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Relevant bibliographies by topics / Inotropic interventions

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Academic literature on the topic 'Inotropic interventions'

Author: Grafiati

Published: 14 March 2023

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Journal articles on the topic "Inotropic interventions"

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Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. "Effect of inotropic interventions on contraction and Ca2+ transients in the human heart." Journal of Applied Physiology 83, no. 2 (1997): 652–60. http://dx.doi.org/10.1152/jappl.1997.83.2.652.

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Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. Effect of inotropic interventions on contraction and on Ca2+ transients in the human heart. J. Appl. Physiol. 83(2): 652–660, 1997.—The present study investigated the influences of inotropic intervention on the intracellular Ca2+ transient {intracellular Ca2+concentration ([Ca2+]i)} and contractile twitch. Isometric twitch and [Ca2+]i(fura 2 ratio method) were measured simultaneously (1 Hz, 37°C) after stimulation with Ca2+(0.9–3.2 mM), the cardiac glycoside ouabain (Oua; 0.1 μM), the β1- and β2

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Bing, O. H., N. L. Hague, C. L. Perreault, et al. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (1994): H1112—H1121. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h1112.

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To examine the mechanisms by which thyroid hormone modulates the inotropic state of rat myocardium, we studied the effects of thyroid state on isolated rat left ventricular papillary muscle function and intracellular calcium transients in the baseline state and in response to calcium and isoproterenol. Marked differences in contractile state of papillary muscles from hypothyroid and thyroid hormone-treated rats seen under baseline conditions (1.0 mM bath calcium, 30 degrees C, stimulation rate 12/min) do not appear to be due to differences in intracellular calcium concentration ([Ca2+]i) or to

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Bahler, R. C., and P. Martin. "Effects of loading conditions and inotropic state on rapid filling phase of left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (1985): H523—H533. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h523.

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Afterload, activation sequence, inotropism, and extent of shortening affect the time constant (T) of left ventricular (LV) isovolumic pressure decay, yet it is unknown if they modify peak lengthening velocity of the LV minor axis [(dD/dt)/D]. Accordingly, we studied their effects on (dD/dt)/D, measured by sonomicrometry, in nine anesthetized open-chest dogs during atrial pacing at 2 Hz. Afterload was increased 20-40 mmHg by 1) constricting the ascending aorta and 2) occluding the descending aorta for four beats. Activation was altered by right ventricular pacing. These interventions, plus cons

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Binkley, P. F., D. B. Van Fossen, G. J. Haas, and C. V. Leier. "Increased ventricular contractility is not sufficient for effective positive inotropic intervention." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (1996): H1635—H1642. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1635.

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Positive inotropic intervention with dobutamine in patients with congestive heart failure is accompanied by complementary vascular changes, as measured by the aortic input impedance spectrum, that promote the efficient transfer of augmented myocardial contractile power. It is unknown whether this is a nonspecific response to increased ventricular contractility or is a function of the properties of the positive inotropic agent employed. Therefore, the influence of two different positive inotropic interventions, dobutamine and dopamine, on ventricular-vascular coupling was examined in 15 patient

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Rose, Horst, Stefanie Pöpping, Stefan Mruck, and Helmut Kammermeier. "Influence of inotropic interventions on efficiency of cardiomyocyte contraction." Journal of Molecular and Cellular Cardiology 24 (August 1992): S110. http://dx.doi.org/10.1016/0022-2828(92)91811-i.

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Neumann, J. "A renaissance of positive inotropic interventions to treat heart failure?" Cardiovascular Research 59, no. 3 (2003): 534–35. http://dx.doi.org/10.1016/s0008-6363(03)00557-1.

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Furukawa, Yasuyuki, and Paul Martin. "Attenuation of the responses to repeated cholinergic interventions in the isolated dog atrium." Canadian Journal of Physiology and Pharmacology 64, no. 2 (1986): 206–12. http://dx.doi.org/10.1139/y86-031.

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In the isolated, blood-perfused canine right atrium, which was pretreated with propranolol, negative chronotropic and inotropic responses were evoked by stimulation of the intramural parasympathetic nerve fibers or by intra-arterial infusion of acetylcholine (ACh). Successive cholinergic interventions were applied; first, a conditioning intervention for 2 min was given, then this was followed by a test intervention for 4 min. The two interventions were separated by a rest period that varied from 15 to 240 s. The cardiac responses to the conditioning parasympathetic nerve stimulation quickly re

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Krstic, Anna, and Marie-Louise Ward. "CA2+ Handling in Non-Failing Hypertrophic Cardiomyocytes Subjected to Inotropic Interventions." Biophysical Journal 120, no. 3 (2021): 110a—111a. http://dx.doi.org/10.1016/j.bpj.2020.11.891.

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Langione, Marianna, J. Manuel Pioner, Sonette Steczina, et al. "Engineered heart tissues for studying twitch tension and inotropic pharmacological interventions." Biophysical Journal 121, no. 3 (2022): 396a. http://dx.doi.org/10.1016/j.bpj.2021.11.778.

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van der Linden, L. P., E. T. van der Velde, H. C. van Houwelingen, A. V. Bruschke, and J. Baan. "Determinants of end-systolic pressure during different load alterations in the in situ left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (1994): H1895—H1906. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h1895.

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Because of the strong dependency of the end-systolic pressure-volume relation on the type of transient loading intervention in the in situ left ventricle (LV), experiments in the basal inotropic state in 16 open-chest anesthetized dogs were reanalyzed to find additional variables to model and predict end-systolic pressure (ESP) of both afterloading and preloading interventions by a single equation. Random-coefficients regression analysis was performed on 22 experiments in the basal inotropic state simultaneously, yielding an overall R2 of 0.97. The major part of total variance of ESP was due t

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Dissertations / Theses on the topic "Inotropic interventions"

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Governali, Serena. "Action mechanisms of physiological and pharmacological inotropic interventions on the slow/cardiac striated muscle." Doctoral thesis, Università di Siena, 2020. http://hdl.handle.net/11365/1107309.

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ACTION MECHANISMS OF PHYSIOLOGICAL AND PHARMACOLOGICAL INOTROPIC INTERVENTIONS ON THE SLOW/CARDIAC STRIATED MUSCLE. The mechanical performance of striated muscle is under the control of both thin and thick filament regulation. The start signal is the increase of intracellular Ca2+ concentration, promoted by cell membrane depolarization by the action potential, followed by Ca2+ binding to troponin in the thin filament and structural changes in the troponin–tropomyosin complex that release the actin sites for binding of myosin motors. The second regulatory mechanism, based on thick filament m

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Books on the topic "Inotropic interventions"

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Partanen, Juhani. Cardiovascular responses induced by haemodynamic interventions and inotropics: A series of noninvasive studies. University Central Hospital, 1989.

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Schwarte, Lothar A., Stephan A. Loer, J. K. Götz Wietasch, and Thomas W. L. Scheeren. Cardiovascular drugs in anaesthetic practice. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0019.

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Anaesthetists should be familiar with currently available cardiovascular drugs used to maintain cardiovascular stability and achieve haemodynamic goals in surgical patients. The first part of this chapter summarizes antihypertensive agents, and the second part discusses positive inotropic drugs and vasopressors, which can be used perioperatively. Selection of vasoactive agents should be guided by the therapeutic goal (e.g. decreasing or increasing blood pressure or blood flow) and the underlying pathophysiology. Choice of catecholamines in a given situation should be based on the desired effec

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Fogelman, Patricia Maani, and Janine A. Gerringer. Withdrawal of Cardiology Technology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190204709.003.0011.

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The care of the cardiac patient requires exquisite assessment including history, physical examinations, and diagnostic data in order to make differential diagnoses and formulate individualized treatment plans. Interventions include education about lifestyle modifications, the introduction and titration of cardiac medications, and referral for more advanced treatments such as vasoactive or inotropic medications, cardiovascular implantable electronic devices, and ventricular assist devices. Often, patients decide to discontinue these therapies. Standardized protocols for withdrawal of life-susta

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Thiele, Holger, and Uwe Zeymer. Cardiogenic shock in patients with acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0049.

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Cardiogenic shock complicating an acute coronary syndrome is observed in up to 10% of patients and is associated with high mortality still approaching 50%. The extent of ischaemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis of the cardiogenic shock patient. Careful risk assessment for each patient, based on clinical criteria, is mandatory, to decide appropriately regarding revascularization by primary percutaneous coronary intervention or coronary artery bypass grafting, drug treatment by inotropes and vasopressors, mechanical left

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Thiele, Holger, and Uwe Zeymer. Cardiogenic shock in patients with acute coronary syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0049_update_001.

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Cardiogenic shock complicating an acute coronary syndrome is observed in up to 10% of patients and is associated with high mortality still approaching 50%. The extent of ischaemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis of the cardiogenic shock patient. Careful risk assessment for each patient, based on clinical criteria, is mandatory, to decide appropriately regarding revascularization by primary percutaneous coronary intervention or coronary artery bypass grafting, drug treatment by inotropes and vasopressors, mechanical left

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Thiele, Holger, and Uwe Zeymer. Cardiogenic shock in patients with acute coronary syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0049_update_002.

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Cardiogenic shock complicating an acute coronary syndrome is observed in up to 10% of patients and is associated with high mortality still approaching 50%. The extent of ischaemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis of the cardiogenic shock patient. Careful risk assessment for each patient, based on clinical criteria, is mandatory, to decide appropriately regarding revascularization by primary percutaneous coronary intervention or coronary artery bypass grafting, drug treatment by inotropes and vasopressors, mechanical left

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Thiele, Holger, and Uwe Zeymer. Cardiogenic shock in patients with acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0049_update_003.

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Cardiogenic shock complicating an acute coronary syndrome is observed in up to 10% of patients and is associated with high mortality still approaching 50%. The extent of ischaemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis of the cardiogenic shock patient. Careful risk assessment for each patient, based on clinical criteria, is mandatory, to decide appropriately regarding revascularization by primary percutaneous coronary intervention or coronary artery bypass grafting, drug treatment by inotropes and vasopressors, mechanical left

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Kevin Luk, K. H., and Deepak Sharma. Subarachnoid Hemorrhage. Edited by David E. Traul and Irene P. Osborn. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850036.003.0024.

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Subarachnoid hemorrhage (SAH) is commonly caused by rupture of an intracranial aneurysm, arteriovenous malformation, or due to trauma. Prompt diagnosis and intervention are required to control intracranial pressure, maintain cerebral perfusion, and prevent rebleeding. Clinical grading of the bleed predicts morbidity and mortality, whereas imaging grading predicts risk of cerebral vasospasm. Hydrocephalus can occur as a result of SAH, which requires treatment with an external ventricular drain. Endovascular and open microsurgical procedures are available for securing the vascular abnormalities.

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Clarkin, Andrew J., and Nigel R. Webster. Pre-surgical optimization of the high-risk patient. Edited by Neil Soni and Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0088.

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There is a small group of patients undergoing surgery who comprise the majority of perioperative deaths. Morbidity and mortality resulting from tissue hypoxia in the perioperative period can be predicted and prevented by identification of the at-risk group and targeted interventions. Management of these patients requires an understanding of oxygen delivery, the use of cardiac output monitoring to guide fluid and inotrope administration to attain a predefined goal of supranormal oxygen delivery, and the attainment of physiological goals. There are both patient outcome and economic benefits to t

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Book chapters on the topic "Inotropic interventions"

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Hasenfuss, Gerd, Ch Holubarsch, H. Just, E. Blanchard, L. A. Mulieri, and N. R. Alpert. "Energetic aspects of inotropic interventions in rat myocardium." In Cardiac Energetics. Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-11289-2_24.

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Bavendiek, U., K. Brixius, G. Münch, C. Zobel, J. Müller-Ehmsen, and R. H. G. Schwinger. "Effect of inotropic interventions on the force-frequency relation in the human heart." In Heart rate as a determinant of cardiac function. Steinkopff, 2000. http://dx.doi.org/10.1007/978-3-642-47070-7_9.

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Orchard, C. H., F. Brette, A. Chase, and M. R. Fowler. "Role of the T-Tubules in the Response of Cardiac Ventricular Myocytes to Inotropic Interventions." In Heart Rate and Rhythm. Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-17575-6_13.

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Novotny, Mark J., and Patricia M. Hogan. "Inotropic Interventions in the Assessment of Myocardial Failure Associated with Taurine Deficiency in Domestic Cats." In Advances in Experimental Medicine and Biology. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0182-8_32.

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Blanchard, E. M., L. A. Mulieri, and Norman R. Alpert. "The effects of acute and chronic inotropic interventions on tension independent heat of rabbit papillary muscle." In Cardiac Energetics. Steinkopff, 1987. http://dx.doi.org/10.1007/978-3-662-11289-2_13.

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Drexler, M., E. Mayer, H. Oelert, R. Erbel, and J. Meyer. "Transesophageal Echocardiographic Monitoring During Positive Inotropic Drug Intervention and Balloon Pumping." In Transesophageal Echocardiography. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74257-6_25.

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Saeed, Diyar. "Role of Inotropes, Pulmonary Vasodilators, and Other Pharmacologic Interventions for Right Ventricular Dysfunction." In Mechanical Circulatory Support in End-Stage Heart Failure. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-43383-7_21.

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Thiele, Holger, and Suzanne de Waha-Thiele. "Low cardiac output states and cardiogenic shock." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0048.

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Low cardiac output and cardiogenic shock are associated with high mortality. Among the multiple heterogeneous reasons for low cardiac output and cardiogenic shock acute coronary syndromes are the most frequent cause. Mortality is still approaching 50%. The extent of ischaemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis of the cardiogenic shock patient. Careful risk assessment for each patient, based on clinical criteria, is mandatory, to decide appropriately regarding revascularization by primary percutaneous coronary intervention or coronary artery bypass grafting, drug treatment by inotropes and vasopressors, mechanical circulatory support, additional intensive care treatment, triage among alternative hospital care levels, and allocation of clinical resources. This chapter will outline the underlying causes and diagnostic criteria, pathophysiology, and treatment of cardiogenic shock focussing on acute coronary syndromes, including mechanical complications and shock from right ventricular failure. There will be a major focus on potential therapeutic issues from an interventional cardiologist's and also an intensive care physician's perspective on the advancement of new therapeutical arsenals, both percutaneous mechanical circulatory support and pharmacological support. Since studying the cardiogenic shock population in randomized trials remains challenging, this chapter will also touch upon the specific challenges encountered in previous clinical trials and the implications for future perspectives in cardiogenic shock.

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Smith, Daniel, Eric Ness, and Amanda M. Kleiman. "Evaluation and Anesthetic Management for Patients With Cardiac Trauma." In Cardiac Anesthesia: A Problem-Based Learning Approach, edited by Mohammed M. Minhaj. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190884512.003.0035.

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Cardiac trauma, either blunt or penetrating, is a life-threatening condition often requiring immediate intervention. Cardiac trauma causes varied hemodynamic effects, from stable arrhythmia to cardiovascular collapse. The diagnosis of cardiac trauma relies on a high level of clinical suspicion paired with imaging, including transthoracic echocardiography. Anesthetic management for cardiac trauma focuses primarily on maintenance of preload and cardiac function while optimizing operating conditions for surgical repair. Depending on the injuries involved, support that includes inotropes, vasopressors, and potentially mechanical support may be required. This chapter discusses the pathophysiology and presentation of cardiac trauma and explores the intricate anesthetic management of these complex patients.

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Daniels, Justin. "Hypertrophic Obstructive Cardiomyopathy With Systolic Anterior Motion of the Mitral Valve." In Critical Care. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780190885939.003.0015.

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Abstract Hypertrophic cardiomyopathy (HCM) is the most common genetic cardiovascular disease, affecting 1 in 500 people. It’s a disease with hypertrophic myocytes in disarray, leading to either diffuse or focal ventricular wall thickening and associated with the development of fibrosis. The penetrance and presentation of the disease spans a wide spectrum. The most concerning sequalae is the occurrence of sudden cardiac death (SCD) in young patients. Besides SCD, HCM is associated with left ventricular outflow tract obstruction, systolic anterior motion of the mitral valve, diastolic heart failure, atrial fibrillation, cardiac ischemia, and end-stage systolic heart failure. The goals of treatment for acute symptoms include volume replacement, vasoconstrictors, and controlling tachycardia. Long-term treatment is centered around negative inotropes, negative chronotropes, and invasive interventions to reduce obstruction.

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Conference papers on the topic "Inotropic interventions"

1

Mazhar, Fazeelat, Francesco Regazzoni, Chiara Bartolucci, et al. "Electro-Mechanical Coupling in Human Atrial Cardiomyocytes: Model Development and Analysis of Inotropic Interventions." In 2021 Computing in Cardiology (CinC). IEEE, 2021. http://dx.doi.org/10.23919/cinc53138.2021.9662766.

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