Titlebook: Cardiovascular Hemodynamics; An Introductory Guid Arman T. Askari,Adrian W. Messerli Book 2019Latest edition Springer Nature Switzerland AG

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书目名称Cardiovascular Hemodynamics影响因子(影响力)




书目名称Cardiovascular Hemodynamics影响因子(影响力)学科排名




书目名称Cardiovascular Hemodynamics网络公开度




书目名称Cardiovascular Hemodynamics网络公开度学科排名




书目名称Cardiovascular Hemodynamics被引频次




书目名称Cardiovascular Hemodynamics被引频次学科排名




书目名称Cardiovascular Hemodynamics年度引用




书目名称Cardiovascular Hemodynamics年度引用学科排名




书目名称Cardiovascular Hemodynamics读者反馈




书目名称Cardiovascular Hemodynamics读者反馈学科排名

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Afterload expel blood into the vasculature and can be understood in the whole heart as the stress encountered by left ventricular myofibers as they contract against the end-diastolic volume. Wall tension can be at least in part described by LaPlace’s equation and aids in the explanation of why a dilated vent

Sinus-Rhythm

Renin–Angiotensin–Aldosterone Axis Modulators and Other Vasodilators in the pathophysiology of cardiac diseases, especially hypertension and systolic heart failure. Aldosterone leads to local effects of vasoconstriction and sodium resorption, and potentiates inflammation and fibrosis in several organs, including the heart. Inhibitors of the RAAS, particularly angiot

LEER

Beta Blockers and Calcium Channel Blockersrgic receptors at the nerve endings of the sympathetic nervous system and therefore reduce systolic pressure, heart rate, and cardiac contractility and output. Calcium channel blockers block voltage-gated calcium channels and inhibit the influx of calcium ions into cardiac and smooth muscle cells. T

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Recently Approved Pharmacologic Agents to Improve Outcomes in Heart Failureormonal inhibition on a background of hemodynamic effects. The agents that have been shown to be associated with improved outcomes in this patient population are inhibitors of the renin-angiotensin-aldosterone (RAAS) system, mineralocorticoids, and beta-blockers. More recently, two agents were FDA-a

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Mechanical Circulatory Supports a state in which cardiac dysfunction is either wholly or partially responsible for an inadequate level of cardiac output to support end-organ function. CS is an especially dangerous state, with in-hospital mortality as high as 27–51% (van Diepen et al., Circulation. 136:e232–68, 2017). Therefore,

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