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Nanomedicines for the Treatment of Respiratory Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Brahmeshwar Mishra, Sundeep Chaurasia
Pulmonary hypertension is high blood pressure in the arteries going to the lung. In healthy individuals, the blood pressure in these arteries is much lower than in the rest of the body. In a healthy individual, the blood pressure of the arteries going to the rest of the body is around 120/80 millimeters of mercury (mm Hg), and pulmonary artery blood pressure is about 25/10 mm Hg. If the pulmonary arterial pressure exceeds about 40/20 mm Hg or the average pressure exceeds 25 mm Hg, then pulmonary hypertension is present. If pulmonary hypertension persists or becomes very high, the right ventricle of the heart, which supplies blood to the pulmonary arteries, is unable to pump effectively, and the person experiences symptoms that include shortness of breath, loss of energy, and edema, which is a sign of right heart failure. Many diseases and conditions increase the pulmonary artery pressure.
Pulmonary complications of illicit drug use
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Patients present with progressive dyspnoea on exertion and an unproductive cough. Precocious emphysema has been well documented in these patients. Pulmonary function tests show reduced DLCO. Right-heart catheterization may show pulmonary hypertension depending on the stage of the disease. Radiographically, injection talcosis may appear as irregular nodular areas of increased opacity in the middle and upper areas of the lungs that may coalesce to form conglomerate masses.31 Diffuse small nodules may be the first manifestation of talc-induced lung disease, with coalescence and enlargement of the nodules being observed as the disease progresses.32 On occasion, lymphadenopathy is present.31 In the later stages of talc-induced pulmonary disease, upper-lobe conglomerate masses that resemble progressive massive fibrosis as seen in silicosis may develop.32 These areas of increased opacity are often superimposed on a background of numerous small nodules and lower lobe-predominant emphysema (see below).
Comparison of mechanical cardiopulmonary support strategies during lung transplantation
Published in Expert Review of Medical Devices, 2020
Noah Weingarten, Dean Schraufnagel, Gilman Plitt, Anthony Zaki, Kamal S. Ayyat, Haytham Elgharably
CPB’s disadvantages relate to inflammation and coagulopathy. CPB induces a systemic inflammatory response when blood interacts with the circuit’s nonendothelial surface thereby activating the coagulation cascade. This activation in turn leads to the elaboration of a broad set of inflammatory mediators [27–29]. Leukocyte-depleting filters have been added to CPB circuits to decrease systemic inflammation, but their clinical benefit has not been definitively proven [30]. CPB induces coagulopathy by subjecting blood to non-laminar flow in an oxygenator, causing blood stasis in its venous reservoir, hemodiluting clotting factors via the infusion of priming fluids, and inducing fibrinolysis and platelet consumption [31–34]. To prevent life-threatening clotting, CPB requires high dose heparinization protocols that aim to maintain activated clotting times greater than 400 seconds [35]. Protamine, which is used to reverse heparin, has been linked to a paradoxical anticoagulant effect at excessive doses, as well as anaphylaxis, pulmonary edema, and pulmonary hypertension [34,36]. Following successful reversal of heparin with protamine, patients may be subject to a heparin rebound effect that increases risk of postoperative bleeding [34,36]. Whether prolonged time on CPB exacerbates these risks during LT is unknown, though evidence suggests that prolonged time on CPB is associated with various worse clinical outcomes in patients undergoing other surgeries like coronary artery bypass grafting [37].
The role of robotic technology in minimally invasive surgery for mitral valve disease
Published in Expert Review of Medical Devices, 2021
Johannes Bonatti, Bob Kiaii, Cem Alhan, Stepan Cerny, Gianluca Torregrossa, Gianluigi Bisleri, Caroline Komlo, T. Sloane Guy
A report from Chemtob et al. [12] describes an extremely conservative approach to patient selection that uses an echocardiographic and computed tomographic (CT) imaging-based algorithm to identify low-risk surgical candidates with isolated mitral valve pathology (Table 1). Thus, contraindications for a robotic approach to mitral valve surgery using this algorithm include patients with echocardiographic findings of moderate or severe aortic regurgitation (AR), mitral annular calcification (MAC), severe pulmonary hypertension, and endocarditis. Other contraindications demonstrated on CT imaging include mild aortoiliac atherosclerosis, a femoral artery diameter <7 mm, or chest wall deformity (Table 1).
Mechanical circulatory support for the right ventricle in combination with a left ventricular assist device
Published in Expert Review of Medical Devices, 2019
Shogo Shimada, Kan Nawata, Osamu Kinoshita, Minoru Ono
Late RHF post-LVAD implant, which is defined as heart failure requiring readmission and medical or surgical intervention after an index hospitalization for LVAD implant, is an underappreciated complication compared to early RHF. Its mechanism remains elusive, but it can be due primarily to intrinsic RV disease or can be secondary to a number of causes, including suboptimal LVAD pump speed, ventricular arrhythmias, progressive tricuspid regurgitation, pulmonary hypertension, or pulmonary embolism. It is potentially distinct from early RHF as the parameters predictive of early RHF are not necessarily useful for predicting late RHF [12,27,28].