of cor pulmonale include increased alveolar pressure, loss of capillary beds, medial hypertrophy in the arterioles, and vasoconstriction. Increased alveolar pressure may be due to mechanical ventilation. Loss of capillary beds may be caused by thrombosis in pulmonary embolism or because of bullous changes as part of COPD. Medial hypertrophy of the arterioles is often related to pulmonary hypertension caused by a variety of factors, and vasoconstriction can be caused by hypercapnia, hypoxia, or both. Afterload on the RV is increased by pulmonary hypertension. There is then an event cascade that is like the steps of LV failure. They include elevated end-diastolic and central venous pressure, with ventricular hypertrophy and dilation. Increased blood viscosity may increase demands upon the RV. The increased viscosity may be caused by hypoxia-influenced polycythemia. In rare cases, RV failure affects the LV when a septum is dysfunctional and bulges into the LV. This interferes with filling and results in diastolic dysfunction.
Thoracic Trauma
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
The thorax contains the heart, lungs, great vessels (aorta, inferior and superior vena cava, pulmonary arteries and veins), lower trachea, oesophagus and thoracic duct. The lower ribs overlie the ‘intrathoracic abdomen’, including the liver, spleen and biliary apparatus. The bulk of the thoracic volume is taken up by the two lungs, with the mediastinum—principally the heart and great vessels—between them. Each lung is cloaked in visceral pleura, which is continuous with the parietal pleura that lines the thoracic cage. A tiny amount of fluid between the two layers lubricates the movements of the lungs. The pressure gradient required to generate inspiratory flow is achieved largely by flattening the diaphragm to increase the volume of the thorax, creating a sub-atmospheric pressure in the lungs. During expiration the intra-alveolar pressure becomes slightly higher than atmospheric pressure and gas flow to the mouth results. The normal adult respiratory rate is 12–16 breaths per minute with a tidal volume (the normal amount of air inhaled and exhaled per breath at rest) of around 500 mL.
Mechanical Properties of the Lungs
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In the nitrogen washout technique, 100% O2 is used, and the total amount of nitrogen eliminated in the expired gas collected is measured (expired volume × nitrogen concentration). The second method uses the wash-in of helium as a tracer gas. These two methods only measure FRC contributed by the communicating airways and do not include gas trapped distal to closed airways. The body plethysmograph technique measures FRC contributed by the communicating as well as non-communicating airways. The subject is contained in a closed gas-tight box and breathes against an occluded airway. Alveolar pressure changes recorded at the mouth are compared with the small changes in lung volume, which are derived from pressure changes in the plethysmograph using Boyle's law.
A teenaged patient with spontaneous pneumopericardium after hookah smoking
Published in Clinical Toxicology, 2022
To our knowledge, the present case appears to be the first documented of SPP associated with smoking a hookah, which was the only causal factor identified with his condition. There are a few case reports of spontaneous pneumothorax and spontaneous pneumomediastinum associated with hookah smoking [1]. We know of no data reporting the incidence of barotrauma after hookah use either in adult or pediatric patients. The pathogenesis of SPP is likely related to the technique associated with hookah smoking; characterized as deep and prolonged inspiration, followed by forced exhalation. Increased alveolar pressure significantly above normal peak inspiratory pressures can induce alveolar rupture, leading to air leakage into the broncho-vascular sheath, and tracking along broncho-vascular bundles; this can dissect/deposit in the subcutaneous tissues. Air deposit can occur in the thorax, neck, pericardium, retroperitoneum; or even the epidural space via the posterior mediastinum and intervertebral foramen [2]. Various precipitating factors associated with airway rupture involve voluntary and involuntary alterations in breathing patterns, such as bronchial asthma, cannabis smoking, cocaine inhalation, and barotrauma occurring with a Valsalva maneuver [3,4].
Epidemiological, clinical, and echocardiographic features of twenty ‘Takotsubo-like’ reversible myocardial dysfunction cases with normal coronarography following immersion pulmonary oedema
Published in Acta Cardiologica, 2021
Raphaël Demoulin, Raphaël Poyet, Olivier Castagna, Emmanuel Gempp, Arnaud Druelle, Paul Schmitt, Eléonore Capilla, Gwénolé Rohel, Frédéric Pons, Christophe Jégo, François-Xavier Brocq, Gilles R. Cellarier
IPE was first described by Wilmshurst et al. [7]. Despite numerous reported cases, its pathophysiology and its risk factors have not been fully established. It affects 1.1% of divers without prior pathology [8]. It generally affects patients who are at least 50 years of age who show CVRFs, or young subjects engaged in substantial physical exertion. It is thought to be linked with a multifactorial increase in the hydrostatic pressure of the pulmonary capillaries during immersion [9,10]. This increase is linked with an elevation of the cardiac output due to the exertion of the dive, as well as an increase in the preload in relation to redistribution of the peripheral blood volume towards the chest vessels by a blood shift and vasoconstriction phenomenon, itself possibly accentuated by the wearing of a diving wetsuit that is too tight. It also results from an increase of the afterload linked with peripheral arterial vasoconstriction secondary to the low temperature of the water during the dive. In parallel, this increase in the hydrostatic pressure is associated with a lowering of the pulmonary intra-alveolar pressure, linked both with respiratory demands enhanced by diving and with the gradient of hydrostatic pressure between the pressure regulator and the diver’s lungs during the ascent.
Targeting transpulmonary pressure to prevent ventilator-induced lung injury
Published in Expert Review of Respiratory Medicine, 2019
Luciano Gattinoni, Lorenzo Giosa, Matteo Bonifazi, Iacopo Pasticci, Mattia Busana, Matteo Macri, Federica Romitti, Francesco Vassalli, Michael Quintel
Anyway, even if Plateau pressure does not always reflect alveolar pressure, it represents the best clinical way to assess the airway pressure under static conditions, and thus estimate PL. Plateau pressure has actually two components, P1 and P2 (see Figure 1). The difference between P1 and P2 is almost completely explained by a viscoelastic property of the respiratory system [33] which is called stress relaxation (a progressive reduction of stress at a constant level of strain) [34]. Part of this difference is instead explained by the so-called pendelluft [35] which is a redistribution of gas between alveoli with different time constants once the flow has been stopped. It has been shown in dogs, however, that pendelluft has a much smaller role than stress relaxation in explaining the difference between P1 and P2 [36]. It is clear that in order for plateau pressure to better reflect the real pressure distending the respiratory system P2 should be preferred to P1 in the estimation of PL. With the exception of very high inspiratory flows, however, the difference between P1 and P2 is minimal [37] and, in the clinical practice, a mean value of plateau pressure can be used to calculate PL.