Relevant bibliographies by topics / Inotropic interventions

Academic literature on the topic 'Inotropic interventions'

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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 (August 1, 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-adrenoceptor-agonist isoprenaline (Iso; 1–10 nM), and the Ca2+ sensitizer EMD-57033 (30 μM) by using isolated human nonfailing right auricular trabeculae ( n = 19). Inotropic interventions increased force of contraction and peak rate of tension rise (+ T) significantly. Only Iso stimulated peak rate of tension decay (− T) higher than + T ( P< 0.05), thereby reducing time of contraction ( T twitch). EMD-57033 increased + T more effectively than − T and prolonged T twitch( P < 0.05). Ca2+, Oua, and Iso, but not EMD-57033, increased systolic Ca2+. Diastolic Ca2+ increased after stimulation with Oua or Ca2+, but not in the presence of EMD-57033. Iso shortened the Ca2+ transient and did not influence diastolic Ca2+. In conclusion, positive inotropic agents differently affect force and [Ca2+]idepending on their mode of action. Inotropic interventions influence diastolic Ca2+ and thus may be less advantageous in a situation with altered intracellular Ca2+ homeostasis (e.g., heart failure due to dilated cardiomyopathy).
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Bing, O. H., N. L. Hague, C. L. Perreault, C. H. Conrad, W. W. Brooks, S. Sen, and J. P. Morgan. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 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 changes in myofilament calcium sensitivity but correlate with shifts in myosin isozyme distribution. In response to superimposed inotropic interventions (calcium, 0.625-5.0 mM, or isoproterenol, 10(-8)-10(-6) M), myocardial thyroid state modulates peak [Ca2+]i and inotropy, both of which are increased in thyroid hormone-treated relative to hypothyroid myocardium. The change in inotropy appears to be proportional to peak [Ca2+]i, whether mediated directly by calcium or as a result of beta-adrenergic stimulation. Thus, whereas baseline differences between hypothyroid and thyroid hormone-treated myocardium appear to be due to differences in myosin isozymes and presumed changes in adenosinetriphosphatase activity and cross-bridge cycling, superimposed inotropic responses appear to be mediated by changes in [Ca2+]i.
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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 (April 1, 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 constriction of venae cavae, were studied during four inotropic states. Aortic stenosis increased (dD/dt)/D (P less than 0.05), whereas occlusion of the descending aorta, vena caval constriction, and right ventricular pacing decreased (dD/dt)/D (P less than 0.05). Left atrial pressure was constant except during vena caval constriction. Alterations in inotropic state modified (dD/dt)/D (P less than 0.001). Extent of shortening and (dD/dt)/D were directly related (r = 0.80, P less than 0.001). Changes in (dD/dt)/D and T were inversely related (r = 0.70, P less than 0.001), and alterations in the interval from -dP/dtpeak to the end of rapid filling were directly related to changes in T (r = 0.75, P less than 0.001). We conclude that (dD/dt)/D can be modified by systolic and diastolic load perturbations, activation sequence, and inotropic interventions. These effects relate to changes in extent of shortening, time course of inactivation, or both.
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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 (October 1, 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 patients with congestive heart failure. Significant reductions in characteristic aortic impedance, wave reflection, and low-frequency impedance moduli were noted with dobutamine and were not seen with dopamine. Consequently, a significantly (P = 0.0008) greater increase in pulsatile, rather than steady-state, power output was noted with dopamine that was reflective of a significantly diminished efficiency of power transfer. Therefore, optimal transfer of increased ventricular contractile power in patients with congestive heart failure requires increases in large vessel compliance and complementary changes in ventriculoarterial coupling.
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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 (September 1, 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 (February 1, 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 reached maximum levels, and then they "faded" or progressively diminished back toward the control level. The inotropic responses to the conditioning infusion of ACh (1 μg/min) faded slightly but the chronotropic response did not. After the rest period, the test nerve stimulation evoked responses that also gradually faded with time. The maximal amplitude of the responses to the test simuli were less than those to the conditioning stimuli. This reduction in the maximal amplitude of the cardiac responses to the test stimuli was more pronounced with high frequency stimulation (30 Hz) than with low frequency stimulation (5 Hz). The decrement was also more pronounced the shorter the rest period, and it was greater at earlier times after beginning the stimulation. Conversely, the maximal cardiac responses to test infusions of ACh were not appreciably less than the responses to the conditioning infusions. We conclude, therefore, that the diminution of the cardiac responses to the second test stimulation of the parasympathetic nerve fibers was mainly ascribable to a prejunctional rather than to a postjunctional mechanism.
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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 (February 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, Giulia Vitale, Elisabetta Cerbai, Chiara Tesi, Raffaele Coppini, Michael Regnier, Corrado Poggesi, and Cecilia Ferrantini. "Engineered heart tissues for studying twitch tension and inotropic pharmacological interventions." Biophysical Journal 121, no. 3 (February 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 (November 1, 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 to linear terms of end-systolic volume (ESV) (74%) and stroke volume (SV) (19%). The SV effect was consistently negative and quantitatively quite important. An average load-independent end-systolic elastance of 6.7 mmHg/ml and an average SV effect of -5.7 mmHg/ml ejected were estimated, separating the “force-length” property from shortening effects in the in situ LV. History-related effects appeared to be only minor.
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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 mechano-sensing, recruits myosin motors from their OFF state, in which they lie along the surface of the thick filament folded toward its centre, unable to bind actin and hydrolyze ATP. In cardiac myocytes it has been demonstrated that inotropic interventions potentiate the mechanical output by mechanisms that imply increase in Ca2+ sensitivity of the thin filament but also mobilisation of myosin heads from their OFF state. During my doctorate I investigated the molecular mechanisms responsible for the regulation of the performance of the heart by defining how physiological and pharmacological inotropic interventions modulate the thick filament regulatory mechanisms and its interaction with the thin filament and the mechanokinetic properties of the slow/cardiac myosin motor. In the first part of my PhD research activity , combined mechanical and X-ray diffraction experiments on electrically paced intact trabeculae of rat heart (frequency 0.5 Hz, temperature 27°C) were used to investigate the effect on the thick filament regulatory state of physiological interventions able to potentiate up to twofold the peak of the twitch force in physiological solution with 1 mM Ca2+, such as increase in sarcomere length (SL) from 1.95 to 2.22 μm and addition of the β-adrenergic effector isoprenaline (10-7 M) to the bathing solution. The results show that, in diastole, none of the diffraction signals attributed to the OFF state of the thick filament were significantly affected by either increase in SL or phosphorylation of myofilament proteins, suggesting that the control of thick filament activation is downstream from the Ca2+-dependent thin filament activation, solidifying the idea that in the intact myocyte myosin motors are switched ON only during systole by an energetically well-suited downstream mechanism as thick filament mechano-sensing (Caremani et al., J. Gen. Physiol. 151:53,2019). In the second part of my PhD, the action mechanism of the inotropic agent Omecamtiv Mecarbil (OM) was studied by combining fast-sarcomere level mechanics and ATPase measurements in Ca2+-demembranated fibres from rabbit soleus (SL 2.4 μm, temperature 12°C), which express the β/slow myosin heavy chain isoform. OM is a cardiac myosin activator in phase three clinical trial as a potential treatment for systolic heart failure with reduced ejection fraction. The results show that, at any [Ca2+], OM depresses the force per motor, by preventing the OM-bound motors to complete the force-generating working stroke, but at low [Ca2+] it increases the sarcomere force by increasing the number of attached motors. Increase in the concentration of inorganic phosphate (Pi) in the physiological range (1-10 mM) causes a partial recovery of the force per myosin motor, suggesting that an allosteric competition between OM and Pi allows the no force-generating motors that release OM to re-enter the force-generating cycle (Governali et al., submitted to Nat Commun). This mechanism could underpin an energetically efficient reduction of systolic tension cost in OM-treated patients under exercise, when [Pi] increases with heart-beat frequency.
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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. Helsinki: 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 effects, that is, goals that can be monitored. Generally speaking, it is easier to affect blood pressure than cardiac output, and how to optimize regional and microcirculatory blood flow remains uncertain. Regardless of the chosen intervention, its haemodynamic effects should be closely monitored and always evaluated against the clinical effects. Recent developments include the definition of haemodynamic goals (goal-directed therapy) and clinical end-points, which seem to decrease morbidity and mortality, regardless of the goals defined and interventions used. With regard to mortality, use of inotropic agents has been associated with adverse outcomes, whereas the use of vasodilators has not. Inotropes in combination with vasodilators have the highest mortality.
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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-sustaining respiratory therapies provide structured guidance, reduce variation in practice, and improve satisfaction of families and healthcare providers. This chapter reviews such therapies and the process for cessation while simultaneously attending to symptom management.
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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 ventricular 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 complicating acute coronary syndromes, including mechanical complications and shock from right heart failure. There will be a major focus on potential therapeutic issues from an interventional cardiologist’s and an intensive care physician’s perspective on the advancement of new therapeutical arsenals, both mechanical percutaneous 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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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 ventricular 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 complicating acute coronary syndromes, including mechanical complications and shock from right heart failure. There will be a major focus on potential therapeutic issues from an interventional cardiologist’s and an intensive care physician’s perspective on the advancement of new therapeutical arsenals, both mechanical percutaneous 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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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 ventricular 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 complicating acute coronary syndromes, including mechanical complications and shock from right heart failure. There will be a major focus on potential therapeutic issues from an interventional cardiologist’s and an intensive care physician’s perspective on the advancement of new therapeutical arsenals, both mechanical percutaneous 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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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 ventricular 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 complicating acute coronary syndromes, including mechanical complications and shock from right heart failure. There will be a major focus on potential therapeutic issues from an interventional cardiologist’s and an intensive care physician’s perspective on the advancement of new therapeutical arsenals, both mechanical percutaneous 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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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. Patients are typically monitored in a neurocritical care unit for up to 21 days post-bleed to monitor for the development of cerebral vasospasm/delayed cerebral ischemia (DCI). Mainstay of treatment for DCI includes induced hypertension, balloon angioplasty, and intraarterial vasodilator therapy. In addition, patient may experience significant derangement in their cardiac, pulmonary, and endocrine systems, requiring inotropic support, mechanical ventilation, or insulin infusion therapy.
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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 this management strategy which support the individualized goal-directed therapy approach to managing high-risk patients.
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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, 251–59. Heidelberg: 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, 125–39. Heidelberg: 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, 255–66. Berlin, Heidelberg: 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, 305–14. Boston, MA: 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, 127–35. Heidelberg: 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, 218–20. Berlin, Heidelberg: 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, 227–33. Cham: 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, 633–50. 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, 348–59. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190884512.003.0035.

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Abstract:
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, 107–16. 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"

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Mazhar, Fazeelat, Francesco Regazzoni, Chiara Bartolucci, Cristiana Corsi, Luca Dede, Alfio Quarteroni, and Stefano Severi. "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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