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Shock and blood transfusion
Published in Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie, Bailey & Love's Short Practice of Surgery, 2018
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie
Endocrine shock may present as a combination of hypovolaemic, cardiogenic or distributive shock. Causes of endocrine shock include hypo- and hyperthyroidism and adrenal insufficiency. Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines. Cardiac output falls due to low inotropy and bradycardia. There may also be an associated cardiomyopathy. Thyrotoxicosis may cause a high-output cardiac failure.
Mechanical circulatory support for thyrotoxicosis-induced cardiomyopathy
Published in Baylor University Medical Center Proceedings, 2023
Nikita Dhir, Travis Haneke, Timothy Mixon
Thyrotoxicosis is a serious condition that can lead to high-output heart failure and possible cardiogenic shock.1 It usually presents with extreme symptoms of hyperthyroidism, including tachycardia, fever, hypotension, agitation, nausea, vomiting, and/or diarrhea. Thyroid function tests will show high free T4 and T3, with low thyroid-stimulating hormone. Treatment for thyroid storm includes beta-blockers, iodine solution, thionamides, and glucocorticoids.2 Complications of heart failure can potentially require temporary mechanical circulatory support (MCS) with an Impella device or extracorporeal membrane oxygenation (ECMO).1 In patients with hemodynamic instability, beta-blockers are avoided to prevent worsening of high-output cardiac failure. MCS can be a useful bridging tool during the treatment of reversible causes of cardiogenic shock, such as thyroid storm.
Hepatorenal syndrome: a Nationwide Trend Analysis from 2008 to 2018
Published in Annals of Medicine, 2021
Jagmeet Singh, Dushyant Singh Dahiya, Asim Kichloo, Gurdeep Singh, Katayoun Khoshbin, Hafeez Shaka
The exact pathophysiological mechanism implicated in the development of HRS is not completely understood and an area of active research, but it is believed to be secondary to renal vasoconstriction and systemic inflammation leading to impairment in renal function [5]. In patients with advanced liver disease, the development of portal hypertension leads to splanchnic vasodilation due to excessive production of vasodilators, particularly nitrous oxide [6]. This causes a significant decrease in the systemic vascular resistance thereby promoting the activation of hypotension-induced vasoconstrictor systems such as the renin-angiotensin-aldosterone system (RAAS) and Endothelin [7]. As a result, renal vasoconstriction ensues leading to decreased renal perfusion and HRS. Additionally, increased cardiac output in patients with progressive liver disease may also result in high-output cardiac failure, which induces renal vasoconstriction [2]. Furthermore, recent literature has suggested that systemic inflammation may also have a key role to play. In cirrhotics, bacterial translocation (usually gram-negative) and endotoxemia can activate the inflammatory cascade due to the release of pro-inflammatory cytokines after recognition of bacterial by-products [pathogen-associated molecular patterns (PAMS)] by immune cells [8]. This causes splanchnic vasodilation and cardiomyocyte dysfunction leading to decreased effective arterial blood volume and activation of homeostatic neurohormonal mechanisms which, in turn, decrease renal perfusion and promote the development of HRS [8].
Coronary artery fistula between the left anterior descending artery and pulmonary artery
Published in Baylor University Medical Center Proceedings, 2018
Abdul Al-Douri, Ari Cedars, Dat Tran
Based on a study by Zamani et al,6 CAFs are usually asymptomatic during the first 2 decades of life, after which the frequency of both symptoms and complications increases. They reported that most cases of CAF with LAD origin, like that presented in this case, were first diagnosed in adulthood.6 Complications from CAF include steal mediated myocardial ischemia, thrombosis and embolism, high-output cardiac failure, atrial fibrillation, rupture, endocarditis/endarteritis, and arrhythmia.7 Patients most commonly present with symptoms of dyspnea or angina pectoris and occasionally arrhythmias. In patients with high-flow CAFs, a continuous precordial murmur may be auscultated. Steal phenomena may occur in previously asymptomatic patients possibly due to a small fistula increasing in size or secondary to changes in coronary physiology related to the onset of age-related vascular disease or endothelial dysfunction.8