For explanation of unfamiliar terms, go to Glossary of Terms.
For a detailed discussion of new concepts of systemic hemodynamics and hemodynamic management, click on the reference listed at the bottom of this page.
Hemodynamics is an important part of cardiovascular physiology dealing
with the forces the pump (the heart) has to develop to circulate blood
through the cardiovascular system. Adequate blood circulation (blood flow) is a necessary
condition for adequate supply of oxygen to all tissues, which, in return,
is synonymous with cardiovascular health, survival of surgical patients, longevity
and quality of life. To an outside observer (a physician or a nurse) these
hemodynamic forces demonstrate themselves as blood pressure and blood flow
paired values at different nodes of the cardiovascular system. We will concentrate
on systemic hemodynamics – the blood pressure and blood flow at the output
of the left heart. The interest in systemic hemodynamics is obvious: A significant
majority of all cardiovascular diseases and disorders is related to systemic hemodynamic
dysfunction. Hypertension and congestive heart failure are two best
known systemic hemodynamic disorders.
Understanding and teaching of hemodynamics at medical and nursing schools has
not significantly changed over the last forty years. Measurement of arterial blood
pressure is considered to be a "hemodynamic measurement." Measurement of
Cardiac Output, CO [liter/min], or measurement of the wedge pressure by the flow-directed
pulmonary artery catheter (sometimes called the Swan-Ganz or the thermodilution catheter)
are considered to be "hemodynamic measurements." Hemodynamics is taught
at the level made available in the ’70s by introduction of this catheter. Since this
measurement is very expensive, risky, require a sterile environment and a highly
skilled physician for catheter insertion, it is only used in about 2% of patient
population. In addition, it propagated myths about its "ability" to assess
intravascular volume, which have subsequently been disputed [Calvin JE et al: Does
the pulmonary capillary wedge pressure predict left ventricular performance in critically
ill patients? Crit Care Med, Vol 9, No 6:437]. It propagated a myth that in a stable
patient the hemodynamics do not change and, therefore, it is adequate to measure
hemodynamics only intermittently, several times a day. The use of the catheter almost
become a cult [Robin ED: The Cult of Swan-Ganz Catheter. Intens & Crit Care Digest,
Vol 5, No 1, June 1986:18]. However, its most negative impact has been the way it
affected hemodynamic thinking of several generations of medical professionals: Though
everybody understands that an adequate oxygen delivery to all organs is an essential
condition for the organs’ health, and that oxygen delivery is a blood flow and not
blood pressure-related phenomenon (blood is the vehicle, oxygen is the cargo), the
blood flow is measured today only in very small percentage of patient population.
Most of hemodynamic management decisions are made just upon the arterial blood pressure
measurement (such as in management of hypertension,….). There is no intellectual
need to simultaneously measure both blood pressure and blood
flow in every patient. Equally, there is no clear understanding that both
normotension and normodynamic state (blood flow within normal range) must
be part of the therapeutic goal.
Though adequately clinically accurate noninvasive measurement of CO has been available from the end of the ’80s and hemodynamic management since the mid ’90s, they have not become a part of routine armament for hemodynamic assessment, monitoring and management.
As a result of these misconceptions, the only available methodology for hemodynamic management is trial and error.
Click here for a detailed discussion of Systemic Hemodynamics – Fiction and Facts
By the beginning of the ’90s, it was discovered that the cardiovascular system
actually forms a new hemodynamic state for every heart beat. The hemodynamically
significant blood flow, therefore, is not the CO (flow/minute) but the Stroke Index
(an indexed blood flow per beat). Also, a new theory of beat hemodynamics and hemodynamic
management was formulated and published.
They are summarized below:
A healthy cardiovascular system maintains adequate supply of oxygen to all tissues
under all metabolic conditions by a dynamic variation of levels of four
modulators. Three of them are the systemic hemodynamic modulators, one
is the perfusion flow modulator.
The body changes levels of these four modulators for every heart beat in response to a varying oxygen demand of all tissues.
The three hemodynamic modulators are the causes of changes of levels of blood pressure (MAP = Mean Arterial Pressure) and blood flow (SI = Stroke Index). These modulators are:
Subsequently, the fourth modulator
affects the perfusion flow (CI = Cardiac Index) by a variation of heart rate (HR). CI = SI x HR.
Note 1: Only a patient who has all four modulators at their respective normal levels, i.e., who is normovolemic, normoinotropic, normovasoactive and normochronotropic can be in a normohemodynamic and normoperfusion state.
Note 2: In a healthy patient, between the rest (the lowest oxygen demand) and a strenuous exercise, such as running a marathon (the highest oxygen demand), the SI increases by 66%, CI by 500%, while MAP changes a little or not at all.
As a human body produces changes in hemodynamic and perfusion modulators to adjust the hemodynamic state in order to respond to a varying oxygen demand, a clinician treating any hemodynamic disorder (abnormal hemodynamic state) can affect therapeutically only the levels of the three hemodynamic modulators and of the perfusion modulator. He cannot affect directly the consequences of their modulating effect, i.e., either only the level of blood pressure or only the level of blood flow, even he may be misled by current trial-and-error concepts of management of cardiovascular system to believe so. The following pharmacological agents are available to him:
volume-reducing drugs (diuretics),
positive and negative inotropes,
vasodilators and vasoconstrictors,
positive and negative chronotropes.
Note 3: All current cardio- and vasoactive drugs consist of these components and/or their mixtures. Each commercially-produced cardio- and vasoactive drug has a specific vector on the hemodynamic map below.
Note 4: There is no pharmacological agent available to perform volume expansion; volume expansion can only be accomplished by intake of fluids – orally or intravenously.
Note 5: A change of level of any of these modulating agents always changes both MAP and SI, and, subsequently, the CI level.
To a clinician, the systemic hemodynamic state of a patient is represented by simultaneously measured MAP and SI values. Hemodynamic state can, therefore, be graphically expressed as a point on the hemodynamic map, shown below. Whereas on a geographic map a singular spot on earth is determined by its latitude and longitude, the hemodynamic state/hemodynamic point of a patient is determined by simultaneously measured values of MAP and SI. As you can see from this map, the three levels of flow and three levels of pressure result in 9 classes of hemodynamic states, described by 9 rectangles, into which the hemodynamic point of a patient may fall. Out of these 9 combinations, 8 are associated with abnormal hemodynamic states and only one – the normohemodynamic state (a simultaneous normotension and normodynamic circulation) – is the only legitimate therapeutic goal for treatment of any abnormal hemodynamic state, caused by hemodynamic reasons (and not by endocrinologic or conduction disorders, or by sepsis).
Current hemodynamic assessment, relying heavily on blood pressure and ECG measurements, is not assessing the most important function of cardiovascular system – transport of oxygen. (The only exception to this polarized view are the high-risk, critically-ill patients, in whom flow is measured by highly invasive, risky and expensive catheters – about 2% of hospitalized patients). What makes the current infatuation with blood pressure as an important tool in assessing hemodynamics even more complicated is that all cardioactive and vasoactive drugs (for instance, all antihypertensive medications) always alter both blood pressure and blood flow, though, only the hemodynamic effect on blood pressure is measured.
Example: Though all antihypertensive drugs decrease blood pressure, some of them simultaneously decrease blood flow (diuretics and beta blockers), some leave it about at the same level (calcium channel blockers) and some increase it (vasodilators, ACE [Angiotensin Converting Enzyme] Inhibitors, or ARBs). In addition, beta blockers, being negative inotropes + negative chronotropes, also reduce heart rate and, as a consequence, the perfusion flow (CI).
In absence of simultaneous SI and CI measurement, the physician has to resort to trial-and-error as his hemodynamic management methodology. Because of that, he tends to treat a symptom and not the cause. For instance, if the symptom is hypertension, the causes may be hypervolemia and/or hyperinotropy and/or vasoconstriction and/or any linear combination of them.
A popular methodology of trial-and-error antihypertensive therapy has been the "step therapy." It instructs the physician to start an antihypertensive therapy with diuretics. If the patient remains hypertensive, he should be switched to beta blockers, if unsuccessful, another antihypertensive drug(s) should be added and/or combined, and so on….
Let’s explain the fallacy of this approach on a patient who is hypertensive & hypodynamic, i.e., in the north-west corner of the hemodynamic map above. While diuretics will lower his blood pressure, they also will further decrease his already-low blood flow. Such a patient may become normotensive, however, he now will be profoundly hypodynamic. If even an increase in heart rate does not result in an adequate level of perfusion flow, this patient will exhibit digestive disorders (gut is not adequately perfused), will have problems with temperature control (skin flow reduced), will be "sleep-walking" and tired (muscles not adequately perfused) and, if a male, becomes impotent (blood flow to sexual organs reduced). Unfortunately, these clear indications of low-flow state are today frequently labeled as the "side-effects of antihypertensive therapy."
What is a correct drug and/or drug combination for one patient may be totally inappropriate therapy for another. A patient-specific therapy can be determined only from the measured, patient-specific hemodynamic state. However, since the hemodynamic state is formed for every heart beat and can be affected by multitude of stimuli, it is important to perform a continuous hemodynamic measurement of the patient for about ten minutes to determine the "actual hemodynamic state" and to eliminate treating him for a ghost-abnormal hemodynamic state based upon a single blood pressure measurement, which could be actually caused by talking or emotions ("the white coat syndrome").
A movement toward modern medicine shows the importance of knowing the hemodynamic baseline and determining the adequacy of oxygen delivery in every patient. A complete hemodynamic assessment and normohemodynamic management has to become the mainstream of patient care, both in a hospital and physician’s office. It will enable an optimization of cardio- and vasoactive drugs used during the therapies.
Note 6: A different set of MAP & SI values represents an ideal normohemodynamic state for different ages, genders and metabolic states. These normal values have to be known in all these groups before a correct and effective cardio- and vasoactive therapy can be implemented.
Normal hemodynamic values for adult males and postmenopausal females, for gravidas and nongravidas and for neonatal and pediatric patients are now published.
Availability of new hemodynamic computer programs and network communications (including the Internet and Intranet) will make the hemodynamic profile of a patient instantly available to any of his physicians and health care providers.
Utilization of new findings in hemodynamics shall considerably improve medical services to the patient and will assist the physician with more comprehensive knowledge of a specific hemodynamic abnormality of a patient. It will significantly shorten a duration of treatment of hypertension and congestive heart failure in the outpatients and improve the outcomes in inpatients.
The mission of IHS is to make a complete hemodynamic assessment,
which includes a simultaneous measurement of both blood pressure and blood flow,
an inherent part of every patient’s cardiovascular evaluation. Utilizing
new concepts in systemic hemodynamic management, a maintenance of normohemodynamic
state, rather than treatment of hemodynamic disorders only if and/or when they
are diagnosed or discovered, should become a standard of cardiovascular care.
The mission of IHS is to debunk some myths surrounding current approach to hemodynamics, such as the treatment of hypertension, especially in the older patients. If you want to learn more, read the HEMODYNAMICS FOR THE SENIORS.
IHS’ mission will be to popularize and clinically evaluate and verify the noninvasive techniques for assessment of hemodynamic and oxygen transport parameters. Use of noninvasive procedures will eliminate the risk, cost, need for sterile environment and a highly skilled clinician associated with use of catheters.
If you want to learn more about
New Concepts in Systemic Hemodynamics and Hemodynamic Management,