(Hemodynamic analysis of a patient with resistant hypertension by the HOTMAN System)


The patient, a 66 year-old female, 164 cm, 60 kg, has been hypertensive for 30 years. Her hypertension has been treated with ARB (angiotensin receptor blocker), CCB (calcium channel blocker) and BB (beta-blocker), however, in spite of this complex antihypertensive therapy coctail, she remains hypertensive with side effects. Her hemodynamics was measured by the HOTMAN System on September 6, 2016 at 10:18.

The Monitoring Page of the HOTMAN System


One of the System’s data presentations is the Monitoring Page, depicted above.


The digital values of her hemodynamic parameters are in the yellow windows on the right; the relationship of each value to its normal range is described as the position of yellow diamond within the blue bars. The normal values for each parameter, a function of gender and age, are the white numbers within the blue bar – normal minima in the left column, normal maxima in the right column.


The patient has an infranormal level of the perfusion blood flow (Cardiac Index, CI = 2.1), a borderline minimum value of hemodynamically-significant blood flow (Stroke Index, SI = 35), is hypertensive (S/D = 170/98; MAP = 122), has infranormal levels of myocardial contractility parameters (Ejection Phase Contractility Index, EPCI = 0.029; and Inotropic State Index, ISI = 0.65), and has significantly elevated level of afterload (Stroke Systemic Vascular Resistance Index, SSVRI = 270).

The picture below is the Hemodynamic Management Page of the HOTMAN System at the same time as data in the Monitoring Page, utilizing the format of hemodynamic map to present the status of patient’s hemodynamics. Whereas the Monitoring Page provides information about the status of a patient’s hemodynamics at a given time, the Hemodynamic Management Page provides information what therapy to administer to produce the normohemodynamic state.

The map has two orthogonal systems on two different planes:

The Hemodynamic State map has as its axes the values of SI and MAP. The Map of Hemodynamic Modulators (represented by isolines of total contractility [LSWI] and vasoactivity [SSVRI]), also orthogonal, has its coordinate system positioned at +45o in respect to the Hemodynamic State map. Hemodynamic state of the patient’s is depicted as yellow dot with the actual MAP & SI values as its coordinates (see and compare their values in the Monitoring Page). The point shares its position with the hemodynamic modulator’s map, where it identifies the percentage deviation in total contractility and vasoactivity from their respective ideal levels.


Thoracic Electrical Bioimpedance (TEB) technology, utilized in the HOTMAN System blood flow hardware module EXT-TEBCO, provides a unique hemodynamic capability: It measures directly the inotropic state (as the Inotropic State Index, ISI), thus enabling the System to separate the percentage deviation in volemia from the known total contractility (Left Stroke Work Index. LSWI)

Position of the hemodynamic point in the Map of Hemodynamic Modulators is the consequence of function of 3 hemodynamic modulators: (intravascular volume + inotropy), i.e., the total contractility, and vasoactivity.  The white hexagon delineates the loci of normohemodynamic states, i.e., the Therapeutic Goal.

The position of the hemodynamic point within the Hemodynamic State map is verbally described in the left column under the chart. The therapeutic conclusions derived from the position of the hemodynamic point in the Map of Hemodynamic Modulators (defining the deviation in hemodynamic and perfusion flow modulators from their respective ideal levels), are described in the right column under the Chart. The therapeutic correction of the identified deviations then produces normovolemia, normoinotropy, normovasoactivity and normochronotropy and, as a result, the normotension and normodynamic circulation – the Therapeutic Goal.



The Hemodynamic Management Page



Since the relationship between the hemodynamic state and hemodynamic modulators is bi-directional, we can predict the vectorial effect of changes of status of any modulator on the hemodynamic state.  This feature is called the Hemodynamic Modeling Page. When switched into this mode, the pane with analog signals is replaced with sliders, enabling the operator to adjust the selected modulator’s level, as depicted below.

Patient’s current status (the red dot) is the starting point from which the status of each modulator can be changed using its slider.



The Hemodynamic Modeling Page


Since the patient is already being treated with existing therapy described above, first we have to predict where this patient’s hemodynamics would be without the current therapy. Two pharmacological agents already used (ARB & CCB) were supposed to reduce vasoconstriction, however, it still stands at 96% level. One of them, or both, will, therefore, be part of her future therapy. However, the major problem with her current therapy is the beta-blocker (negative inotrope + negative chronotrope); she was administered this drug though she was never diagnosed as hyperinotropic and hyperchronotropic at the onset of the therapy, though, this is what BB treats.

Also, we will not address at this point the deviation in chronotropy, as its level will change as a result of hemodynamic management, therefore, the resulting level of SI.

The image of the Hemodynamic Modeling Page below addresses the correction of 84% level of hypoinotropy, caused by the beta-blocker therapy: The inotropy slider has been moved to increase the level of inotropy to reverse the effects of negative inotrope therapy (the starting hemodynamic point is yellow, the end-result red). The inotropy level in the HEMODYNAMIC MODULATORS identifiers now shows NORMOINOTROPY.



Correction of 84% of Hypoinotropy till Normoinotropy is reached

Since we have at this stage corrected the deviation in inotropy, there are two remaining hemodynamic modulators at their abnormal level: the 86% hypervolemia and 90% vasoconstriction. We will address first the 86% deviation in volume by “administering” diuretics:

Correction of 86% of Hypervolemia till Normovolemia is reached


Note that the vectorial effects of changes in volemia are superimposed onto the effects of inotropy (they move the hemodynamic point along the same isoline of vasoactivity).


So far the hemodynamic modeling corrected the deviations in two hemodynamic modulators – the inotropy and volemia – and the patient is now normovolemic and normoinotropic. What is left to address the correction of the remaining modulator – the vasoactivity.  This task is explained in the following image:


Correction of 96% deviation in vasoconstriction


As it was already mentioned in the introduction, the patient is currently on two separate therapies reducing the afterload – the ARB and CCB – though she still remains 96% vasoconstricted. Increasing the vasodilation (either increasing the titration of ARB or CCB) is addressed in the image above. The patient’s hemodynamic point is now residing in the center of normohemodynamic states delineated by the white hexagon 35 < SI < 75 and 70 < MAP < 105.


Producing the normohemodynamic state increased the SI level, so the patient became normochronotropic without need for any additional chronotropy therapy.


For the explanation of the theory of hemodynamic management click here.