Cardiac Output And Regional Blood Flow Introduction By Kw Donald With A Bibliography

Cardiac output has always been a subject of interest to both clinicians and researchers in different branches of medicine and surgery. In the last decade more attention has also been paid to its application in pediatrics, neonatology, fetal medicine and pregnancy. Better understanding of the peripheral circulation has provided more insight into the patholophysiology of different diseases. Many cardiac and non-cardiac disorders affect cardiac outputs. Monitoring of the changes in cardiac output is also important in the acutely ill patient. There are several methods to measure cardiac output, each with advantages and pitfalls. This book deals with all relevant aspects of cardiac output in eight parts: part one describes the methods of measuring cardiac output and a comparison between the catheterisation based and the noninvasive techniques, while part two describes the changes in cardiac output due to physiological causes. Part three describes cardiac output in cardiac diseases and systemic hypertension. Cardiac output in acutely ill patients is discussed in part four. Effect of cardiac medications, temporary atrial pacing, permanent pacing, pharmacologic stress testing and anesthesia are covered in detail in part six, while changes in cardiac output in noncardiac diseases are described in part seven. Finally great attention has been paid in part eight to the regional circulation including cerebral, coronary, skeletal and splanchnic circulations. A separate chapter discusses in detail the dynamics of blood flow. This book will be useful both to the cardiologists as well as to physicians in other fields of surgery and medicine and to their trainees. Readers will find this book an interesting and a useful reference on the topic of cardiac output.

Although cardiac output is measured as the flow of blood from the left ventricle into the aorta, the system that controls cardiac output includes many other components besides the heart itself. The heart’s rate of output cannot exceed the rate of venous return to it, and therefore, the factors governing venous return are primarily responsible for control of output from the heart. Venous return is affected by its pressure gradient and resistance to flow throughout the vascular system. The pressure gradient for venous return is a function of several factors including the blood volume flowing through the system, the unstressed vascular volume of the circulatory system, its capacitance, mean systemic pressure, and right atrial pressure. Resistance to venous return is the sum of total vascular resistance from the aortic valve to the right atrium. The sympathetic nervous system and vasoactive circulating hormones affect short-term resistance, whereas local tissue blood flow autoregulatory mechanisms are the dominant determinants of long-term resistance to venous return. The strength of contraction of the heart responds to changes in atrial pressure driven by changes in venous return, with small changes in atrial pressure eliciting large changes in strength of contraction, as described by the Frank–Starling mechanism. In addition, the autonomic nervous system input to the heart alters myocardial pumping ability in response to cardiovascular challenges. The function of the cardiovascular system is strongly affected by the operation of the renal sodium excretion–body fluid volume–arterial pressure negative feedback system that maintains arterial blood pressure at a controlled value over long periods. The intent of this volume is to integrate the basic knowledge of these cardiovascular system components into an understanding of cardiac output regulation. Table of Contents: Introduction / Venous Return / Cardiac Function / Integrated Analysis of Cardiac Output Control / Analysis of Cardiac Output Regulation by Computer Simulation / Analysis of Cardiac Output Control in Response to Challenges / Conclusion / References / Author Biography

​This book traces the development of the basic concepts in cardiovascular physiology in the light of the accumulated experimental and clinical evidence and, rather than making the findings fit the standard pressure-propulsion mold, let the phenomena ‘speak for themselves’. It starts by considering the early embryonic circulation, where blood passes through the valveless tube heart at a rate that surpasses the contractions of its walls, suggesting that the blood is not propelled by the heart, but possesses its own motive force, tightly coupled to the metabolic demands of the tissues. Rather than being an organ of propulsion, the heart, on the contrary, serves as a damming-up organ, generating pressure by rhythmically impeding the flow of blood. The validity of this model is then confirmed by comparing the key developmental stages of the cardiovascular system in the invertebrates, the insects and across the vertebrate taxa. The salient morphological and histological features of the myocardium are reviewed with particular reference to the vortex. The complex, energy-dissipating intracardiac flow-patterns likewise suggest that the heart functions as an organ of impedance, whose energy consumption closely matches the generated pressure, but not its throughput. Attention is then turned to the regulation of cardiac output and to the arguments advanced by proponents of the ‘left ventricular’ and of the ‘venous return’ models of circulation. Hyperdynamic states occurring in arteriovenous fistulas and congenital heart defects, where communication exists between the systemic and pulmonary circuits at the level of atria or the ventricles, demonstrate that, once the heart is unable to impede the flow of blood, reactive changes occur in the pulmonary and systemic circulations, leading to pulmonary hypertension and Eisenmenger syndrome. Finally, the key points of the nook are summarized in the context of blood as a ‘liquid organ’ with autonomous movement.​