Copyright B. Bo Sramek


B. Bo Sramek, Ph.D.

(For explanation of new terms, go to Glossary of Terms)

A detailed discussion of systemic hemodynamics, its old ("per-minute’) and new ("per-beat") concepts, methods for measurement of cardiac output, case studies, normal hemodynamic values for neonates, pediatrics, adult males, nongravidas, gravidas and postmenopausal females and more can be found in a textbook Systemic Hemodynamics and Hemodynamic Management.

Hemodynamics is concerned with the forces generated by the heart and the resulting motion of blood through the cardiovascular system. Milnor W: Hemodynamics, Williams & Wilkins 1982

Hemodynamics is a subchapter of cardiovascular physiology. 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..

1) Current "Per-minute" Concepts (State of the Art)

Current (incorrect) understanding of hemodynamics and hemodynamic modulation is based upon the clinical capabilities of the flow-directed pulmonary artery catheter (most often called the thermodilution – TD – catheter, or the Swan-Ganz catheter), introduced in the ’70s of the last century. Though the TD catheter is utilized only in small stratum of patients in critical care setting (less that 2% of hospitalized patients in the U.S. get catheterized), it profoundly influenced the formulation of hemodynamics as is known and taught today. TD technique has become a measurement base of what is being called the "hemodynamic parameters." It has become an accepted standard for CO (Cardiac Output), CVP (Central Venous Pressure) and PAOP (Pulmonary Artery Occluded Pressure = "Wedge" pressure) measurements and management of patients in critical care setting. 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.e., invasive) measurement, it must be accurate, whereas it actually converts a measurement of temperature change over time into CO value and its accuracy is, at best, 20% from the actual (never known) CO value. Since this concept considers CO, with a physical dimension liters/min, to be the hemodynamically significant blood flow, let’s call this concept "per-minute hemodynamics."

CO is today, probably, the most misunderstood cardiovascular parameter. On one hand, Braunwald calls CO "the ultimate expression of cardiovascular performance" (Braunwald E: Assessment of cardiac function. Heart Disease, A Textbook of Cardiovascular Medicine. WB Saunders Co, 1984:467). According to him, CO is one of the most important hemodynamic/perfusion base assessment parameters, related to a true definition of cardiovascular health. On the other hand, many physicians have left medical schools with a belief that CO need not be indexed, its normal value in an adult human is CO = 5.5 l/min, its determination is unimportant in outpatients and in a majority of inpatients, and its measurement is of value only in high risk and/or critically ill patients.

Since the normal value of CO in all resting mammals (of normal weight) is a linear function of their body weight at 0.1 l/min/kg (Milnor WR: Hemodynamics, Williams & Wilkins, 1982:155), the normal CO = 5.5 l/min is a valid value for a 55 kg female only, while a normal CO value for an 85 kg male is 8.5 l/min… Only indexed values of all blood flow and blood flow-related parameters (such as vascular resistance or cardiac or ventricular work) exhibit a normal value and normal range. Indexing by Body Surface Area (BSA) has become a medical standard: CI = CO/BSA. Normal CI for resting, supine adults is CI = 3.5 l/min/mSuperscript2 20%.

The DuBois & DuBois formula for determination of BSA [mSuperscript2] is

The "per-minute" concepts of systemic hemodynamics can be best expressed by the following functional diagram of cardiovascular system (Fig.1):

Fig.1: Functional diagram of systemic hemodynamic modulation as utilized in current clinical practice. Hemodynamically significant blood flow is the Cardiac Index (CI) [l/min/mSuperscript2], hemodynamically significant blood pressure is the Mean Arterial Pressure (MAP) [torr]. Either the level of CI or MAP is an end result of hemodynamic modulation by preload, contractility and afterload. CI is then the only dynamic modulator of Oxygen Delivery Index (DOSubscript2I) [ml/min/mSuperscript2]. Hgb is the Hemoglobin [g/dl],
SaOSubscript2 is the Saturation level of oxygen in arterial blood [%]. HR is the Heart Rate [beats/min], SI is the Stroke Index (blood flow per beat) [ml/beat/mSuperscript2].

This concept starts with a correct notion that the primary function of cardiovascular system is transport of oxygen, and the Oxygen Delivery Index, DOSubscript2I, 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:

The hemodynamic management under current concepts can be described as follows:

2) New "Per-beat" Concepts

A scientist studying respiratory pattern-related cardiovascular response phenomena has obtained the following recordings (see Fig.2 below), from which we clearly can conclude that the cardiovascular system actually adjusts to a new hemodynamic state for every heart beat and that the “slow" or "per-minute" concepts of hemodynamics described above are fundamentally flawed. The beat-by-beat variations of SI are the leading cause of continuous hemodynamic changes; the beat-by-beat variations of HR are the chronotropic compensatory responses as to keep the perfusion flow (CI) constant (CI = SI x HR); the beat-by-beat variations of MAP then are a result of per-beat variations of SI and per-beat variations of vascular resistance (if the vascular resistance would be constant, the MAP recording would have to be the exact image of the SI recording).
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.e., as the paired values of Mean Arterial Pressure (MAP) and Stroke Index (SI). A new and different hemodynamic state (a new pair of MAP & SI values) is thus formed for every heart beat:

Fig.2: These recordings of the beat-by-beat values of MAP, SI and HR (courtesy of David Shannahoff-Khalsa, The Research Group for Mind-Body Dynamics, Institute for Nonlinear Science University of California San Diego, California) were obtained from a resting, reclining adult over a 10-minute period. Please note that the hemodynamic state (MAP & SI) varies continuously, though, in such a stable patient, the mean values of each monitored parameter over the 10-minute period are fairly stable. The semiperiodic and sudden drops of SI taking place every 10 – 120 sec (the Mayer waves) are met by simultaneous step increases of HR as to maintain the perfusion flow (i.e., CI = SI x HR) at a steady-state level, corresponding to a steady-state level of oxygen demand in this patient. Since MAP is formed across the vascular resistance (SSVRI) by the blood flow (SI) for every heart beat {i.e., MAP = [SSVRI x SI/80] – 4}, and both SSVRI and SI attain a new value for every beat, the instantaneous values of MAP are not direct images of SI. 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.4 below for details), therefore, is as follows (please note that a change of level of any modulator affects both the MAP and the SI value):

1) The inertia forces of flowing blood from pulmonary circulation fill the heart chambers during diastole and, as a consequence, stretch the myocardial fibers, thus storing mechanical energy in them. 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 atrial + ventricular filling (i.e., the preload) and increases both MAP and SI.
Volume reduction (diuresis) decreases preload and, subsequently, decreases both MAP and SI values.
2) The forces causing contraction of myocardial fibers during systole are called contractility and are modulated either mechanically by preload (i.e., by changes in intravascular volume [the Frank-Starling Law] => more stretched fibers during diastole have more energy stored in them and, therefore, contract with a higher force during the following ejection phase) or pharmacologically by agents called inotropes.

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.
Positive inotropes increase the contractility during the entire electro-mechanical systole (pre-ejection period + ejection phase) and increase simultaneously both MAP and SI.

Volume reduction (diuresis)
decreases the ejection phase contractility and, as a result, decrease both MAP and SI.
Negative inotropes decrease the contractility of the entire electro-mechanical systole (pre-ejection period + ejection phase) 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.2a below.
Fig.2a: Frank-Starling Law and Inotropy: Three Frank-Starling curves shown – normoinotropy, hyperinotropy and hypoinotropy.
A patient, who is normovolemic and normoinotropic, exhibits a normal level of Ejection Phase Contractility (EPC). 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.
3) The resistive forces of systemic vasculature, which the pump has to overcome during every heart beat to deliver boluses of blood (SI) into the aorta, are called the afterload. 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 "per-beat" systemic vascular resistance is, therefore, determined via the Stroke Systemic Vascular Resistance Index,
SSVRI = 80 (MAP-4)/SI, and not by currently used SVRI, discussed in detail below.
The primary component of afterload is vasoactivity:
Vasoconstriction increases afterload and, as a result increases MAP while decreasing SI.
Vasodilation reduces afterload and, subsequently, decreases MAP while increasing 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.
The hemodynamically-incorrect focus on CI discussed in Current "per-minute" concepts above, leads to an incorrect assessment of afterload via the SVRI [Systemic Vascular Resistance Index, where SVRI = 80 (MAP-4)/CI]. 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. This subject is briefly discussed below and in detail in the REFERENCE publications.
Table1: This table has in the first row the ideal hemodynamic and perfusion values (MAP, SI, HR and CI) for supine resting adults (Hurst JW. The Heart. McGraw Hill, 5th Edit, 1982:93) with calculated ideal values of SVRI (SVRI = 80[MAP-4]/CI) and SSVRI (SSVRI = 80[MAP-4]/SI). The second row has the same parameters for a hemodynamically compromised patient in the ICU: This patient is still normotensive (MAP = 85 Torr), however his hypodynamic state (SI = 31 ml/m2) is chronotropically compensated in such a way (HR = 110 bpm) that the resulting CI still has the same value of 3.4 l/min/m2 as for the ideal patient. Should the clinician wishing to correct this hypodynamic state utilize SVRI to assess the status of vasoactivity, he would conclude that his vasoactivity is normal (SVRI = 1905, i.e., ideal normovasoactivity), and concentrate on therapy involving the two remaining hemodynamic modulators – volume and inotropy (volume expansion and positive inotropic support). However, in spite of his expectations and to his surprise, this patient’s hemodynamics would not improve, since the actual major cause of his compromised hemodynamic state is vasoconstriction. The true state of vasoconstiction becomes visible only by using SSVRI for its assessment.
The value SSVRI = 209 clearly documents a 51% vasoconstriction. 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 per-beat variation of SI then is chronotropically compensated by a per-beat variation of Heart Rate (HR) as to produce the perfusion flow, called Cardiac Index (CI), responding to varying global oxygen demand:

CI = SI x HR

Since CI is the only dynamic modulator of global oxygen delivery (see the discussion which follows, and Fig.4), a patient with a constant and stable oxygen demand needs CI at a certain, stable level. 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.3 below.

Fig.3: These recordings of MAP, SI and HR (courtesy of David Shannahoff-Khalsa, The Research Group for Mind-Body Dynamics, Institute for Nonlinear Science University of California San Diego,, California) are, in contrast to Fig.1, the sliding averages over 200 heart beats. 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 200-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.1), the absolute value of HR continually adjusts to the absolute value of SI as well, in order to maintain CI at a level providing an adequate CI. Since the patient was supine and sleeping, the variation of SI, compensated by HR as to maintain CI steady, and the 1.5 hour step-drop of MAP, independent of SI, were produced by other phenomena (dreams?).

When the perfusion-significant blood flow (CI) is established through the hemodynamic modulation of SI plus the chronotropic compensation of HR, the global Oxygen Delivery Index (DOSubscript2I) is formed as a product of CI, Hemoglobin (Hgb) and saturation percentage of oxygen in arterial blood (SaOSubscript2):

DOSubscript2I = CI x 10 Hgb x SaOSubscript2 x 1.34

(1.34 is the oxygen affinity constant: 1 gram of Hgb binds 1.34 ml of oxygen)

(Please note that in the HOTMAN System, the pulse oximetry value, SpOSubscript2, which can be obtained noninvasively and which approximates the SaOSubscript2 value, is used in the equation above in place of SaOSubscript2)
In a patient who is not hemorrhaging and whose lungs are functioning normally, Hgb and SaOSubscript2 do not exhibit rapid changes and can be considered constants over longer periods of time. CI thus is the only dynamic modulator of DOSubscript2I. In young, healthy and athletic subject, CI can increase five-fold between the rest and strenuous exercise (see Fig.5).

Adequate DOSubscript2I (under all metabolic conditions) equates to health, good quality of life and longevity. Adequacy of DOSubscript2I in surgical patients has been directly linked to their survival rates. Hospitalized patient with adequate DOSubscript2I exhibit a shorter duration of their hospitalization.

The functional diagram of hemodynamic and perfusion flow modulation under per-beat hemodynamics is depicted in Fig.4 below:


Fig.4: The functional diagram of hemodynamic and oxygen delivery modulation (black arrows indicate the direction of modulation): The Intravascular Volume and Inotropic State affect the Myocardial Contractility. The Vascular Resistance affects the Vasoactivity. They, together, are vectorially responsible for the Hemodynamic State (SI @ MAP). The SI level, established by the hemodynamic modulation, together with the Chronotropic compensation by HR are responsible for the Perfusion Flow (CI). CI is then the only dynamic modulator of DOSubscript2I.

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. However, the augmentation of SI is not taking place over the entire HR range, but only between the resting HR and HR = 120 bpm, at which the augmentation of SI stops and the human heart becomes only a constant volume pump, as seen in Fig.5.

Fig.5: Percentage increase of SI as a function of HR in a normal, athletic adult with a resting HR = 60 bpm. Below the HR = 120 bpm (the end of augmentation range in human hearts), his heart is both a variable frequency and a variable volume pump. The augmentation of SI stops approximately at HR = 120 bpm, at which frequency the heart becomes a constant volume pump. As you can see, CI increases quadratically with HR from the resting HR until HR = 120 bpm; further increase of CI is then only a linear function of HR. So lower the resting HR (as in athletes), so longer the augmentation range with HR. This example shows a typical 500% increase in CI and in DOSubscript2I observed in a healthy, athletic adult between rest and peak exercise. In contrast, in patients with compromised heart or in obese patients, the resting HR is close to the end of augmentation range of HR = 120 bpm. The dynamic range of their oxygen delivery increase is then only a linear function of HR, leading to 200-250% rather than 500% capability of oxygen delivery increase and explaining the shortness of breath under a workload conditions.

3) Therapeutic Goal

The hemodynamic state of a patient can be graphically expressed as a point in a two-dimensional hemodynamic map having blood flow (SI) on horizontal axis and blood pressure (MAP) on vertical axis (see Fig.6 below). The hemodynamic point’s coordinates are the actual values of MAP and SI.

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.

Fig.6: As a result of three levels of MAP (hypertension, normotension and hypotension) and three levels of SI (hyper-, normo- and hypodynamic blood flow), there are nine different classes of hemodynamic states, documented by nine rectangles in the hemodynamic map above. 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. Each cardio- or vasoactive therapy moves a patient’s hemodynamic state along a vector, which length is determined by the therapy’s titration: The vector of volume expansion or positive inotropic therapy points north-east (producing an increase in both pressure and flow), the vector of diuresis or negative inotropic therapy points south-west. The vector of vasoconstriction points north-west, the vector of vasodilation (or therapy using ACE inhibitors) points south-east. The combination drugs have their vectorial effect formed by the sum of individual components (for instance, the vector of calcium channel blockers, being vasodilators and negative inotropes, points essentially south…)

We can derive a simple conclusion from this discussion so far:
a) We cannot administer a proper therapy affecting hemodynamics without measuring the patient’s current hemodynamic state (MAP @ SI). The hemodynamic measurement has to include measurement of blood flow in every patient!
We cannot administer a proper therapy involving a cardio- or vasoactive drug without knowing the vectorial hemodynamic effect of each cardio- and vasoactive drug.

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.6). 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.e., the simultaneous normohemodynamic state and normoperfusion state, are clinically desirable and become the therapeutic goal. Please note that different normohemodynamic and normoperfusion states exist for different ages and genders and/or for different metabolic or clinical states.

We have been able to define this bidirectional physiologic/mathematical relationship between the causes of abnormal hemodynamic and perfusion state (i.e., the deviations in intravascular volume, inotropy, vasoactivity and chronotropy from their ideal levels) and its consequences (the actual MAP, SI and CI values). See the THERAPEUTIC MANAGEMENT CHART below.

As a result, we can utilize this knowledge in either direction:

4) Therapeutic Management Chart

The inter-relationship between the hemodynamic state and hemodynamic modulators for resting, supine adults is expressed graphically in the proprietary hemodynamic management chart, depicted in Fig.7 below. 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 chart has two separate system of coordinates: the orthogonal system of lines belongs to the hemodynamic state (MAP & SI), the diagonal system of lines to hemodynamic modulators (volume, inotropy + vasoactivity). 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). [Detailed information about the theory of beat systemic hemodynamics and the hemodynamic management chart can be found in the References]

Fig.7: Sramek’s Hemodynamic Management Chart for supine, resting adults. The hemodynamic map is formed by the orthogonal system of coordinates of SI and MAP. A map of hemodynamic modulators (an orthogonal system of coordinates on a different plane) is formed by sets of diagonal lines. Location of a patient’s hemodynamic point is shared by both systems of coordinates. Its location within the map of hemodynamic modulators determines the status of hemodynamic modulators responsible for the hemodynamic state. The isolines of LSWI are the isolines of total myocardial contractility, representing the sum of modulating effect of volume and/or inotropy. Isolines of SSVRI (marked in Italic) are the isolines of vasoactivity. The loci of normohemodynamic states are defined by gray hexagon.

These hemodynamic management charts have been implemented in the hemodynamic management software of the HOTMAN System.

5) Problems Directly Attributable to Current Methods of Assessment of the Cardiovascular System

As a consequence of fragmented and incomplete hemodynamic information (as documented by the data presentation of any current patient monitor, which does not display blood flow parameters, or by data acquisition in current cardiovascular evaluation, relying on ECG and blood pressure measurement) and an exclusion of evaluation of oxygen transport dynamics from the therapeutic decision process in every patient, the medical practice has to embrace a management philosophy of trial-and-error. This practice does not strive for identification and treatment of hemodynamic causes (abnormal level of hemodynamic and/or perfusion modulators) but attempts to treat the symptom (for instance, the blanket treatment of "hypertension" with random selection of antihypertensive drugs while ignoring their different hemodynamic vectors, treatment of male impotence with Viagra with its potent cardioactive effects, while ignoring a patient’s quite frequently abnormal hemodynamic state, or treatment of a low-flow state of ICU patients with blanket administration of volume expansion, positive inotropic support and afterload reduction). Unfortunately, this trial-and-error therapeutic methodology wastes time, money, the patients’ quality of life and, generally, results in poor patient outcomes.

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.e., the causes of abnormal hemodynamics and perfusion dynamics) and correcting them therapeutically as to achieve normovolemia, normoinotropy, normovasoactivity and normochronotropy. Only this approach leads to normohemodynamic and normoperfusion state.

6) Solutions

This normohemodynamic therapy described above can be performed today at low cost, noninvasively and in every patient with the HOTMAN System.

The HOTMAN System measures all the hemodynamic and oxygen delivery parameters noninvasively in all adults. It has a built-in normal and postoperative hemodynamic management goal. It also provides the clinician with complete monitoring and management information of a patient’s systemic hemodynamics and oxygen transport dynamics. 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).

[Please note that the clinical utilization of beat hemodynamics, discussed above and utilized in HOTMAN System, represents a major improvement in diagnostic specificity when compared to the currently-accepted and clinically implemented concepts of "per-minute" hemodynamics.]

See the REFERENCES for list of publications related to the new concepts of hemodynamics and hemodynamic management.

Do you want to see the improved outcomes of management of hypertension? Read the abstract of a paper presented at the 1996 Meeting of the American Society of Hypertension, or read a related featured article Treatment of Hypertension as a Hemodynamic Disorder.

Do you want to read more how important is HEMODYNAMICS FOR THE SENIORS? Just click on this title.