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Complications of hemodialysis access
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Mia Miller, Prakash Jayanthi, William Oppat
Development of high-output heart failure is an underappreciated complication in patients. As a fistula shunts blood from the arterial circulation to venous circulation bypassing capillary resistance, there is increased preload, as well as decreased systemic arterial flow. Fistula flow in a well-functioning fistula is approximately 700–1500 mL/min.73 Over time, this leads to left ventricular hypertrophy, reduced ejection fraction, and heart failure. Symptoms include tachycardia, elevated pulse pressure, dyspnea on exertion, fluid retention, and jugular venous distension.74 On physical examination, the fistula appears large with rapid flow and aneurysmal growth, often times referred to as a “mega-fistula”.75 Workup begins with an echocardiogram to document left ventricular function, and investigation to rule out other etiologies of high-output heart failure. Elevated levels of biochemical assays such as ANP and BNP confirm volume expansion. To determine high-output heart failure as the definitive cause, a right heart catheterization is required. Characteristic findings include pulmonary hypertension with normal pulmonary vascular resistance and high cardiac output with low-normal systemic vascular resistance.74
Pulmonary Circulation
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
Pulmonary vascular resistance is equally divided between arteries, capillaries and veins, unlike the systemic circulation, where the greatest part of the resistance is in the arterioles. Pulmonary arteries and arterioles which are mostly extra-alveolar are involved in active mechanisms (neural, humoral and gaseous) that control pulmonary vascular resistance. The resistance of the pulmonary capillaries is influenced by alveolar volume and pressure.
Acute coronary syndrome with haemodynamic instability
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Davinder Singh Chadha, Keshavamurthy Ganapathy Bhat
The systemic vascular resistance is often high, but it may be in the normal or low range. The fall in blood pressure may in part be moderated by a marked elevation in systemic vascular resistance (SVR), a response that is mediated by increased release of endogenous vasopressors such as norepinephrine and angiotensin II.
Acute kidney injury in COVID 19 – an update on pathophysiology and management modalities
Published in Archives of Physiology and Biochemistry, 2023
Manoj Khokhar, Purvi Purohit, Dipayan Roy, Sojit Tomo, Ashita Gadwal, Anupama Modi, Mithu Banerjee, Praveen Sharma
The careful monitoring of intravascular volume status is a crucial tenet of conservative fluid management in cardiovascular and renal injury (Matthay et al.2020, p. 19). In the backdrop of sepsis-induced coagulopathy, mechanical ventilation with high PEEP can increase the risk of development of pulmonary hypertension, right heart failure, and hypoperfusion (Tang et al.2020). The currently available standard monitors have a low capability of identifying end-organ damage, thus contributing to increased risk of morbidity and mortality (Table 3). Pulmonary artery catheter (PAC) has shown promise in this regard because it can measure right atrial and right ventricular pressures as well as continuous mixed venous oxygen saturation (SvO2). Additionally, systemic vascular resistance (SVR), and cardiac output can also be measured (D'Alto et al.2018). This helps in minimising the expenditure of hospital resources and maximises monitoring sensitivity. The vigilant monitoring of hemodynamic status and fluid imbalance in COVID-19 associated AKI would help to tide over the period of renal impairment with better outcomes. Further, Ponce et al. (2020) described the workflow for the delivery and monitoring of peritoneal dialysis for patients without the risk of respiratory impairment.
Enhanced bioavailability and pharmacokinetics parameters of Enalapril solid self nanoemulsifying oral dispersible tablet: formulation, in vitro and in vivo evaluation
Published in Pharmaceutical Development and Technology, 2023
Doaa H. Hassan, Amal A. Ammar, Afaf A. Ramadan, Mona K. Younis
Enalapril (EN) is an angiotensin-converting enzyme inhibitor (ACE). EN is used to treat hypertension. It decreases blood pressure via lowering peripheral vascular resistance without significantly increasing cardiac output, rate, or contractility. EN can treat essential hypertension of all grades, particularly in people with diabetes and other chronic renal disorders like glomerulosclerosis (Verbeeck et al. 2017). EN is sparingly soluble and has poor membrane permeability, which ultimately limits the oral bioavailability of EN up to 60% (Maheen et al. 2020). There were numerous strategies for improving oral bioavailability and controlling the release of EN. These involved the formulation of EN as biodegradable microspheres (Nanjwade et al. 2014), cryogels (Ipate et al. 2018), lipospheres (Maheen et al. 2020), and as floating microspheres (Abbas and Alhamdany 2020). This study aimed to improve the oral bioavailability of EN through self-nanoemulsion formulation. The optimized SNES was converted to SSNES and then directly incorporated into a more convenient and easily administered ODT. In vivo pharmacokinetics study for optimum ODT was done in healthy human volunteers compared to the market product.
Secondary erythrocytosis
Published in Expert Review of Hematology, 2023
Rodrick Babakhanlou, Srdan Verstovsek, Naveen Pemmaraju, Cristhiam M. Rojas-Hernandez
Patients with CCHD and erythrocytosis represent a complex management problem. In CCHD, a compensatory erythrocytosis aids to deliver oxygen to the tissues [2,6,9]. With the increase of erythrocytosis, patients may experience symptoms of hyperviscosity and have an increased risk of arterial and venous thrombosis [2,7,11]. These patients may respond to venesection with the aim to reduce peripheral vascular resistance and increase stroke volume and cardiac output [7]. There is no general target hematocrit, and treatment should be individualized on a case-to-case base [11,13]. Excessive venesection may also increase the risk of iron deficiency, and thus, compromise oxygen delivery to the tissue [11]. Facing all those challenges, management of these patients should occur in a specialized CCHD unit.