The rate of mean blood flow depends on both blood pressure and the resistance to flow presented by the blood vessels. Mean blood pressure decreases as the circulating blood moves away from the heart through arteries and capillaries due to viscous losses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries and arterioles. Other major arteries have similar levels of blood pressure recordings indicating very low disparities among major arteries. Pressure drops gradually as blood flows from the major arteries, through the arterioles, the capillaries until blood is pushed up back into the heart via the venules, the veins through the vena cava with the help of the muscles. At any given pressure drop, the flow rate is determined by the resistance to the blood flow.

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Bo Sramek, Ph. Hemodynamics is concerned with the forces generated by the heart and the resulting motion of blood through the cardiovascular system. We will be discussing here the systemic hemodynamics, dealing with interactive forces of pulmonary vasculature, the left heart and systemic vasculature.

To a clinician, these forces demonstrate themselves as a pressure-flow relationships at the output node of the left heart.

The interest in systemic hemodynamics is clear: On one hand, a significant majority of cardiovascular disorders and diseases is related to systemic hemodynamics. On the other hand, proper hemodynamic management, resulting in the normohemodynamic state and producing adequate perfusion of all organs, is attributable to improved outcomes, lower mortality rates and better quality of life.. TD technique has become a measurement base of what is being called the "hemodynamic parameters.

TD-influenced hemodynamic thinking has not changed over the last 30 years. Most clinicians believe that since the CO measurement by the TD catheter is the "direct" i. On one hand, Braunwald calls CO "the ultimate expression of cardiovascular performance" Braunwald E: Assessment of cardiac function. WB Saunders Co, Since the normal value of CO in all resting mammals of normal weight is a linear function of their body weight at 0.

Either the level of CI or MAP is an end result of hemodynamic modulation by preload, contractility and afterload. This concept starts with a correct notion that the primary function of cardiovascular system is transport of oxygen, and the Oxygen Delivery Index, DO I, is its ultimate expression.

Oxygen delivery is a blood flow and not blood pressure-related phenomenon blood is the vehicle, oxygen is the cargo. It then assumes that in a stable, resting patient who has, therefore, a constant oxygen demand , the hemodynamics does not change rapidly. As a result, if the patient has a TD catheter inserted, an infrequent measurement of CI with this philosophy is quite adequate. Current understanding of hemodynamic modulation is as follows: Hemodynamic State — blood flow and blood pressure — is represented by CI and MAP [incorrect — see the discussion below].

CI is the result of hemodynamic modulation of preload, contractility and afterload [incorrect — see the discussion below]. MAP is a result of hemodynamic modulation of preload, contractility and afterload [incorrect — see the discussion below].

In inpatients with TD catheter, hemodynamic management concentrates on management of CI for instance, to manage a low flow state , or management of PAOP in management of intravascular volume hypovolemia or hypervolemia. In outpatients, hemodynamic management is reduced to management of arterial blood pressure for instance, systolic and diastolic blood pressure measurement in management of hypertension.

Preload level i. Contractility is not routinely measured. The general knowledge of its physiologic understanding is vague. Quite often, contractility and inotropy are considered to by synonymous medical terms [incorrect — see the discussion below]. The Frank-Starling mechanism is simplified as pressure-volume relationship [incorrect — see the discussion below — see Fig.

The principal hemodynamic management methodology is trial-and-error. Current hemodynamic management tends to treat the symptom i. As a result of this finding, the systemic hemodynamic state has to be defined as the mean value of blood pressure and the mean value of blood flow over one heart beat interval, i.

The semiperiodic and sudden drops of SI taking place every 10 — sec the Mayer waves are met by simultaneous step increases of HR as to maintain the perfusion flow i. We, therefore, can conclude that the vascular resistance adjusts itself to a new value for every heart beat as well.

In respect to systemic hemodynamics, the cardiovascular system is an interactive system involving a dynamic interaction between 1 the preceding pulmonary vasculature, 2 the pump [left heart] and 3 the systemic vasculature.

The sequence of systemic hemodynamic modulation see Fig. These forces are called the preload. Preload is a diastolic phenomenon. Preload is modulated by a variation in intravascular volume volemia. Volume expansion increases the ejection phase contractility rate of contraction of fibers in time during the ejection phase and thus increases simultaneously both MAP and SI.

Volume reduction diuresis decreases the ejection phase contractility and, as a result, decrease both MAP and SI. The mutually independent modulating effects of intravascular volume and of inotropy on the Ejection Phase Contractility are depicted in Fig. However, a patient who is hypovolemic can exhibit the same normal level of EPC if administered positive inotropes, and, a patient who is volume overloaded hypervolemic can also have normal level of EPC if administered negative inotropes.

As a result of pulsatile blood flow through the vascular resistance which also changes dynamically its value for every heart beat , a pulsatile arterial blood pressure develops its mean value being the MAP. The primary component of afterload is vasoactivity: Vasoconstriction increases afterload and, as a result increases MAP while decreasing SI. The secondary component of afterload is blood viscosity; however, with the exception of extreme hemoconcentration or hemodilution, it can be neglected in the clinical assessment of afterload.

Since CI used in the SVRI equation already includes the chronotropic compensation by the Heart Rate HR see Fig4, The Functional Diagram of Hemodynamic Modulation , this "per-minute" assessment of afterload may lead to misdiagnoses, incorrect selection and administration of cardio- and vasoactive drugs and to a prolonged therapy. The Heart. Administration of a vasodilator will then result in a rapid improvement. As a consequence of beat-by-beat variation of volume, inotropy and vasoactivity, a new set of MAP and SI the hemodynamic state is produced for every heart beat.

The beat-by-beat hemodynamic changes, responsible for producing the beat variation of the hemodynamically-significant blood flow component SI on one side of the hemodynamic regulation equation, and the demand for oxygen delivery requiring a certain level of the perfusion flow CI on the other, are tied together through the chronotropic modulation by HR. These longer-term biofeedback changes are documented in Fig. The raw data were obtained in a beat-by-beat fashion during a sleep study the time period covers approximately 6 hours of night and then subjected to the beat sliding average calculation and plotting.

These recordings document that in addition to the dynamic, beat-by-beat adjustments of HR to beat-by-beat variation of SI as shown in Fig. Since the patient was supine and sleeping, the variation of SI, compensated by HR as to maintain CI steady, and the 1. CI thus is the only dynamic modulator of DO I. In young, healthy and athletic subject, CI can increase five-fold between the rest and strenuous exercise see Fig.

Adequate DO I under all metabolic conditions equates to health, good quality of life and longevity. Adequacy of DO I in surgical patients has been directly linked to their survival rates. Hospitalized patient with adequate DO I exhibit a shorter duration of their hospitalization.

The functional diagram of hemodynamic and perfusion flow modulation under per-beat hemodynamics is depicted in Fig. The Vascular Resistance affects the Vasoactivity.

CI is then the only dynamic modulator of DO I. Heart is, therefore, not only a variable frequency pump by a variation of HR but a variable volume pump by a variation of SI as well. So lower the resting HR as in athletes , so longer the augmentation range with HR. This hemodynamic map clearly shows there are nine classes of hemodynamic states into which the hemodynamic point of a patient can fall, however, only one of them, called the normohemodynamic state, containing a simultaneous normotension and normodynamic flow, can serve as the Therapeutic Goal.

Eight of them represent abnormal hemodynamic states and only one — simultaneous normotension and normodynamic state the normohemodynamic state — is the Therapeutic Goal. Please note that normotension alone — the therapeutic goal of current antihypertensive therapy — contains two abnormal hemodynamic states. The vector of vasoconstriction points north-west, the vector of vasodilation or therapy using ACE inhibitors points south-east. The hemodynamic measurement has to include measurement of blood flow in every patient!

As a result of three levels of MAP hypertension, normotension and hypotension and three levels of SI hyper-, normo- and hypodynamic state , there are nine different classes of hemodynamic states, documented by nine rectangles in the hemodynamic map Fig. In addition, there are three classes of perfusion flow states hypo-, normo- and hyperperfusion flow , determined by three levels of CI.

Out of these twelve linear combinations, only two of them, i. As a result, we can utilize this knowledge in either direction: Either determine the deviations in hemodynamic and perfusion modulators from the measured MAP, SI and CI values. Similar charts can be constructed for other normal hemodynamic states in different groups of patients, such as for neonates, pediatric patients or for gravidas.

The center of the chart represents the ideal hemodynamic state. The hemodynamic state of a patient is expressed as a point with the coordinates of MAP and SI values. Location of this point in the system of hemodynamic modulators the diagonal lines identifies exact and specific causes of the observed hemodynamic state.

When the hemodynamic point falls within the dark hexagon, outlining the loci of normohemodynamic states, the patient is normohemodynamic this state is a result of simultaneous normovolemia, normoinotropy and normovasoactivity. A map of hemodynamic modulators an orthogonal system of coordinates on a different plane is formed by sets of diagonal lines. Its location within the map of hemodynamic modulators determines the status of hemodynamic modulators responsible for the hemodynamic state.

The loci of normohemodynamic states are defined by gray hexagon. Please be aware that the only way of rapidly establishing the normohemodynamic and normoperfusion state is to identify those hemodynamic and perfusion modulators which are at abnormal levels i. Only this approach leads to normohemodynamic and normoperfusion state. It has a built-in normal and postoperative hemodynamic management goal.

It can help the drug companies to establish the vectorial effects of all of their cardio- and vasoactive drugs, or drugs with a potent cardioactive effect such as Viagra. Do you want to see the improved outcomes of management of hypertension? Read the abstract of a paper presented at the Meeting of the American Society of Hypertension , or read a related featured article Treatment of Hypertension as a Hemodynamic Disorder.

Just click on this title.


Arterial hemodynamics in human hypertension.

Abstract Aims Carotid—femoral pulse wave velocity PWV , a direct measure of aortic stiffness, has become increasingly important for total cardiovascular CV risk estimation. Its application as a routine tool for clinical patient evaluation has been hampered by the absence of reference values. The aim of the present study is to establish reference and normal values for PWV based on a large European population. Methods and results We gathered data from 16 subjects and patients from 13 different centres across eight European countries, in which PWV and basic clinical parameters were measured. Prior to data pooling, PWV values were converted to a common standard using established conversion formulae. Subjects were categorized by age decade and further subdivided according to BP categories.



DeepDyve Hemodynamics, William R. Eigler, Neal tory and is thus a more practical text for the practicing physician. Despite the complexity of the topics, the book is well organized and easy to read. Milnor presents the topics in a clear and concise fashion with ample references and in a style which provides an historical perspective on the various developments in the field. Notwithstanding the narrow range of highly technical interests to which this book is directed, it is well worth recommending to those who are not easily frightened by the rigors of a little mathematics and physics. Sanbom Alan R.

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